FN Thomson Reuters Web of Science™ VR 1.0 PT J AU ZHANG, YJ RUTLEDGE, BJ ROLLINS, BJ AF ZHANG, YJ RUTLEDGE, BJ ROLLINS, BJ TI STRUCTURE-ACTIVITY ANALYSIS OF HUMAN 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 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 A27 EP A27 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200095 ER PT J AU KAHN, CR AF KAHN, CR TI IDENTIFICATION OF THE INSULIN-RECEPTOR TYROSINE KINASE-ACTIVITY - A CITATION-CLASSIC COMMENTARY ON INSULIN STIMULATES THE PHOSPHORYLATION OF THE 95,000 DALTON SUBUNIT OF ITS OWN RECEPTOR BY KASUGA,M., KARLSSON,F.A., KAHN,C.R. SO CURRENT CONTENTS/LIFE SCIENCES LA English DT Article ID SIGNAL TRANSDUCTION; PROTEIN RP KAHN, CR (reprint author), JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU INST SCI INFORM INC PI PHILADELPHIA PA 3501 MARKET ST, PHILADELPHIA, PA 19104 SN 0011-3409 J9 CC/LIFE SCI PD NOV 15 PY 1993 IS 46 BP 9 EP 9 PG 1 WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary SC Science & Technology - Other Topics; Social Sciences - Other Topics GA MD703 UT WOS:A1993MD70300002 ER PT J AU SHIPLEY, WU AF SHIPLEY, WU TI THE ADVANTAGE OP AN X-RAY VISIBLE MARKER OF THE PROSTATIC APEX SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Editorial Material RP SHIPLEY, WU (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,GENITOURINARY ONCOL UNIT,BOSTON,MA 02114, USA. NR 4 TC 9 Z9 11 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD NOV 15 PY 1993 VL 27 IS 4 BP 985 EP 985 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA MH970 UT WOS:A1993MH97000033 PM 8244834 ER PT J AU NAGAYA, T JAMESON, JL AF NAGAYA, T JAMESON, JL TI DISTINCT DIMERIZATION DOMAINS PROVIDE ANTAGONIST PATHWAYS FOR THYROID-HORMONE RECEPTOR ACTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIGAND-BINDING DOMAIN; 9-CIS RETINOIC ACID; C-ERBA PROTOONCOGENES; DNA-BINDING; X-RECEPTOR; TRANSCRIPTIONAL REGULATION; RESPONSE ELEMENTS; HUMAN TESTIS; RXR-BETA; PROTEIN AB Transcriptional regulation by thyroid hormone is mediated through its nuclear receptors, which bind to target response elements as homodimers or as heterodimers with proteins such as retinoid X receptors (RXR). Thyroid hormone response elements exhibit remarkable flexibility in that the receptor binding half-sites can be arranged as direct repeats, inverted repeats, or everted repeats. We report that a limited region at the carboxyl-terminal end of the thyroid hormone receptor differentially contributes to the formation of receptor homo- and heterodimers. The functionally inactive thyroid hormone receptor splicing variant alpha2, which is altered at the juncture of the homo- and heterodimerization domains, cannot form homodimers. However, alpha2 can form a heterodimer when bound to half-sites arranged as a direct repeat spaced by 4 base pairs (DR4), but not with other arrangements of response element half-sites. The alpha2-RXR heterodimer strongly inhibits wild type receptor function mediated by the DR4 element, suggesting that the alpha2 isoform modulates thyroid hormone action by binding as an antagonist to a subset of response elements. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,THYROID UNIT,BOSTON,MA 02114. OI Jameson, James/0000-0001-9538-4059 FU NIDDK NIH HHS [DK42144] NR 40 TC 49 Z9 50 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 15 PY 1993 VL 268 IS 32 BP 24278 EP 24282 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MF294 UT WOS:A1993MF29400084 PM 8226975 ER PT J AU PLATT, OS LUX, SE FALCONE, JF AF PLATT, OS LUX, SE FALCONE, JF TI A HIGHLY CONSERVED REGION OF HUMAN ERYTHROCYTE ANKYRIN CONTAINS THE CAPACITY TO BIND SPECTRIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FILAMENT-MEMBRANE INTERACTIONS; ANION-EXCHANGER; BRAIN ANKYRIN; HEREDITARY SPHEROCYTOSIS; CYTOPLASMIC DOMAIN; FUNCTIONAL DOMAINS; SITE-SPECIFICITY; STRUCTURAL BASIS; ATTACHMENT SITE; PLASMA-MEMBRANE AB Ankyrin has a spectrin-binding region within a central 62-kDa chymotryptic peptide. We examined the spectrin binding ability of a series of smaller ankyrin fragments and recombinant peptides within the 62-kDa domain using a ligand blot assay. The smallest proteolytic fragment that bound was a 12-kDa tryptic peptide starting at amino acid 1068. Peptides containing this region expressed as glutathione S-transferase fusion products also bound spectrin and suggested that residues 1101-1192 were important. In contrast, a fusion protein containing residues 826-898 did not bind spectrin, a surprising finding since this region is known to influence binding affinity. Proteins that bound spectrin on ligand blots also competed for binding in solution, but did so with one-tenth the affinity of the native peptide. Comparing the 62-kDa domains of erythrocyte and brain ankyrins (species that bind spectrin but with 10-fold differences in affinity), the NH2-terminal regions are 0-40% identical, while the regions (1136-1160) common to all binding peptides are 80-90% identical. We hypothesize that the highly conserved region contains an important spectrin-binding site, while the poorly conserved region controls the binding affinity. We speculate that this unique NH2-terminal region is what gives different members of the ankyrin family their signature set of affinities, and accordingly their distinctive cellular localization. C1 CHILDRENS HOSP MED CTR,DEPT LAB MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP PLATT, OS (reprint author), CHILDRENS HOSP MED CTR,DEPT MED,DIV HEMATOL ONCOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [5P01 HL32262, 2P60 HL15157] NR 47 TC 30 Z9 30 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 15 PY 1993 VL 268 IS 32 BP 24421 EP 24426 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MF294 UT WOS:A1993MF29400104 PM 8226993 ER PT J AU JAYARAMAN, S HEILIGENHAUS, A RODRIGUEZ, A SOUKIASIAN, S DORF, ME FOSTER, CS AF JAYARAMAN, S HEILIGENHAUS, A RODRIGUEZ, A SOUKIASIAN, S DORF, ME FOSTER, CS TI EXACERBATION OF MURINE HERPES-SIMPLEX VIRUS-MEDIATED STROMAL KERATITIS BY TH2 TYPE T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID GLYCOPROTEIN-D; MONOCLONAL-ANTIBODY; INTERFERON-GAMMA; MICE; PROTECTION; TOLERANCE; LEISHMANIASIS; INTERLEUKIN-4; INDUCTION; RESPONSES AB Corneal infection of susceptible mice with HSV-1 causes herpetic stromal keratitis (HSK), which serves as a model of human HSK. To study the properties of the T lymphocytes involved in HSK, susceptible mice were immunized with the synthetic peptide corresponding to the amino terminal of HSV-1-associated glycoprotein D (gD 5-23). A CD4+ long-term T cell line and a clone bearing Vbeta 8.2 TCR were derived from peptide-primed lymph node cells. These T cells recognize gD 5-23 peptide in the context of I-E(d) and require CD4 and LFA-1 for Ag-specific proliferation. Significantly, a truncated peptide gD 15-23 induced vigorous proliferation, indicating that these 9 amino acids constitute an epitope recognized by these T cells. The gD-specific T cells produced IL-4 and used it as the autocrine growth factor and hence belong to the Th2 subtype. Adoptive transfer of gD-specific Th2 cells into susceptible mice increased both the onset and severity of HSK after corneal HSV-1 infection. Injection of gD-specific Th2 cells without HSV-1 infection failed to cause eye damage. In addition, an irrelevant Ag-specific Th2 clone failed to induce similar tissue damage when the corresponding Ag was applied to the eye. These data indicate that the T cell-mediated exacerbation of HSK in these studies is dependent on the specific recognition of gD after corneal HSV-1 infection. Finally, gD-specific Th2 cell transfer also rendered HSK-resistant mice susceptible for HSK, suggesting that the freedom from HSK in resistant mice may primarily be due to their inability to produce the pathogenic Th2 cells. The data collectively implicate an important role for Th2 cells in the induction of HSV-mediated keratitis in mice. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. RP JAYARAMAN, S (reprint author), JAMES N GAMBLE INST MED RES,DIV CLIN VIROL,2141 AUBURN AVE,CINCINNATI,OH 45219, USA. OI Rodriguez-Garcia, Alejandro/0000-0002-1419-2109 NR 38 TC 68 Z9 68 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 NOV 15 PY 1993 VL 151 IS 10 BP 5777 EP 5789 PG 13 WC Immunology SC Immunology GA MF995 UT WOS:A1993MF99500067 PM 8228262 ER PT J AU TRUEDSSON, L ALPER, CA AWDEH, ZL JOHANSEN, P SJOHOLM, AG STURFELT, G AF TRUEDSSON, L ALPER, CA AWDEH, ZL JOHANSEN, P SJOHOLM, AG STURFELT, G TI CHARACTERIZATION OF TYPE-I COMPLEMENT C2-DEFICIENCY MHC HAPLOTYPES - STRONG CONSERVATION OF THE COMPLOTYPE/HLA-B-REGION AND ABSENCE OF DISEASE ASSOCIATION DUE TO LINKED CLASS-II GENES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; SYSTEMIC LUPUS-ERYTHEMATOSUS; C2 DEFICIENCY; DEFINED POPULATION; 4TH COMPONENT; DNA; POLYMORPHISM; HLA; ANTIGEN; POLYMERASE AB Fourteen individuals with complete C2 deficiency from 11 families and 3 heterozygous C2-deficient individuals from two families were investigated. In all the 24 independent C2-deficient haplotypes, the complotype S042 was present and the majority (21/24) was [HLA-B18,S042,DR2]. All carried the type I C2 deficiency C2 pseudogene with its characteristic 28 bp deletion. All but two haplotypes had 10 AC/GT repeats in the TNFalpha microsatellite polymorphism and all but one of the haplotypes were identical at or near HLA-B as assessed by RFLP using BstEII digestion and two genomic probes, R5A and M20A, located 100 and 38 kb centromeric to HLA-B, respectively. The exceptional haplotype was HLA-B40 with four AC/GT repeats at TNF-alpha. Three of the haplotypes were not DR2 based on generic and sequence-specific oligonucleotide typing. Another four haplotypes showed different DO-variants detected by RFLP analysis using Bg/II and Mspl digestion. Thus, the [HLA-B18,S042,DR2] haplotype appears to be more fixed in the region between the complement genes and the HLA-B locus (96%) than in the region between the complement genes and DR (88%) and DO loci (71 %). Of the 14 individuals studied, six had SLE or SLE-like syndromes and six had a history of severe infections although two were apparently healthy. Three of the six SLE patients and two individuals with repeated infections were homozygous for [HLA-B18,S042,DR2] and also homozygous for DQB1*0602 and the common DO variant. Thus, MHC class II genes linked to the C2 pseudogene do not appear to determine different clinical consequences of C2 deficiency. C1 LUND UNIV,DEPT RHEUMATOL,S-22362 LUND,SWEDEN. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02118. RP TRUEDSSON, L (reprint author), LUND UNIV,DEPT MED MICROBIOL,CLIN IMMUNOL SECT,SOLVEGATAN 23,S-22362 LUND,SWEDEN. FU NIAID NIH HHS [AI14157] NR 38 TC 31 Z9 31 U1 1 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 NOV 15 PY 1993 VL 151 IS 10 BP 5856 EP 5863 PG 8 WC Immunology SC Immunology GA MF995 UT WOS:A1993MF99500073 PM 7901282 ER PT J AU CAPE, EG KIM, YH HEINRICH, RS GRIMES, RY MURALIDHARAN, E BRODER, JD SCHWAMMENTHAL, E YOGANATHAN, AP LEVINE, RA AF CAPE, EG KIM, YH HEINRICH, RS GRIMES, RY MURALIDHARAN, E BRODER, JD SCHWAMMENTHAL, E YOGANATHAN, AP LEVINE, RA TI CARDIAC MOTION CAN ALTER PROXIMAL ISOVELOCITY SURFACE-AREA CALCULATIONS OF REGURGITANT FLOW SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID COLOR DOPPLER FLOW; MITRAL REGURGITATION; VALVULAR REGURGITATION; CONVERGENCE REGION; QUANTIFICATION; INVITRO; ORIFICE; JETS; SIZE; VISUALIZATION AB Objectives. This study addressed the hypothesis that motion of the surface containing a regurgitant orifice relative to the Doppler ultrasound transducer can cause differences between actual flow rate and calculations based on the proximal flow convergence technique. Background. In vitro studies quantitating regurgitant flow rate by proximal how convergence have been limited to stationary orifices. Clinically, however, valve leaflets generally move relative to the ultrasound transducer during the cardiac cycle and can move at velocities important relative to the measured color aliasing velocities. The transducer therefore senses the vector sum of actual flow velocity toward the orifice and orifice velocity relative to the transducer. This can cause potential overestimation or underestimation of true flow rate, depending on the direction of surface motion. Methods. The hypothesis was explored computationally and tested by pumping fluid at a constant flow rate through an orifice in a plate moving at 0 to 8 cm/s (velocities comparable to those described clinically for mitral and tricuspid annulus motion toward an apical transducer). Results. Surface motion in the same direction as flow caused overestimation of the aliasing radius and calculated flow rate. Surface motion opposite to the direction of flow (typical for mitral and tricuspid regurgitation viewed from the apex or esophagus) caused underestimation of actual flow rate. The underestimation was greater for lower aliasing velocities (36 +/- 11% for 10 cm/s vs. 23 +/- 6% for 20 cm/s). Correcting for surface motion provided excellent agreement with actual values (y = 0.97x + 0.10, r = 0.99, SEE = 0.17 liters/min). Conclusions. Physiologic motion of the surface containing a regurgitant orifice can cause substantial differences between actual flow rate and that calculated by the proximal flow convergence technique. Low aliasing velocities used to optimize that technique can magnify this effect. Such errors can be minimized by using higher aliasing velocities (compatible with the need to measure the aliasing radius) or eliminated by correcting for surface velocity determined by an M mode ultrasound scan. C1 GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID MECH LAB,ATLANTA,GA 30332. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC ULTRASOUND LAB,BOSTON,MA. RP CAPE, EG (reprint author), UNIV PITTSBURGH,CHILDRENS HOSP PITTSBURGH,DIV PEDIAT CARDIOL,3705 5TH AVE,PITTSBURGH,PA 15213, USA. FU NHLBI NIH HHS [R29 HL 38176, R01 HL 45485] NR 35 TC 17 Z9 17 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD NOV 15 PY 1993 VL 22 IS 6 BP 1730 EP 1737 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ365 UT WOS:A1993MQ36500027 PM 8227847 ER PT J AU CRUMP, AL GRUSBY, MJ GLIMCHER, LH CANTOR, H AF CRUMP, AL GRUSBY, MJ GLIMCHER, LH CANTOR, H TI THYMOCYTE DEVELOPMENT IN MAJOR HISTOCOMPATIBILITY COMPLEX-DEFICIENT MICE - EVIDENCE FOR STOCHASTIC COMMITMENT TO THE CD4 AND CD8 LINEAGES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-CELL SELECTION; T-CELL SUBSETS; THYMOCYTE DIFFERENTIATION ID T-CELL-RECEPTOR; NEGATIVE SELECTION; TRANSGENIC MICE; ANTIGEN RECEPTOR; THYMIC SELECTION; DELETION; DIFFERENTIATION; PRECURSORS; EXPRESSION; KINETICS AB The mechanism resulting in commitment of precursor cells in the thymus to either the CD4 or CD8 lineage remains poorly understood. In principle, this may reflect a stochastic process or may reflect instructional signals from host major histocompatibility complex (MHC) molecules. We have examined the role of MHC products in subset commitment by using mice deficient in class I or class II MHC products. Normal numbers of committed CD4 intermediates (CD4+ CD8lo) develop in the thymus in the absence of class II molecules. Similarly, CD8 transitional cells (CD4loCD8+) are present in the thymus of mice lacking class I products. These findings suggest that commitment of CD4+8+ precursor cells to either lineage is a stochastic process that does not depend on instructive signals from MHC molecules (i.e., expression of alternative differentiative options by uncommitted precursor cells is independent of this environmental signal). These studies also suggest that an interaction between the T-cell antigen receptor (TCR) and MHC molecules that is independent of CD4/CD8 coreceptor engagement enhances stochastic coreceptor downregulation substantially and leads to upregulation of TCR expression as a prelude to selective events that require joint coreceptor/TCR engagement. We suggest that this initial interaction molds the TCR repertoire of stochastically generated T-cell subsets toward recognition of self-MHC products. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,IMMUNOPATHOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI31541, AI12184, AI13600] NR 27 TC 59 Z9 59 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 NOV 15 PY 1993 VL 90 IS 22 BP 10739 EP 10743 DI 10.1073/pnas.90.22.10739 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MH322 UT WOS:A1993MH32200068 PM 7902569 ER PT J AU YEOMAN, H GRESS, RE BARE, CV LEARY, AG BOYSE, EA BARD, J SHULTZ, LD HARRIS, DT DELUCA, D AF YEOMAN, H GRESS, RE BARE, CV LEARY, AG BOYSE, EA BARD, J SHULTZ, LD HARRIS, DT DELUCA, D TI HUMAN BONE-MARROW AND UMBILICAL-CORD BLOOD-CELLS GENERATE CD4+ AND CD8+ SINGLE-POSITIVE T-CELLS IN MURINE FETAL THYMUS ORGAN-CULTURE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID THYMOCYTES; INVITRO; DIFFERENTIATION; EXPRESSION; INVIVO AB Murine fetal thymus lobes isolated from both normal and scid/scid mice can be colonized by donor cells from either human bone marrow or human umbilical cord blood in vitro. Subsequent organ culture results in a transient production of a few CD4+ CD8+ (double-positive) cells and then the accumulation of CD4+ or CD8+ (single-positive) T cells. A significant number of immature T-cell intermediates (e.g., CD8low, CD3-/low cells) were present in early organ cultures, suggesting that these were progenitors of the mature CD3+/high single-positive T cells that dominated late cultures. Depletion of mature T cells from the donor-cell populations did not affect their ability to colonize thymus lobes. However, colonization depended on the presence of CD7+ progenitor T cells. Limiting dilution experiments using mature T-cell populations (human peripheral blood leukocytes, human bone marrow cells, and human umbilical cord blood cells) suggested that thymic organ culture supports the growth of progenitor T cells but does not support the growth of mature human T cells. Each of these donor populations produced single-positive populations with different CD4/CD8 ratios, suggesting that precursor cells from different sources differ qualitatively in their capacity to differentiate into T cells. C1 UNIV ARIZONA,DEPT MICROBIOL & IMMUNOL,TUCSON,AZ 85721. NCI,BETHESDA,MD 20892. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29403. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29403. JACKSON LAB,BAR HARBOR,ME 04609. FU NCI NIH HHS [CA 39827]; NIAID NIH HHS [AI 30389, AI/GM 29407] NR 22 TC 50 Z9 51 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 NOV 15 PY 1993 VL 90 IS 22 BP 10778 EP 10782 DI 10.1073/pnas.90.22.10778 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MH322 UT WOS:A1993MH32200076 PM 7902570 ER PT J AU SU, Y BROOKS, DG LI, LY LEPERCQ, J TROFATTER, JA RAVETCH, JV LEBO, RV AF SU, Y BROOKS, DG LI, LY LEPERCQ, J TROFATTER, JA RAVETCH, JV LEBO, RV TI MYELIN PROTEIN ZERO GENE MUTATED IN CHARCOT-MARIE-TOOTH TYPE-1B PATIENTS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MULTICOLOR INSITU HYBRIDIZATION; NEUROPATHY TYPE-I; HEREDITARY MOTOR; DISEASE TYPE-1A; DNA-SEQUENCE; LINKAGE; MOUSE; REGION; HETEROGENEITY; CHROMOSOME-1 AB Autosomal dominant of Charcot-Marie-Tooth disease (CMT), whose gene is type 1B (CMT1B), has slow nerve conduction with demyelinated Schwann cells. In this study the abundant peripheral myelin protein zero (MPZ) gene, MPZ, was mapped 130 kb centromeric to the Fc receptor immunoglobulin gene cluster in band 1q22, and a major MPZ point mutation was found to cosegregate with CMT1B in one large CMT1B family. The MPZ point mutation in 18 of 18 related CMT1B pedigree 1 patients converts a positively charged lysine in codon % to a negatively charged glutamate. The same MPZ locus cosegregates with the CMT1B disease gene in a second CMT1B family [total multipoint logarithm of odds (lod) = 11.4 at theta = 0.00] with a splice junction mutation. Both mutations occur in MPZ protein regions otherwise conserved identically in human, rat, and cow since these species diverged 100 million years ago. MPZ protein, expressed exclusively in myelinated peripheral nerve Schwann cells, constitutes >50% of myelin protein. These mutations are anticipated to disrupt homophilic MPZ binding and result in CMT1B peripheral nerve demyelination. C1 UNIV CALIF SAN FRANCISCO,DEPT OBSTET & GYNECOL,U-262,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. SLOAN KETTERING INST CANC RES,MOLEC BIOL PROGRAM,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. NR 31 TC 73 Z9 75 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 15 PY 1993 VL 90 IS 22 BP 10856 EP 10860 DI 10.1073/pnas.90.22.10856 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MH322 UT WOS:A1993MH32200092 PM 7504284 ER PT J AU YELLEN, G AF YELLEN, G TI CALCIUM CHANNELS - STRUCTURE AND SELECTIVITY SO NATURE LA English DT Editorial Material ID PERMEATION; PORES C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP YELLEN, G (reprint author), HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115, USA. OI Yellen, Gary/0000-0003-4228-7866 NR 11 TC 15 Z9 15 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD NOV 11 PY 1993 VL 366 IS 6451 BP 109 EP 110 DI 10.1038/366109a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MG216 UT WOS:A1993MG21600027 PM 7901764 ER PT J AU JOSEPH, PM MARK, EJ MCLOUD, TC MACLEAN, JA AF JOSEPH, PM MARK, EJ MCLOUD, TC MACLEAN, JA TI A 23-YEAR-OLD ASTHMATIC MAN WITH PULMONARY-INFILTRATES AND HILAR LYMPHADENOPATHY - ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID BRONCHOCENTRIC GRANULOMATOSIS; CRITERIA; ANGIITIS; DISEASE; COCAINE C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JOSEPH, PM (reprint author), MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 35 TC 6 Z9 6 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 11 PY 1993 VL 329 IS 20 BP 1484 EP 1491 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA MF292 UT WOS:A1993MF29200009 ER PT J AU MEYER, GS AF MEYER, GS TI OCCUPATIONAL INFECTION IN HEALTH-CARE - THE CENTURY-OLD LESSONS FROM SYPHILIS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID UNIVERSAL PRECAUTIONS; HOUSE OFFICERS; BLOOD; HIV AB The dangers of occupational infection (where the infectious agent was acquired during the provision or receipt of a medical service) have received renewed interest in the era of the human immunodeficiency virus. The dilemmas raised by this phenomenon, however, are far from novel and were the subject of considerable debate in the medical literature at the turn of the century with regard to syphilis. After recognition of the problem, it took time to manage syphilis effectively through technical innovation, personal prophylaxis, education, and regulation. These efforts led to the development of a strategy remarkably similar to that of the ''universal precautions'' approach applied to human immunodeficiency virus today. C1 MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,FAC DEV PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 65 TC 5 Z9 5 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 8 PY 1993 VL 153 IS 21 BP 2439 EP 2447 DI 10.1001/archinte.153.21.2439 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA ME659 UT WOS:A1993ME65900005 PM 8215748 ER PT J AU HUNG, AY HAASS, C NITSCH, RM QIU, WQ CITRON, M WURTMAN, RJ GROWDON, JH SELKOE, DJ AF HUNG, AY HAASS, C NITSCH, RM QIU, WQ CITRON, M WURTMAN, RJ GROWDON, JH SELKOE, DJ TI ACTIVATION OF PROTEIN-KINASE-C INHIBITS CELLULAR PRODUCTION OF THE AMYLOID BETA-PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID FAMILIAL ALZHEIMERS-DISEASE; PRECURSOR PROTEIN; IDENTIFICATION; DERIVATIVES; SECRETION; MUTATION; CLEAVAGE; PEPTIDE; CELLS; LOCALIZATION AB The 39-43-amino acid amyloid beta-protein (Abeta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer's disease (AD), is released by cultured human cells during normal metabolism. Here we show that agents which activate protein kinase C or otherwise enhance protein phosphorylation caused a substantial decrease in Abeta production in vitro. Protein kinase C activation also markedly decreased Abeta release from cells that express mutant forms of the beta-amyloid precursor protein genetically linked to familial AD. Inhibition of Abeta secretion could also be effected by direct stimulation of m1 muscarinic acetylcholine receptors with carbachol. These results demonstrate that activation of the protein kinase C signal transduction pathways down-regulates the generation of the amyloidogenic Abeta peptide. Pharmacologic agents that activate this system, including a variety of first messengers, could potentially slow the development or growth of some Abeta plaques during the early stages of AD. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,BOSTON,MA 02115. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP HUNG, AY (reprint author), HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115, USA. NR 33 TC 352 Z9 356 U1 1 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 5 PY 1993 VL 268 IS 31 BP 22959 EP 22962 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MF515 UT WOS:A1993MF51500002 PM 8226807 ER PT J AU PING, J SCHILDBACH, JF SHAW, SY QUERTERMOUS, T NOVOTNY, J BRUCCOLERI, R MARGOLIES, MN AF PING, J SCHILDBACH, JF SHAW, SY QUERTERMOUS, T NOVOTNY, J BRUCCOLERI, R MARGOLIES, MN TI EFFECT OF HEAVY-CHAIN SIGNAL PEPTIDE MUTATIONS AND NH(2)-TERMINAL CHAIN-LENGTH ON BINDING OF ANTIDIGOXIN ANTIBODIES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SITE-DIRECTED MUTAGENESIS; SEQUENCE CLEAVAGE SITES; B-CELL DEVELOPMENT; 3-DIMENSIONAL STRUCTURE; SOMATIC MUTATION; ANTIDIGOXIN ANTIBODIES; IMMUNOGLOBULIN GENES; INCREASED AFFINITY; A-II; SPECIFICITY AB In certain instances, antibody variable region mutations outside of the antigen-combining site influence antigen binding. We reported previously that a heavy chain mutation (Ser-94 --> Arg) decreased binding of the anti-digoxin antibody 40-150, whereas an additional signal peptide mutation at the -2 position (Gln --> Pro) causing NH2-terminal 2-residue truncation partially restored binding. To assess the combined effects on binding of two seemingly distant mutations, we constructed signal peptide mutations and NH2-terminal deletions in the presence of Ser-94 and Arg-94. Deletions of one to three amino acids had little effect on binding for Ser-94 mutants, whereas 2-residue truncations produced directly or by signal peptide mutation increased affinity approximately 40-fold for Arg-94 mutants. These observations are consistent with the reported computer-generated model of antibody 40-150. Introduction of Pro at the signal peptide -3 position in 40-150 resulted in cleavage at alternative sites, with varying effects on affinity. Introduction of Pro at -2 into the anti-digoxin antibody 26-10 resulted, unexpectedly, in expression of heavy chains with 3 extra NH2-terminal residues,.causing an approximately 100-fold reduction in affinity. Thus, both extensions and deletions of the heavy chain amino terminus can enhance or reduce antigen binding, depending on the structural context of specific antigen combining sites. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,JACKSON 4,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ 08543. FU NHLBI NIH HHS [R01 HL47415-01A1] NR 49 TC 13 Z9 13 U1 3 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 5 PY 1993 VL 268 IS 31 BP 23000 EP 23007 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MF515 UT WOS:A1993MF51500010 PM 8226814 ER PT J AU RAVICHANDRAN, KS LEE, KK ZHOU, SY CANTLEY, LC BURN, P BURAKOFF, SJ AF RAVICHANDRAN, KS LEE, KK ZHOU, SY CANTLEY, LC BURN, P BURAKOFF, SJ TI INTERACTION OF SHC WITH THE ZETA-CHAIN OF THE T-CELL RECEPTOR UPON T-CELL ACTIVATION SO SCIENCE LA English DT Article ID MITOGENIC SIGNAL TRANSDUCTION; PROTEIN TYROSINE KINASE; ANTIGEN RECEPTOR; CYTOPLASMIC TAIL; RAS; DOMAIN; PHOSPHORYLATION; IDENTIFICATION; INDUCTION; PATHWAYS AB The shc oncogene product is tyrosine-phosphorylated by Src family kinases and after its phosphorylation interacts with the adapter protein Grb2 (growth factor receptor-bound protein 2). In turn, Grb2 interacts with the guanine nucleotide exchange factor for Ras, mSOS. Because several Src family kinases participate in T cell activation and Shc functions upstream of Ras, the role of Shc in T cell signaling was examined. Shc was phosphorylated on tyrosine after activation through the T cell receptor (TCR), and subsequently interacted with Grb2 and mSOS. The Src homology region 2 (SH2) domain of Shc directly interacted with the tyrosine-phosphorylated zeta chain of the TCR. Thus, Shc may couple TCR activation to the Ras signaling pathway. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. F HOFFMANN LA ROCHE & CO LTD,PHARMACEUT RES NEW TECHNOL,DEPT BIOL,CH-4002 BASEL,SWITZERLAND. RI Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 FU NIAID NIH HHS [AI-17258] NR 46 TC 342 Z9 344 U1 1 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 5 PY 1993 VL 262 IS 5135 BP 902 EP 905 DI 10.1126/science.8235613 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MF438 UT WOS:A1993MF43800036 PM 8235613 ER PT J AU FREEMAN, GJ BORRIELLO, F HODES, RJ REISER, H HATHCOCK, KS LASZLO, G MCKNIGHT, AJ KIM, J DU, LN LOMBARD, DB GRAY, GS NADLER, LM SHARPE, AH AF FREEMAN, GJ BORRIELLO, F HODES, RJ REISER, H HATHCOCK, KS LASZLO, G MCKNIGHT, AJ KIM, J DU, LN LOMBARD, DB GRAY, GS NADLER, LM SHARPE, AH TI UNCOVERING OF FUNCTIONAL ALTERNATIVE CTLA-4 COUNTER-RECEPTOR IN B7-DEFICIENT MICE SO SCIENCE LA English DT Article ID T-CELL ACTIVATION; INVIVO; EXPRESSION; MOLECULE; ANTIGEN; CLONES AB B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,IMMUNOL RES DIV,BOSTON,MA 02115. REPLIGEN CORP,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NIA,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA 40216] NR 21 TC 378 Z9 379 U1 0 U2 4 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 5 PY 1993 VL 262 IS 5135 BP 907 EP 909 DI 10.1126/science.7694362 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MF438 UT WOS:A1993MF43800038 PM 7694362 ER PT J AU FREEMAN, GJ GRIBBEN, JG BOUSSIOTIS, VA NG, JW RESTIVO, VA LOMBARD, LA GRAY, GS NADLER, LM AF FREEMAN, GJ GRIBBEN, JG BOUSSIOTIS, VA NG, JW RESTIVO, VA LOMBARD, LA GRAY, GS NADLER, LM TI CLONING OF B7-2 - A CTLA-4 COUNTER-RECEPTOR THAT COSTIMULATES HUMAN T-CELL PROLIFERATION SO SCIENCE LA English DT Article ID ACTIVATION; INTERLEUKIN-2; ANTIGEN-B7; INDUCTION; ANERGY AB Although presentation of antigen to the T cell receptor is necessary for the initiation of an immune response, additional molecules expressed on antigen-presenting cells deliver essential costimulatory signals. T cell activation, in the absence of costimulation, results in T cell anergy. The B7-1 protein is a costimulator molecule that regulates interleukin-2 (IL-2) secretion by signaling through the pathway that uses CD28 and CTLA-4 (hereafter referred to as the CD28 pathway). We have cloned a counter-receptor of CD28 and CTLA-4, termed B7-2. Although only 26 percent identical to B7-1, B7-2 also costimulates IL-2 production and T cell proliferation. Unlike B7-1, B7-2 messenger RNA is constitutively expressed in unstimulated B cells. It is likely that B7-2 provides a critical early costimulatory signal determining if the T cell will contribute to an immune response or become anergic. C1 REPLIGEN CORP,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP FREEMAN, GJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 40216] NR 18 TC 820 Z9 827 U1 2 U2 9 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 5 PY 1993 VL 262 IS 5135 BP 909 EP 911 DI 10.1126/science.7694363 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MF438 UT WOS:A1993MF43800039 PM 7694363 ER PT J AU KAUFMAN, DS SHIPLEY, WU GRIFFIN, PP HENEY, NM ALTHAUSEN, AF EFIRD, JT AF KAUFMAN, DS SHIPLEY, WU GRIFFIN, PP HENEY, NM ALTHAUSEN, AF EFIRD, JT TI SELECTIVE BLADDER PRESERVATION BY COMBINATION TREATMENT OF INVASIVE BLADDER-CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID TRANSITIONAL CELL-CARCINOMA; ADJUVANT CHEMOTHERAPY; CISPLATIN; RADIOTHERAPY; METHOTREXATE; VINBLASTINE; TRIAL; DOXORUBICIN; IRRADIATION; MANAGEMENT AB Background. For patients with invasive bladder cancer the usual recommended treatment is radical cystectomy, although transurethral resection of the tumor, systemic chemotherapy, and radiotherapy are each effective in some patients. We sought to determine whether these treatments in combination might be as effective as radical cystectomy and thus might allow the bladder to be preserved and the cancer cured. Methods. We enrolled 53 consecutive patients with muscle-invading bladder cancer (stages T2 through T4, NXMO) in a trial of transurethral surgery, combination chemotherapy, and irradiation (4000 cGy) with concurrent cisplatin administration. Urologic evaluation of the tumor response directed further therapy: radical cystectomy in the 8 patients who had incomplete responses, additional chemotherapy and radiotherapy (6480 cGy) in the 34 patients who had complete responses or who were unsuited for cystectomy, and alternative care in the 11 patients who could not tolerate either irradiation or chemotherapy. Results. After a median follow-up of 48 months, 24 of the 53 patients (45 percent) were alive and free of detectable tumor. In 31 patients (58 percent) the bladder was free of invasive tumor and functioning well, even though in 9 (17 percent) a superficial tumor recurred and required further transurethral surgery and intravesical drug therapy. Of the 28 patients who had complete responses after initial treatment, 89 percent had functioning tumor-free bladders. Conclusions. Conservative combination treatment may be an acceptable alternative to immediate cystectomy in selected patients with bladder cancer, although a randomized clinical trial that included a group for simultaneous comparison would be required to produce definitive results. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KAUFMAN, DS (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DEPT MED ONCOL,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-56381-01] NR 24 TC 159 Z9 161 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 NOV 4 PY 1993 VL 329 IS 19 BP 1377 EP 1382 DI 10.1056/NEJM199311043291903 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA MD949 UT WOS:A1993MD94900003 PM 8413433 ER PT J AU BREWER, TF WILSON, ME GONZALEZ, E FELSENSTEIN, D AF BREWER, TF WILSON, ME GONZALEZ, E FELSENSTEIN, D TI BACON THERAPY AND FURUNCULAR MYIASIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Note ID DERMATOBIA-HOMINIS; CUTANEOUS MYIASIS; TUMBU FLY; LARVAE AB Objective.-To evaluate a simple, noninvasive method for removing fly larvae from patients with furuncular myiasis. Design.-Case series. Setting.-Ambulatory office of a tertiary care center. Patients.-Three patients who presented with Dermatobia hominis infestation. Intervention.-The patients with D hominis infestation were treated with the application of bacon fat over the larval apertures. Main Outcome Measure.-Removal of intact larvae. Results.-Within 3 hours of the application of bacon, the larvae had migrated sufficiently far out of the skin to be removed with tweezers. Ten larvae were removed with this method. There were no treatment failures or complications. Conclusions.-Furuncular myiasis will be seen more frequently in temperate areas as individuals travel to endemic areas. We describe the clinical characteristics of myiasis and a simple method of treatment that permits rapid diagnosis and cure. C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. MT AUBURN HOSP,DIV INFECT DIS,CAMBRIDGE,MA 02138. RP BREWER, TF (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,GRAY 5,BOSTON,MA 02114, USA. NR 26 TC 67 Z9 69 U1 0 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD NOV 3 PY 1993 VL 270 IS 17 BP 2087 EP 2088 DI 10.1001/jama.270.17.2087 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MD882 UT WOS:A1993MD88200029 PM 8411575 ER PT J AU REHEMTULLA, A BARR, PJ RHODES, CJ KAUFMAN, RJ AF REHEMTULLA, A BARR, PJ RHODES, CJ KAUFMAN, RJ TI PACE4 IS A MEMBER OF THE MAMMALIAN PROPEPTIDASE FAMILY THAT HAS OVERLAPPING BUT NOT IDENTICAL SUBSTRATE-SPECIFICITY TO PACE SO BIOCHEMISTRY LA English DT Article ID PROPROTEIN PROCESSING ENZYME; YEAST KEX2 PROTEASE; VONWILLEBRAND-FACTOR; COMPLEMENT PRO-C3; FURIN; EXPRESSION; SEQUENCE; ENDOPROTEASE; PROALBUMIN; PRECURSOR AB Proteins that transit the constitutive pathway of secretion frequently require proteolytic processing after a pair of basic amino acids to attain their full functional activity. A ubiquitously expressed calcium-dependent subtilisin-like serine protease, named PACE or furin, can cleave precursor polypeptides specifically at pairs of basic amino acids where an arginine residue is present in the P4 position. Another member of this protease family, PACE4, was cloned recently by a PCR-based strategy and was also shown to be ubiquitously expressed. We have expressed PACE4 by transient DNA transfection of COS-1 cells and have shown that the cDNA encodes a 120-kDa polypeptide that is present in cell extracts but not in conditioned medium of transfected cells. The substrate specificities of PACE and PACE4 for cleavage of pro-von Willebrand factor were studied in parallel using a transient DNA cotransfection system. Like PACE, PACE4 was able to process pro-vWF to its mature form, and efficient cleavage required both the P4 arginine and the P2 lysine. These data, taken together with previously published data showing that PACE4 cannot process pro-factor IX, demonstrate that PACE and PACE4 have overlapping but not identical substrate specificities. Further differences between PACE and PACE4 specificities were elucidated by monitoring inhibition of processing activity mediated by the serine protease inhibitor alpha1-antitrypsin Pittsburgh mutant. Pro-vWF processing by PACE was inhibited by expression of the alpha1-antitrypsin Pittsburgh mutant, whereas processing of pro-vWF by PACE4 was not affected. Processing of pro-vWF by the endogenous COS-1 cellular enzyme was also inhibited by the alpha1-antitrypsin Pittsburgh mutant, suggesting the COS-1 cell endogenous processing enzyme is more closely related to PACE than to PACE4. The unique property of the alpha1-antitrypsin Pittsburgh mutant to differentiate between these two enzymes provides an important tool to dissect the relative significance of these two processing enzymes. C1 GENET INST INC,DEPT MOLEC & CELLULAR GENET,CAMBRIDGE,MA 02148. CHIRON CORP,EMERYVILLE,CA 94608. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,EP JOSLIN RES LAB,BOSTON,MA 02215. NR 25 TC 59 Z9 59 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 2 PY 1993 VL 32 IS 43 BP 11586 EP 11590 DI 10.1021/bi00094a015 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA ME656 UT WOS:A1993ME65600015 PM 8218226 ER PT J AU BUSH, RK AF BUSH, RK TI FUNGAL EXTRACTS IN CLINICAL-PRACTICE SO ALLERGY PROCEEDINGS LA English DT Article AB Sensitivity to fungi is a common clinical problem. Although many commercial extracts for diagnosis and treatment of fungal sensitivity are available, there is a lack of standardized materials. New research into the isolation and purification of fungal allergens may improve upon this situation. Controlled immunotherapy trials with fungal extracts have identified selected populations who may benefit from this type of therapy. RP BUSH, RK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 0 TC 16 Z9 17 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 SN 1046-9354 J9 ALLERGY PROC JI Allergy Proc. PD NOV-DEC PY 1993 VL 14 IS 6 BP 385 EP 390 DI 10.2500/108854193778792803 PG 6 WC Allergy SC Allergy GA MR585 UT WOS:A1993MR58500001 PM 8157160 ER PT J AU RIVITZ, SM DELUCA, SA AF RIVITZ, SM DELUCA, SA TI PERFUSION IMAGING IN ISCHEMIC-HEART-DISEASE SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Myocardial perfusion imaging with thallium-201 has been used extensively for many years in the evaluation of ischemic heart disease. It is a valuable adjunct to exercise treadmill testing and is especially helpful in evaluating cardiac perfusion in patients who have abnormal resting electrocardiograms, who are unable to exercise, and whose clinical history and exercise test results are discordant. Perfusion imaging is useful for both diagnosis and prognosis in patients with coronary artery disease. In patients unable to exercise, the coronary vasodilators dipyridamole and adenosine may be used in conjunction with thallium imaging. Two recently approved technetium agents, sestamibi and teboroxime, may be used in place of thallium. RP RIVITZ, SM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD NOV 1 PY 1993 VL 48 IS 6 BP 1071 EP 1078 PG 8 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA MF796 UT WOS:A1993MF79600010 PM 8237730 ER PT J AU PRINCE, M FRISOLI, J AF PRINCE, M FRISOLI, J TI A MODIFIED METHOD OF HYDRODENSITOMETRY IN YOUNG-CHILDREN - REPLY SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Letter RP PRINCE, M (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD NOV PY 1993 VL 58 IS 5 BP 713 EP 713 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA ME259 UT WOS:A1993ME25900028 ER PT J AU JOHNSON, LA PEARLMAN, JD MILLER, CA YOUNG, TI THULBORN, KR AF JOHNSON, LA PEARLMAN, JD MILLER, CA YOUNG, TI THULBORN, KR TI MR QUANTIFICATION OF CEREBRAL VENTRICULAR VOLUME USING A SEMIAUTOMATED ALGORITHM SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE BRAIN, VENTRICLES; BRAIN, VOLUME; BRAIN, OCCIPITAL LOBE; BRAIN, MAGNETIC RESONANCE; MAGNETIC RESONANCE, 3-D; DEGENERATIVE BRAIN DISEASE ID CEREBROSPINAL-FLUID VOLUMES; COMPUTED-TOMOGRAPHY; GRAY-MATTER; BRAIN; SIZE; CT; VALIDATION; FEATURES; DISEASE; IMAGES AB PURPOSE: A semiautomated border identification algorithm, insensitive to user bias, is evaluated for accuracy and speed in the measurement of ventricular volumes from three-dimensional MR images. METHODS: A three-dimensional gradient-echo technique was implemented on a Signa clinical imaging system. Data from phantoms and patients were analyzed for volume using a segmentation algorithm designed with: 1) correction for partial volume averaging; 2) insensitivity to user bias; and 3) speed. Accuracy, precision, and intra- and interobserver variability were determined. RESULTS: Average error for phantom studies was 4% to 6%, or 1 to 2 cc across the volumes, which ranged from normal to mild hydrocephalus (<60 cc). Patient studies showed intra- and interobserver error of 2.3% and 7.8%, respectively. The correction for partial volume averaging resulted in a threefold decrease in error. Data were acquired and reconstructed within 7 minutes. Experienced radiologists required less than 15 minutes to perform each analysis. CONCLUSIONS: This algorithm allows accurate measurement of ventricular volumes in an efficient, minimally supervised manner. C1 MASSACHUSETTS GEN HOSP,NUCL MAGNET RESONANCE CTR,13TH ST,BLDG 149,BOSTON,MA 02129. RI Thulborn, Keith/D-9183-2015 OI Thulborn, Keith/0000-0001-6197-4296 FU NHLBI NIH HHS [R01HL45176] NR 29 TC 35 Z9 35 U1 0 U2 1 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD NOV-DEC PY 1993 VL 14 IS 6 BP 1373 EP 1378 PG 6 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA MG537 UT WOS:A1993MG53700022 PM 8279334 ER PT J AU MOORREES, CFA AF MOORREES, CFA TI REFLECTIONS ON AN ACADEMIC CAREER IN TEACHING AND RESEARCH SO AMERICAN JOURNAL OF ORTHODONTICS AND DENTOFACIAL ORTHOPEDICS LA English DT Article AB It is alleged that Coenraad Moorrees retired last January. I do not believe it. That he has retired as Professor of Orthodontics at Harvard and as Director of Orthodontics at Forsythe, yes, but that he truly retired, never. Coenraad came to the United States from the Netherlands ''to do a bit of orthodontics.'' He surely did do a bit and more. Prof. Moorrees is a leading authority on the development of the dentition, for his papers and those of his colleagues constitute the very bedrock base of our knowledge in this field. He designed and conducted one of the few longitudinal studies of twins dedicated to dental and craniofacial growth and development. His students chair a disproportionately large number of the orthodontic departments in the world. Whether in teaching or clinical practice, you will find that all of his students display the same quiet fervor for new ideas. To Coenraad and his students, teaching and practice are simply different ways to apply and deliver new ideas and research findings. He has a rare trait that is much appreciated, namely, the ability to confront important topics with the courage which provides directness and objectivity which grants fair presentation, while his quiet, courtly, poise guarantees ready listeners. Think how many times in orthodontic discussions Coenraad's calm Dutch charm has captured our attention, while his easy irrefutable logic cleared the air of a debate going nowhere until he rose to talk. In this generation of academic orthodontists, Coenraad Moorrees has set standards few others have met. Ladies and gentlemen, Professor Coenraad Moorrees of Harvard. C1 HARVARD UNIV,SCH DENT MED,BOSTON,MA 02115. RP MOORREES, CFA (reprint author), FORSYTH DENT CTR,BOSTON,MA 02115, USA. NR 26 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0889-5406 J9 AM J ORTHOD DENTOFAC JI Am. J. Orthod. Dentofac. Orthop. PD NOV PY 1993 VL 104 IS 5 BP 516 EP 522 DI 10.1016/0889-5406(93)70077-2 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MH332 UT WOS:A1993MH33200015 PM 8237903 ER PT J AU GARCIA, CE CUNNINGHAM, MJ CLARY, RA JOSEPH, MP AF GARCIA, CE CUNNINGHAM, MJ CLARY, RA JOSEPH, MP TI THE ETIOLOGIC ROLE OF FRONTAL SINUSITIS IN PEDIATRIC ORBITAL ABSCESSES SO AMERICAN JOURNAL OF OTOLARYNGOLOGY LA English DT Article C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. NR 0 TC 5 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0196-0709 J9 AM J OTOLARYNG JI Am. J. Otolaryngol. PD NOV-DEC PY 1993 VL 14 IS 6 BP 449 EP 452 DI 10.1016/0196-0709(93)90122-N PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA MG535 UT WOS:A1993MG53500013 PM 8285318 ER PT J AU MONTGOMERY, WW AF MONTGOMERY, WW TI DURAL DEFECTS OF THE TEMPORAL BONE SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article AB Cerebrospinal fluid leakage (otorrhea or otorhinorrhea) from the temporal bone is the end result of rupture of the arachnoid membrane or herniation of the brain through a defect in the protective dura mater and calvarium. The rupture may be small, admitting only a herniation of arachnoid (meningocele), or be large enough to accommodate brain tissue (encephalocele). Flow of cerebrospinal fluid through either type of fistula may be a trickle or profuse, chronic or intermittent, and usually ceases temporarily for a few weeks following an attack of meningitis. The etiology, anatomy, signs and symptoms, and various methods of treatment for cerebrospinal fluid otorrhea and otorhinorrhea are discussed. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP MONTGOMERY, WW (reprint author), MASSACHUSETTS GEN HOSP,DEPT OTOLARYNGOL,BOSTON,MA 02114, USA. NR 6 TC 8 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD NOV PY 1993 VL 14 IS 6 BP 548 EP 551 PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA MF334 UT WOS:A1993MF33400005 PM 8296856 ER PT J AU DOWNING, JR HEAD, DR PARHAM, DM DOUGLASS, EC HULSHOF, MG LINK, MP MOTRONI, TA GRIER, HE CURCIOBRINT, AM SHAPIRO, DN AF DOWNING, JR HEAD, DR PARHAM, DM DOUGLASS, EC HULSHOF, MG LINK, MP MOTRONI, TA GRIER, HE CURCIOBRINT, AM SHAPIRO, DN TI DETECTION OF THE (11 22)(Q24 Q12) TRANSLOCATION OF EWINGS-SARCOMA AND PERIPHERAL NEUROECTODERMAL TUMOR BY REVERSE TRANSCRIPTION-POLYMERASE CHAIN-REACTION SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID CHROMOSOME-TRANSLOCATION; T(11-22)(Q24-Q12); NEUROEPITHELIOMA; CONSISTENCY; PCR AB Ewing's sarcoma and the related primitive neuroectodermal tumor (PNET) share a unique and specific t(11;22)(q24;q12) chromosomal translocation. The breakpoints have recently been cloned and shown to involve the EWS gene on chromosome 22 and the FLI-1 gene on chromosome 11. Translocation results in the fusion of these genes on the der(22) chromosome, resulting in the production of a novel chimeric EWS/FLI-1 message. Using oligonucleotide primers derived from EWS and FLI-1 complementary DNAs, we were able to amplify a specific fusion transcript from 18 of 18 cases containing t(11;22) and 10 of 14 cases of Ewing's sarcoma/PNET that had unsuccessful cytogenetics. No EWS/FLI-1 fusion transcripts were detected in five cell lines derived from cases of pediatric sarcomas having a histological diagnosis other than Ewing's sarcoma/PNET. The sensitivity and specificity of this PCR analysis demonstrates the usefulness of this approach for the primary diagnosis of t(11;22)-containing Ewing's sarcoma/PNET and for the detection of metastatic or residual disease. C1 ST JUDE CHILDRENS RES HOSP, DEPT TUMOR CELL BIOL, MEMPHIS, TN 38105 USA. ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL & ONCOL, MEMPHIS, TN 38105 USA. ST JUDE CHILDRENS RES HOSP, DEPT EXPTL ONCOL, MEMPHIS, TN 38105 USA. ST CHRISTOPHERS HOSP CHILDREN, DEPT HEMATOL & ONCOL, PHILADELPHIA, PA 19133 USA. STANFORD UNIV, MED CTR, SCH MED, DEPT PEDIAT, STANFORD, CA 94305 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV PEDIAT ONCOL, BOSTON, MA 02115 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. RP DOWNING, JR (reprint author), ST JUDE CHILDRENS RES HOSP, DEPT PATHOL, 575 ST JUDE PL, MEMPHIS, TN 38105 USA. FU NCI NIH HHS [CA-21765, CA-01429, P01-CA27165] NR 23 TC 115 Z9 118 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD NOV PY 1993 VL 143 IS 5 BP 1294 EP 1300 PG 7 WC Pathology SC Pathology GA MF656 UT WOS:A1993MF65600009 PM 8238248 ER PT J AU GRAEMECOOK, F BHAN, AK HARRIS, NL AF GRAEMECOOK, F BHAN, AK HARRIS, NL TI IMMUNOHISTOCHEMICAL CHARACTERIZATION OF INTRAEPITHELIAL AND SUBEPITHELIAL MONONUCLEAR-CELLS OF THE UPPER AIRWAYS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID MONOCLONAL-ANTIBODY HML-1; HUMAN MUCOSAL LYMPHOCYTES; DELTA-T-CELLS; GAMMA-DELTA; NASAL-MUCOSA; MEMBRANE MOLECULE; EPITHELIAL-CELLS; LANGERHANS CELLS; CELIAC-DISEASE; LYMPHOMA AB The upper airway is the first site of exposure to inhaled antigens and the site of initiation of mucosal immunity to certain antigens; however, the intraepithelial lymphoid populations of this region have not been well characterized. We studied 6-mu frozen tissue sections from tonsils, adenoids, and nasal mucosae using immunohistochemistry and a panel of antibodies to mononuclear antigens to determine whether nasal mucosa contained distinctive populations of mononuclear cells. Intraepithelial lymphocytes (IELs) of nasal mucosa were CD3+, CD8+, and mainly CD5+. Tonsil and adenoid both showed diffuse CD8+ IELs, clusters of CD4+ IELs were associated with B cells within the crypt epithelium. All nasal IELs were uniformly negative for Leu8 (homing receptor analog of Mel14). Scattered Leu8-positive cells were present within tonsil and adenoid crypt epithelium only. Nasal IELs rarely expressed HML1 and were often CD7-, whereas the majority of tonsillar and adenoidal IELs were HML1+ and variably CD7+. In nasal mucosa and in deep submucosa of tonsil and adenoid, 80 to 90% of T cell receptor expression was of alpha/beta type. There was a concentration of gamma/delta T cell receptor-positive cells in intraepithelial and subepithelial zones of tonsil and adenoid, with areas of up to 30% gamma/delta T cell receptor positivity. A population of intraepithelial dendritic cells was identified in all three tissues expressing mononuclear phagocyte system antigens CD14 and KiM1P, but lacking CD1a. Virtually no B cells and no organized subepithelial lymphoid tissue were identified in nasal mucosa. Nasal mucosal lymphoid tissue seems to differ from that of endodermally derived mucosae, tonsil, and adenoid to share similarities with both mucosa-associated lymphoid tissue abd peripheral lymph nodes. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GRAEMECOOK, F (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK33506, DK43351] NR 39 TC 38 Z9 41 U1 0 U2 2 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD NOV PY 1993 VL 143 IS 5 BP 1416 EP 1422 PG 7 WC Pathology SC Pathology GA MF656 UT WOS:A1993MF65600021 PM 8238257 ER PT J AU LEVITSKY, LL STONESTREET, BS MINK, K ZHENG, QJ AF LEVITSKY, LL STONESTREET, BS MINK, K ZHENG, QJ TI GLUTAMINE CARBON DISPOSAL AND NET GLUTAMINE UPTAKE IN FETUSES OF FED AND FASTED EWES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE OVINE FETUS; ISOTOPIC TRACER STUDY; GLUTAMINE UTILIZATION ID AMINO-ACID-METABOLISM; HUMAN-PLACENTA; OVINE FETAL; HYPERINSULINEMIA; INVITRO; PLASMA; SHEEP; LAMB AB We have traced ovine fetal glutamine carbon uptake and disposal in 7 chronically catheterized fetuses of fed ewes and 10 fetuses of 48-h fasted ewes. Net fetal glutamine uptake (Fick principle, antipyrine blood flow) was 10.0 +/- 2.0 mumol - kg-1 . min-1 in fed fetuses and 6.4 +/- 1.4 mumol . kg-1 . min-1 in fasted fetuses [not significant (NS)]. However, net fetal glutamine uptake was linearly related to the umbilical vein glutamine level (P < 0.05) in fed and fasted fetuses. In contrast, fetal glutamate transfer to the placenta was 4.0 +/- 0.8 mumol . kg-1 . min-1 in the fed state and 2.7 +/- 0.1 mumol - kg-1 . min-1 in the fasted state. Net fetal glutamine uptake and fetal glutamate transfer to the placenta were directly correlated (P < 0.05). Fetal glutamine carbon disposal was measured using a primed continuous infusion of [U-C-14]glutamine over a 3-h period and blood sampling during the last hour of infusion (steady state). Disposal was 20.9 +/- 2.6 mumol . kg-1 . min-1 in the fed state and 18.6 +/- 2.3 mumol . kg-1 . min-1 in the maternal fasted state (NS). Glutamine carbon disposal did not correlate with fetal arterial glutamine levels and was not influenced by maternal nutritional state. C1 BROWN UNIV,WOMEN & INFANTS HOSP,SCH MED,DEPT PEDIAT,PROVIDENCE,RI 02905. RP LEVITSKY, LL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILDRENS SERV,PEDIAT ENDOCRINE UNIT,709 WACC,BOSTON,MA 02114, USA. FU NICHD NIH HHS [HD-22891, P50 HD-11343] NR 25 TC 3 Z9 3 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 NOV PY 1993 VL 265 IS 5 BP E722 EP E727 PN 1 PG 6 WC Physiology SC Physiology GA MJ167 UT WOS:A1993MJ16700038 PM 8238498 ER PT J AU SHIBA, T INOGUCHI, T SPORTSMAN, JR HEATH, WF BURSELL, S KING, GL AF SHIBA, T INOGUCHI, T SPORTSMAN, JR HEATH, WF BURSELL, S KING, GL TI CORRELATION OF DIACYLGLYCEROL LEVEL AND PROTEIN-KINASE-C ACTIVITY IN RAT RETINA TO RETINAL CIRCULATION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HYPERGLYCEMIA; ENDOTHELIAL CELLS; DIABETES ID DIABETIC RATS; ENDOTHELIAL-CELLS; GLUCOSE; INSULIN; COMPLICATIONS; PATHOGENESIS; ACTIVATION; EXPRESSION; GLOMERULI; ISOZYMES AB The increases in diacylglycerol (DAG) level and protein kinase C (PKC) activity have been characterized biochemically and functionally in the retina and the brain of diabetic rats as well as in cultured vascular cells. PKC specific activities were increased in the membraneous fraction of retina from streptozotocin (STZ)-induced diabetic rats and the genetically determined diabetic BB rats, respectively, after 1 or 2 wk of diabetes, compared with control. The ratio of total PKC activities from membraneous and cytosol fractions was also increased in the retina of diabetic rats. With diabetes, all the isoenzymes and the total DAG level were increased in the rat retina, whereas no changes were found in the rat brain. Insulin treatment normalized plasma glucose levels and partially prevented the increases in the membraneous PKC activity and all the isoenzymes in the retina. In the retinal endothelial cells, the total DAG level and PKC specific activities are increased by 36 and 22%, respectively, in the membraneous pool when the glucose levels are changed from 5.5 to 22 mM. Activation of PKC activity and isoform betaII by the vitreal injection of phorbol dibutyrate mimicked the abnormal retinal blood circulation observed in diabetic rats (2.22 +/- 0.24 vs. 1.83 +/- 0.40 s). Thus diabetes and elevated glucose levels will increase DAG level and PKC activities and its isoenzyme specifically in vascular cells and may affect retinal hemodynamics. C1 ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. RP SHIBA, T (reprint author), HARVARD UNIV,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY-05110, EY-09602]; NIDDK NIH HHS [DK-36836] NR 34 TC 222 Z9 225 U1 1 U2 5 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 NOV PY 1993 VL 265 IS 5 BP E783 EP E793 PN 1 PG 11 WC Physiology SC Physiology GA MJ167 UT WOS:A1993MJ16700046 PM 8238505 ER PT J AU CHOUDHURY, GG BISWAS, P GRANDALIANO, G ABBOUD, HE AF CHOUDHURY, GG BISWAS, P GRANDALIANO, G ABBOUD, HE TI INVOLVEMENT OF PKC-ALPHA IN PDGF-MEDIATED MITOGENIC SIGNALING IN HUMAN MESANGIAL CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE KIDNEY; GROWTH FACTORS; SIGNAL TRANSDUCTION ID PROTEIN-KINASE-C; GROWTH-FACTOR; TYROSINE PHOSPHORYLATION; PHOSPHOLIPASE-C; MESSENGER-RNAS; RECEPTOR; EPSILON; RAT; EXPRESSION; ACTIVATION AB Platelet-derived growth factor (PDGF) is a potent mitogen for a variety of cells. The calcium/phospholipid-dependent protein kinase C (PKC) represents a major signal transduction pathway for many growth stimuli including PDGF. Various isoforms of PKC are differentially expressed in the same or in different cells and tissues, and diverse stimuli may selectively activate one or more PKC isoforms. We studied the effect of PDGF on DNA synthesis and on the activity of PKC in human mesangial cells and vascular pericytes in the glomerular microvascular bed. PKC activity was measured as the amount of phosphorylated myelin basic protein-derived peptide substrate in the absence and presence of an inhibitor, a peptide spanning the pseudosubstrate region of PKC. PDGF (15 ng/ml) stimulated PKC activity within 5 min, and the effect was sustained for 60 min. Pretreatment of mesangial cells with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), an inhibitor of PKC, abolished the stimulation of PKC and DNA synthesis in response to PDGF. This effect of H-7 was specific, because H-7 did not inhibit the tyrosine phosphorylation of the PDGF receptor in vivo when added to the cells or the in vitro kinase activity in the PDGF beta-receptor immunoprecipitates. Utilizing isotype-specific antibodies against PKC-alpha, -beta, or -gamma for immunoprecipitation of PDGF-treated mesangial cell extracts, followed by assay of PKC activity, we demonstrated the activation of PKC-alpha only. Northern blot analysis of mRNA prepared from mesangial cells also revealed two transcripts, 3.7 kb and 1.8 kb, that hybridized with cDNA specific for PKC-alpha. Moreover, specific ribonuclease (RNase) protection assay using cRNAs specific for PKC-alpha, -beta, and -gamma as probes revealed predominantly the presence of PKC-alpha in mesangial cells. These studies demonstrate that in mesangial cells stimulation of DNA synthesis in response to PDGF is dependent on activation of PKC and that the alpha-isoform of this kinase may mediate the mitogenic effect of PDGF. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP CHOUDHURY, GG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK-33665, DK-43988] NR 30 TC 39 Z9 39 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 NOV PY 1993 VL 265 IS 5 BP F634 EP F642 PN 2 PG 9 WC Physiology SC Physiology GA MJ168 UT WOS:A1993MJ16800087 PM 8238543 ER PT J AU CONHAIM, RL ROSENFELD, DJ SCHREIBER, MA BAASKE, DM HARMS, BA AF CONHAIM, RL ROSENFELD, DJ SCHREIBER, MA BAASKE, DM HARMS, BA TI EFFECTS OF INTRAVENOUS PENTAFRACTION ON LUNG AND SOFT-TISSUE LIQUID EXCHANGE IN HYPOPROTEINEMIC SHEEP SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PLASMA PROTEIN DEPLETION; PLASMA VOLUME EXPANDERS; MICROVASCULAR FILTRATION; LYMPH FLOW; PLASMA OSMOTIC PRESSURE ID TRANS-VASCULAR FLUID; AWAKE SHEEP; PROTEIN FLUX; LYMPH; FILTRATION; PERMEABILITY; COAGULATION; MUSCLE; FLOW AB Effects of infusing pentafraction (Pen), a synthetic hydroxyethyl starch plasma volume expander, on lung and soft tissue lymph flux were compared in nonanesthetized sheep that were protein depleted by batch plasmapheresis. Pen (5%) was infused to raise pulmonary arterial wedge pressure by 5 mmHg for 2 h (1.8 +/- 0.3 1). Pen raised plasma osmotic pressure from plasmapheresis baseline (10.7 +/- 2.2 mmHg; preplasmapheresis baseline, 19.6 +/- 0.6 mmHg) to 16.6 +/- 2.4 mmHg. After Pen, lung lymph flows peaked at 3.9 +/- 2.0 times a preplasmapheresis baseline value of 1.0 (plasmapheresis baseline, 2.7 +/- 0.7), but soft tissue lymph flows rose insignificantly. Plasma Pen concentrations were 2.3 +/- 1.0% postinfusion and 1.6 +/- 0.3% at 12 h. Pen mean molecular masses at these times, measured by high-performance liquid chromatography, were 160 +/- 44 and 129 +/- 23 kDa, respectively. In lung lymph, Pen concentrations were 0.8 +/- 0.6% postinfusion and 0.7 +/- 0.2% at 12 h, with mean molecular masses of 125 +/- 44 and 112 +/- 18 kDa, respectively. In soft tissue lymph Pen was nearly undetectable postinfusion, but at 12 h concentrations averaged 0.3 +/- 0.2% with a mean molecular mass of 80 +/- 10 kDa. The osmotic effectiveness of Pen may be related to its molecular mass, which was large enough to restrict filtration so that the plasma-to-lung lymph osmotic pressure gradient widened. Pen remained effective in the circulation for at least 24 h. C1 UNIV WISCONSIN,DEPT SURG,MADISON,WI 53705. DUPONT MERCK PHARMACEUT CO,WILMINGTON,DE 19880. RP CONHAIM, RL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT SURG,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 26 TC 9 Z9 9 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 NOV PY 1993 VL 265 IS 5 BP H1536 EP H1543 PN 2 PG 8 WC Physiology SC Physiology GA MJ168 UT WOS:A1993MJ16800010 ER PT J AU SHIMOUCHI, A JANSSENS, SP BLOCH, DB ZAPOL, WM BLOCH, KD AF SHIMOUCHI, A JANSSENS, SP BLOCH, DB ZAPOL, WM BLOCH, KD TI CAMP REGULATES SOLUBLE GUANYLATE-CYCLASE BETA-1-SUBUNIT GENE-EXPRESSION IN RFL-6 RAT FETAL LUNG FIBROBLASTS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GUANOSINE 3',5'-CYCLIC MONOPHOSPHATE; NITRIC OXIDE ID SMOOTH-MUSCLE CELLS; INHALED NITRIC-OXIDE; RELAXING FACTOR; GUANOSINE-MONOPHOSPHATE; PLATELET-AGGREGATION; MOLECULAR-CLONING; ENDOTHELIUM; VASODILATORS; SUBUNITS; ENZYME AB Endothelium-derived relaxing factor (EDRF)/nitric oxide (NO) activates soluble guanylate cyclase, thereby stimulating the synthesis of guanosine 3',5'-cyclic monophosphate (cGMP). To investigate the regulation of this important EDRF/NO receptor, we studied soluble guanylate cyclase gene expression in a rat fetal lung fibroblast cell line (RFL-6). 3-Isobutyl-1-methylxanthine, forskolin, and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP), agents which increase intracellular cAMP, decreased the concentration of mRNA encoding the beta1-subunit of soluble guanylate cyclase in RFL-6 cells. To investigate whether a decrease in beta1-subunit mRNA concentration was reflected in diminished capacity to produce cGMP, forskolin-treated RFL-6 cells were exposed to the NO-donor compound sodium nitroprusside. Exposure to forskolin reversibly reduced the ability of RFL-6 cells to increase cGMP in response to NO. These observations suggest that cAMP can modulate the cellular response to EDRF/NO by decreasing the expression of one of the subunits of soluble guanylate cyclase. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114. RP SHIMOUCHI, A (reprint author), HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-42397, HL-45896]; NIAMS NIH HHS [AR-01866] NR 23 TC 39 Z9 39 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 NOV PY 1993 VL 265 IS 5 BP L456 EP L461 PN 1 PG 6 WC Physiology SC Physiology GA MJ167 UT WOS:A1993MJ16700081 PM 7694505 ER PT J AU JOHNSON, DC BURT, CT PERNG, WC HITZIG, BM AF JOHNSON, DC BURT, CT PERNG, WC HITZIG, BM TI EFFECTS OF TEMPERATURE ON MUSCLE PHI AND PHOSPHATE METABOLITES IN NEWTS AND LUNGLESS SALAMANDERS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INTRACELLULAR ACID-BASE REGULATION; ALPHA-IMIDAZOLE; OXYGEN DELIVERY; BODY TEMPERATURE REGULATION; AMPHIBIANS ID P-31 MAGNETIC-RESONANCE; ACID-BASE REGULATION; INTRACELLULAR PH; BODY-TEMPERATURE AB The effect of acute alterations in body temperature (BT) on intracellular pH (pH(i)) and phosphate metabolites was assessed in white skeletal muscle of intact newts and lungless red-backed salamanders using P-31-nuclear magnetic resonance spectroscopy. pH(i) decreased with increasing BT in the tail muscle of both newts and lungless red-backed salamanders. The change in pH with change in temperature from 10 to 30-degrees-C was -0.018 U/degrees-C in newts and -0.041 U/degrees-C in red backs. The calculated alpha-imidazole for skeletal muscle cytosol did not change (0.56) in newts from 10 to 30-degrees-C but fell from 0.69 to 0.43 in red-backed salamanders. Phosphocreatine (PCr)/P(i) fell and P(i)/beta-ATP rose with increasing temperature in both newts and red backs; however, the change was much greater in red backs. Providing the red backs with O2 at 30-degrees-C led to higher pH and alpha-imidazole, comparable to that of newts, along with increased PCr/P(i) and lower P(i)/beta-ATP. Thus newts maintain white skeletal muscle cell cytosol alpha-imidazole constant with changes in BT, whereas red backs apparently do not. However, at the BT of preference, red backs and newts maintain similar muscle pH(i) and alpha-imidazole. The method of gas exchange appears to strongly influence the ability of an animal to maintain its acid-base status over a range of temperatures, and our results suggest that behavioral regulation of BT may involve alpha-imidazole regulation as well. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PHYSIOL,BOSTON,MA 02114. BIOMECH INST,BOSTON,MA 02114. RP JOHNSON, DC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 29 TC 7 Z9 7 U1 1 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 NOV PY 1993 VL 265 IS 5 BP R1162 EP R1167 PN 2 PG 6 WC Physiology SC Physiology GA MJ168 UT WOS:A1993MJ16800076 ER PT J AU BAER, L BROWNBEASLEY, MW SORCE, J HENRIQUES, AI AF BAER, L BROWNBEASLEY, MW SORCE, J HENRIQUES, AI TI COMPUTER-ASSISTED TELEPHONE ADMINISTRATION OF A STRUCTURED INTERVIEW FOR OBSESSIVE-COMPULSIVE DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note AB A computer-assisted telephone system using digitized human speech was developed to administer two rating scales for obsessive-compulsive disorder. For 18 patients, scores derived with this system agreed well with scores from human administration of the scales by telephone and paper-and-pencil scales returned by mail. This approach provides reliable, low-cost, and instantaneous data acquisition. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. GTE LABS INC,WALTHAM,MA 02254. RP BAER, L (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BLDG 149,9TH FLOOR,13TH ST,BOSTON,MA 02129, USA. NR 9 TC 118 Z9 118 U1 0 U2 5 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 1993 VL 150 IS 11 BP 1737 EP 1738 PG 2 WC Psychiatry SC Psychiatry GA MF102 UT WOS:A1993MF10200024 PM 8214187 ER PT J AU WOLF, AM GORTMAKER, SL CHEUNG, L GRAY, HM HERZOG, DB COLDITZ, GA AF WOLF, AM GORTMAKER, SL CHEUNG, L GRAY, HM HERZOG, DB COLDITZ, GA TI ACTIVITY, INACTIVITY, AND OBESITY - RACIAL, ETHNIC, AND AGE-DIFFERENCES AMONG SCHOOLGIRLS SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note ID PHYSICAL-ACTIVITY AB Physical activity, inactivity, and obesity were assessed by questionnaire among a multiethnic sample of 552 girls in grades 5 through 12. Hispanics and Asians reported lower activity levels than other racial groups. Only 36% of the entire sample and less than one fifth of either Asians or Hispanics met the year 2000 goal for strenuous physical activity. Physical activity was inversely associated with age and age-adjusted body mass index. Obesity was unrelated to inactivity. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT HLTH & SOCIAL BEHAV,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,CTR HLTH COMMUN,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,EATING DISORDER UNIT,BOSTON,MA 02114. RP WOLF, AM (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,CHANNING LAB,180 LONGWOOD AVE,BOSTON,MA 02215, USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NCRR NIH HHS [2507 RR05446-30]; NIMH NIH HHS [R01 MH38333-05] NR 14 TC 123 Z9 124 U1 0 U2 5 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD NOV PY 1993 VL 83 IS 11 BP 1625 EP 1627 DI 10.2105/AJPH.83.11.1625 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MF808 UT WOS:A1993MF80800025 PM 8238692 ER PT J AU BOLAND, GW LEE, MJ MUELLER, PR MAYOSMITH, W DAWSON, SL SIMEONE, JF AF BOLAND, GW LEE, MJ MUELLER, PR MAYOSMITH, W DAWSON, SL SIMEONE, JF TI EFFICACY OF SONOGRAPHICALLY GUIDED BIOPSY OF THYROID MASSES AND CERVICAL LYMPH-NODES SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID NEEDLE ASPIRATION BIOPSY; FOLLOW-UP; US; CARCINOMA AB OBJECTIVE. We performed a prospective study in 96 patients to determine accuracy of sonographically guided fine-needle aspiration biopsy of thyroid masses and cervical lymph nodes. MATERIALS AND METHODS. Real-time sonography was used to guide biopsy of 112 cervical masses in 96 patients (71 patients with impalpable masses, 16 with failed unguided attempts, patient's or physician's preference in nine). The diameters of all masses were less than 3 cm, with a mean of 1.5 cm and a median of 1.5 cm. Twenty-nine masses measured 1 cm or less in diameter, 60 masses between 1.1 and 2.0 cm, and 23 masses between 2.1 and 3.0 cm. Cervical masses that were sampled by biopsy included 75 thyroid masses and 37 lymph nodes. RESULTS. Diagnostic specimens were obtained in 102 (91%) of 112 masses sampled. Sixty-eight (91%) of 75 biopsies of thyroid tissue and 34 (92%) of 37 biopsies of lymph nodes were diagnostic. Nondiagnostic thyroid biopsies included four of complex cysts and three of solid nodules. Sonographic follow-up (1 year) revealed no change or decrease in size of those seven lesions. Sixty of 68 diagnostic thyroid biopsies showed benign processes: 42 macrofollicular adenomas, six colloid adenomas, five microfollicular adenomas, four probable cases of thyroiditis, and three hemorrhagic cysts. The remaining eight diagnostic thyroid biopsies showed malignant processes: seven papillary carcinomas and one metastatic small-cell carcinoma. Of 34 diagnostic biopsies of lymph nodes, 26 showed malignant processes and eight showed benign processes. Surgery in the three patients with nondiagnostic biopsies of lymph nodes revealed two recurrent medullary cancers and one benign node. CONCLUSION. Sonographically guided fine-needle aspiration biopsy of neck masses has a high sensitivity (91%) and should be routinely used to evaluate indeterminate masses in the neck. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 13 TC 61 Z9 63 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1993 VL 161 IS 5 BP 1053 EP 1056 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MD368 UT WOS:A1993MD36800032 PM 8273609 ER PT J AU BOLAND, GW LEE, MJ DAWSON, SL MUELLER, PR AF BOLAND, GW LEE, MJ DAWSON, SL MUELLER, PR TI PERCUTANEOUS INJECTION OF ETHANOL IN A PATIENT WITH A SOLITARY HEPATOCELLULAR-CARCINOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note ID ARTERIAL EMBOLIZATION; THERAPY; LIVER; CHEMOEMBOLIZATION; NEOPLASMS C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,55 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 32 TC 1 Z9 1 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1993 VL 161 IS 5 BP 1071 EP 1077 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MD368 UT WOS:A1993MD36800037 PM 8273613 ER PT J AU PICOU, MA ANTONOVIC, R HOLDEN, WE AF PICOU, MA ANTONOVIC, R HOLDEN, WE TI POSITION-DEPENDENT MEDIASTINAL MASS - ANEURYSM OF THE SUPERIOR VENA-CAVA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP PICOU, MA (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97201, USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1993 VL 161 IS 5 BP 1110 EP 1111 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MD368 UT WOS:A1993MD36800048 PM 8273622 ER PT J AU KABUS, D SIDHU, GS WIECZOREK, RL CHOI, HSH AF KABUS, D SIDHU, GS WIECZOREK, RL CHOI, HSH TI METASTATIC MENINGIOMA - HEMANGIOPERICYTOMA OR ANGIOBLASTIC MENINGIOMA SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE MENINGIOMA; HEMANGIOPERICYTOMA; ANGIOBLASTIC MENINGIOMA ID MENINGEAL HEMANGIOPERICYTOMA; ELECTRON-MICROSCOPY; CULTURE; TISSUE AB The question of whether meningeal hemangiopericytoma is a variant of meningioma (''angioblastic meningioma'') or a nosologically distinct entity remains controversial. We present the case histories of an intracranial meningioma and of a meningeal hemangiopericytoma, both of which developed extracranial metastases. The metastatic lesions in both cases were studied by electron microscopy, which demonstrated pericytomatous differentiation in one instance and meningothelial differentiation in the other. This report supports the opinion that meningeal hemangiopericytomas and meningiomas of the CNS are distinct pathological entities. C1 VET AFFAIRS MED CTR,DEPT PATHOL,LAB SERV,NEW YORK,NY 10010. BRONX VET AFFAIRS MED CTR,DEPT PATHOL,NEW YORK,NY. NYU,SCH MED,DEPT PATHOL,NEW YORK,NY. NR 26 TC 23 Z9 25 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 1993 VL 17 IS 11 BP 1144 EP 1150 DI 10.1097/00000478-199311000-00007 PG 7 WC Pathology; Surgery SC Pathology; Surgery GA ME250 UT WOS:A1993ME25000007 PM 8214259 ER PT J AU JONES, EC CLEMENT, PB YOUNG, RH AF JONES, EC CLEMENT, PB YOUNG, RH TI INFLAMMATORY PSEUDOTUMOR OF THE URINARY-BLADDER - REPLY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter ID PSEUDOTUMOR; TUMOR C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA. RP JONES, EC (reprint author), UNIV BRITISH COLUMBIA,VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER V5Z 1M9,BC,CANADA. NR 6 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 1993 VL 17 IS 11 BP 1193 EP 1194 DI 10.1097/00000478-199311000-00016 PG 2 WC Pathology; Surgery SC Pathology; Surgery GA ME250 UT WOS:A1993ME25000016 ER PT J AU FERRY, JA HARRIS, NL AF FERRY, JA HARRIS, NL TI NASAL LYMPHOMAS IN PERU SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter RP FERRY, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 1993 VL 17 IS 11 BP 1194 EP 1195 DI 10.1097/00000478-199311000-00017 PG 2 WC Pathology; Surgery SC Pathology; Surgery GA ME250 UT WOS:A1993ME25000017 PM 8214268 ER PT J AU ROSOW, C AF ROSOW, C TI REMIFENTANIL - A UNIQUE OPIOID ANALGESIC SO ANESTHESIOLOGY LA English DT Editorial Material DE ANALGESICS, OPIOID; REMIFENTANIL; GI87084B ID ALFENTANIL RP ROSOW, C (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,FRUIT ST,BOSTON,MA 02114, USA. NR 8 TC 78 Z9 83 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD NOV PY 1993 VL 79 IS 5 BP 875 EP 876 PG 2 WC Anesthesiology SC Anesthesiology GA MF835 UT WOS:A1993MF83500001 PM 7902031 ER PT J AU GOUDSOUZIAN, NG DENMAN, W SCHWARTZ, A SHORTEN, G FOSTER, V SAMARA, B AF GOUDSOUZIAN, NG DENMAN, W SCHWARTZ, A SHORTEN, G FOSTER, V SAMARA, B TI PHARMACODYNAMIC AND HEMODYNAMIC-EFFECTS OF MIVACURIUM IN INFANTS ANESTHETIZED WITH HALOTHANE AND NITROUS-OXIDE SO ANESTHESIOLOGY LA English DT Article DE ANESTHESIA, PEDIATRIC; INFANTS; NEUROMUSCULAR RELAXANTS; MIVACURIUM ID VECURONIUM INFUSION REQUIREMENTS; CHLORIDE BW B1090U; CLINICAL-PHARMACOLOGY; NARCOTIC ANESTHESIA; PEDIATRIC-PATIENTS; CHILDREN; BW-B1090U; ATRACURIUM; DURATION; AGENTS AB Background: The newly developed neuromuscular blocking agent, mivacurium, has been evaluated in adults and children, but there are no data on its effects in infants. This study was designed to evaluate the neuromuscular effects of mivacurium by dose-response analysis, and its cardiovascular effects in 90 infants 2-11 months of age anesthetized with 1% halothane and nitrous oxide:oxygen. Methods: The neuromuscular response was measured by recording the force of contraction of the adductor pollicis during train-of-four stimulation at 0.1 Hz. The infants were divided according to age into two equal groups of 45; group A infants were 2-6 months of age, and group B infants were 7-11 months of age. Each group was further subdivided into five subgroups of nine. Infants in group A received mivacurium at sequential doses of 40, 50, 55, 75, and 150 mug/kg, while those in group B received mivacurium at doses 40, 50, 60, 75, and 150 mug/kg. The first four doses in each group were used to determine dose-response relationships. The last two doses of 75 and 150 mug/kg were based on the observed preceding dose-response data to approximate the ED95 and 2XED95. Heart rate and blood pressure were determined every minute for a minimum of 3 min after mivacurium. Results. The effective doses for 50% depression of the first twitch response of the train-of-four (ED50) were 44-50 mug/kg (confidence limits 29-74 mug/kg), without any significant difference between groups A and B. In both groups, a larger dose of mivacurium, 150 mug/kg, caused complete ablation of the twitch response in 1.3 +/- 0.2 min (mean +/- SE) with recovery to 5, 25, and 95% of control in 7,6 +/- 0.5, 9.4 +/- 0.6, and 16.2 +/-0.9 min, respectively. In infants, the 25-75% recovery index was 3.8 +/- 0.4 min, and the 5-95% recovery index was 8.5 +/-0.8 min. In 28 infants, in whom surgical relaxation was required for more than 20 min, the infusion requirements to maintain 90-99% neuromuscular block in infants 2-6 and 7-11 months of age were 12.1 +/- 1 and 9.9 +/- 1 mug - kg-1 . min-1, respectively (NS). No significant changes of heart rate or blood pressure occurred in infants, except in the subgroup of infants 7-11 months of age who received 150 mug/kg mivacurium. In this group, a 13-mmHg increase in mean systolic blood pressure was seen without any significant change in diastolic pressure or heart rate. In addition, in 7 of 36 patients receiving 75-150 mug/kg mivacurium, a greater than 29% change in systolic or diastolic pressure occurred. One infant with cholinesterase deficiency had a prolonged neuromuscular block from mivacurium. Conclusions. The ED50 duration of action and infusion requirements of mivacurium in infants 2-6 months of age are comparable with those of infants 7-11 months of age. C1 BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. RP GOUDSOUZIAN, NG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 20 TC 13 Z9 13 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD NOV PY 1993 VL 79 IS 5 BP 919 EP 925 DI 10.1097/00000542-199311000-00008 PG 7 WC Anesthesiology SC Anesthesiology GA MF835 UT WOS:A1993MF83500007 PM 8239009 ER PT J AU DEARMENDI, AJ TONNER, PH BUGGE, B MILLER, KW AF DEARMENDI, AJ TONNER, PH BUGGE, B MILLER, KW TI BARBITURATE ACTION IS DEPENDENT ON THE CONFORMATIONAL STATE OF THE ACETYLCHOLINE-RECEPTOR SO ANESTHESIOLOGY LA English DT Article DE HYPNOTICS, BARBITURATES; RECEPTORS, NICOTINIC ACETYLCHOLINE ID CENTRAL NERVOUS-SYSTEM; CHANNELS; TORPEDO; ANESTHETICS; MEMBRANES; POTENCIES AB Background. Barbiturates act on many neuronal ion channels by poorly understood mechanisms. The authors investigated the hypothesis that barbiturates inhibit the transient open-channel conformation of the nicotinic acetylcholine receptor (nAchR) by binding to a discrete site. Methods. Inhibition curves of the agonist-stimulated efflux of Rb-86+ from nAchR-rich membrane vesicles prepared from the electric tissue of Torpedo nobiliana were obtained for 14 barbiturates using a filter assay. Results: When added simultaneously with agonist, all agents inhibited the ion efflux with half-inhibitory concentrations (IC50), varying from 23 mum for pentobarbital to 880 mum for barbital, and with Hill coefficients of one. The effect of several barbiturates on the agonist concentration-response curve for carbachol-stimulated efflux indicated that this inhibitory action was not competitive. Conclusions: The IC50s of these agents did not correlate with their octanol/water partition coefficients, nor with general anesthetic potency, although a degree of channel inhibition occurred with many agents at general anesthetic concentrations. The existence of a barbiturate-inhibitory site of action was indicated by the structural specificity. This conclusion was supported by the Hill coefficient of one, and by the high inhibitory potencies, which ruled out membrane perturbations as a mechanism. This site on the transient open-channel conformation exhibits different structure-activity relationships than an allosteric site established by equilibrium barbiturate binding on the resting conformation of the AchR. Thus, barbiturate action depends on the nAchR's conformational state. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. UNIV BONN,INST ANASTHESIOL,W-5300 BONN,GERMANY. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIGMS NIH HHS [GM 015904, GM 07592] NR 25 TC 17 Z9 17 U1 2 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD NOV PY 1993 VL 79 IS 5 BP 1033 EP 1041 DI 10.1097/00000542-199311000-00022 PG 9 WC Anesthesiology SC Anesthesiology GA MF835 UT WOS:A1993MF83500021 PM 8238981 ER PT J AU HAUPTMAN, O ALBERT, DM PLOWMAN, MC HOPFER, SM SUNDERMAN, FW AF HAUPTMAN, O ALBERT, DM PLOWMAN, MC HOPFER, SM SUNDERMAN, FW TI OCULAR MALFORMATIONS OF XENOPUS-LAEVIS EXPOSED TO NICKEL DURING EMBRYOGENESIS SO ANNALS OF CLINICAL AND LABORATORY SCIENCE LA English DT Article ID EMBRYO TERATOGENESIS ASSAY; FETAX PROCEDURE; METAL-IONS; COLOBOMATOUS MICROPHTHALMIA; LIPID-PEROXIDATION; CHLORIDE; DOPACHROME; INDUCTION; COMPLEXES; TOXICITY AB The pathogenesis of eye anomalies induced by exposure to Ni2+ (as nickel chloride) during embryogenesis was studied in the frog, Xenopus laevis. Eyes of control and Ni2+-exposed tadpoles were examined without staining using a dissecting microscope, by light microscopy of histological sections, and by electron microscopy. The ocular abnormalities of Ni2+-exposed tadpoles included (a) microphthalmia, (b) hypopigmentation, (c) hernias and cysts of the choroid and retina, and (d) iris coloboma; cataracts were uncommon. The pathogenesis of the ocular lesions appears to involve diffuse or focal dysplasia and loss of the retinal pigment epithelium, with dystrophy of photoreceptor outer segments and protrusion of neuroretina through gaps in the pigment epithelium. This study confirms that Ni2+ is a potent ocular teratogen for Xenopus embryos and points to the retinal pigment epithelium as a primary cellular target for Ni2+-induced embryotoxicity. C1 UNIV CONNECTICUT SCH MED,CTR HLTH,DEPT LAB MED,MC-2225,263 FARMINGTON AVE,FARMINGTON,CT 06030. UNIV CONNECTICUT,SCH MED,DEPT PHARMACOL,FARMINGTON,CT 06030. MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [EY-01917]; NIEHS NIH HHS [ES-05331] NR 37 TC 10 Z9 10 U1 0 U2 1 PU INST CLINICAL SCIENCE INC PI PHILADELPHIA PA 1833 DELANCEY PLACE, PHILADELPHIA, PA 19103 SN 0091-7370 J9 ANN CLIN LAB SCI JI Ann. Clin. Lab. Sci. PD NOV-DEC PY 1993 VL 23 IS 6 BP 397 EP 406 PG 10 WC Medical Laboratory Technology SC Medical Laboratory Technology GA MJ173 UT WOS:A1993MJ17300001 PM 8291895 ER PT J AU CARR, PL FRIEDMAN, RH MOSKOWITZ, MA KAZIS, LE AF CARR, PL FRIEDMAN, RH MOSKOWITZ, MA KAZIS, LE TI COMPARING THE STATUS OF WOMEN AND MEN IN ACADEMIC MEDICINE SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID FEMALE PHYSICIANS; INTERNAL-MEDICINE; FACULTY; RANK AB Objective: To explore the status and academic productivity of women compared with men in academic internal medicine. Design: Mail survey done in 1986. Setting: A total of 107 major teaching hospitals in the United States. Participants: Full-time (1693 of 2510) faculty in cardiology, rheumatology, and general internal medicine; 67% of eligible men and 70% of eligible women. Measurements: Academic productivity defined as research grants awarded, abstracts accepted, and papers published in refereed journals; academic advancement as determined by academic rank and tenure status; and monetary compensation. Results: Women entered academic medicine with shorter periods of fellowship training and were less likely to be members in the Alpha Omega Alpha honor society, but they had job descriptions similar to those of men, with similar allocation of work between research, clinical, and teaching activities. After adjustment, women and men were similar in the numbers of research grants funded as principal investigator (1.9 compared with 2.0), abstracts accepted (6.8 compared with 6.1), and papers published in refereed journals (28.8 compared with 29.2; all with P > 0.20). Women were as likely as men to have tenure, but they had lower academic rank (full or associate professor; 33% compared with 47%, P < 0.001) and received less compensation ($72 000 compared with $79 600 annually; P < 0.001). Conclusion: Although women do similar professional tasks and achieve similar levels of academic productivity, they receive fewer rewards for their work, both in academic rank and monetary compensation. C1 BOSTON UNIV,SCH MED,BOSTON,MA 02118. BOSTON UNIV,SCH PUBL HLTH,BOSTON,MA 02215. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP CARR, PL (reprint author), MASSACHUSETTS GEN HOSP,GEN MED UNIT,BULFINCH 1,FRUIT ST,BOSTON,MA 02114, USA. NR 13 TC 91 Z9 91 U1 0 U2 5 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 1 PY 1993 VL 119 IS 9 BP 908 EP 913 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA MD711 UT WOS:A1993MD71100008 PM 8215004 ER PT J AU ASHTON, CM WU, L AF ASHTON, CM WU, L TI SLEEP-APNEA AND THE RISK FOR PERIOPERATIVE MYOCARDIAL-INFARCTION - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP ASHTON, CM (reprint author), DEPT VET AFFAIRS MED CTR,HOUSTON,TX 77030, USA. NR 2 TC 0 Z9 0 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 1 PY 1993 VL 119 IS 9 BP 953 EP 953 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MD711 UT WOS:A1993MD71100021 ER PT J AU STROH, EM CHEN, S JALKH, AE AF STROH, EM CHEN, S JALKH, AE TI MELARNOCYTOMA WITH JUXTAPAPILLARY NEVUS - PREMALIGNANT OR BENIGN SO ANNALS OF OPHTHALMOLOGY LA English DT Article ID OPTIC DISK; MALIGNANT-MELANOMA; MELANOCYTOMA AB A melanocytoma is a benign heavily pigmented tumor that usuatly arises at the optic nerve. Originally thought to be a malignant neoplasm, currently, it is believed to be a variant of the melanocytic nevus. Recently, several cases of malignant transformation to malignant melanoma have been reported. We present the case of a 63-year-old man with a melanocytoma and juxtapapillary choroidal nevus that remained stable for more than six years. Although the overwhelming majority of such neoplasms are benign, regular follow-up examinations are recommended because there is a small risk of malignant transformation. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,SCHEPENS EYE RES INST,BOSTON,MA 02114. NR 9 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CONTEMPORARY OPHTHALMOLOGY PI SKOKIE PA 4711 GOLF RD, SUITE 408, SKOKIE, IL 60076-1242 SN 0003-4886 J9 ANN OPHTHALMOL JI Ann. Ophthalmol. PD NOV PY 1993 VL 25 IS 11 BP 429 EP 430 PG 2 WC Ophthalmology SC Ophthalmology GA MN389 UT WOS:A1993MN38900007 PM 8109886 ER PT J AU GAISSERT, HA LOFGREN, RH GRILLO, HC AF GAISSERT, HA LOFGREN, RH GRILLO, HC TI UPPER AIRWAY COMPROMISE AFTER INHALATION INJURY - COMPLEX STRICTURES OF THE LARYNX AND TRACHEA AND THEIR MANAGEMENT SO ANNALS OF SURGERY LA English DT Article ID INTUBATION; SEQUELAE AB Objective Strictures of the upper airway caused by burns have features distinct from other benign stenoses. The authors reviewed their experience with burn-related stenoses to define the principles of treatment. Summary Background Data The combined effects of inhaled irritant gases and heat in burn victims produce an intense, often transmural, inflammation of the airway, further complicated by intubation. The incidence of laryngotracheal strictures in survivors of inhalation injury is high, but the reported experience with their treatment is limited and often unduly separated into injuries of larynx and trachea. Methods Presentation, treatment, and long-term follow-up are reviewed in 9 women and 9 men age 9 to 63 years, who were evaluated over a 22-year period for chronic airway compromise after inhalation injury. There were 18 tracheal stenoses, 14 subglottic strictures, and 2 main bronchial stenoses. Laryngotracheal strictures developed in three patients without history of intubation. Six underwent resection of subglottic stenosis. T-tubes were placed in 15 patients, in low subglottic or tracheal stenosis below the vocal cords, in high subglottic stenosis through the vocal cords, and as a stent after resection of subglottic stenosis. Results There were two deaths during follow-up, one from respiratory failure and one from an unrelated cause. Two patients underwent evaluation only. Early in this series, one tracheal and one laryngotracheal resection resulted in prompt restenosis. Of the remaining 14 patients, 9 are without airway support from 2 to 20 years later. Four have permanent tracheal tubes. One patient required tracheostomy 8 years after successful subglottic reconstruction. Conclusions Strictures of the upper airway related to inhalation injury are associated with prolonged inflammation and involve larynx and trachea in a majority of patients. These complex injuries respond to prolonged tracheal stenting (mean, 28 months) and resection or stenting of subglottic stenoses with recovery of a functional airway and voice in most patients. Early tracheal resection should be avoided C1 MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,OTOLARYNGOL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. NR 15 TC 36 Z9 37 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD NOV PY 1993 VL 218 IS 5 BP 672 EP 678 PG 7 WC Surgery SC Surgery GA MH024 UT WOS:A1993MH02400014 PM 8239783 ER PT J AU DAMBRA, M AF DAMBRA, M TI IS INTRAOPERATIVE ECHOCARDIOGRAPHY A USEFUL MONITOR IN THE OPERATING-ROOM SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT SYMP ON RISK MANAGEMENT AND OUTCOME ANALYSIS IN OPEN HEART SURGERY CY JAN 23, 1993 CL SAN ANTONIO, TX ID SURGERY AB Few cardiac surgeons or anesthesiologists would argue with the view that intraoperative echocardiography, both transesophageal and epicardial, has become an important diagnostic tool. Specific diagnostic applications primarily involve valve reconstruction and replacement, as well as complex congenital heart disease repairs. Routine echocardiographic monitoring in cardiac operations is, however, controversial. Three specific modalities may benefit from this technology. Aortic root scanning before cannulation/proximal coronary anastomoses using surface echocardiography is one. Areas with significant atherosclerosis can be identified and manipulation avoided. Another is quantification of global left-ventricular function using transesophageal echocardiography. This method may have specific relevance to patients requiring mechanical circulatory assistance. Using echocardiography to monitor ischemic regional wall-motion abnormalities and using the findings to predict an unfavorable outcome is a third suggested use for perioperative monitoring in cardiac surgery. RP DAMBRA, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 8 Z9 9 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 NOV PY 1993 VL 56 IS 5 SU S BP S83 EP S85 PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA MF703 UT WOS:A1993MF70300005 PM 8239843 ER PT J AU TEICHER, BA HOLDEN, SA ARA, G NORTHEY, D AF TEICHER, BA HOLDEN, SA ARA, G NORTHEY, D TI RESPONSE OF THE FSAII FIBROSARCOMA TO ANTIANGIOGENIC MODULATORS PLUS CYTOTOXIC AGENTS SO ANTICANCER RESEARCH LA English DT Article DE ANTIANGIOGENIC MODULATORS; BETA-CYCLODEXTRIN TETRADECASULFATE; FSAII FIBROSARCOMA; CYTOTOXIC THERAPIES ID MELPHALAN ANTITUMOR-ACTIVITY; ANGIOGENESIS INHIBITION; ANGIOSTATIC STEROIDS; BASEMENT-MEMBRANE; MESSENGER-RNA; FLUOSOL-DA; MR 72,000; COLLAGENASE; MINOCYCLINE; METASTASIS AB The formation of a blood supply (angiogenesis) is critical to the growth of solid tumors. The naturally occurring steroid tetrahydrocortisol, the synthetic cyclodextrin derivative beta-cyclodextrin tetradecasulfate, and the tetracycline derivative minocycline have antiangiogenic activity. Tetrahydrocortisol (125 mg/kg) and beta-cyclodextrin tetradecasulfate (1000 mg/kg) in a 1:1 molar ratio by continous infusion over 14 days and minocycline (10 mg/kg) administered i.p. daily from day 4 to day 18 postimplantation of the FSaII fibrosarcoma did not alter the growth of the tumor. These antiangiogenic modulators were not cytotoxic toward FSaIIC tumor cells or bone marrow CFU-GM when tumor-bearing animals were treated and cytotoxicity determined by colony formation in culture. The antiangiogenic modulators markedly increased the cytotoxicity of cyclophosphamide toward FSaIIC tumor cells and to a much lesser degree toward bone marrow CFU-GM. The cytotoxicity of CDDP and radiation was enhanced only by administration of the three modulators in combination. In tumor growth delay studies, the three modulator combination increased the effectiveness of CDDP by 1.5-fold, of cyclophosphamide by 1.9-fold and of radiation by 1.4-fold. Although the antiangiogenic therapies alone did not substantially reduce the number of lung metastases compared with the untreated controls, addition of the antiangiogenic agents to treatment with the cytotoxic therapies reduced not only the number of lung metastases formed from the primary tumor but also reduced the number of large metastases. Thus, antiangiogenic therapies can potentiate the efficacy of standard anticancer therapies. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01-CA19589, P01-CA38493] NR 36 TC 25 Z9 27 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD NOV-DEC PY 1993 VL 13 IS 6A BP 2101 EP 2106 PG 6 WC Oncology SC Oncology GA MT983 UT WOS:A1993MT98300026 PM 7507654 ER PT J AU WEINBERG, JM ROOK, AH LESSIN, SR AF WEINBERG, JM ROOK, AH LESSIN, SR TI MOLECULAR DIAGNOSIS OF LYMPHOCYTIC INFILTRATES OF THE SKIN SO ARCHIVES OF DERMATOLOGY LA English DT Article ID T-CELL RECEPTOR; GENE REARRANGEMENT ANALYSIS; REGRESSING ATYPICAL HISTIOCYTOSIS; CUTANEOUS LYMPHOID HYPERPLASIA; POLYMERASE CHAIN-REACTION; SOUTHERN BLOT ANALYSIS; MYCOSIS-FUNGOIDES; LYMPHOMATOID PAPULOSIS; B-CELL; PERIPHERAL-BLOOD AB Background: Advances in our understanding of the molecular genetics of lymphocyte antigen receptors (B-cell immunoglobulin and T-cell antigen receptor), have led to the application of molecular biologic techniques to molecularly characterize lymphocytic infiltrates of the skin. Molecular diagnosis refers to the application of these techniques as a diagnostic aid in the clinicopathologic evaluation of cutaneous lymphocytic infiltrates. Observation: Molecular studies have clinical application in the determination of lineage and detection of retroviruses in cutaneous lymphoid neoplasms, distinguishing between lymphoproliferative and reactive infiltrates, and staging and monitoring response to therapy in cutaneous T-cell lymphoma. Southern blot analysis of immunoglobulin and T-cell antigen receptor gene rearrangements may fail to aid the clinician in establishing a diagnosis of a cutaneous malignancy due to the limits of detection sensitivity in minimally infiltrated lesions (eg, parapsoriasis and patch-stage mycosis fungoides) or the still uncertain prognostic significance of clonality in benign cutaneous diseases (eg, follicular mucinosis, pityriasis lichenoides et varioliformis acuta, lymphomatoid papulosis, and cutaneous lymphoid hyperplasia). Conclusions: Molecular studies have enormous research value, providing new means to explore the pathogenesis and clonal evolution of lymphoproliferative skin diseases. Presently, however, they have limited applications as an independent diagnostic tool. As our understanding of the clinical and biologic significance of the molecular detection of clonal lymphocyte populations in the skin expands and as the application of polymerase chain reaction amplification provides us with greater detection sensitivity and specificity, the clinical utility of molecular diagnosis of lymphocytic infiltrates of the skin will be enhanced. C1 UNIV PENN, DEPT DERMATOL, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. FU NCI NIH HHS [R29 CA-55017] NR 97 TC 31 Z9 31 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-987X EI 1538-3652 J9 ARCH DERMATOL JI Arch. Dermatol. PD NOV PY 1993 VL 129 IS 11 BP 1491 EP 1500 DI 10.1001/archderm.129.11.1491 PG 10 WC Dermatology SC Dermatology GA MG677 UT WOS:A1993MG67700015 PM 8239706 ER PT J AU GUSELLA, JF MACDONALD, ME AMBROSE, CM DUYAO, MP AF GUSELLA, JF MACDONALD, ME AMBROSE, CM DUYAO, MP TI MOLECULAR-GENETICS OF HUNTINGTONS-DISEASE SO ARCHIVES OF NEUROLOGY LA English DT Review ID FRAGILE-X SYNDROME; BULBAR MUSCULAR-ATROPHY; POLYMORPHIC DNA MARKER; MYOTONIC-DYSTROPHY; CANDIDATE REGION; TRINUCLEOTIDE REPEAT; LINKAGE DISEQUILIBRIUM; CTG REPEAT; RECOMBINATION; CHROMOSOME-4 AB Huntington's disease is an inherited disorder in which selective neuronal loss in the brain leads to a characteristic choreic movement disorder. The successful mapping of the Huntington's disease gene to chromosome 4 set off a torrent of similar studies in other inherited disorders as investigators attempted to locate and isolate human disease genes with this new approach. Although it took a decade-long quest since the initial mapping of the genetic defect, the gene causing Huntington's disease has recently been isolated. Discovery of the mutational mechanism causing Huntington's disease has explained some of the peculiarities of inheritance of this intriguing disorder and creates hope for a better understanding of the cause of neuronal cell death that could eventually lead to a treatment. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. FU NINDS NIH HHS [NS22031, NS16367] NR 58 TC 84 Z9 85 U1 3 U2 16 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD NOV PY 1993 VL 50 IS 11 BP 1157 EP 1163 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA MF530 UT WOS:A1993MF53000003 PM 8215974 ER PT J AU BERSON, EL ROSNER, B SANDBERG, MA HAYES, KC NICHOLSON, BW WEIGELDIFRANCO, C WILLETT, W AF BERSON, EL ROSNER, B SANDBERG, MA HAYES, KC NICHOLSON, BW WEIGELDIFRANCO, C WILLETT, W TI VITAMIN-A SUPPLEMENTATION FOR RETINITIS-PIGMENTOSA SO ARCHIVES OF OPHTHALMOLOGY LA English DT Letter RP BERSON, EL (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BERMAN GUND LAB,243 CHARLES ST,BOSTON,MA 02114, USA. NR 2 TC 53 Z9 54 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD NOV PY 1993 VL 111 IS 11 BP 1456 EP 1458 PG 3 WC Ophthalmology SC Ophthalmology GA MG678 UT WOS:A1993MG67800001 PM 8240091 ER PT J AU BERSON, EL ROSNER, B SANDBERG, MA HAYES, KC NICHOLSON, BW WEIGELDIFRANCO, C WILLET, W AF BERSON, EL ROSNER, B SANDBERG, MA HAYES, KC NICHOLSON, BW WEIGELDIFRANCO, C WILLET, W TI A RANDOMIZED TRIAL OF VITAMIN-A AND VITAMIN-E SUPPLEMENTATION FOR RETINITIS-PIGMENTOSA - REPLY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Letter RP BERSON, EL (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. NR 3 TC 2 Z9 2 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD NOV PY 1993 VL 111 IS 11 BP 1463 EP 1465 PG 3 WC Ophthalmology SC Ophthalmology GA MG678 UT WOS:A1993MG67800008 ER PT J AU GULLEY, ML RAABTRAUB, N AF GULLEY, ML RAABTRAUB, N TI DETECTION OF EPSTEIN-BARR-VIRUS IN HUMAN TISSUES BY MOLECULAR-GENETIC TECHNIQUES SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID POLYMERASE CHAIN-REACTION; INSITU HYBRIDIZATION; HODGKINS-DISEASE; NASOPHARYNGEAL CARCINOMA; VIRAL-DNA; CELL LINES; LYMPHOPROLIFERATIVE DISORDERS; REACTION AMPLIFICATION; TRANSPLANT RECIPIENTS; EPITHELIAL-CELLS AB In the past few years, there has been an explosion of new data on the association of Epstein-Barr virus (EBV) with human disease. Many of these discoveries have come as a direct result of the application of DNA technology. The nucleic acid hybridization techniques most commonly used to detect EBV in human tissues include Southern blot analysis, in situ hybridization to viral DNA or RNA, and polymerase chain reaction. An advantage of Southern blotting is the ability to distinguish latent from infectious EBV and to determine the clonality of infected tumors with respect to the structure of the viral terminal repeat sequences. In situ hybridization has the advantage of precise localization of the virus in infected tissues or tumors. Polymerase chain reaction is exquisitely sensitive in detecting viral DNA, perhaps too sensitive for disease-specific purposes given the ubiquitous nature of EBV. Each of these molecular genetic methods of EBV analysis is currently used in research laboratories, while some methods have found their way into routine diagnostic pathology because they are faster, more sensitive, or more informative than previous assays. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. UNIV N CAROLINA, DEPT MICROBIOL IMMUNOL, CHAPEL HILL, NC 27514 USA. RP UNIV TEXAS, HLTH SCI CTR, DEPT PATHOL, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. FU NCI NIH HHS [R01-CA32979, K08-CA01615] NR 58 TC 27 Z9 27 U1 0 U2 0 PU COLL AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA SN 0003-9985 EI 1543-2165 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD NOV PY 1993 VL 117 IS 11 BP 1115 EP 1120 PG 6 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MF095 UT WOS:A1993MF09500012 PM 8239932 ER PT J AU MARCINIAK, CM HEINEMANN, AW MONGA, T AF MARCINIAK, CM HEINEMANN, AW MONGA, T TI CHANGES IN MEDICAL STABILITY UPON ADMISSION TO A REHABILITATION UNIT SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article ID CARE C1 NORTHWESTERN UNIV,SCH MED,DEPT REHABIL MED,CHICAGO,IL 60611. BAYLOR COLL MED,HOUSTON VET ADM MED CTR,DEPT PM&R,DEPT RMS,HOUSTON,TX 77030. RI Heinemann, Allen /K-6283-2012; OI Heinemann, Allen /0000-0003-2782-7326; Marciniak, Christina/0000-0003-3300-0050 NR 6 TC 5 Z9 5 U1 0 U2 0 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 NOV PY 1993 VL 74 IS 11 BP 1157 EP 1160 PG 4 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA MD088 UT WOS:A1993MD08800006 PM 8239953 ER PT J AU WEHNER, JM PAYLOR, R JOHNSON, R SPIEGELMAN, BM PAPAIOANNOU, V CAO, W COLLINS, AC AF WEHNER, JM PAYLOR, R JOHNSON, R SPIEGELMAN, BM PAPAIOANNOU, V CAO, W COLLINS, AC TI BEHAVIORAL CHARACTERIZATION OF C-FOS NULL MUTANTS - LEARNING AND ETHANOL EXPERIMENTS SO BEHAVIOR GENETICS LA English DT Meeting Abstract C1 UNIV COLORADO,INST BEHAV GENET,BOULDER,CO 80309. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. TUFTS UNIV,DEPT PATHOL,BOSTON,MA 02111. NR 1 TC 0 Z9 0 U1 0 U2 2 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD NOV PY 1993 VL 23 IS 6 BP 569 EP 569 PG 1 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA MP039 UT WOS:A1993MP03900104 ER PT J AU GARG, HG LIPPAY, EW CARTER, EA DONELAN, MB REMENSNYDER, JP SIEBERT, JW AF GARG, HG LIPPAY, EW CARTER, EA DONELAN, MB REMENSNYDER, JP SIEBERT, JW TI COMPARISON OF THE EFFECTS OF INTERLEUKIN-1-BETA ON PROTEOGLYCAN SYNTHESIS BY HUMAN SKIN AND POSTBURN NORMAL SCAR EXPLANT CULTURES SO BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL LA English DT Article ID ANIMAL GLYCOSAMINOGLYCANS; CARTILAGE; COLLAGEN; SEPARATION; BREAKDOWN; DECORIN; TENDON C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. NYU,INST RECONSTRUCT PLAST SURG,NEW YORK,NY 10016. RP GARG, HG (reprint author), SHRINERS BURNS INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 23 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 1039-9712 J9 BIOCHEM MOL BIOL INT JI Biochem. Mol. Biol. Int. PD NOV PY 1993 VL 31 IS 3 BP 583 EP 591 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MG757 UT WOS:A1993MG75700023 PM 8118432 ER PT J AU LAFER, B FAVA, M HAMMERNESS, P ROSENBAUM, JF AF LAFER, B FAVA, M HAMMERNESS, P ROSENBAUM, JF TI THE INFLUENCE OF DST AND TRH TEST ADMINISTRATION ON DEPRESSION ASSESSMENTS - A CONTROLLED-STUDY SO BIOLOGICAL PSYCHIATRY LA English DT Article DE DST; TRH TEST; MAJOR DEPRESSIVE DISORDER; NEUROENDOCRINE TESTS; DEPRESSION ASSESSMENTS; RATING SCALES ID THYROTROPIN-RELEASING-HORMONE; RELAPSE; MARKER AB Significant antidepressant effects have been reported after administration of dexamethasone and thyrotropin-releasing hormone (TRH). The purpose of this study was to evaluate whether or not the administration of the dexamethasone suppression test (DST) and TRH test in depressed patients, just before their entering clinical trials, has any impact on their symptoms. The Hamilton Rating Scale for Depression was administered to 166 subjects at screen visit, 1 week later (baseline visit), and 1 week after beginning treatment with fluoxetine 20 mg/day (week-1). Between screen and baseline visits, 62 patients were administered the DST alone, 6 underwent the TRH test alone, and 26 received both the DST and the TRH test. Seventy-two patients were not administered either test. No statistically significant differences in depression scores were found at screen, baseline and week-1 visits between patients who underwent neuroendocrine tests and those who did not. Our data suggest that the administration of neuroendocrine tests such as the DST and the TRH test does not have a statistically significant effect on depressive symptoms and, therefore, does not interfere with study results and interpretation. RP LAFER, B (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,DEPRESS RES PROGRAM,ACC815,15 PARKMAN ST,BOSTON,MA 02114, USA. RI Lafer, Beny/C-1055-2012; Lafer, Beny/F-9390-2015 OI Lafer, Beny/0000-0002-6132-9999; Lafer, Beny/0000-0002-6132-9999 NR 12 TC 5 Z9 5 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD NOV 1 PY 1993 VL 34 IS 9 BP 650 EP 653 DI 10.1016/0006-3223(93)90158-A PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MH048 UT WOS:A1993MH04800010 PM 8292694 ER PT J AU KAUFMAN, DW KELLY, JP JOHANNES, CB SANDLER, A HARMON, D STOLLEY, PD SHAPIRO, S AF KAUFMAN, DW KELLY, JP JOHANNES, CB SANDLER, A HARMON, D STOLLEY, PD SHAPIRO, S TI ACUTE THROMBOCYTOPENIC PURPURA IN RELATION TO THE USE OF DRUGS SO BLOOD LA English DT Article ID QUININE; HEPARIN C1 MASSACHUSETTS GEN HOSP,DEPT HEMATOL ONCOL,BOSTON,MA 02114. UNIV MARYLAND,SCH MED,DEPT EPIDEMIOL & PREVENT MED,BALTIMORE,MD 21201. RP KAUFMAN, DW (reprint author), BOSTON UNIV,SCH PUBL MED,SLONE EPIDEMIOL UNIT,1371 BEACON ST,BROOKLINE,MA 02146, USA. FU NHLBI NIH HHS [R01 HL31768] NR 36 TC 55 Z9 58 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 1 PY 1993 VL 82 IS 9 BP 2714 EP 2718 PG 5 WC Hematology SC Hematology GA ME657 UT WOS:A1993ME65700014 PM 8219224 ER PT J AU SOIFFER, RJ ROBERTSON, MJ MURRAY, C COCHRAN, K RITZ, J AF SOIFFER, RJ ROBERTSON, MJ MURRAY, C COCHRAN, K RITZ, J TI INTERLEUKIN-12 AUGMENTS CYTOLYTIC ACTIVITY OF PERIPHERAL-BLOOD LYMPHOCYTES FROM PATIENTS WITH HEMATOLOGIC AND SOLID MALIGNANCIES SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; NATURAL-KILLER-CELL; STIMULATORY FACTOR NKSF; CHRONIC MYELOGENOUS LEUKEMIA; VERSUS-HOST DISEASE; RECOMBINANT INTERLEUKIN-2; CYTO-TOXICITY; HETERODIMERIC CYTOKINE; COMPLETE REMISSION; MATURATION FACTOR C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA41619]; NIAID NIH HHS [AI29530] NR 46 TC 81 Z9 81 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 1 PY 1993 VL 82 IS 9 BP 2790 EP 2796 PG 7 WC Hematology SC Hematology GA ME657 UT WOS:A1993ME65700023 PM 8106018 ER PT J AU ADKINS, D ENCARNACION, C SALZMAN, D BOLDT, D FREYTES, C VONHOFF, DD LEMAISTRE, CF AF ADKINS, D ENCARNACION, C SALZMAN, D BOLDT, D FREYTES, C VONHOFF, DD LEMAISTRE, CF TI DURABLE COMPLETE REMISSION IN A PATIENT WITH REFRACTORY MEDIASTINAL NONSEMINOMATOUS GERM-CELL TUMOR AFTER TANDEM HIGH-DOSE CHEMOTHERAPY AND AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO BONE MARROW TRANSPLANTATION LA English DT Note ID CANCER; CARBOPLATIN; IFOSFAMIDE; CISPLATIN; ETOPOSIDE; VP-16; PLUS AB The prognosis of patients with relapsed or refractory mediastinal germ cell tumors is uniformly poor. There have been no reports of long-term disease-free survivors using any currently available salvage regimen. We describe a patient with primary mediastinal non-seminomatous germ cell tumor refractory to initial and salvage chemotherapy, who entered his first complete remission after surgical resection and tandem autologous bone marrow transplantation. The patient remains without evidence of disease 19 months after the first BMT. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 15 TC 4 Z9 4 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD NOV PY 1993 VL 12 IS 5 BP 541 EP 546 PG 6 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA MG557 UT WOS:A1993MG55700019 PM 7507767 ER PT J AU SPOHR, U BACH, M SPIRO, RG AF SPOHR, U BACH, M SPIRO, RG TI INHIBITORS OF ENDO-ALPHA-MANNOSIDASE .1. DERIVATIVES OF 3-O-(ALPHA-D-GLUCOPYRANOSYL)-D-MANNOPYRANOSE SO CANADIAN JOURNAL OF CHEMISTRY-REVUE CANADIENNE DE CHIMIE LA English DT Article ID N-LINKED OLIGOSACCHARIDES; GLUCOSIDASE-II-DEFICIENT; ENDOMANNOSIDASE PATHWAY; RAT-LIVER; GLYCOPROTEINS; CELLS AB Golgi membrane endo-alpha-D-mannosidase releases the disaccharide alphaDGlc(1 --> 3)DMan (34) from the GlcMan9Glc-NAc2 oligosaccharide of immature N-linked glycoproteins. To convert the hydrolysis product 34 into a potent inhibitor of the enzyme, chemical modifications at the 1- and 2-positions of the mannose unit of 34 were performed. These include replacement of OH-1 by hydrogen (6), fluorine (12), and p-nitrophenoxy (5). Two potent inhibitors resulted, as reported recently, when both OH-1 and OH-2 of 34 were replaced by a double bond (glucal derivative 8) or replaced by hydrogen (1,2-dideoxy 9). 9 proved 40 times stronger as an inhibitor than 1-deoxy 6. However, further modifications at the 4- and 6-positions of 9, namely deoxygenation, methylation, and replacement of OH-6 by an amino group, were now found to largely abolish the activity, demonstrating that OH-4 and OH-6 of 9 are involved in H-bonding with the enzyme. C1 UNIV ALBERTA,DEPT CHEM,EDMONTON T6G 2G2,ALBERTA,CANADA. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. ELLIOTT P JOSLIN RES LAB,BOSTON,MA 02215. RP SPOHR, U (reprint author), CHEMBIOMED LTD,EDMONTON,AB,CANADA. NR 26 TC 15 Z9 15 U1 0 U2 7 PU NATL RESEARCH COUNCIL CANADA PI OTTAWA PA RESEARCH JOURNALS, MONTREAL RD, OTTAWA ON K1A 0R6, CANADA SN 0008-4042 J9 CAN J CHEM JI Can. J. Chem.-Rev. Can. Chim. PD NOV PY 1993 VL 71 IS 11 BP 1919 EP 1927 DI 10.1139/v93-239 PG 9 WC Chemistry, Multidisciplinary SC Chemistry GA MM244 UT WOS:A1993MM24400020 ER PT J AU SPOHR, U BACH, M SPIRO, RG AF SPOHR, U BACH, M SPIRO, RG TI INHIBITORS OF ENDO-ALPHA-MANNOSIDASE .2. 1-DEOXY-3-0-(ALPHA-D-GLUCOPYRANOSYL)-MANNOJIRIMYCIN AND CONGENERS MODIFIED IN THE MANNOJIRIMYCIN UNIT SO CANADIAN JOURNAL OF CHEMISTRY-REVUE CANADIENNE DE CHIMIE LA English DT Article ID BLOOD-GROUP DETERMINANT; MAGNETIC-RESONANCE SPECTROSCOPY; MOLECULAR RECOGNITION; CONFORMATIONAL-ANALYSIS; MONOCLONAL-ANTIBODY; ULEX-EUROPAEUS; RAT-LIVER; D-GLUCOSE; LEWIS-B; BINDING AB The syntheses of 1-deoxy-3-O-(alpha-D-glucopyranosyl)-mannojirimycin (9) and its 2-deoxy, 2-O-methyl, 4-deoxy, 4-O-methyl, 6-deoxy, 6-O-methyl, N-methyl, and N-propyl congeners are described. Since 9 was previously shown to effectively inhibit endo-alpha-D-mannosidase, a glycoprotein-processing hydrolase, these chemical modifications were designed to assist in the assessment of intermolecular hydrogen bonds of the inhibitor-enzyme complex. The previously reported data require that all hydroxyl groups of the deoxymannojirimycin unit of 9, namely, OH-2, OH-4, OH-6, and also the NH-5 group, interact with charged and polar groupings of the enzyme, since deoxygenations and alkylations abolished or significantly reduced activities. Conformational analysis of 9 and some of its congeners based on NMR chemical shifts, experimental and theoretical nuclear Overhauser enhancements, and HSEA calculations were performed. The chemical modifications of the glucose unit of 9 are described in the accompanying paper. C1 UNIV ALBERTA,DEPT CHEM,EDMONTON T6G 2G2,ALBERTA,CANADA. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. ELLIOTT P JOSLIN RES LAB,BOSTON,MA 02215. RP SPOHR, U (reprint author), CHEMBIOMED LTD,EDMONTON,AB,CANADA. NR 38 TC 18 Z9 18 U1 0 U2 2 PU NATL RESEARCH COUNCIL CANADA PI OTTAWA PA RESEARCH JOURNALS, MONTREAL RD, OTTAWA ON K1A 0R6, CANADA SN 0008-4042 J9 CAN J CHEM JI Can. J. Chem.-Rev. Can. Chim. PD NOV PY 1993 VL 71 IS 11 BP 1928 EP 1942 DI 10.1139/v93-240 PG 15 WC Chemistry, Multidisciplinary SC Chemistry GA MM244 UT WOS:A1993MM24400021 ER PT J AU POLLACK, MH AF POLLACK, MH TI INNOVATIVE USES OF BENZODIAZEPINES IN PSYCHIATRY SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Article; Proceedings Paper CT 42nd Annual Meeting of the Canadian-Psychiatric-Association CY SEP 17, 1992 CL MONTREAL, CANADA SP CANADIAN PSYCHIAT ASSOC ID NEGATIVE SCHIZOPHRENIC SYMPTOMS; OBSESSIVE-COMPULSIVE DISORDER; TERM THERAPEUTIC USE; SOCIAL PHOBIA; PANIC DISORDER; DOUBLE-BLIND; PSYCHOGENIC CATATONIA; PSYCHOTIC AGITATION; ALPRAZOLAM; CLONAZEPAM AB Over the last three decades, a greater understanding of the phenomenology and etiology of illness has fostered progress in psychopharmacology. While research has yielded important new psychopharmacologic compounds, the field continues to benefit from the discovery of innovative clinical applications of established agents. For instance, benzodiazepines - among the most commonly used medications in the pharmacopeia - have demonstrated their efficacy in the treatment of a wide variety of syndromes. Recently, much attention has focused on the use of high-potency benzodiazepines (for example, clonazepam, alprazolam, lorazepam) in the treatment of panic disorder and mania. This paper presents the uses of benzodiazepines to treat other conditions, including psychotic and agitated states, social phobia, obsessive-compulsive disorder pain syndromes, seizures, drug withdrawal and side-effects induced by antidepressants and neuroleptics. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP POLLACK, MH (reprint author), MASSACHUSETTS GEN HOSP,ANXIETY DISORDERS PROGRAM,ACC-815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 55 TC 5 Z9 6 U1 1 U2 3 PU CANADIAN PSYCHIATRIC ASSOC PI OTTAWA PA SUITE 200, 237 ARGYLE AVE, OTTAWA ON K2P 1B8, CANADA SN 0706-7437 J9 CAN J PSYCHIAT JI Can. J. Psychiat.-Rev. Can. Psychiat. PD NOV PY 1993 VL 38 IS 9 SU 4 BP S122 EP S126 PG 5 WC Psychiatry SC Psychiatry GA ML975 UT WOS:A1993ML97500005 PM 7905781 ER PT J AU ANTMAN, K AF ANTMAN, K TI REIMBURSEMENT ISSUES FACING PATIENTS, PROVIDERS, AND PAYERS SO CANCER LA English DT Article; Proceedings Paper CT INTERACTIVE WORKSHOP ON MEDICAL ETHICS VERSUS MEDICAL ECONOMICS : A HEALTH CARE DILEMMA IN CANCER PATIENT CARE CY FEB 16-17, 1993 CL WASHINGTON, DC SP AMER CANC SOC, ROCHE LABS DE REIMBURSEMENT; CLINICAL TRIALS; CANCER; ETHICS ID COST-EFFECTIVENESS; HEALTH-CARE; CANCER; CRISIS; TRIAL AB Escalating costs of health care delivery and the current constraints imposed by the federal budget deficit seriously threaten to compromise patient care and innovative biomedical research. Recent third-party refusal to cover some patients treated in protocols has had considerable impact on trial research.1,2 In addition, reimbursement for conventional care sometimes has been refused if delivered as part of a study (e.g., MOPP therapy versus ABVD therapy) or for an indication that is not specifically cited on the Food and Drug Administration label. Who should cover the patient care costs of patients participating in clinical trials? One approach would have patients cover these costs themselves.3 A second approach is the reinstitution of patient care costs into research grants. A third possibility is that the pharmaceutical industry support patient care costs of clinical research. Historically, hospital expenses of patients participating in studies have been paid by health insurance policies. In the absence of a clinical trial, many patients would be treated with Food and Drug Administration-approved therapies despite a lack of substantial benefit. Such marginal treatments are compensated by third-party payers routinely. The current system is arbitrary and expensive, compromises research and development, and equates new treatment with no treatment. By refusing to reimburse the patient care costs of investigational therapy, third-party carriers are, in fact, making medical decisions.4 There is a growing and legitimate concern that the pace of clinical research will be impeded significantly at a time when many exciting developments will be ready for clinical trials.5 The molecular steps in carcinogenesis are being documented rapidly for common malignancies, such as colon cancer. Immunologic, biologic, and hormonal approaches, and emerging technologies, such as marrow transplant or antibody toxin conjugates, already are being studied in the clinic. Health policy legislation and decisions by the insurance industry have a direct impact on physicians, facilitating, or often impeding, the care physicians are able to provide. Who makes health policy decisions? Increasingly, these decisions are being made not hy physicians, but by public health experts, economists, and, more recently, large industries grappling with the cost of providing insurance coverage (and its effects on competitive pricing in a world market).4 Therefore, physicians need to position themselves to influence the development of medical policy, particularly as it relates to the prevention, diagnosis, and treatment of patients with cancer. RP ANTMAN, K (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 23 TC 11 Z9 11 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD NOV 1 PY 1993 VL 72 IS 9 SU S BP 2842 EP 2845 DI 10.1002/1097-0142(19931101)72:9+<2842::AID-CNCR2820721514>3.0.CO;2-I PG 4 WC Oncology SC Oncology GA MD661 UT WOS:A1993MD66100012 PM 8402516 ER PT J AU BERKMAN, BJ SAMPSON, SE AF BERKMAN, BJ SAMPSON, SE TI PSYCHOSOCIAL EFFECTS OF CANCER ECONOMICS ON PATIENTS AND THEIR FAMILIES SO CANCER LA English DT Article; Proceedings Paper CT INTERACTIVE WORKSHOP ON MEDICAL ETHICS VERSUS MEDICAL ECONOMICS : A HEALTH CARE DILEMMA IN CANCER PATIENT CARE CY FEB 16-17, 1993 CL WASHINGTON, DC SP AMER CANC SOC, ROCHE LABS DE CANCER; SOCIOECONOMIC; PSYCHOSOCIAL; FINANCIAL AB Cancer frequently follows an unpredictable course, with patients experiencing numerous disruptions in their lives. Concomitantly, the enormous financial burdens that accompany the onset and subsequent treatment of cancer become even more overwhelming. Regardless of socioeconomic status, almost all families confronted with cancer and its treatment will have financial problems. Poor people are more likely to be diagnosed with cancer when the disease is advanced and treatment options are significantly more limited. Limited access to medical care carries the additional risk of denied access to community resources, which often are made through referrals from the health care system. For the middle-class family with insurance, as medication costs increase (whether they are covered or not), financial deprivations accumulate as out-of-pocket expenditures, because of required insurance deductibles and copayments and wages lost because of aspects of the treatment. Therefore, even those who are insured can be financially devastated by substantial gaps in coverage. A diagnosis of cancer compounds the struggle for survival and introduces new financial, physical, and psychologic demands. As a nation, we must ensure that cancer prevention, detection, treatment, and rehabilitation services are accessible and available to all who need them, regardless of their ability to pay. C1 HARVARD UNIV,SCH MED,CTR GERIATR EDUC,BOSTON,MA 02115. RP BERKMAN, BJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT SOCIAL SERV,55 FRUIT ST,BOSTON,MA 02114, USA. NR 20 TC 26 Z9 26 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD NOV 1 PY 1993 VL 72 IS 9 SU S BP 2846 EP 2849 DI 10.1002/1097-0142(19931101)72:9+<2846::AID-CNCR2820721515>3.0.CO;2-3 PG 4 WC Oncology SC Oncology GA MD661 UT WOS:A1993MD66100013 PM 8402517 ER PT J AU FREI, E HOLDEN, SA GONIN, R WAXMAN, DJ TEICHER, BA AF FREI, E HOLDEN, SA GONIN, R WAXMAN, DJ TEICHER, BA TI ANTITUMOR ALKYLATING-AGENTS - IN-VITRO CROSS-RESISTANCE AND COLLATERAL SENSITIVITY STUDIES SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE CROSS RESISTANCE; COLLATERAL SENSITIVITY; ALKYLATING AGENTS ID BONE-MARROW SUPPORT; TUMOR-CELL-LINES; CANCER-CHEMOTHERAPY; CARCINOMA; TRANSPORT; INVITRO; CIS-DIAMMINEDICHLOROPLATINUM(II); MELPHALAN; MELANOMA; ANALOG AB Cell lines resistant to five antitumor alkylating agents (CDDP, PAM, 4-HC, HN2, and BCNU) were developed from five parental human tumor lines representative of solid tumors with a range of sensitivities to antitumor alkylating agents. The parental cell lines were SCC-25 squamous carcinoma of the head and neck, MCF7 breast carcinoma, SW2 small-cell lung cancer, SL6 non-small-cell lung carcinoma, and G3361 melanoma. Survival curves using colony formation as the endpoint were generated for each of the 25 cell lines to each of the five alkylating agents. Comparison of the drug concentrations that reduced the survival of the alkylating agent-resistant cell lines by 90% (IC90 values) with the IC90 values obtained for the corresponding parental cell lines was used as a measure of the resistance/sensitivity of the alkylating agent-resistant lines to each drug tested. Although cross-resistance among the alkylating agents was generally uncommon, several patterns of response emerged. Cross-resistance occurred in 27 of the 105 determinations and occurred most frequently in the cell lines in which resistance was developed to PAM (57%) or BCNU (38%). Cross-resistance to HN2 occurred most frequently. Collateral sensitivity was equally as common, occurring in 25 of the 105 determinations. Collateral sensitivity occurred most frequently in the cell lines made resistant to 4-HC. The 4-HC-resistant cell lines were most frequently collaterally sensitive to PAM and to BCNU. Cross-resistance developed most frequently in the MCF-7 breast carcinoma and SCC-25 squamous-cell carcinoma cell lines, whereas collateral sensitivity developed most frequently in the SW2 small-cell lung cancer line and the G3361 melanoma cell line and least frequently in the MCF-7 breast carcinoma cell line and the SL6 non-small-cell lung cancer cell line. The implication of these findings for the development of strategies for clinical treatment are discussed. C1 HARVARD UNIV,DANA FARBER CANC INST,BOSTON,MA 02115. FU PHS HHS [P01-38493] NR 56 TC 21 Z9 21 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 NOV PY 1993 VL 33 IS 2 BP 113 EP 122 DI 10.1007/BF00685328 PG 10 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA ME526 UT WOS:A1993ME52600003 PM 8261570 ER PT J AU BARSKY, AJ CLEARY, PD BRENER, J RUSKIN, JN AF BARSKY, AJ CLEARY, PD BRENER, J RUSKIN, JN TI THE PERCEPTION OF CARDIAC ACTIVITY IN MEDICAL OUTPATIENTS SO CARDIOLOGY LA English DT Article DE PALPITATION; CARDIAC AWARENESS; HOLTER MONITOR ID SOMATOSENSORY AMPLIFICATION; HYPOCHONDRIASIS; HEARTBEAT; ARRHYTHMIAS; SYMPTOMS; AWARENESS; STIMULI; ANXIETY AB This study compared several measures of cardiac perception and related them to patient' spontaneous reports of palpitations. One hundred and forty-five ambulatory patients referred for Holter monitoring for the evaluation of palpitations were compared with 70 asymptomatic nonpatients. Reports of palpitations during monitoring were compared with the ECG to determine whether they coincided with an arrhythmia. Subjects also completed a heartbeat detection task to determine whether they were accurately aware of cardiac systole while at rest. 20.7% of palpitation patients and 4.7% of asymptomatic controls demonstrated an accurate awareness of resting heartbeat (p = 0.01). Performance was unrelated to bodily amplification, somatization, hypochondriacal symptoms, ECG findings, or psychiatric morbidity. 34.3% of palpitation patients reported symptoms that consistently coincided with arrhythmias on ECG. These accurate patients had significantly lower levels of amplification, somatization, hypochondriacal symptoms, and psychiatric morbidity. Accuracy of symptom reporting and accuracy of heartbeat awareness were not statistically associated. Although accurate awareness of resting heartbeat appears to be unrelated to medical experiences and psychiatric status, the accurate perception of arrhythmias during daily activity is inversely correlated with clinical variables such as somatization and psychiatric distress. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. SUNY STONY BROOK,STONY BROOK,NY. MASSACHUSETTS GEN HOSP,MED SERV,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL43216] NR 49 TC 19 Z9 19 U1 2 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0008-6312 J9 CARDIOLOGY JI Cardiology PD NOV-DEC PY 1993 VL 83 IS 5-6 BP 304 EP 315 DI 10.1159/000175986 PG 12 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MT684 UT WOS:A1993MT68400003 PM 8111763 ER PT J AU MARGOLIS, HC ZHANG, YP VANHOUTE, J MORENO, EC AF MARGOLIS, HC ZHANG, YP VANHOUTE, J MORENO, EC TI EFFECT OF SUCROSE CONCENTRATION ON THE CARIOGENIC POTENTIAL OF POOLED PLAQUE FLUID FROM CARIES-FREE AND CARIES-POSITIVE INDIVIDUALS SO CARIES RESEARCH LA English DT Article DE CARIES; DEMINERALIZATION; PLAQUE FLUID; PLAQUE ID HUMAN DENTAL PLAQUE; AMINO-ACID PROFILES; SUSCEPTIBLE INDIVIDUALS; PH; ENAMEL AB Pooled plaque samples were obtained from (1) coronal surfaces of two groups of caries-free (CF) subjects, (2) coronal 'white-spot' surface areas of a group of caries-positive (CP) subjects, and (3) exposed, sound root surfaces of root caries-free (RCF) and root caries-positive (RCP) subjects. The plaque samples were obtained before and 3 min after a 1 min rinse with a 0.5, 1, 2, 5 and 10% sucrose solution. Plaque fluid was then isolated from each plaque sample by centrifugation and analyzed for inorganic ions, organic acids, and pH values. With increasing sucrose concentration: (1) plaque fluid pH and the degree of saturation (DS) with respect to tooth mineral decreased; (2) the pH and DS values of CP and RCP samples were consistently lower than those of CF and RCF samples, respectively; (3) plaque fluid lactic acid concentrations increased and were consistently higher in the CP and RCP samples than in the CF and RCF samples, respectively, and (4) plaque fluid lactic acid concentrations leveled off between 1 and 5% sucrose; this occurred at lower sucrose concentrations with CP and RCP samples than with CF and RCF samples, respectively. RCP samples contained consistently higher levels of mutans streptococci than RCF samples. The chemical composition of plaque fluids, following sucrose exposure, were found to correlate well with caries history. The observed differences in lactic acid concentrations in samples from CF and CP subjects are discussed with regard to differences in microbiological composition and possible differences in plaque permeability to sucrose. RP MARGOLIS, HC (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009, DE-07493, DE-03187] NR 17 TC 25 Z9 27 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0008-6568 J9 CARIES RES JI Caries Res. PD NOV-DEC PY 1993 VL 27 IS 6 BP 467 EP 473 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MK685 UT WOS:A1993MK68500004 PM 8281560 ER PT J AU FERRELL, MA DOHERTY, M ZUSMAN, RM NASH, IS AF FERRELL, MA DOHERTY, M ZUSMAN, RM NASH, IS TI TOTAL AORTIC OCCLUSION CAUSED BY SUSTAINED BALLOON INFLATION - A PREVIOUSLY UNREPORTED COMPLICATION OF INTRAAORTIC BALLOON COUNTERPULSATION SO CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS LA English DT Note DE COUNTERPULSATION; COMPLICATIONS; ACUTE LOWER-BODY ISCHEMIA ID ACUTE MYOCARDIAL-INFARCTION; LIMB ISCHEMIA; PUMP AB A case of acute lower-body ischemia 2 days following intraaortic balloon pump insertion is reported. Fluoroscopy revealed persistent balloon inflation throughout the cardiac cycle with distal aortic occlusion. Attempts to manually deflate the balloon were unsuccessful until a guidewire was advanced through the gas-exchange lumen into the body of the balloon. The balloon catheter was removed without clinical sequelae other than transient oliguria and an asymptomatic increase in creatinine phosphokinase (CPK). This is a previously unreported complication of intraaortic balloon counterpulsation. (C) 1993 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP FERRELL, MA (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,CARDIAC UNIT,KNIGHT CARDIAC CATHETERIZAT LAB,BULFINCH BASEMENT,BOSTON,MA 02114, USA. NR 9 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 0098-6569 J9 CATHETER CARDIO DIAG JI Catheter. Cardiovasc. Diagn. PD NOV PY 1993 VL 30 IS 3 BP 211 EP 213 DI 10.1002/ccd.1810300306 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MF123 UT WOS:A1993MF12300005 PM 8269491 ER PT J AU GUO, YJ MA, J WONG, JH LIN, SC CHANG, HC BIGBY, M SY, MS AF GUO, YJ MA, J WONG, JH LIN, SC CHANG, HC BIGBY, M SY, MS TI MONOCLONAL ANTI-CD44 ANTIBODY ACTS IN SYNERGY WITH ANTI-CD2 BUT INHIBITS ANTI-CD3 OR T-CELL RECEPTOR-MEDIATED SIGNALING IN MURINE T-CELL HYBRIDOMAS SO CELLULAR IMMUNOLOGY LA English DT Article ID LYMPHOCYTE-HOMING RECEPTOR; TRANSMEMBRANE GLYCOPROTEIN; B-CELLS; CD44; ACTIVATION; PGP-1; HYALURONATE; MOLECULE; BINDS; PROTEOGLYCAN C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. RP GUO, YJ (reprint author), CASE WESTERN RESERVE UNIV,SCH MED,INST PATHOL,2085 ADALBERT RD,CLEVELAND,OH 44106, USA. FU NIAID NIH HHS [R0-1 AI-27740]; NIAMS NIH HHS [AR-38018] NR 50 TC 35 Z9 37 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD NOV PY 1993 VL 152 IS 1 BP 186 EP 199 DI 10.1006/cimm.1993.1278 PG 14 WC Cell Biology; Immunology SC Cell Biology; Immunology GA MJ781 UT WOS:A1993MJ78100018 PM 7694807 ER PT J AU NOJIMA, Y HIROSE, T TACHIBANA, K TANAKA, T SHI, LK DOSHEN, J FREEMAN, GJ SCHLOSSMAN, SF MORIMOTO, C AF NOJIMA, Y HIROSE, T TACHIBANA, K TANAKA, T SHI, LK DOSHEN, J FREEMAN, GJ SCHLOSSMAN, SF MORIMOTO, C TI THE 4F9 ANTIGEN IS A MEMBER OF THE TETRA SPANS TRANSMEMBRANE PROTEIN FAMILY AND FUNCTIONS AS AN ACCESSORY MOLECULE IN T-CELL ACTIVATION AND ADHESION SO CELLULAR IMMUNOLOGY LA English DT Note ID HUMAN LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; SYNCYTIUM FORMATION; RECEPTOR COMPLEX; CD4 CELLS; EXPRESSION; CLONING; LFA-1; CD28; SUPERFAMILY RP NOJIMA, Y (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI29530, AI12609]; NIAMS NIH HHS [AR33713] NR 43 TC 51 Z9 52 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD NOV PY 1993 VL 152 IS 1 BP 249 EP 260 DI 10.1006/cimm.1993.1285 PG 12 WC Cell Biology; Immunology SC Cell Biology; Immunology GA MJ781 UT WOS:A1993MJ78100025 PM 8242765 ER PT J AU SUGITA, K TANAKA, T DOSHEN, JM SCHLOSSMAN, SF MORIMOTO, C AF SUGITA, K TANAKA, T DOSHEN, JM SCHLOSSMAN, SF MORIMOTO, C TI DIRECT DEMONSTRATION OF THE CD27 MOLECULE INVOLVED IN THE NEGATIVE REGULATORY EFFECT ON T-CELL ACTIVATION SO CELLULAR IMMUNOLOGY LA English DT Note ID GROWTH-FACTOR RECEPTOR; TUMOR-NECROSIS-FACTOR; ANTIGEN; EXPRESSION; CLONING; FAMILY; MEMBER; CDNA; DIFFERENTIATION; RECOGNITION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. RP SUGITA, K (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI29530, AI12609]; NIAMS NIH HHS [AR33713] NR 32 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD NOV PY 1993 VL 152 IS 1 BP 279 EP 285 DI 10.1006/cimm.1993.1288 PG 7 WC Cell Biology; Immunology SC Cell Biology; Immunology GA MJ781 UT WOS:A1993MJ78100028 PM 8242768 ER PT J AU KADHIM, HJ BHIDE, PG FROST, DO AF KADHIM, HJ BHIDE, PG FROST, DO TI TRANSIENT AXONAL BRANCHING IN THE DEVELOPING CORPUS-CALLOSUM SO CEREBRAL CORTEX LA English DT Article ID DEVELOPING VISUAL-CORTEX; FETAL RHESUS-MONKEY; PROJECTION NEURONS; WHITE MATTER; ASSOCIATION PROJECTIONS; TRANSITORY MACROPHAGES; POSTNATAL-DEVELOPMENT; REGRESSIVE EVENTS; GROWTH CONES; OPTIC-NERVE AB During development, there is a transient overproduction of axons in the corpus callosum; this overproduction of axons is due, in part, to a transient excess of neurons that send an axon through the corpus callosum. However, transient axonal branching could also contribute to the developmental overproduction of callosal axons. To investigate this possibility, we filled developing callosal axons in the Syrian hamster with the carbocyanine dye 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (Dill. Light microscopic analysis showed that, indeed, developing callosal axons branch transiently in the hamster: branching was robust on postnatal day [1 (PO) and P3 (PO = the first 24 hr after birth), less prominent on P6 and P8, and absent by P11. Immature callosal axons branched before or after crossing the midline and at all rostral-caudal and medial-lateral levels within the corpus callosum. The majority of callosal axon collaterals that were contained within individual 100-mu m-thick sections were relatively short (mean = 15.1 mu m) but some collaterals extended up to similar to 135 mu m from the main axon trunk before passing out of the section in which tNearly all of the collaterals emanated from the main axon trunk; higher-order collaterals were rare. Some callosal axon trunks had multiple collaterals. Branching callosal axons originated from multiple cortical areas, including area 17. Electron microscopic observations indicated that the processes designated as axon collaterals by light microscopic criteria would have been included in electron microscopic counts of developing callosal axons. Some callosal axon trunks and branches had ultrastructural features that suggested they were degenerating. In cats, developing callosal axons branch on embryonic day 57 (E57; the first 24 hr after conception = EO) and PO. Thus, it is likely that transient branching of immature callosal axons is a generalized feature of mammalian cortical development and that it contributes to the overproduction of callosal axons, albeit perhaps to varying degrees, in multiple species. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. OI Bhide, Pradeep/0000-0003-4236-9415 FU NEI NIH HHS [EY-03465] NR 42 TC 16 Z9 16 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 1047-3211 J9 CEREB CORTEX JI Cereb. Cortex PD NOV-DEC PY 1993 VL 3 IS 6 BP 551 EP 566 DI 10.1093/cercor/3.6.551 PG 16 WC Neurosciences SC Neurosciences & Neurology GA MP581 UT WOS:A1993MP58100004 PM 8136653 ER PT J AU KOSSLYN, SM DALY, PF MCPEEK, RM ALPERT, NM KENNEDY, DN CAVINESS, VS AF KOSSLYN, SM DALY, PF MCPEEK, RM ALPERT, NM KENNEDY, DN CAVINESS, VS TI USING LOCATIONS TO STORE SHAPE - AN INDIRECT EFFECT OF A LESION SO CEREBRAL CORTEX LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL BLOOD-FLOW; EXTRASTRIATE CORTEX; METABOLISM; STIMULI; DISSOCIATION; LOCALIZATION; RECOGNITION; PERFORMANCE; COMPONENTS AB This study had three general points. First, it examined possible visual consequences of frontal lesions. A patient with focal damage to the subcortical regions of the left frontal lobe, and a small amount of damage near Broca's area, was predicted to have impaired brain function in posterior regions that are anatomically connected to the damaged site. Second, it showed the utility of using positron emission tomography (PET) in conjunction with magnetic resonance imaging to characterize ''functional lesions.'' PET revealed reduced metabolism in posterior cortical loci that are innervated by fibers from the damaged regions. Some of the affected areas are hypothesized to be involved in visual functions, specifically the encoding of lines and edges. Third, a series of tests was designed to document that the patient had difficulty encoding visual stimuli, and then to distinguish among alternative possible causes of this deficit. The results suggested that the patient encoded shapes as sets of filled locations if possible, which allowed him to use intact processes subserved by brain areas that were not affected by the damage, The data were best explained if the lesion slowed processing in the ventral system (which encodes object properties), allowing the dorsal system (which encodes spatial properties) to produce a response more quickly than the ventral system. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,DEPT RADIOL,CAMBRIDGE,MA 02138. RP KOSSLYN, SM (reprint author), HARVARD UNIV,DEPT PSYCHOL,CAMBRIDGE,MA 02138, USA. RI Kennedy, David/H-3627-2012 NR 44 TC 17 Z9 17 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 1047-3211 J9 CEREB CORTEX JI Cereb. Cortex PD NOV-DEC PY 1993 VL 3 IS 6 BP 567 EP 582 DI 10.1093/cercor/3.6.567 PG 16 WC Neurosciences SC Neurosciences & Neurology GA MP581 UT WOS:A1993MP58100005 PM 8136654 ER PT J AU SHANNON, DC AF SHANNON, DC TI YOU SEE BUT YOU DO NOT OBSERVE SO CHEST LA English DT Editorial Material C1 HARVARD UNIV,MASSACHUSETTS INST TECHNOL,CAMBRIDGE,MA 02138. RP SHANNON, DC (reprint author), MASSACHUSETTS GEN HOSP,PULM UNIT,BOSTON,MA 02114, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD NOV PY 1993 VL 104 IS 5 BP 1320 EP 1321 DI 10.1378/chest.104.5.1320 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MF615 UT WOS:A1993MF61500004 PM 8222777 ER PT J AU XU, XP CHRISTIANI, DC AF XU, XP CHRISTIANI, DC TI OCCUPATIONAL EXPOSURES AND PHYSICIAN-DIAGNOSED ASTHMA SO CHEST LA English DT Article ID RESPIRATORY SYMPTOMS; BRONCHIAL REACTIVITY; GENERAL-POPULATION AB Data from a community-based random sample of 3,606 adults 40 to 69 years of age residing in Beijing, China, were used to examine the relationship between occupational exposures to dusts and gases/fumes and physician-diagnosed asthma. The prevalence of asthma was 3.9 percent for men and 3.8 percent for women. After adjusting for sex, age, education, residential areas, indoor coal combustion, and smoking status, the attributable risks of asthma were 1.7 percent and 1.2 percent for dust and gas/fume exposure, respectively. The adjusted odds ratios of asthma for dust and gas/fume exposed groups were 1.6 (95 percent confidence interval [CI], 1.1 to 2.2) and 1.4 (95 percent CI, 0. 9 to 2. 1), which were independent of sex and smoking status. When subjects were classified into none, dust-only, gas/fume-only, and both-exposure groups, the estimated odds ratios of asthma were 1.3 (95 percent CI, 0.9 to 2.1) in dust-only group, 0.9 (95 percent CI, 0.5 to 1.9) in fume-only group, and 2.1 (95 percent CI, 1.2 to 3.6) in both-exposure group, suggesting a combining effect of the two agents. There was an exposure-response relationship between dust and gas/fume exposures and asthma. In analysis of specific occupational agents, our findings are consistent with previously reported airway effects of organic dusts, but they also suggest that exposure to organic solvents may result in asthma, particularly when combined with dust. C1 MASSACHUSETTS GEN HOSP,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP XU, XP (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA 02115, USA. FU NIEHS NIH HHS [NIEHS ES00002] NR 28 TC 43 Z9 45 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD NOV PY 1993 VL 104 IS 5 BP 1364 EP 1370 DI 10.1378/chest.104.5.1364 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MF615 UT WOS:A1993MF61500016 PM 8222789 ER PT J AU KROENKE, K LAWRENCE, VA THEROUX, JF TULEY, MR HILSENBECK, S AF KROENKE, K LAWRENCE, VA THEROUX, JF TULEY, MR HILSENBECK, S TI POSTOPERATIVE COMPLICATIONS AFTER THORACIC AND MAJOR ABDOMINAL-SURGERY IN PATIENTS WITH AND WITHOUT OBSTRUCTIVE LUNG-DISEASE SO CHEST LA English DT Article ID PREOPERATIVE PULMONARY EVALUATION; SURGICAL PROCEDURES; RISK; SPIROMETRY; ANESTHESIA; PREDICTION AB Study objective: To determine the risk of thoracic and major abdominal surgery in patients with chronic obstructive pulmonary disease (COPD). Design: Retrospective cohort study with controls. Setting: A 692-bed teaching hospital. Patients: A cohort of 26 patients with severe COPD (FEV1 < 50 percent predicted) undergoing thoracic and major abdominal surgery was matched by age and type of operation to 52 patients with mild-moderate COPD and 52 patients with no COPD. Measurements and results: The 26 patients with severe COPD had rates of cardiac, vascular, and minor pulmonary complications similar to patients with mild-moderate COPD and without COPD, but experienced higher rates of serious pulmonary complications (23 percent vs 10 percent vs 4 percent, p = 0.03) and death (19 percent vs 4 percent vs 2 percent, p = 0.02). All deaths and instances of ventilatory failure in the patients with severe COPD occurred in the subset undergoing coronary artery bypass surgery. Logistic regression revealed that increased age, higher American Society of Anesthesiologists class, an abnormal chest radiograph, and perioperative bronchodilator administration were associated with higher cardiac or serious pulmonary complication rates. Spirometry was not an independent predictor of postoperative complications. Conclusions: Clinical variables appear better than preoperative spirometry in predicting postoperative cardiopulmonary complications. The utility of preoperative spirometry as well as the benefits of perioperative bronchodilators in patients in stable condition remain to be determined. C1 WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. RP KROENKE, K (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814, USA. NR 38 TC 100 Z9 107 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD NOV PY 1993 VL 104 IS 5 BP 1445 EP 1451 DI 10.1378/chest.104.5.1445 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MF615 UT WOS:A1993MF61500031 PM 8222804 ER PT J AU CASALE, LM SIEGEL, RE AF CASALE, LM SIEGEL, RE TI NEUROMUSCULAR BLOCKADE IN THE ICU SO CHEST LA English DT Letter RP CASALE, LM (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PULM & CRIT CARE MED,BRONX,NY, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD NOV PY 1993 VL 104 IS 5 BP 1639 EP 1640 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MF615 UT WOS:A1993MF61500084 PM 8222855 ER PT J AU ZOLDHELYI, P WEBSTER, MWI FUSTER, V GRILL, DE GASPAR, D EDWARDS, SJ CABOT, CF CHESEBRO, JH AF ZOLDHELYI, P WEBSTER, MWI FUSTER, V GRILL, DE GASPAR, D EDWARDS, SJ CABOT, CF CHESEBRO, JH TI RECOMBINANT HIRUDIN IN PATIENTS WITH CHRONIC, STABLE CORONARY-ARTERY DISEASE - SAFETY, HALF-LIFE, AND EFFECT ON COAGULATION PARAMETERS SO CIRCULATION LA English DT Article DE ANTITHROMBOTICS; THROMBOLYSIS; ATHEROSCLEROSIS; HIRUDIN; THROMBOSIS ID TICK ANTICOAGULANT PEPTIDE; THROMBIN INHIBITOR; MONOCLONAL-ANTIBODIES; PLATELET-AGGREGATION; HEPARIN-ANTITHROMBIN; VENOUS THROMBOSIS; BLEEDING-TIME; VESSEL WALL; PROTEIN-C; ANGIOPLASTY AB Background. Because the specific antithrombin hirudin prevents platelet-rich arterial thrombus and accelerates thrombolysis in a variety of animal models, it has promise as antithrombotic therapy. We therefore studied the half-life, effect on anticoagulant parameters, and safety of hirudin in patients with coronary artery disease. Methods and Results. Thirty-eight men and 1 woman (age [mean+/-SD], 60.4+/-6.9 years) with angiographic coronary disease were allocated in a single-blind ascending dosage study to a 6-hour IV infusion of recombinant hirudin (CGP 39 393) or matching placebo. The median terminal half-life for hirudin, measured by ELISA, was 2.7, 2.3, 2.9, 3.1, and 2.0 hours for the 0.02, 0.05, 0.1, 0.2, and 0.3 mg . kg-1 . h-1 groups, respectively. Activated partial thromboplastin times (aPTT) at 3, 4, and 6 hours were averaged into a plateau value. The aPTT plateau-to-baseline ratios were 1.5+/-0.1, 2.0+/-0.1, 2.3+/-0.1, 2.7+/-0.1, and 2.9+/-0.1, respectively, with hirudin infused at 0.02, 0.05, 0.1, 0.2, and 0.3 mg . kg-1 . h-1. From 62% to 77% of the aPTT plateau value was seen within 30 minutes of starting the infusions and was directly related to dose. The aPTT-to-baseline ratios correlated well with plasma hirudin levels (r=.88), whereas poor correlation and sensitivity were observed between plasma hirudin levels and activated coagulation time (ACT)-to-baseline ratios (r=.44). Plasma levels of hirudin and ACT in seconds correlated overall well (r=.80), but considerable overlap occurred between baseline ACT and ACT at plasma hirudin concentrations <1000 ng/mL. Prothrombin times were significantly prolonged only at a dosage of greater-than-or-equal-to 0.05 mg . kg-1 . h-1 and were 11.8+/-0.5 (INR=1.0), 12.3+/-0.7 (INR=1.1), 13.3+/-1.2 (INR=1.4), 14.2+/-0.4 (INR=1.7), and 15.8+/-0.9 (INR=2.3) seconds for each respective hirudin dosage. Thrombin times were beyond range (>600 seconds) at 6 hours in all except 2 patients who received the lowest dosage. All parameters returned to baseline between 8 and 18 hours after the infusion. Bleeding times were not significantly prolonged. No side effects occurred. No antibodies to hirudin were detected 2 weeks after the infusion. Conclusions. Recombinant hirudin has a terminal half-life of 2 to 3 hours. The aPTT correlates well with plasma levels of hirudin and allows close titration over a wide range of anticoagulation, while ACT and prothrombin time are relatively insensitive for monitoring hirudin administration. At anticoagulant levels effective in experimental thrombosis, a 6-hour infusion of hirudin is well tolerated and safe in a predominantly male group of patients with stable coronary atherosclerosis. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,JACKSON 1402,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV CARDIOVASC DIS & INTERNAL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CIBA GEIGY CORP,SUMMIT,NJ 07901. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 61 TC 97 Z9 100 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV PY 1993 VL 88 IS 5 BP 2015 EP 2022 PN 1 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ME833 UT WOS:A1993ME83300003 PM 8222093 ER PT J AU NARULA, J CHOPRA, P TALWAR, KK REDDY, KS VASAN, RS TANDON, R BHATIA, ML SOUTHERN, JF AF NARULA, J CHOPRA, P TALWAR, KK REDDY, KS VASAN, RS TANDON, R BHATIA, ML SOUTHERN, JF TI DOES ENDOMYOCARDIAL BIOPSY AID IN THE DIAGNOSIS OF ACTIVE RHEUMATIC CARDITIS SO CIRCULATION LA English DT Article DE RHEUMATIC HEART DISEASE; RHEUMATIC FEVER; PHARYNGITIS ID FEVER; MYOCARDITIS; AREA AB Background. Carditis is the only component of rheumatic fever that leads to permanent disability. The diagnosis of carditis is presently made by using composite clinical criteria based on the. revised Jones' criteria. Since myocardial involvement is ap important component of rheumatic carditis, right ventricular endomyocardial biopsies were performed in 54 patients with clinical acute rheumatic fever and quiescent rheumatic heart disease to evaluate the role of biopsy for the diagnosis of rheumatic carditis. Methods and Results. In 11 of the 54 patients, clinical consensus was certain about rheumatic fever and carditis based on the revised Jones' criteria (group 1). Histomorphological abnormalities in these patients were scarce. The diagnostic features of rheumatic myocarditis including Aschoff nodules or histiocytic aggregates were encountered in 3 patients (27%). Lymphocytic infiltration was sparse. A majority of patients demonstrated myocyte degeneration, interstitial degeneration, or occasional interstitial mononuclear cell infiltration, but since these histopathological lesions may occur in other conditions also, they were considered nondiagnostic. In 33 of the 54 patients with preexisting rheumatic heart disease, the diagnosis of carditis was suspected based on varied clinical presentations. Since previous cardiac findings were not available in these patients, the clinical diagnosis of carditis could not be made without equivocation (group 2). Twenty-three patients presented with unexplained acute onset of congestive heart failure and evidence of recent streptococcal infection (group 2A). While 13 of them had one or more other major manifestations, 10 patients had only minor manifestations. Mimetic carditis was suspected in the remaining 10 of 33 patients based on carditis having occurred in previous episodes of rheumatic fever (group 2B). The endomyocardial biopsy provided confirmatory evidence of rheumatic myocarditis in 9 patients of group 2A but in none of the 10 patients with suspected mimetic carditis. Nondiagnostic myocyte or interstitial alterations were frequently observed in group 2. Ten of the 54 patients had no clinical evidence of active carditis (group 3). No histological alterations diagnostic of rheumatic carditis were noted in these patients. Twenty-two follow-up biopsies were performed in the first 10 consecutive patients. Diagnostic histiocytic aggregates or Aschoff nodules were observed in initial biopsies in 4 of 10 patients, and nonspecific myocyte or interstitial alterations were observed in 9. All patients with diagnostic changes in initial biopsy demonstrated fibrohistiocytic nodules in 6- or 12-week biopsy samples. Nondiagnostic alterations, similar to those seen in acute cases, were present in 5 of 8 patients at 6 weeks, 5 of 8 patients at 12 weeks, and 3 of the 6 patients at 24 weeks despite the presumed adequate immunosuppressive therapy. No complications related to biopsy were encountered. Conclusions. The present study highlights the low frequency of diagnostic features in the biopsy specimens of patients with definite clinical rheumatic carditis. Although such alterations are not observed in patients with chronic rheumatic heart disease, endomyocardial biopsy does not appear to provide additional diagnostic information where clinical consensus is certain about diagnosis of rheumatic carditis. Our study, however, substantiates the concept of carditis underlying unexplained congestive heart failure of acute onset in patients with preexisting rheumatic heart disease and elevated antistreptolysin-O titers. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ALL INDIA INST MED SCI,NEW DELHI 110016,INDIA. OI Ramachandran, Vasan/0000-0001-7357-5970 NR 32 TC 41 Z9 42 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV PY 1993 VL 88 IS 5 BP 2198 EP 2205 PN 1 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ME833 UT WOS:A1993ME83300026 PM 8222115 ER PT J AU FIFER, MA LEE, JS HUTTER, AM BUCKLEY, MJ AF FIFER, MA LEE, JS HUTTER, AM BUCKLEY, MJ TI SYSTOLIC OBLITERATION OF THE LEFT ANTERIOR DESCENDING CORONARY-ARTERY SO CIRCULATION LA English DT Note C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT SURG,SURG CARDIOVASC UNIT,BOSTON,MA 02114. RP FIFER, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,WACC 478,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV PY 1993 VL 88 IS 5 BP 2437 EP 2437 PN 1 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ME833 UT WOS:A1993ME83300049 PM 8222136 ER PT J AU KNAPP, RG SCHREINER, PJ SUTHERLAND, SE KEIL, JE GILBERT, GE KLEIN, RL HAMES, C TYROLER, HA AF KNAPP, RG SCHREINER, PJ SUTHERLAND, SE KEIL, JE GILBERT, GE KLEIN, RL HAMES, C TYROLER, HA TI SERUM LIPOPROTEIN(A) LEVELS IN ELDERLY BLACK-AND-WHITE MEN IN THE CHARLESTON HEART-STUDY SO CLINICAL GENETICS LA English DT Article DE AGING; ETHNICITY; LIPOPROTEIN(A); LIPOPROTEINS ID LP(A) LIPOPROTEIN; MYOCARDIAL-INFARCTION; RISK FACTOR; DISEASE; PLASMA; CHILDREN; DENSITY AB Lipoprotein(a) [Lp(a)l is an important genetic trait associated with cardiovascular disease. While Lp(a) levels have been demonstrated to be approximately twice as high in black adults and children compared with whites, this relationship:has not been assessed in the elderly. During the 1987 recall of the Charleston Heart Study cohort, plasma Lp(a) [mg/dl] was measured on 113 white men and 83 black men. The average age of those having Lp(a) measurements was 71 years (+/-6) for white men and 72 years (+/-9) for black men. The distribution of Lp(a) was skewed in both whites (mean = 14.8, median = 8.2 mg/dl) and blacks (mean = 18.1, median = 12.8 mg/dl). The skewed distribution in elderly black men was in contrast to the bell-shaped distribution commonly reported for younger blacks. The Charleston Heart Study data suggest a shift to lower values among elderly as compared to younger men, with the greatest shift occurring among the black men. For black men who have survived to the 7th, 8th, and 9th decades of life, Lp(a) levels appear to be approaching the lower levels of white men. Despite this shift in distribution among black men, there remained a statistically significant difference in Lp(a) between racial groups. C1 UNIV N CAROLINA,DEPT EPIDEMIOL,CHAPEL HILL,NC. RALPH H JOHNSON VET ADM MED CTR,CHARLESTON,SC. CURTIS HAMES CLIN,CLAXTON,GA. RP KNAPP, RG (reprint author), MED UNIV S CAROLINA,DEPT BIOSTAT EPIDEMIOL & SYST SCI,CHARLESTON,SC 29425, USA. RI Gilbert, Gregory/C-7735-2016 OI Gilbert, Gregory/0000-0003-0879-5496 FU NHLBI NIH HHS [HL 31397] NR 33 TC 12 Z9 12 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD NOV PY 1993 VL 44 IS 5 BP 225 EP 231 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA MM211 UT WOS:A1993MM21100001 PM 8313620 ER PT J AU DORIA, A WARRAM, JH KROLEWSKI, AS AF DORIA, A WARRAM, JH KROLEWSKI, AS TI DNA REPORT SO CLINICAL GENETICS LA English DT Note ID HUMAN INSULIN-RECEPTOR; GENE C1 JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET SECT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. FU NIDDK NIH HHS [NIDDK/RO1 DK 41526, 5 P30 DK 36836] NR 4 TC 1 Z9 1 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD NOV PY 1993 VL 44 IS 5 BP 279 EP 280 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA MM211 UT WOS:A1993MM21100014 PM 7906213 ER PT J AU DEKEYSER, F TAKEI, M DANG, H DEKEYSER, H ISENBERG, DA TALAL, N AF DEKEYSER, F TAKEI, M DANG, H DEKEYSER, H ISENBERG, DA TALAL, N TI CHARACTERIZATION OF A CROSS-REACTIVE IDIOTYPE ON 2 HUMAN AUTOANTIBODIES ASSOCIATED WITH SYSTEMIC AUTOIMMUNE-DISEASE SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID ANTI-SM AUTOANTIBODY; LUPUS-ERYTHEMATOSUS; INTERSPECIES IDIOTYPE; RETROVIRAL PROTEINS; ANTIBODIES; SLE; IDIOTOPES; SEQUENCE; HEAVY; SERA C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. BLOOMSBURY RHEUMATOL UNIT,LONDON,ENGLAND. FU NIDCR NIH HHS [DE-09311] NR 23 TC 2 Z9 2 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 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD NOV PY 1993 VL 69 IS 2 BP 155 EP 160 DI 10.1006/clin.1993.1164 PG 6 WC Immunology; Pathology SC Immunology; Pathology GA MC285 UT WOS:A1993MC28500005 PM 7691456 ER PT J AU WHARTON, RH LEVINE, K JELLENIK, MS AF WHARTON, RH LEVINE, K JELLENIK, MS TI PEDIATRICIANS ROLE AFTER HOSPITAL-BASED DEATH AND PERMANENT DISABILITY IN SCHOOL-AGED CHILDREN SO CLINICAL PEDIATRICS LA English DT Note ID CHILDHOOD INJURIES; UNITED-STATES C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP WHARTON, RH (reprint author), SPAULDING REHABIL HOSP,125 NASHUA ST,BOSTON,MA 02114, USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 SN 0009-9228 J9 CLIN PEDIATR JI Clin. Pediatr. PD NOV PY 1993 VL 32 IS 11 BP 675 EP 680 DI 10.1177/000992289303201106 PG 6 WC Pediatrics SC Pediatrics GA MG957 UT WOS:A1993MG95700006 PM 8299298 ER PT J AU FRASER, RA ZAJAC, JD HARVEY, S AF FRASER, RA ZAJAC, JD HARVEY, S TI EXPRESSION OF PARATHYROID HORMONE-RELATED PEPTIDE GENE IN THE RAT HYPOTHALAMUS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY LA English DT Article ID HUMORAL HYPERCALCEMIA; CELL-LINE; PROTEIN; MALIGNANCY; GLANDS; IMMUNOREACTIVITY; TISSUES; PLASMA AB 1. Parathyroid hormone-related peptide (PTHrP), originally isolated from human malignant tumors, is present in a variety of normal mammalian tissues, including the brain. 2. The expression and translation of the PTHrP gene within the rat hypothalamus was demonstrated in this study by the specific hybridization of a 1.8 kb mRNA product with a PTHrP cDNA probe and by the crossreactivity of rat hypothalamic extracts in a PTHrP radioimmunoassay. 3. These results suggest roles for PTHrP in neural or hypophysiotropic regulation. C1 UNIV ALBERTA,DEPT PHYSIOL,EDMONTON T6G 2E1,ALBERTA,CANADA. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 27 TC 7 Z9 7 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0305-0491 J9 COMP BIOCHEM PHYS B JI Comp. Biochem. Physiol. B-Biochem. Mol. Biol. PD NOV PY 1993 VL 106 IS 3 BP 647 EP 650 DI 10.1016/0305-0491(93)90143-S PG 4 WC Biochemistry & Molecular Biology; Zoology SC Biochemistry & Molecular Biology; Zoology GA MD826 UT WOS:A1993MD82600024 PM 8281759 ER PT J AU CONN, AKT AF CONN, AKT TI OUTCOME OF THE ELDERLY AFTER OUT-OF-HOSPITAL CARDIAC-ARREST SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE CARDIAC ARREST; CARDIOPULMONARY EMERGENCIES; CARDIOPULMONARY RESUSCITATION; PREHOSPITAL EMERGENCY CARE RP CONN, AKT (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD NOV PY 1993 VL 21 IS 11 BP 1619 EP 1619 DI 10.1097/00003246-199311000-00001 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA MF983 UT WOS:A1993MF98300001 PM 8222669 ER PT J AU KARLSSON, JOM CRAVALHO, EG TONER, M AF KARLSSON, JOM CRAVALHO, EG TONER, M TI INTRACELLULAR ICE FORMATION - CAUSES AND CONSEQUENCES SO CRYO-LETTERS LA English DT Article ID DROSOPHILA-MELANOGASTER EMBRYOS; ISOLATED PROTOPLASTS; COLD-ACCLIMATION; FREEZING-INJURY; NUCLEATION; CELLS; CRYOSURGERY; HEPATOCYTES; TRANSPORT; OOCYTES C1 SHRINERS BURN INST,RES CTR,CAMBRIDGE,MA 02139. MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,SURG RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02114. NR 71 TC 58 Z9 59 U1 2 U2 7 PU CRYO LETTERS PI CAMBRIDGE PA 7 WOOTTON WAY, CAMBRIDGE, CAMBS, ENGLAND CB3 9LX SN 0143-2044 J9 CRYO-LETT JI Cryo-Lett. PD NOV-DEC PY 1993 VL 14 IS 6 BP 323 EP 336 PG 14 WC Biology; Physiology SC Life Sciences & Biomedicine - Other Topics; Physiology GA MK361 UT WOS:A1993MK36100001 ER PT J AU KUSHWAHA, S FUSTER, V AF KUSHWAHA, S FUSTER, V TI THE NEED FOR CORONARY SURGERY IN 1993 SO CURRENT OPINION IN CARDIOLOGY LA English DT Article AB Coronary surgery remains an important therapeutic option for coronary revascularization, particularly in the elderly with coronary disease, in whom recent studies have demonstrated improvement of quality of life and long-term survival compared with medical treatment. Morbidity and mortality in the elderly may be predicted by stratification of preoperative risk factors into scoring systems. Interim results from multicenter trials comparing coronary surgery and coronary angioplasty for the treatment of multivessel coronary disease suggest that coronary surgery may be better for symptom relief in angina, with fewer hospital admissions and therapeutic interventions. Surgery for single- or double-vessel disease is appropriate when initial attempts at revascularization by coronary angioplasty have failed. Coronary surgery may be a therapeutic option in the treatment of cardiogenic shock, particularly in the presence of three-vessel disease or the presence of complex lesions not amenable to angioplasty. Long-term survival after myocardial infarction may be improved by revascularization of the infarct-related artery. Recent studies of myocardial viability have examined the use of positron-emission tomography scanning to determine which patients may benefit most from myocardial revascularization. RP KUSHWAHA, S (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BULLFINCH 105,BOSTON,MA 02114, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 0 TC 1 Z9 1 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0268-4705 J9 CURR OPIN CARDIOL JI Curr. Opin. Cardiol. PD NOV PY 1993 VL 8 IS 6 BP 889 EP 896 DI 10.1097/00001573-199311000-00001 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MG147 UT WOS:A1993MG14700001 PM 10146518 ER PT J AU WALKER, WA AF WALKER, WA TI IMMUNOLOGY SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Editorial Material RP WALKER, WA (reprint author), MASSACHUSETTS GEN HOSP EAST,MUCOSAL IMMUNOL LAB,149 13TH ST,BOSTON,MA 02129, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD NOV PY 1993 VL 9 IS 6 BP 943 EP 945 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ME054 UT WOS:A1993ME05400009 ER PT J AU ACHIM, CL MINERS, DK BURROLA, PG MARTIN, FC WILEY, CA AF ACHIM, CL MINERS, DK BURROLA, PG MARTIN, FC WILEY, CA TI IN-VIVO MODEL OF HIV-INFECTION OF THE HUMAN BRAIN SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE CENTRAL NERVOUS SYSTEM, FETAL; HIV, IN VIVO; MACROPHAGE; SCID MICE ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY-SYNDROME; AIDS DEMENTIA COMPLEX; DISEASE; NEUROPATHOLOGY; MACROPHAGES; PATHOLOGY AB Approximately one quarter of the AIDS patients have severe HIV encephalitis with diffuse neuronal damage that may be mediated by immune factors secreted by CNS macrophages. Based on an in vitro brain microsphere model, we developed an in vivo system in which human embryonic brain tissue survives for several months in the interscapular fat pad of SCID mice. Coculture of human brain tissue with macrophages prior to transplantation resulted in infiltration of the microspheres by activated macrophages. When the macrophages were infected in vitro with a neurotropic HIV strain, viral particles were detected in vivo up to 3 months after transplantation. HIV-infected transplants contained multinucleated giant cells similar to those seen in HIV encephalitis. However, the neuroglial component degenerated in the fat pad of SCID mice. The absence of synaptogenesis in the human transplants suggests that the murine fat pad lacks adequate stimuli or support for human neuronal differentiation. To study neurologic damage associated with HIV infection, sites of implantation that stimulate synaptogenesis (e.g. murine CNS) will need to be explored. Based on these findings we conclude that transplantation of brain microspheres with HIV-infected macrophages into SCID mice may be an achievable model of HIV encephalitis. C1 UNIV PITTSBURGH,MED CTR,DIV NEUROPATHOL,PITTSBURGH,PA. UNIV CALIF SAN DIEGO,DEPT PATHOL,LA JOLLA,CA 92093. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. FU NIMH NIH HHS [MH43298, MH45294]; NINDS NIH HHS [NS-2578] NR 18 TC 9 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PD NOV-DEC PY 1993 VL 15 IS 6 BP 423 EP 432 DI 10.1159/000111368 PG 10 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA PM203 UT WOS:A1993PM20300006 PM 7835248 ER PT J AU DELAHANTY, LM HALFORD, BN AF DELAHANTY, LM HALFORD, BN TI THE ROLE OF DIET BEHAVIORS IN ACHIEVING IMPROVED GLYCEMIC CONTROL IN INTENSIVELY TREATED PATIENTS IN THE DIABETES CONTROL AND COMPLICATIONS TRIAL SO DIABETES CARE LA English DT Article ID SELF-CARE; EDUCATION AB OBJECTIVE- To determine whether specific diet-related behaviors practiced by IDDM patients in the intensive treatment group of the Diabetes Control and Complications Trial were associated with lower HbA1c values. RESEARCH DESIGN AND METHODS- A questionnaire addressing various aspects of their dietary behavior during the previous year in the DCCT was completed by 623 DCCT intensive treatment group subjects. The association between self-reported diet behaviors and the subject's mean HbA1c during the previous year was evaluated using a linear rank test for trend. The goal of intensive treatment was to achieve blood glucose and HbA1c levels as close to the nondiabetic range as possible without hypoglycemia. RESULTS- Adherence to the prescribed meal plan and adjusting food and/or insulin in response to hyperglycemia were significantly associated with lower HbA1c levels. Over-treating hypoglycemia and consuming extra snacks beyond the meal plan were associated with higher HbA1c levels. Adjusting insulin dose for meal size and content and consistent consumption of an evening snack were associated, albeit to a lesser degree, with lower HbA1c. CONCLUSIONS- The average HbA1c among intensively managed patients who reported that they followed specific diet-related behaviors was 0.25 to 1.0 lower than among subjects who did not follow these behaviors. Health-care providers may wish to use these results to focus clinical care for intensively treated IDDM patients by emphasizing counseling on meal plans, prompt response to high blood glucose levels, appropriate treatment of hypoglycemia, and consistent snacking behaviors. C1 JOSLIN DIABET CTR, DIABET CONTROL & COMPLICAT TRIAL, BOSTON, MA USA. RP DELAHANTY, LM (reprint author), MASSACHUSETTS GEN HOSP, DEPT DIETET, DIABET CONTROL & COMPLICAT TRIAL, BOSTON, MA 02114 USA. NR 25 TC 134 Z9 140 U1 1 U2 5 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 EI 1935-5548 J9 DIABETES CARE JI Diabetes Care PD NOV PY 1993 VL 16 IS 11 BP 1453 EP 1458 DI 10.2337/diacare.16.11.1453 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MD404 UT WOS:A1993MD40400005 PM 8299434 ER PT J AU HOLZ, GG LEECH, CA KUHTREIBER, WM HABENER, JF AF HOLZ, GG LEECH, CA KUHTREIBER, WM HABENER, JF TI GLUCAGON-LIKE PEPTIDE-1 AND GLUCOSE - BIDIRECTIONAL SIGNAL-TRANSDUCTION CROSS-TALK AND THE GLUCOSE COMPETENCE CONCEPT SO DIGESTION LA English DT Article; Proceedings Paper CT International Symposium on Glucagon-Like Peptide-1 CY MAY 17-19, 1993 CL COPENHAGEN, DENMARK SP NOVO NORDISK, BAYER AG RP HOLZ, GG (reprint author), HARVARD MED SCH,MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. RI Holz, George/A-3386-2012 NR 3 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0012-2823 J9 DIGESTION JI Digestion PD NOV-DEC PY 1993 VL 54 IS 6 BP 351 EP 351 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MN780 UT WOS:A1993MN78000014 ER PT J AU HABENER, JF MCMANUS, K NATHAN, DM AF HABENER, JF MCMANUS, K NATHAN, DM TI INSULINOTROPIC ACTIONS OF GLUCAGON-LIKE PEPTIDE-1(7-37) IN DIABETIC AND NONDIABETIC SUBJECTS SO DIGESTION LA English DT Article; Proceedings Paper CT International Symposium on Glucagon-Like Peptide-1 CY MAY 17-19, 1993 CL COPENHAGEN, DENMARK SP NOVO NORDISK, BAYER AG ID HORMONE; CELLS C1 MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. RP HABENER, JF (reprint author), MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. NR 9 TC 1 Z9 1 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0012-2823 J9 DIGESTION JI Digestion PD NOV-DEC PY 1993 VL 54 IS 6 BP 376 EP 377 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MN780 UT WOS:A1993MN78000033 ER PT J AU DYKE, MM EARNHARDT, R HANKS, JB PRUETT, T MINAKER, KL HABENER, JF ANDERSEN, DK GINGERICH, RL ELAHI, D AF DYKE, MM EARNHARDT, R HANKS, JB PRUETT, T MINAKER, KL HABENER, JF ANDERSEN, DK GINGERICH, RL ELAHI, D TI INSULINOTROPIC EFFECT OF GLP-1(7-37) IN PORTALLY OR SYSTEMICALLY DRAINED PANCREAS TRANSPLANT PATIENTS SO DIGESTION LA English DT Article; Proceedings Paper CT International Symposium on Glucagon-Like Peptide-1 CY MAY 17-19, 1993 CL COPENHAGEN, DENMARK SP NOVO NORDISK, BAYER AG C1 HARVARD UNIV,BETH ISRAEL HOSP,THORNDIKE LAB,DIV GERONTOL,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA. UNIV CHARLOTTSVILLE,DEPT SURG,CHARLOTTESVILLE,VA. UNIV CHICAGO,PRITZKER SCH MED,DEPT SURG,CHICAGO,IL 60637. UNIV CHICAGO,PRITZKER SCH MED,DEPT MED,CHICAGO,IL 60637. BARNES HOSP,ST LOUIS,MO 63110. RP DYKE, MM (reprint author), HARVARD UNIV,SCH MED,CHARLES A DANA RES INST,DIV AGING,BOSTON,MA 02215, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0012-2823 J9 DIGESTION JI Digestion PD NOV-DEC PY 1993 VL 54 IS 6 BP 390 EP 392 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MN780 UT WOS:A1993MN78000045 ER PT J AU DEMULDER, A TAKAHASHI, S SINGER, FR HOSKING, DJ ROODMAN, GD AF DEMULDER, A TAKAHASHI, S SINGER, FR HOSKING, DJ ROODMAN, GD TI ABNORMALITIES IN OSTEOCLAST PRECURSORS AND MARROW ACCESSORY CELLS IN PAGETS-DISEASE SO ENDOCRINOLOGY LA English DT Article ID MULTINUCLEATED CELLS; PROGENITOR CELLS; BONE-MARROW; CULTURES; INTERLEUKIN-6 AB Paget's disease of bone is characterized by increased numbers of abnormal osteoclasts. To determine if osteoclast precursors were increased or abnormal in this disease, we examined CFU-GM, the committed granulocyte-macrophage progenitor and the most likely precursor for osteoclasts. In cultures of unfractionated marrow mononuclear cells, CFU-GM colony formation was significantly increased in Paget's marrow cultures compared to that in normal cells (356 +/- 44 vs. 271 +/- 15/10(5) cells; P < 0.05). However, when we enriched hematopoietic precursors from Paget's and normal marrow samples using an antibody that recognizes the CD34 antigen present on most hematopoietic precursors, we found that similar numbers of CFU-GM colonies were formed (87 +/- 13/10(4) cells plated vs. 83 +/- 13). Coculture experiments with highly purified hematopoietic precursors (CD34+ cells) and non-hematopoietic marrow accessory cells (CD34- cells) revealed that the growth of Paget's precursors was significantly enhanced above expected levels by normal or Pagetic CD34- cells (P < 0.05). CFU-GM colony formation was also significantly enhanced when normal CD34+ cells were cocultured with Pagetic, but not with normal, CD34- cells. In addition, CFU-GM colony-derived cells from Paget's patients were hyperresponsive to 1,25-dihydroxyvitamin D3 and could form osteoclast-like multinucleated cells with 1,25-dihydroxyvitamin D3 concentrations one tenth of that required for normal multinucleated formation (10(-11) vs. 10(-10) m). These data suggest that osteoclast precursors may be abnormal in Paget's disease, and other cells in the Pagetic marrow microenvironment may further enhance the growth and differentiation of these abnormal precursors. C1 VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. CEDARS SINAI MED CTR,LOS ANGELES,CA 90404. CITY HOSP NOTTINGHAM,NOTTINGHAM NG5 1PD,ENGLAND. FU NCI NIH HHS [NCI CA-40035]; NIADDK NIH HHS [NIDDK AM-35188]; NIAMS NIH HHS [NIDDK AR39539] NR 13 TC 49 Z9 49 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1993 VL 133 IS 5 BP 1978 EP 1982 DI 10.1210/en.133.5.1978 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ME080 UT WOS:A1993ME08000009 PM 7691583 ER PT J AU TSUANG, MT FARAONE, SV LYONS, MJ AF TSUANG, MT FARAONE, SV LYONS, MJ TI IDENTIFICATION OF THE PHENOTYPE IN PSYCHIATRIC GENETICS SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE LA English DT Review DE GENETICS; NOSOLOGY; METHODOLOGY; LINKAGE ANALYSIS ID FAMILIAL ALZHEIMERS-DISEASE; AMYLOID PRECURSOR PROTEIN; ATTENTION-DEFICIT DISORDER; DSM-III-R; MAJOR AFFECTIVE-DISORDERS; EYE-MOVEMENT DYSFUNCTION; COMPLEX DISEASES; DNA MARKERS; HYPERACTIVITY DISORDER; SPORADIC SCHIZOPHRENIA AB Statistical procedures and molecular genetic techniques have attained a fine degree of resolution. Their ability to find disease genes has revolutionized medicine and raised hopes for breakthroughs in psychiatry. However, such breakthroughs may require an equally discriminating nosology. A psychiatric genetic nosology seeks to classify patients into categories that correspond to distinct genetic entities by addressing the problem of diagnostic accuracy: the degree to which a diagnosis correctly classifies people with and without a putative genetic illness. We review methods that deal with misclassification in genetic studies. These are clinical and epidemiological approaches that deal directly with how to define the observable manifestation of a putative genotype. We discuss two groups of methods: those that use known phenotypes and those that design new phenotypes. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. BOSTON UNIV,DEPT PSYCHOL,BOSTON,MA 02215. RP TSUANG, MT (reprint author), HARVARD UNIV,SCH MED,BROCKTON W ROXBURY VET AFFAIRS MED CTR,DEPT PSYCHIAT,940 BELMONT ST,BROCKTON,MA 02401, USA. RI Lyons, Michael/B-6119-2011; OI Lyons, Michael/0000-0001-6516-9219; Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [1 R01MH41874-01, 1 R37MH43518-01, 5 UO1 MH46318-02] NR 116 TC 119 Z9 120 U1 3 U2 4 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0940-1334 J9 EUR ARCH PSY CLIN N JI Eur. Arch. Psych. Clin. Neurosci. PD NOV PY 1993 VL 243 IS 3-4 BP 131 EP 142 DI 10.1007/BF02190719 PG 12 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MG699 UT WOS:A1993MG69900003 PM 8117756 ER PT J AU MATTIA, AR DOERN, GV CLARK, J HOLDEN, J WU, L FERRARO, MJ AF MATTIA, AR DOERN, GV CLARK, J HOLDEN, J WU, L FERRARO, MJ TI COMPARISON OF 4 METHODS IN THE DIAGNOSIS OF CLOSTRIDIUM-DIFFICILE DISEASE SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Note ID LATEX AGGLUTINATION-TEST; TOXIN-A; ENZYME-IMMUNOASSAY; REACTIVE PROTEIN AB Nine hundred forty-five stool specimens from patients suspected of having,ing Clostridium difficile disease were examined using a cell culture cytotoxicity assay (CTA), two enzyme immunoassay (EIA) kits (Cytoclone for toxins A and B; VIDAS for toxin A) and a latex agglutination assay (CDT). One hundred nineteen specimens had positive titers (greater than or equal to 90) in the CTA; clinical review of 16 discordant samples and 49 controls supported the significance of 90 as the positive cut-off titer. The performance of the two EIAs and the latex assay was assessed relative to CTA titers of the samples. Sensitivity was less than or equal to 50% for all three assays for the 24 specimens with CTA titers of 90, but it reached 97-100% for the two EIAs and 84% for the latex assay at titers of greater than or equal to 2,250. The Cytoclone EIA exhibited higher sensitivity at the lower positive titers. Overall, specificity of the methods ranged from 96.7% (CDT latex assay)to 99.1% (Cytoclone EIA). C1 UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA. HARVARD UNIV,SCH MED,BOSTON,MA. RP MATTIA, AR (reprint author), MASSACHUSETTS GEN HOSP,CLIN MICROBIOL LABS,GRAY 5,BOSTON,MA 02114, USA. NR 15 TC 19 Z9 19 U1 0 U2 0 PU FRIEDR VIEWEG SOHN VERLAG GMBH PI WIESBADEN 1 PA PO BOX 5829, W-6200 WIESBADEN 1, GERMANY SN 0934-9723 J9 EUR J CLIN MICROBIOL JI Eur. J. Clin. Microbiol. Infect. Dis. PD NOV PY 1993 VL 12 IS 11 BP 882 EP 886 DI 10.1007/BF02000416 PG 5 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA MM849 UT WOS:A1993MM84900017 PM 8112366 ER PT J AU RODRIGUEZ, CL NUEDA, A GROSPIERRE, B SANCHEZMADRID, F FISCHER, A SPRINGER, TA CORBI, AL AF RODRIGUEZ, CL NUEDA, A GROSPIERRE, B SANCHEZMADRID, F FISCHER, A SPRINGER, TA CORBI, AL TI CHARACTERIZATION OF 2 NEW CD18 ALLELES CAUSING SEVERE LEUKOCYTE ADHESION DEFICIENCY SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE ADHESION DEFICIENCY; BETA(2) INTEGRIN; CD18 ID CELL-SURFACE EXPRESSION; MOLECULAR-BASIS; MESSENGER-RNA; BETA-SUBUNIT; GLANZMANN THROMBASTHENIA; NONSENSE MUTATIONS; RECEPTOR GENE; LFA-1; IDENTIFICATION; P150,95 AB Leukocyte adhesion deficiency (LAD) is an autosomal recessive disease caused by heterogeneous mutations within the gene encoding the common beta subunit (CD18) of the three leukocyte integrins LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18), and p150,95 (CD11c/CD18). Based on the level of expression of CD18 on patient leukocytes, two phenotypes of LAD have been defined (severe and moderate) which correlate with the severity of the disease. We have investigated the molecular basis of the disease in two unrelated severe patients (HS and ZJO). Both patients share a complete absence of CD18 protein precursor and cell surface expression, but they differ in the level of CD18 mRNA, which is normal in HS and undetectable by Northern blot in ZJO. Determination of the primary structure of the patient HS CD18 mRNA revealed a 10-base pair deletion between nucleotides 190-200 (CD18 exon 3),which eliminates residues 41-43 and causes a frameshift into a premature termination codon 17 base pairs downstream from the deleted region. The 10-base pair frameshift deletion maps to a region of the CD18 gene where aberrant mRNA processing has been detected in HS and two other unrelated LAD patients. In the ZJO patient, amplification of lymphoblast CD18 mRNA demonstrated the presence of a non-sense mutation in the third nucleotide of the triplet encoding Cys(534) (TGC --> TGA),within exon 12. Both genetic abnormalities were also detected at the genomic level, and affect the restriction pattern of their corresponding genes, thus enabling the detection of the mutant alleles among healthy heterozygous alleles in family studies. The identification of two new LAD CD18 alleles, either carrying a non-sense mutation (ZJO) or a partial gene deletion (HS), further illustrates the heterogeneity of the genetic alterations in LAD. C1 HOSP LA PRINCESA,UNIDAD BIOL MOLEC PLANTA 9,E-28006 MADRID,SPAIN. HOSP LA PRINCESA,SECC INMUNOL,E-28006 MADRID,SPAIN. HOP NECKER ENFANTS MALAD,INSERM,U132,F-75743 PARIS,FRANCE. HARVARD UNIV,CTR BLOOD RES,SCH MED,BOSTON,MA. RI Lopez-Rodriguez, C/G-4482-2014; Corbi, Angel/B-7194-2011; Sanchez-Madrid, Francisco/M-7889-2016 OI Lopez-Rodriguez, C/0000-0002-2311-2406; Corbi, Angel/0000-0003-1980-5733; Sanchez-Madrid, Francisco/0000-0001-5303-0762 NR 40 TC 15 Z9 15 U1 0 U2 1 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD NOV PY 1993 VL 23 IS 11 BP 2792 EP 2798 DI 10.1002/eji.1830231111 PG 7 WC Immunology SC Immunology GA MH526 UT WOS:A1993MH52600010 ER PT J AU BROWN, RH AF BROWN, RH TI MUTATIONS IN CU/ZN SUPEROXIDE-DISMUTASE (SOD1) ARE ASSOCIATED WITH FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS (ALS) SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DAY NEUROMUSCULAR RES LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 471 EP 471 DI 10.1016/0891-5849(93)90187-Y PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700002 ER PT J AU GULATI, S DHAUNSI, GS SINGH, AK ORAK, JK SINGH, I AF GULATI, S DHAUNSI, GS SINGH, AK ORAK, JK SINGH, I TI EFFECT OF CIPROFIBRATE ON PEROXISOMAL ANTIOXIDANT-ENZYME SYSTEM IN RAT-LIVER SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,CHARLESTON,SC 29403. NR 0 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 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 505 EP 505 DI 10.1016/0891-5849(93)90316-M PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700132 ER PT J AU SINGH, AK GULATI, S SINGH, I AF SINGH, AK GULATI, S SINGH, I TI ISCHEMIA-REPERFUSION ALTERATIONS IN THE STRUCTURE-FUNCTION OF PEROXISOMES SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,DEPT PATHOL,CHARLESTON,SC 29403. NR 0 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 522 EP 522 DI 10.1016/0891-5849(93)90380-D PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700194 ER PT J AU SINGH, I DHAUNSI, GS ORAK, JK SINGH, AK AF SINGH, I DHAUNSI, GS ORAK, JK SINGH, AK TI ANTIOXIDANT ENZYME-SYSTEM IN PEROXISOMES SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,DEPT PATHOL,CHARLESTON,SC 29403. 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 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 536 EP 536 DI 10.1016/0891-5849(93)90429-X PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700245 ER PT J AU GULATI, S SINGH, I ORAK, JK SINGH, AK AF GULATI, S SINGH, I ORAK, JK SINGH, AK TI EXPRESSION OF ANTIOXIDANT ENZYMES IN RAT-KIDNEY DURING ISCHEMIA-REPERFUSION INJURY SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,DEPT PATHOL,CHARLESTON,SC 29403. NR 0 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 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 545 EP 545 DI 10.1016/0891-5849(93)90462-4 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700277 ER PT J AU DIGNASS, AU PODOLSKY, DK AF DIGNASS, AU PODOLSKY, DK TI CYTOKINE MODULATION OF INTESTINAL EPITHELIAL-CELL RESTITUTION - CENTRAL ROLE OF TRANSFORMING GROWTH-FACTOR-BETA SO GASTROENTEROLOGY LA English DT Article ID INVITRO MODEL; EXPRESSION; ENTEROCYTE; MIGRATION; RECEPTOR; CULTURE; ACID; PROLIFERATION; LOCALIZATION; INJURY C1 MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,JACKSON 7,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NERPRC CTR STUDY INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 41557, DK 43351] NR 37 TC 391 Z9 393 U1 0 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD NOV PY 1993 VL 105 IS 5 BP 1323 EP 1332 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ME594 UT WOS:A1993ME59400009 PM 8224636 ER PT J AU BARSKY, AJ AF BARSKY, AJ TI A RESEARCH AGENDA FOR OUTPATIENT CONSULTATION-LIAISON PSYCHIATRY SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article AB Primary care settings are increasingly important sites for psychiatric research. A broader range of many psychiatric disorders is encountered here than in the mental health arena, and their study will therefore provide us with a more representative picture of the true nature of these disorders. This is also the setting in which to investigate the medical care process itself, including such phenomena as nonadherence with the medical regimen, patient delay before seeking appropriate medical attention, the placebo phenomenon, patient satisfaction, and the nature of the doctor-patient relationship. Much of primary care practice consists of the management and palliation of somatic symptoms, yet the phenomenology of somatic symptoms has barely been investigated. Outpatient psychiatric researchers are in an ideal position to study the entire process of symptom perception, formation, experience, and reporting, including the phenomenon of somatization. However, ambulatory medical settings impose particular constraints and demands upon consultation-liaison researchers. They may be met with indifference and even suspicion, and in turn they too often fail to appreciate the nature of the primary care setting and the research questions that are important to primary care providers, whose interest and involvement must be enlisted from the outset. Consultation-liaison researchers must acquire the substantive skills, knowledge, and techniques that are demanded by this type of research, because this work must be rigorous and of high caliber. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP BARSKY, AJ (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,WARREN 631,FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL43216]; NIMH NIH HHS [MH40487] NR 7 TC 10 Z9 10 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD NOV PY 1993 VL 15 IS 6 BP 381 EP 385 DI 10.1016/0163-8343(93)90006-A PG 5 WC Psychiatry SC Psychiatry GA MM995 UT WOS:A1993MM99500006 PM 8112561 ER PT J AU CANNISTRA, SA AF CANNISTRA, SA TI UNTITLED SO GYNECOLOGIC ONCOLOGY LA English DT Letter ID OVARIAN-CANCER; 2ND-LOOK RP CANNISTRA, SA (reprint author), DANA FARBER CANC INST,DIV MED ONCOL,PROGRAM GYNECOL ONCOL,BOSTON,MA 02115, USA. NR 3 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 NOV PY 1993 VL 51 IS 2 BP 292 EP 294 PG 3 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA MQ993 UT WOS:A1993MQ99300039 PM 8276314 ER PT J AU WILENS, TE BIEDERMAN, J AF WILENS, TE BIEDERMAN, J TI PSYCHOPATHOLOGY IN PREADOLESCENT CHILDREN AT HIGH-RISK FOR SUBSTANCE-ABUSE - A REVIEW OF THE LITERATURE SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review ID 15-YEAR FOLLOW-UP; ILLICIT DRUG-USE; PSYCHIATRIC-DISORDERS; PARENTAL ALCOHOLISM; YOUNG ADULTHOOD; PERSONALITY-CHARACTERISTICS; CHILDHOOD PERSONALITY; DIFFICULT TEMPERAMENT; BEHAVIORAL-INHIBITION; ENVIRONMENTAL-FACTORS AB Despite the high prevalence of the psychoactive substance use disorders (PSUDs), relatively little is known about the childhood antecedents of these disorders. To examine this issue a comprehensive review of the English-language literature on studies of preadolescents (< 12 years) who subsequently developed PSUDs or were offspring of parents with PSUDs was undertaken. In all, nine longitudinal studies and 13 cross-sectional studies were identified. Data from studies of subjects at high risk for PSUDs indicate that children of parents with PSUDs are at increased risk for the development of temperamental, personality, non-PSUD psychiatric, cognitive, and psychosocial disturbances. Longitudinal studies also indicate that children with these neuropsychiatric disturbances are at increased risk for the development of PSUDs in adolescence and adulthood. We conclude that neuropsychiatrically impaired children of parents with PSUDs may represent those ot highest risk for later development of PSUDs. Because these neuropsychiatric disorders are potentially treatable, their identification may lead to effective early intervention strategies. C1 MASSACHUSETTS GEN HOSP, DEPT PSYCHIAT, PEDIAT PSYCHOPHARMACOL CLIN, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. NR 123 TC 34 Z9 34 U1 5 U2 6 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD NOV-DEC PY 1993 VL 1 IS 4 BP 207 EP 218 DI 10.3109/10673229309017081 PG 12 WC Psychiatry SC Psychiatry GA MU382 UT WOS:A1993MU38200002 PM 9384850 ER PT J AU HAMBURG, P STELOVICH, S SABIN, J AF HAMBURG, P STELOVICH, S SABIN, J TI MANAGING THERAPEUTIC DESPAIR SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article ID BORDERLINE PATIENTS C1 DEACONESS HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 10 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD NOV-DEC PY 1993 VL 1 IS 4 BP 238 EP 243 DI 10.3109/10673229309017084 PG 6 WC Psychiatry SC Psychiatry GA MU382 UT WOS:A1993MU38200005 PM 9384853 ER PT J AU FAVA, M ROSENBAUM, JF AF FAVA, M ROSENBAUM, JF TI PSYCHOPHARMACOLOGY OF PATHOLOGICAL AGGRESSION SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article ID ORGANIC MENTAL SYNDROMES; DOUBLE-BLIND; CEREBROSPINAL-FLUID; CONDUCT DISORDER; BRAIN DISEASE; BEHAVIOR; LITHIUM; DISTURBANCES; CROSSOVER; EFFICACY C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,FRUIT ST,BOSTON,MA 02114. NR 26 TC 6 Z9 6 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD NOV-DEC PY 1993 VL 1 IS 4 BP 244 EP 246 DI 10.3109/10673229309017085 PG 3 WC Psychiatry SC Psychiatry GA MU382 UT WOS:A1993MU38200006 PM 9384854 ER PT J AU SEWELL, WF MROZ, EA AF SEWELL, WF MROZ, EA TI FLAVIN ADENINE-DINUCLEOTIDE IS A MAJOR ENDOGENOUS FLUOROPHORE IN THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE HAIR CELL; AUDITORY SYSTEM; AUTOFLUORESCENCE; FLAVINS; GOLDFISH; FORMALDEHYDE ID CARASSIUS-AURATUS; GOLDFISH; AUTOFLUORESCENCE; CELLS AB When illuminated with visible light, hair cells can exhibit autofluorescence (Lewis et al. [1982] Science 215, 1641-1643) concentrated in the basal pole near the synapses (Sento and Furukawa [1987] J. Comp. Neurol. 258, 352-367). The autofluorescence is enhanced by formaldehyde. The level of fluorescence is high enough to interfere with fluorescence microscopy of hair cells and to suggest that the fluorescent substance might have a particular role in hair-cell function. To identify this substance, we extracted a substance with formaldehyde-enhanced fluorescence from the inner ears of goldfish and purified it chromatographically. The substance copurified with FAD and had the same fluorescence emission spectrum. Two further results supported the identity of the endogenous fluorescent substance with FAD. First, as is the case with flavins, the autofluorescence in inner ear tissue examined within a few hours after fixation was reduced by addition of dithionite. Second, as is the case with the formaldehyde-enhanced fluorophore, the fluorescence of FAD was enhanced by formaldehyde. FAD accounted for 90% of flavins in goldfish inner ears; its concentration in the sensory epithelium was estimated to be about 30 nmol/g tissue weight, one of the highest tissue concentrations known. The FAD is probably associated with an unidentified flavoprotein concentrated in the basal, synaptic region of the hair cell. C1 HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP SEWELL, WF (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC 00767, DC 00119, DC 00033] NR 14 TC 8 Z9 8 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1993 VL 70 IS 2 BP 131 EP 138 DI 10.1016/0378-5955(93)90150-Y PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300001 PM 7904988 ER PT J AU MROZ, EA LECHENE, C AF MROZ, EA LECHENE, C TI CALCIUM AND MAGNESIUM TRANSPORT BY ISOLATED GOLDFISH HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; ELECTRON-PROBE ANALYSIS; ION TRANSPORT; CALCIUM; MAGNESIUM ID ION-DEPENDENT CONDUCTANCES; INTRACELLULAR CALCIUM; GUINEA-PIG; EXCHANGE; COCHLEA; DEPOLARIZATION; MECHANISMS; MICROSCOPY; MOTILITY; AXONS AB We used electron-probe analysis (EPA) to investigate the transport of the divalent cations calcium and magnesium across the plasma membranes of hair cells. Unlike ion-sensitive fluorescent dyes, EPA detects these ions regardless of the state of chemical combination inside the cell; changes in these cell ions determined by EPA indicate net transport across the cell membrane. Raising or lowering either extracellular divalent cation within 1 mM of its control level raised or lowered its cell contents, but further increases in extracellular concentration of either ion had little additional effect on the cell content of that ion. New steady-state contents could be obtained within minutes, but the net divalent cation currents required to account for the observed changes would have been smaller than most currents recorded electrophysiologically, less than 1 pA. The effects of replacing extracellular Na+ with other ions were consistent with the presence in hair cells of exchangers for divalent cations thought to occur in other tissues: electrically neutral sodium/magnesium exchange (2 Na+ per Mg2+) and electrogenic sodium/calcium exchange (at least 3 Na+ per Ca2+). The increase in cell Ca after 1 minute of pottasium-depolarization was similar to that expected from electrophysiological studies of voltage-sensitive calcium currents in goldfish hair cells. After that time in elevated potassium, however, either calcium-entry pathways were inhibited or calcium-export mechanisms were enhanced. C1 BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [R01 DC000033, DC00033] NR 37 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1993 VL 70 IS 2 BP 139 EP 145 DI 10.1016/0378-5955(93)90151-P PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300002 PM 8294257 ER PT J AU MROZ, EA LECHENE, C AF MROZ, EA LECHENE, C TI EXTRACELLULAR N-METHYL-D-GLUCAMINE LEADS TO LOSS OF HAIR-CELL SODIUM, POTASSIUM, AND CHLORIDE SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; ION TRANSPORT; PERMEABILITY; PH REGULATION ID EXCHANGE; PUMP AB The organic cation N-methyl-D-glucamine (NMDG) is often used to replace extracellular sodium in experimental studies. Replacing 100 mM of Na+ with NMDG(+) in the fluid bathing isolated goldfish hair cells led to a rapid loss not only of cell sodium, but also of cell potassium and chloride. The loss of inorganic cell solutes was accompanied by acidification of the cells. Cell volume did not change significantly. These results are consistent with passage of the cationic form of NMDG, a titratable amine with a pK(a) 9.6, across the hair-cell membrane. These results should have bearing in interpreting results of experiments in which this cation is used to replace extracellular sodium, particularly for periods of time longer than 3 min. C1 BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC00033, R01 DC000033] NR 20 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1993 VL 70 IS 2 BP 146 EP 150 DI 10.1016/0378-5955(93)90152-Q PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300003 PM 8294258 ER PT J AU HU, FL GU, Z KOZICH, V KRAUS, JP RAMESH, V SHIH, VE AF HU, FL GU, Z KOZICH, V KRAUS, JP RAMESH, V SHIH, VE TI MOLECULAR-BASIS OF CYSTATHIONINE BETA-SYNTHASE DEFICIENCY IN PYRIDOXINE RESPONSIVE AND NONRESPONSIVE HOMOCYSTINURIA SO HUMAN MOLECULAR GENETICS LA English DT Article ID BIOSYNTHESIS; MUTATIONS; GENE AB Cystathionine beta-synthase (CBS) deficiency is an autosomal recessive disorder associated with multisystem clinical disease. We analyzed PCR amplified products from patients' RNA and genomic DNA. Direct sequencing of the entire coding region of the CBS gene revealed a G-919 to A transition in exon 8, resulting in replacement of Gly 307 by Ser (G307S) in the protein. The mutation was detected in one allele of patient L171 of French/Scottish ancestry and in both alleles of patient L198 of Irish ancestry. Amplifying and sequencing exon 8 from the genomic DNA showed that both parents of L198 were heterozygotes for G307S. The pathogenicity of the mutation was demonstrated in an expression experiment. The mutant protein was apparently stable in E.coli extracts and lacked catalytic activity. Sequencing of exon 8 revealed the G307S mutation in five additional families. All patients have pyridoxine nonresponsive homocystinuria. We have now observed this mutation in 9 of 52 apparently unrelated alleles of varied ethnic backgrounds. All 9 are from patients with Celtic (Irish/English/Scottish/French) ancestry in either one or both parents. The G307S mutation was detected in 50% (9 of 18) of the Celtic alleles in our series. The second mutation found in exon 8 is the 1278T mutation, which was described previously in one allele of a pyridoxine responsive patient. This missense mutation was detected in one allele of a pyridoxine nonresponsive patient and in both alleles of a pyridoxine responsive patient. The latter suggests that 1278T is probably associated with pyridoxine responsiveness. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,AMINO ACID DISORDER LAB,BLDG 149,13TH ST,BOSTON,MA 02129. UNIV COLORADO,DENVER,CO 80262. HARVARD UNIV,DEPT NEUROL,BOSTON,MA 02114. RI Kozich, Viktor/A-7672-2008 OI Kozich, Viktor/0000-0001-5820-5277 FU NICHD NIH HHS [HD 08315-18]; NINDS NIH HHS [NS05096] NR 16 TC 73 Z9 77 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD NOV PY 1993 VL 2 IS 11 BP 1857 EP 1860 DI 10.1093/hmg/2.11.1857 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MG827 UT WOS:A1993MG82700017 PM 7506602 ER PT J AU CHURCH, DM BANKS, LT ROGERS, AC GRAW, SL HOUSMAN, DE GUSELLA, JF BUCKLER, AJ AF CHURCH, DM BANKS, LT ROGERS, AC GRAW, SL HOUSMAN, DE GUSELLA, JF BUCKLER, AJ TI IDENTIFICATION OF HUMAN CHROMOSOME-9 SPECIFIC GENES USING EXON AMPLIFICATION SO HUMAN MOLECULAR GENETICS LA English DT Article ID SOMATIC-CELL HYBRIDS; DIRECT CLONING; DNA; CDNAS; REGION; GENERATION; SEQUENCES; SELECTION; PROTEIN; CANCERS AB We have recently developed a method, exon amplification, that is designed for isolation of exon sequences from genomic DNA. To assess the efficacy of this method we have analyzed cosmid genomic clones derived from human chromosome 9, and have cloned several products from this analysis. Approximately 63% of cosmids produced at least one product derived from functioning splice sites within the target genomic fragment, and in many cases multiple products were isolated. In addition, an easily identifiable class of false positives was produced from 56% of cosmids analyzed; these are readily eliminated from subsequent study. Sequence analysis and database searches revealed that the majority (87%) of the putative exon clones were unique, the remainder being derived from repetitive sequences. Analysis of sequence conservation by Southern blotting in addition to cDNA screening experiments suggested that most, if not all, of these unique sequences represent true exons. The results of these studies indicate that exon amplification is a rapid and reliable approach for isolation of exon sequences from mammalian genomic DNA. C1 HARVARD UNIV,DEPT GENET,BOSTON,MA 02114. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. FU NHGRI NIH HHS [HG00169, HG00317, HG00672] NR 29 TC 24 Z9 24 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD NOV PY 1993 VL 2 IS 11 BP 1915 EP 1920 DI 10.1093/hmg/2.11.1915 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MG827 UT WOS:A1993MG82700027 PM 7506603 ER PT J AU CHEN, MA BONIFAS, JM MATSUMURA, K BLUMENFELD, A EPSTEIN, EH AF CHEN, MA BONIFAS, JM MATSUMURA, K BLUMENFELD, A EPSTEIN, EH TI A NOVEL 3-NUCLEOTIDE DELETION IN THE HELIX 2B REGION OF KERATIN-14 IN EPIDERMOLYSIS-BULLOSA SIMPLEX - DELTA-E375 SO HUMAN MOLECULAR GENETICS LA English DT Note ID HYPERKERATOSIS; MUTATION; ABNORMALITIES; CHROMOSOME-12; LINKAGE C1 UNIV CALIF SAN FRANCISCO,DEPT DERMATOL,SAN FRANCISCO,CA 94110. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NIAMS NIH HHS [AR 41120] NR 17 TC 45 Z9 46 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD NOV PY 1993 VL 2 IS 11 BP 1971 EP 1972 DI 10.1093/hmg/2.11.1971 PG 2 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MG827 UT WOS:A1993MG82700041 PM 7506606 ER PT J AU BJORNSDOTTIR, US BUSH, RK AF BJORNSDOTTIR, US BUSH, RK TI LEUKOTRIENE ANTAGONISTS AND INHIBITORS SO IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA LA English DT Review ID ARACHIDONIC-ACID METABOLISM; EXERCISE-INDUCED BRONCHOCONSTRICTION; ASPIRIN-INDUCED ASTHMA; LUNG MAST-CELLS; RECEPTOR ANTAGONIST; GUINEA-PIG; URINARY LEUKOTRIENE-E4; AIRWAY RESPONSIVENESS; POLYMORPHONUCLEAR LEUKOCYTES; BRONCHIAL-ASTHMA C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. NR 121 TC 5 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8561 J9 IMMUNOL ALLERGY CLIN JI Immunol. Allerg. Clin. North Am. PD NOV PY 1993 VL 13 IS 4 BP 861 EP 890 PG 30 WC Allergy; Immunology SC Allergy; Immunology GA ME137 UT WOS:A1993ME13700009 ER PT J AU SORKNESS, CA BUSH, RK AF SORKNESS, CA BUSH, RK TI ALTERNATIVES TO CORTICOSTEROIDS IN THE TREATMENT OF ASTHMA SO IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA LA English DT Article ID STEROID-DEPENDENT ASTHMA; INTRAVENOUS IMMUNE GLOBULIN; DOUBLE-BLIND; RHEUMATOID-ARTHRITIS; BRONCHIAL-ASTHMA; GAMMA-GLOBULIN; GOLD SALT; METHOTREXATE; AURANOFIN; TRIAL C1 UNIV WISCONSIN,SCH MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP SORKNESS, CA (reprint author), UNIV WISCONSIN,SCH PHARM,425 N CHARTER ST,MADISON,WI 53706, USA. NR 55 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 0889-8561 J9 IMMUNOL ALLERGY CLIN JI Immunol. Allerg. Clin. North Am. PD NOV PY 1993 VL 13 IS 4 BP 917 EP 938 PG 22 WC Allergy; Immunology SC Allergy; Immunology GA ME137 UT WOS:A1993ME13700012 ER PT J AU MOUNTZ, JD TALAL, N AF MOUNTZ, JD TALAL, N TI RETROVIRUSES, APOPTOSIS AND AUTOGENES SO IMMUNOLOGY TODAY LA English DT Editorial Material ID ENDOGENOUS RETROVIRUSES; AUTOIMMUNE-DISEASE; ELEMENT ETN; MICE; TRANSPOSON; INFECTION; INSERTION; PROTEINS; SEQUENCE; GENE AB Autoimmunity and autoimmune disease are not the same. Autoimmunity is a normal consequence of aging, potentially reversible and possibly physiological. Autoimmune disease is dependent on genetic, viral, hormonal and psychoneuroimmunological factors. Aside from the apparently normal regulation of autoimmune responses by immune response genes, little is known about other genetic factors. Here, Norman Talal and John Mountz propose the term autogene to describe non-MHC genes which directly or indirectly interfere with important immunoregulatory actions. When mutated or otherwise genetically altered (e.g. by retrotransposon insertion), these genes predispose to immune dysregulation, lymphoproliferation and autoimmunity. C1 UNIV ALABAMA,SCH MED,DEPT MED,DIV CLIN IMMUNOL & RHEUMATOL,BIRMINGHAM,AL 35294. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP MOUNTZ, JD (reprint author), BIRMINGHAM VET HOSP,BIRMINGHAM,AL 35294, USA. NR 36 TC 52 Z9 54 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD NOV PY 1993 VL 14 IS 11 BP 532 EP 536 DI 10.1016/0167-5699(93)90182-K PG 5 WC Immunology SC Immunology GA MF709 UT WOS:A1993MF70900004 PM 8274195 ER PT J AU FISHMAN, SM HOLLISTER, D BONHIEM, NA AF FISHMAN, SM HOLLISTER, D BONHIEM, NA TI SALMONELLA BACTEREMIA WITH GAS-PRODUCING PYOMYOSITIS SO INFECTIOUS DISEASES IN CLINICAL PRACTICE LA English DT Note ID ACQUIRED IMMUNODEFICIENCY SYNDROME; INFECTION; PATIENT C1 GREENWICH HOSP,DEPT INTERNAL MED,GREENWICH,CT. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FISHMAN, SM (reprint author), MASSACHUSETTS GEN HOSP,MGH PAIN CTR,FRUIT ST,BOSTON,MA 02114, USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1056-9103 J9 INFECT DIS CLIN PRAC JI Infect. Dis. Clin. Pract. PD NOV-DEC PY 1993 VL 2 IS 6 BP 431 EP 433 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MK201 UT WOS:A1993MK20100009 ER PT J AU ZAPOL, WM AF ZAPOL, WM TI MINIDOSE INHALED NITRIC-OXIDE - LESS IS BETTER SO INTENSIVE CARE MEDICINE LA English DT Editorial Material ID PERSISTENT PULMONARY-HYPERTENSION; GUINEA-PIGS; NEWBORN RP ZAPOL, WM (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 12 TC 21 Z9 21 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0342-4642 J9 INTENS CARE MED JI Intensive Care Med. PD NOV PY 1993 VL 19 IS 8 BP 433 EP 434 DI 10.1007/BF01711082 PG 2 WC Critical Care Medicine SC General & Internal Medicine GA MJ978 UT WOS:A1993MJ97800002 PM 8294624 ER PT J AU KAHN, RS DAVIDSON, M AF KAHN, RS DAVIDSON, M TI SEROTONIN RECEPTOR RESPONSIVITY IN SCHIZOPHRENIA SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT International Scientific Symposium on Advances in the Pharmacology and Clinical Applications of Serotonin CY JAN 07-09, 1993 CL HI ID META-CHLOROPHENYLPIPERAZINE; NEUROLEPTIC TREATMENT; NEURO-ENDOCRINE; CLOZAPINE; MCPP; 5-HT1C C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY. RP KAHN, RS (reprint author), UNIV HOSP UTRECHT,DEPT PSYCHIAT,HEIDELBERGLAAN 100,3584 CX UTRECHT,NETHERLANDS. FU NIMH NIH HHS [NIMH R01 MH46957-01] NR 23 TC 10 Z9 10 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0268-1315 J9 INT CLIN PSYCHOPHARM JI Int. Clin. Psychopharmacol. PD NOV PY 1993 VL 8 SU 2 BP 47 EP 51 DI 10.1097/00004850-199311002-00007 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA MU110 UT WOS:A1993MU11000007 PM 7911140 ER PT J AU HERZOG, DB HOPKINS, JD BURNS, CD AF HERZOG, DB HOPKINS, JD BURNS, CD TI A FOLLOW-UP-STUDY OF 33 SUBDIAGNOSTIC EATING-DISORDERED WOMEN SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article ID BULIMIA-NERVOSA; BEHAVIORS AB Thirty-three female subjects with subdiagnostic DSM-III-R anorexia nervosa (SAN) and/or subdiagnostic bulimia nervosa (SBN) were reinterviewed 24 to 52 months (mean 41 months) after seeking treatment for an eating disorder. Subjects were administered a semistructured interview by telephone and assessed for level of functioning, eating disorder symptoms, course of illness, and treatment sought. During the course of the follow-up, 15 (46%) subjects went on to meet full DSM-III-R criteria for AN and/or BN. At follow-up, 4 (12%) met full DSM-III-R criteria for AN and/or BN, 22 (67%) were subdiagnostic, and 6 (18%) had recovered. The high percentage of subdiagnostic women that eventually develop full DSM-III-R criteria for AN and/or BN and the low rates of recovery at 2 to 4 years suggest that the current diagnostic criteria may be too restrictive. (C) 1993 by John Wiley & Sons, Inc. RP HERZOG, DB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,EATING DISORDERS UNIT,ACC 725,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [R0I MH38333-01A3] NR 13 TC 65 Z9 68 U1 0 U2 2 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD NOV PY 1993 VL 14 IS 3 BP 261 EP 267 DI 10.1002/1098-108X(199311)14:3<261::AID-EAT2260140304>3.0.CO;2-N PG 7 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA ME127 UT WOS:A1993ME12700003 PM 8275062 ER PT J AU HAFFNER, SM VALDEZ, RA STERN, MP KATZ, MS AF HAFFNER, SM VALDEZ, RA STERN, MP KATZ, MS TI OBESITY, BODY-FAT DISTRIBUTION AND SEX-HORMONES IN MEN SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE BODY FAT DISTRIBUTION; OBESITY; TESTOSTERONE; SEX HORMONE BINDING GLOBULIN; ESTRADIOL; DHEA-SO4; SEX HORMONES; AGE ID ADIPOSE-TISSUE DISTRIBUTION; BINDING-GLOBULIN; POSTMENOPAUSAL WOMEN; DIABETES-MELLITUS; DEHYDROEPIANDROSTERONE SULFATE; CARDIOVASCULAR-DISEASE; CENTRALIZED ADIPOSITY; PREMENOPAUSAL WOMEN; ABDOMINAL ADIPOSITY; MEXICAN-AMERICANS AB An unfavourable body fat distribution may cause metabolic abnormalities including diabetes and dyslipidemia. These effects may be mediated by alterations in sex hormones. In women the available data suggest that upper body adiposity is related to increased androgenicity (especially as indicated by low concentrations of sex hormone binding globulin). Few data, however, are available on these relationships in men. We therefore examined the association of total testosterone, free testosterone, oestradiol, dehydroepiandrosterone sulphate (DHEA-SO4) and sex hormone binding globulin (SHBG) to waist-to-hip ratio (WHR) and conicity index in 178 men from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. The conicity index is equal to the abdominal circumference divided by 0.109 x the square root of (weight/ height). The conicity index and WHR were significantly inversely related to DHEA-SO4 and free testosterone. SHBG was only weakly associated with body mass index (r= -0.18, P< 0.05). After adjustment for age and body mass index, DHEA-SO, remained inversely correlated with WHR (r = -0.22, P < 0.01) and conicity index (r = -0.31, P < 0.001) and free testosterone remained inversely associated with conicity index (r = -0.21, P < 0.01). Thus, in men, the association between unfavourable body fat distribution and increased androgenicity is inverse in contrast to the situation in women. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIAT & GERONTOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU NHLBI NIH HHS [R01HL-24799, R37HL-36820] NR 53 TC 153 Z9 156 U1 1 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD NOV PY 1993 VL 17 IS 11 BP 643 EP 649 PG 7 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA MF383 UT WOS:A1993MF38300005 PM 8281222 ER PT J AU XIAO, M GALANOPOULOS, T NEVILLEGOLDEN, J RICHIE, JP ANTONIADES, HN AF XIAO, M GALANOPOULOS, T NEVILLEGOLDEN, J RICHIE, JP ANTONIADES, HN TI HUMAN PROSTATE ADENOCARCINOMAS EXPRESS IN-VIVO MESSENGER-RNAS AND PROTEIN PRODUCTS FOR PLATELET-DERIVED GROWTH FACTOR-B AND ITS RECEPTOR SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE PROSTATE ADENOCARCINOMAS; PLATELET-DERIVED GROWTH FACTOR ID NORMAL RAT PROSTATE; EPITHELIAL-CELLS; GENE-EXPRESSION; HORMONE ANALOG; FACTOR-BETA; FACTOR PDGF; SERUM-FREE; FACTOR-I; HYPERPLASIA; INSULIN AB In situ hybridization and immunocytochemistry studies have shown the in vivo expression of platelet-derived growth factor B (PDGF-B) and PDGF receptor (PDGF-R) beta mRNAs and their respective protein products in the malignant epithelial cells of eight primary human prostatic adenocarcinomas. Examination of five nonmalignant adjacent prostate tissues did not demonstrate significant expression of PDGF B and PDGF-R beta mRNAs or production of their respective protein products in nonmalignant epithelial cells. Expression of androgen receptor mRNA was shown to be present in the epithelial cells of all of the five nonmalignant adjacent prostate tissues. There was a significant reduction in the expression of androgen receptor mRNA in poorly differentiated regions, and a moderate reduction in the well differentiated regions of the malignant tissues. It appears that dedifferentiation of the tumor cells in prostatic adenocarcinomas is accompanied by a reduction in androgen receptor mRNA expression. The coexpression of PDGF and its receptor in the malignant epithelial cells of prostatic adenocarcinomas signifies an abnormal autocrine loop that may contribute to their growth and maintenance. C1 HARVARD UNIV,SCH PUBL HLTH,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT UROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 35 TC 1 Z9 1 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD NOV PY 1993 VL 3 IS 5 BP 809 EP 815 PG 7 WC Oncology SC Oncology GA MD194 UT WOS:A1993MD19400004 PM 21573435 ER PT J AU SANDBERG, MA MILLER, S GAUDIO, AR AF SANDBERG, MA MILLER, S GAUDIO, AR TI FOVEAL CONE ERGS IN FELLOW EYES OF PATIENTS WITH UNILATERAL NEOVASCULAR AGE-RELATED MACULAR DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE MACULAR DEGENERATION; CHOROIDAL NEOVASCULARIZATION; ELECTRORETINOGRAPHY; AGE; OCULAR PIGMENTATION ID ELECTRORETINOGRAMS; MACULOPATHY AB Purpose. To determine whether fellow eyes with normal visual acuity of patients with unilateral neovascular age-related macular degeneration (AMD) have retinal malfunction. Methods. Foveal cone electroretinograms (ERGs) were recorded from fellow eyes with visual acuities of 20/25 or better of 73 patients with unilateral neovascular AMD and from 28 normal volunteers of comparable age. Responses were elicited with a 4-degrees stimulus flickering at 42 Hz presented by a stimulator-ophthalmoscope. Results. The study eyes of the patients were found to have foveal cone ERGs that, on average, were normal in amplitude but delayed in implicit (peak) time after adjustment of the data for age, sex, iris pigmentation, and refractive error by multiple linear regression. Based on all subjects, amplitude declined with increasing age and was smaller in eyes with darker irides; implicit time increased with increasing age. Conclusions. These findings suggest that fellow eyes with normal visual acuity of patients with unilateral neovascular AMD tend to have foveal cones that are normal in number but that function abnormally. In addition, foveal cone ERG amplitude should be adjusted for both age and iris pigmentation and implicit time should be adjusted for age when assessing retinal function of elderly patients. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BERMAN GUND LAB,BOSTON,MA 02115. FU NEI NIH HHS [EY08398] NR 10 TC 35 Z9 35 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD NOV PY 1993 VL 34 IS 12 BP 3477 EP 3480 PG 4 WC Ophthalmology SC Ophthalmology GA MF621 UT WOS:A1993MF62100029 PM 7693610 ER PT J AU CHEW, FS SMIRNIOTOPOULOS, JG AF CHEW, FS SMIRNIOTOPOULOS, JG TI EDUCATIONAL EFFICACY OF COMPUTER-ASSISTED-INSTRUCTION WITH INTERACTIVE VIDEODISC IN RADIOLOGY SO INVESTIGATIVE RADIOLOGY LA English DT Article DE COMPUTER-ASSISTED INSTRUCTION; INTERACTIVE VIDEODISC; EDUCATION; EDUCATIONAL MEDIA; RADIOLOGY AB RATIONALE AND OBJECTIVES. To create a robust, functional computer-assisted instruction (CAI)-videodisc program and to demonstrate its educational efficacy. METHODS. After creating a CAI-videodisc program in skeletal radiology for a two-screen Macintosh system, 36 medical students and 162 radiology residents entered a controlled study with paired pre- and posttests. Subjects also compared CAI-videodisc with other educational media. RESULTS. Medical students using the CAI-videodisc improved their mean pre- and posttest scores from 50.9 to 70.9 (P < .001, control group scores 50.1 and 50.6) and residents (using a different test) improved from 45.4 to 70.9 (P < .001, control group scores 49.6 and 46.1). Medical students and residents favored CAI-videodisc over teaching files, textbooks, videotapes, and slide-audiotapes. CONCLUSIONS. A functional CAI-videodisc program was created and demonstrated to be educationally effective. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. ARMED FORCES INST PATHOL,DEPT RADIOL PATHOL,WASHINGTON,DC 20306. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. RI Smirniotopoulos, James/D-3726-2011; OI Chew, Felix/0000-0003-2711-2013 NR 20 TC 17 Z9 17 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1993 VL 28 IS 11 BP 1052 EP 1058 DI 10.1097/00004424-199311000-00018 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG179 UT WOS:A1993MG17900013 PM 8276578 ER PT J AU DAWSON, P HILL, JA GRABOWSKI, EF KIDO, DK BERNARDINO, ME AF DAWSON, P HILL, JA GRABOWSKI, EF KIDO, DK BERNARDINO, ME TI NONIONIC CONTRAST USE IN CARDIAC ANGIOGRAPHY - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 ROYAL POSTGRAD MED SCH,DEPT RADIOL,LONDON W12 0HS,ENGLAND. UNIV FLORIDA,COLL MED,DEPT CARDIOL,GAINESVILLE,FL 32611. UNIV FLORIDA,SHANDS HOSP,GAINESVILLE,FL 32611. MASSACHUSETTS GEN HOSP,CARDIOVASC THROMBOSIS LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,DIV NEURORADIOL,ST LOUIS,MO 63110. EMORY UNIV HOSP,DEPT RADIOL,ATLANTA,GA 30322. EMORY UNIV HOSP,WINSHIP CANC CTR,ATLANTA,GA 30322. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1993 VL 28 SU 5 BP S54 EP S54 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG875 UT WOS:A1993MG87500016 ER PT J AU DAWSON, P LATCHAW, RE GRABOWSKI, EF GAVANT, M KIDO, D HILL, JA PORTER, G AF DAWSON, P LATCHAW, RE GRABOWSKI, EF GAVANT, M KIDO, D HILL, JA PORTER, G TI THE CLOTTING ISSUE - ETIOLOGIC FACTORS IN THROMBOEMBOLISM .2. CLINICAL CONSIDERATIONS - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Article C1 ROYAL POSTGRAD MED SCH,DEPT RADIOL,LONDON W12 0HS,ENGLAND. UNIV MINNESOTA,DEPT RADIOL,MINNEAPOLIS,MN 55455. MASSACHUSETTS GEN HOSP,CARDIOVASC THROMBOSIS LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV TENNESSEE CTR HLTH SCI,MEMPHIS COLL MED,DEPT DIAGNOST RADIOL,MEMPHIS,TN 38163. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,DIV NEURORADIOL,ST LOUIS,MO 63110. UNIV FLORIDA,COLL MED,DIV CARDIOL,GAINESVILLE,FL 32611. UNIV FLORIDA,SHANDS HOSP,GAINESVILLE,FL 32611. OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1993 VL 28 SU 5 BP S37 EP S38 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG875 UT WOS:A1993MG87500010 ER PT J AU GRABOWSKI, E BLOMLEY, M SIEGLE, R DAWSON, P PORTER, G GOLDFARB, S BERNARDINO, M MORRIS, T AF GRABOWSKI, E BLOMLEY, M SIEGLE, R DAWSON, P PORTER, G GOLDFARB, S BERNARDINO, M MORRIS, T TI CONTRAST BOLUS DYNAMIC COMPUTED-TOMOGRAPHY FOR THE MEASUREMENT OF SOLID-ORGAN PERFUSION - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HAMMERSMITH HOSP,DEPT RADIOL,LONDON W12 0HS,ENGLAND. UNIV CHICAGO HOSP & CLIN,DEPT RADIOL,CHICAGO,IL 60637. UNIV TEXAS,HLTH SCI CTR,DEPT RADIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. ROYAL POSTGRAD MED SCH,DEPT RADIOL,LONDON W12 0HS,ENGLAND. OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. GRAD HOSP PHILADELPHIA,DIV NEPHROL,PHILADELPHIA,PA 19146. EMORY UNIV HOSP,DEPT RADIOL,ATLANTA,GA 30322. EMORY UNIV HOSP,WINSHIP CANC CTR,ATLANTA,GA 30322. UNIV ROCHESTER,MED CTR,DEPT RADIOL,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT PHYSIOL,ROCHESTER,NY 14642. RP GRABOWSKI, E (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC THROMBOSIS LAB,JACKSON 13,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1993 VL 28 SU 5 BP S78 EP S78 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG875 UT WOS:A1993MG87500024 ER PT J AU GRABOWSKI, EF HEAD, C MICHELSON, AD AF GRABOWSKI, EF HEAD, C MICHELSON, AD TI NONIONIC CONTRAST-MEDIA - PROCOAGULANTS OR CLOTTING INNOCENTS SO INVESTIGATIVE RADIOLOGY LA English DT Article DE NONIONIC VERSUS IONIC CONTRAST MEDIA; PLATELET ADHESION AGGREGATION; DIGITAL IMAGE PROCESSING; EPIFLUORESCENCE VIDEOMICROSCOPY; PLATELET MEMBRANE GLYCOPROTEINS; FLOW CYTOMETRY; PROCOAGULANT; ENDOTHELIAL INJURY; ADEQUACY OF HEPARINIZATION ID AGENTS; MECHANISMS; INHIBITION; BLOOD AB OBJECTIVES. Compared with ionic contrast media, nonionic contrast media cause fewer adverse reactions, including hemodynamic and electrophysiologic complications, and are better tolerated by patients. However, concern as to whether nonionic agents are associated with more thromboembolic complications has been raised in recent years. This article reviews in-vitro and in-vivo coagulation studies with nonionic contrast media, including the authors' current study using blood samples from percutaneous transluminal coronary angioplasty (PTCA) patients. METHODS. Articles for this review were selected on the basis of providing viewpoints representative of both sides of the clotting controversy involving nonionic contrast media. In addition, articles were selected that, in toto, include the several relevant aspects of thrombosis during PTCA: whole blood clotting, angiography catheters, angiography syringes, rheology, and vascular endothelium. The preliminary work described used platelet adhesion/aggregation to a collagen-coated surface under controlled conditions of heparinized, whole blood flow. Adhesion/aggregation was quantified by digital analysis of real-time images obtained by epifluorescence videomicroscopy. In parallel studies, changes in markers (membrane glycoproteins) of platelet activation were measured using whole blood flow cytometry. RESULTs. Although nonionic contrast media are weaker anticoagulants than ionic contrast media, no convincing evidence demonstrates that they are procoagulant. On the contrary, in-vitro studies suggest that ionic media may weaken the antithrombotic properties of vascular endothelium by direct endothelial injury. Certain clinical trials of PTCA patients substantially challenge the use of nonionics. Yet, Grabowski et al found no evidence of platelet activation by ioxaglate or iohexol in preliminary work. This result was obtained with two of the most sensitive platelet assays available: flowing whole blood aggregometry and whole blood flow cytometry. Attention should be given to the adequacy of heparinization in future clinical studies. CONCLUSIONS. Nonionic contrast media are not procoagulant in vitro in the hands of most research groups. The focus of current controversy, therefore, is whether there is a clinical and in-vivo difference in thrombotic events seen with nonionic versus ionic media during PTCA. Elements in this controversy include platelet activation, blood-foreign surface (catheter and syringe) interaction, rheology, vascular endothelium, and adequacy of heparinization. C1 UNIV MASSACHUSETTS,SCH MED,WORCESTER,MA 01605. RP GRABOWSKI, EF (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC THROMBOSIS LAB,JACKSON 13,BOSTON,MA 02114, USA. NR 18 TC 20 Z9 20 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1993 VL 28 SU 5 BP S21 EP S24 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG875 UT WOS:A1993MG87500007 PM 8282498 ER PT J AU LATCHAW, RE HILL, JA COHEN, MD DAWSON, P KIDO, D GRABOWSKI, E AF LATCHAW, RE HILL, JA COHEN, MD DAWSON, P KIDO, D GRABOWSKI, E TI A REVIEW OF THE TOXICITY OF NONIONIC CONTRAST AGENTS IN CHILDREN - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 UNIV FLORIDA,COLL MED,DEPT CARDIOL,GAINESVILLE,FL 32611. UNIV FLORIDA,SHANDS HOSP,GAINESVILLE,FL 32611. INDIANA UNIV,MED CTR,RILEY HOSP CHILDREN,INDIANAPOLIS,IN 46202. ROYAL POSTGRAD MED SCH,DEPT RADIOL,LONDON W12 0HS,ENGLAND. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,DIV NEURORADIOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,CARDIOVASC THROMBOSIS LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LATCHAW, RE (reprint author), UNIV MINNESOTA,DEPT RADIOL,BOX 292,420 DELEWARE ST SE,MINNEAPOLIS,MN 55455, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1993 VL 28 SU 5 BP S94 EP S94 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG875 UT WOS:A1993MG87500028 ER PT J AU LATCHAW, RE KIDO, D GRABOWSKI, E HILL, JA AF LATCHAW, RE KIDO, D GRABOWSKI, E HILL, JA TI THE ROLE OF NONIONIC MYELOGRAPHY IN THE DIAGNOSIS OF LUMBAR DISC HERNIATION - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,DIV NEURORADIOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,CARDIOVASC THROMBOSIS LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV FLORIDA,COLL MED,DEPT CARDIOL,GAINESVILLE,FL 32611. UNIV FLORIDA,SHANDS HOSP,GAINESVILLE,FL 32611. RP LATCHAW, RE (reprint author), UNIV MINNESOTA,DEPT RADIOL,BOX 292,420 DELEWARE ST SE,MINNEAPOLIS,MN 55455, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1993 VL 28 SU 5 BP S67 EP S67 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG875 UT WOS:A1993MG87500020 ER PT J AU FARAONE, SV BIEDERMAN, J LEHMAN, BK SPENCER, T NORMAN, D SEIDMAN, LJ KRAUS, I PERRIN, J CHEN, WJ TSUANG, MT AF FARAONE, SV BIEDERMAN, J LEHMAN, BK SPENCER, T NORMAN, D SEIDMAN, LJ KRAUS, I PERRIN, J CHEN, WJ TSUANG, MT TI INTELLECTUAL-PERFORMANCE AND SCHOOL FAILURE IN CHILDREN WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER AND IN THEIR SIBLINGS SO JOURNAL OF ABNORMAL PSYCHOLOGY LA English DT Article ID ACADEMIC UNDERACHIEVEMENT; FAMILIAL ASSOCIATION; RISK-FACTORS; COMORBIDITY; ANXIETY; PSYCHOPATHOLOGY; ADOLESCENTS; STRATEGIES; RELATIVES; CHILDHOOD AB We made psychiatric and intellectual assessments of 140 children with attention-deficit hyperactivity disorder (ADHD), 120 normal controls, and their 303 siblings. The index children were white, non-Hispanic boys. ADHD children were more likely to have had learning disabilities, repeated grades, been placed in special classes, and received academic tutoring. They also did worse on the Wechsler Intelligence Scale for Children-Revised (WISC-R). Among ADHD probands, comorbid conduct, major depressive, and anxiety disorders predicted school placement more than school failure or WISC-R scores. However, the neuropsychological disability of all ADHD children could not be attributed to comorbid disorders because those without comorbidity had more school failure and lower WISC-R scores than normal controls. Intellectual impairment was also increased among siblings of ADHD children. This provides converging evidence that the ADHD syndrome is familial. C1 MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,CHILD PSYCHIAT SERV,ACC 725,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS MENTAL HLTH CTR,DEPT PSYCHOL,BOSTON,MA 02115. HARVARD COMMUNITY HLTH PLAN,DEPT PEDIAT,BOSTON,MA. MASSACHUSETTS GEN HOSP,PEDIAT SERV,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH-41314-01A2] NR 47 TC 187 Z9 193 U1 2 U2 26 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0021-843X J9 J ABNORM PSYCHOL JI J. Abnorm. Psychol. PD NOV PY 1993 VL 102 IS 4 BP 616 EP 623 DI 10.1037/0021-843X.102.4.616 PG 8 WC Psychology, Clinical; Psychology, Multidisciplinary SC Psychology GA MF719 UT WOS:A1993MF71900015 PM 8282932 ER PT J AU MALONEY, WJ PETERS, P ENGH, CA CHANDLER, H AF MALONEY, WJ PETERS, P ENGH, CA CHANDLER, H TI SEVERE OSTEOLYSIS OF THE PELVIS IN ASSOCIATION WITH ACETABULAR REPLACEMENT WITHOUT CEMENT SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID ARTHROPLASTY AB We reviewed the cases of fourteen patients (fifteen lesions) who had osteolysis following the replacement of the acetabulum without cement. Nine women and rive men, seventeen to sixty-seven years old, were involved in the study. One woman had bilateral pelvic osteolysis. Eight of the fifteen index acetabular reconstructions were done with a titanium-alloy implant and seven, with a chromium-cobalt-alloy implant. Eleven of the fifteen acetabular components had holes in the metal shell that may have acted as a conduit through which wear debris could gain access to the implant-bone interface, but only two of the acetabular components had been fixed with screws. In these two acetabular components, all available screw holes were not filled. The polyethylene liner was eight millimeters thick or less in twelve of the fifteen acetabular components; all of the liners were ten millimeters thick or less. The diameter of the head of eleven of the fifteen femoral components was thirty-two millimeters. Fourteen of the fifteen femoral components were placed without cement, and all but one was radiographically stable. The duration from the index operation to the appearance of pelvic osteolysis ranged from fifty-three to eighty-four months (mean, sixty-five months). At the time of the diagnosis, the patients were functioning well clinically, and all but three had a Harris hip score of 90 points or better, despite extensive destruction of bone in some instances. Since these patients were functioning well, the pelvic osteolysis was diagnosed radiographically at a regular follow-up examination. Only one patient had evidence of migration of the acetabular component on serial radiographs. Wear of the polyethylene liner was evident, on radiographic evaluation, in twelve of the fifteen hips. Nine patients (ten hips) have been managed with a reoperation to date. In two of these hips, osteolysis was diagnosed before extensive destruction of bone had occurred; in both hips, the lytic lesion was curetted and bone-grafting was done in order to salvage the implant. In the other eight hips, the acetabular component was revised because of severe loss of bone, and all needed supplemental allografting. Histologically, the membranes were found to contain numerous macrophages. Particulate debris, consisting predominantly of polyethylene, was present in all hips. Radiographs routinely led to an underestimation of the amount of bone loss; this fact emphasizes the importance of regular follow-up examination with serial radiographs of good quality. C1 ANDERSON ORTHOPAED CLIN,ARLINGTON,VA 22206. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP MALONEY, WJ (reprint author), PALO ALTO MED CLIN,300 HOMER AVE,PALO ALTO,CA 94305, USA. OI Engh, Andy/0000-0002-7303-4776 NR 27 TC 136 Z9 137 U1 1 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 NOV PY 1993 VL 75A IS 11 BP 1627 EP 1635 PG 9 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MK985 UT WOS:A1993MK98500007 PM 8245055 ER PT J AU TEICHER, BA SCHWARTZ, GN SOTOMAYOR, EA ROBINSON, MF DUPUIS, NP MENON, K AF TEICHER, BA SCHWARTZ, GN SOTOMAYOR, EA ROBINSON, MF DUPUIS, NP MENON, K TI OXYGENATION OF TUMORS BY A HEMOGLOBIN SOLUTION SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY LA English DT Article DE TUMOR OXYGENATION; HEMOGLOBIN; OXYGEN PRESSURE; CARBOGEN BREATHING ID CHEMOTHERAPEUTIC ALKYLATING-AGENTS; FSAIIC MURINE FIBROSARCOMA; SQUAMOUS-CELL CARCINOMA; FLUOSOL-DA; BOVINE HEMOGLOBIN; RADIATION-THERAPY; ANTITUMOR-ACTIVITY; PERFLUOROCHEMICAL EMULSION; CLINICAL-TRIAL; CYTO-TOXICITY AB Tumor oxygen tensions were measured using a computer-controlled PO2 microelectrode in two preclinical solid tumor models, the rat 9L gliosarcoma and the rat 13672 mammary carcinoma. Tumor oxygenation profiles were determined under four conditions: (a) during normal air breathing, (b) during carbogen breathing, (c) after intravenous administration of a solution of ultrapurified polymerized bovine hemoglobin with normal air breathing and (d) after intravenous administration of a solution of ultrapurified polymerized bovine hemoglobin with carbogen breathing. Both tumors had severely hypoxic regions under normal air-breathing conditions. Although carbogen breathing increased the oxygenation of the better-oxygenated portions of the tumor, it made no impact on the severely hypoxic tumor regions. Administration of the hemoglobin solution was effective in increasing the oxygenation throughout both tumors under normal air-breathing conditions. The addition of carbogen breathing to administration of the hemoglobin solution eliminated severe hypoxia in the 9L gliosarcoma and markedly reduced the severely hypoxic regions of the 13672 mammary carcinoma. At 24 h after administration of the hemoglobin solution the 13672 mammary carcinoma showed greater hypoxia than before treatment, which was partially corrected with carbogen breathing. 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-CA19589] NR 51 TC 29 Z9 29 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-5216 J9 J CANCER RES CLIN JI J. Cancer Res. Clin. Oncol. PD NOV-DEC PY 1993 VL 120 IS 1-2 BP 85 EP 90 DI 10.1007/BF01200729 PG 6 WC Oncology SC Oncology GA MD995 UT WOS:A1993MD99500014 PM 8270614 ER PT J AU VERBAVATZ, JM BROWN, D SABOLIC, I VALENTI, G AUSIELLO, DA VANHOEK, AN MA, T VERKMAN, AS AF VERBAVATZ, JM BROWN, D SABOLIC, I VALENTI, G AUSIELLO, DA VANHOEK, AN MA, T VERKMAN, AS TI TETRAMERIC ASSEMBLY OF CHIP28 WATER CHANNELS IN LIPOSOMES AND CELL-MEMBRANES - A FREEZE-FRACTURE STUDY SO JOURNAL OF CELL BIOLOGY LA English DT Article ID PROTEIN; RECONSTITUTION; PERMEABILITY; JUNCTIONS; TUBULE; CDNA AB Channel forming integral protein of 28 kD (CHIP28) functions as a water channel in erythrocytes, kidney proximal tubule and thin descending limb of Henle. CHIP28 morphology was examined by freeze-fracture EM in proteoliposomes reconstituted with purified CHIP28, CHO cells stably transfected with CHIP28k cDNA, and rat kidney tubules. Liposomes reconstituted with HPLC-purified CHIP28 from human erythrocytes had a high osmotic water permeability (P(f) 0.04 cm/s) that was inhibited by HgCl2. Freeze-fracture replicas showed a fairly uniform set of intramembrane particles (IMPs); no IMPs were observed in liposomes without incorporated protein. By rotary shadowing, the IMPs had a diameter of 8.5 +/- 1.3 nm (mean +/- SD); many IMPs consisted of a distinct arrangement of four smaller subunits surrounding a central depression. IMPs of similar size and appearance were seen on the P-face of plasma membranes from CHIP28k-transfected (but not mock-transfected) CHO cells, rat thin descending limb (TDL) of Henle, and S3 segment of proximal straight tubules. A distinctive network of complementary IMP imprints was observed on the E-face of CHIP28-containing plasma membranes. The densities of IMPs in the size range of CHIP28 IMPs, determined by nonlinear regression, were (in IMPs/mum2): 2,494 in CHO cells, 5,785 in TDL, and 1,928 in proximal straight tubules; predicted P(f), based on the CHIP28 single channel water permeability of 3.6 x 10(-14) cm3/s (10-degrees-C), was in good agreement with measured P(f) of 0.027 cm/s, 0.075 cm/s, and 0.031 cm/s, respectively, in these cell types. Assuming that each CHIP28 monomer is a right cylindrical pore of length 5 nm and density 1.3 g/cm3, the monomer diameter would be 3.2 nm; a symmetrical arrangement of four cylinders would have a greatest diameter of 7.2 nm, which after correction for the thickness of platinum deposit, is similar to the measured IMP diameter of approximately 8.5 nm. These results provide a morphological signature for CHIP28 water channels and evidence for a tetrameric assembly of CHIP28 monomers in reconstituted proteoliposomes and cell membranes. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,DEPT MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,DEPT PHYSIOL,SAN FRANCISCO,CA 94143. RP VERBAVATZ, JM (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114, USA. OI VALENTI, GIOVANNA/0000-0003-0233-0778 FU NIDDK NIH HHS [DK-35124, DK-38452] NR 33 TC 195 Z9 201 U1 0 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV PY 1993 VL 123 IS 3 BP 605 EP 618 DI 10.1083/jcb.123.3.605 PG 14 WC Cell Biology SC Cell Biology GA ME817 UT WOS:A1993ME81700010 PM 7693713 ER PT J AU MCCORMICK, BA COLGAN, SP DELPARCHER, C MILLER, SI MADARA, JL AF MCCORMICK, BA COLGAN, SP DELPARCHER, C MILLER, SI MADARA, JL TI SALMONELLA-TYPHIMURIUM ATTACHMENT TO HUMAN INTESTINAL EPITHELIAL MONOLAYERS - TRANSCELLULAR SIGNALING TO SUBEPITHELIAL NEUTROPHILS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID CHEMOTACTIC FACTORS; MAMMALIAN-CELLS; URINARY-TRACT; MIGRATION; INVASION; COLONIZATION; INFLAMMATION; PERMEABILITY; INVITRO; ABILITY AB In human intestinal disease induced by Salmonella typhimurium, transepithelial migration of neutrophils (PMN) rapidly follows attachment of the bacteria to the epithelial apical membrane. In this report, we model these interactions in vitro, using polarized monolayers of the human intestinal epithelial cell, T84, isolated human PMN, and S. typhimurium. We show that Salmonella attachment to T84 cell apical membranes did not alter monolayer integrity as assessed by transepithelial resistance and measurements of ion transport. However, when human neutrophils were subsequently placed on the basolateral surface of monolayers apically colonized by Salmonella, physiologically directed transepithelial PMN migration ensued. In contrast, attachment of a non-pathogenic Escherichia coli strain to the apical membrane of epithelial cells at comparable densities failed to stimulate a directed PMN transepithelial migration. Use of the n-formyl-peptide receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine (tBOC-MLP) indicated that the Salmonella-induced PMN transepithelial migration response was not attributable to the classical pathway by which bacteria induce directed migration of PMN. Moreover, the PMN transmigration response required Salmonella adhesion to the epithelial apical membrane and subsequent reciprocal protein synthesis in both bacteria and epithelial cells. Among the events stimulated by this interaction was the epithelial synthesis and polarized release of the potent PMN chemotactic peptide interleukin-8 (IL-8). However, IL-8 neutralization, transfer, and induction experiments indicated that this cytokine was not responsible for the elicited PMN transmigration. These data indicate that a novel transcellular pathway exists in which subepithelial PMN respond to lumenal pathogens across a functionally intact epithelium. Based on the known unique characteristics of the intestinal mucosa, we speculate that IL-8 may act in concert with an as yet unidentified transcellular chemotactic factor(s) (TCF) which directs PMN migration across the intestinal epithelium. C1 BRIGHAM & WOMENS HOSP,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,DIV INFECT DIS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP MCCORMICK, BA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV GASTROINTESTINAL PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. RI Colgan, Sean/B-4573-2009 FU NIDDK NIH HHS [DK 33506, DK 35932, DK34854] NR 68 TC 363 Z9 366 U1 1 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV PY 1993 VL 123 IS 4 BP 895 EP 907 DI 10.1083/jcb.123.4.895 PG 13 WC Cell Biology SC Cell Biology GA MG275 UT WOS:A1993MG27500011 PM 8227148 ER PT J AU KIM, SJ KAHN, CR AF KIM, SJ KAHN, CR TI INSULIN INDUCES RAPID ACCUMULATION OF INSULIN-RECEPTORS AND INCREASES TYROSINE KINASE-ACTIVITY IN THE NUCLEUS OF CULTURED ADIPOCYTES SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID RAT HEPATOMA-CELLS; GROWTH FACTOR-I; MATRIX ASSOCIATION; GENE-TRANSCRIPTION; PHOSPHORYLATION; PROTEIN; LIVER; STIMULATION; BINDING; INVIVO AB To better understand the mechanism by which insulin exerts effects on events at the cell nucleus, we have studied insulin receptors and tyrosine kinase activity in nuclei isolated by sucrose density gradient centrifugation following insulin treatment of differentiated 3T3-F442A cells. Insulin stimulated nuclear accumulation of insulin receptors by approximately threefold at 5 min. The half-maximal effect was observed with 1-10 nM insulin. Following insulin treatment, phosphotyrosine content associated with the nuclear insulin receptor was also increased by twofold at 5 min with a similar insulin concentration dependency. These nuclear insulin receptors differ from the membrane-associated insulin receptors in that they were not efficiently solubilized with 1% Triton X-100. During the same period of time, insulin stimulated nuclear tyrosine kinase activity toward the exogenous substrate poly Glu,:Tyr, tenfold in a time-dependent manner reaching a maximum at 30 min. The insulin receptor substrate protein 1 (IRS-1) could not be detected in the nucleus by immunoblotting. However, a nuclear protein with M(r) almost-equal-to 220 kDa was tyrosine phosphorylated, and insulin further stimulated this process threefold >30 mins. Surface labeling was performed to determine if the nuclear insulin receptors would emerge from the plasma membrane fraction. Using I-125-BPA-insulin with intact cells, the intensity of nuclear insulin receptor labeling was negligible and not increased throughout 30 min incubation at 37-degrees-C. In contrast, there was an increase in labeled receptors in the microsomal fraction following insulin treatment. Taken together, these results indicate that insulin rapidly increases nuclear insulin receptor appearance and activates nuclear tyrosine kinase activity. The insulin-induced accumulation of nuclear insulin receptors cannot be accounted for by internalization of surface membrane receptors. These effects of insulin may play an important role in action of the hormone at the nuclear level. (C) 1993 Wiley-Liss, Inc. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. FU NIDDK NIH HHS [DK 36836, DK 33201] NR 53 TC 34 Z9 34 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD NOV PY 1993 VL 157 IS 2 BP 217 EP 228 DI 10.1002/jcp.1041570203 PG 12 WC Cell Biology; Physiology SC Cell Biology; Physiology GA ME671 UT WOS:A1993ME67100002 PM 8227156 ER PT J AU GLASS, WF KREISBERG, JI AF GLASS, WF KREISBERG, JI TI REGULATION OF INTEGRIN-MEDIATED ADHESION AT FOCAL CONTACTS BY CYCLIC-AMP SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID CULTURED MESANGIAL CELLS; DEPENDENT PROTEIN-KINASE; EXTRACELLULAR-MATRIX; PLASMINOGEN-ACTIVATOR; VITRONECTIN; FIBROBLASTS; FIBRONECTIN; MORPHOLOGY; ACTIN; SHAPE AB Cyclic AMP (cAMP) elevation causes diverse types of cultured cells to round partially and develop arborized cell processes. Renal glomerular mesangial cells are smooth, muscle-like cells and in culture contain abundant actin microfilament cables that insert into substratum focal contacts. cAMP elevation causes adhesion loss, microfilament cable fragmentation, and shape change in cultured mesangial cells. We investigated the roles of the classical vitronectin (alphaVbeta3 integrin) and fibronectin (alpha5beta1 integrin) receptors in these changes. Mesangial cells on vitronectin-rich substrata contained microfilament cables that terminated in focal contacts that stained with antibodies to vitronectin receptor. cAMP elevation caused loss of focal contact and associated vitronectin receptor. Both fibronectin and its receptor stained in a fibrillary pattern at the cell surface under control conditions but appeared aggregated along the cell processes after cAMP elevation. This suggested that cAMP elevation caused loss of adhesion mediated by vitronectin receptor but not by fibronectin receptor. We plated cells onto fibronectin-coated slides to test the effect of ligand immobilization on the cellular response to cAMP. On fibronectin-coated slides fibronectin receptor was observed in peripheral focal contacts where actin filaments terminated, as seen with vitronectin receptor on vitronectin-coated substrata, and in abundant linear arrays distributed along microfilaments as well. Substratum contacts mediated by fibronectin receptor along the length of actin filaments have been termed fibronexus contacts. After cAMP elevation, microfilaments fragmented and fibronectin receptor disappeared from peripheral focal contacts, but the more central contacts along residual microfilament fragments appeared intact. Also, substratum adhesion was maintained after cAMP elevation on fibronectin-but not on vitronectin-coated surfaces. Although other types of extracellular matrix receptors may also be involved, our observations suggest that cAMP regulates adhesion at focal contacts but not at fibronexus-type extracellular matrix contacts. (C) 1993 Wiley-Liss, Inc. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL,CHARLOTTESVILLE,VA 22908. RP GLASS, WF (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK29787] NR 32 TC 50 Z9 50 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 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD NOV PY 1993 VL 157 IS 2 BP 296 EP 306 PG 11 WC Cell Biology; Physiology SC Cell Biology; Physiology GA ME671 UT WOS:A1993ME67100011 PM 7693723 ER PT J AU VORSANGER, GJ ROBERTS, JT AF VORSANGER, GJ ROBERTS, JT TI MIDAZOLAM-INDUCED ATHETOID MOVEMENTS OF THE LOWER-EXTREMITIES DURING EPIDURAL-ANESTHESIA REVERSED BY PHYSOSTIGMINE SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Note DE ANESTHESIA; EPIDURAL; ATHETOID MOVEMENTS; MIDAZOLAM; PHYSOSTIGMINE AB Midazolam is a short-acting, water-soluble benzodiazepine used for induction and maintenance of general anesthesia and as an adjunct to regional anesthesia. This substance produces several types of untoward reactions, including agitated excitement, mental confusion, and uncooperativeness, as well as dystonic extrapyramidal reactions, such as tonic clonic movements, muscle tremor, and athetoid movements. We describe two patients who developed akinesthesia with athetoid movements of the lower extremities after receiving midazolam as a premedication and as all adjunct to epidural anesthesia. These movements occurred with a sensory level of T-4 as assessed by pinprick, even though the patients were unable to move their lower extremities. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD NOV-DEC PY 1993 VL 5 IS 6 BP 494 EP 496 DI 10.1016/0952-8180(93)90068-P PG 3 WC Anesthesiology SC Anesthesiology GA ML641 UT WOS:A1993ML64100012 PM 8123277 ER PT J AU SWEITZER, BJ HOFFMAN, WJ ALLYN, JW DAGGETT, WJ AF SWEITZER, BJ HOFFMAN, WJ ALLYN, JW DAGGETT, WJ TI DIAGNOSIS OF A LEFT-SIDED SUPERIOR VENA-CAVA DURING PLACEMENT OF A PULMONARY-ARTERY CATHETER SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Note DE PULMONARY ARTERY CATHETER COMPLICATIONS; SUPERIOR VENA CAVA, LEFT-SIDED AB We report a case of a left sided superior vena cava (SVC) that was diagnosed during placement of a pulmonary artery (PA) catheter. After entering the left internal jugular, the PA catheter passed into the left side of the heart, through the aortic valve, and into the aorta. This was an unusual cause of right-to-left shunting and persistent cyanosis in a patient who had undergone two open cardiac procedures, including repair of an atrial septal defect. Cardiac catherization and echocardiography also failed to reveal the abnormality. The embryology and physiology of a left sided SVC is reviewed, including an historical perspective. A discussion of the variants of the syndrome is included, as is a review of aberrant placement of central venous catheters. RP SWEITZER, BJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD NOV-DEC PY 1993 VL 5 IS 6 BP 500 EP 504 DI 10.1016/0952-8180(93)90070-U PG 5 WC Anesthesiology SC Anesthesiology GA ML641 UT WOS:A1993ML64100014 PM 8123279 ER PT J AU MICHALOWSKI, P ROSOW, CE AF MICHALOWSKI, P ROSOW, CE TI PERIOPERATIVE DRUG-INTERACTIONS SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Article DE ALPHA-2-ADRENERGIC RECEPTORS; ANESTHETICS INTRAVENOUS, VOLATILE; BENZODIAZEPINES; DRUG INTERACTIONS; HYPNOTICS; MINIMUM ALVEOLAR CONCENTRATION; OPIOIDS C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD NOV-DEC PY 1993 VL 5 IS 6 SU 1 BP S29 EP S33 PG 5 WC Anesthesiology SC Anesthesiology GA MM101 UT WOS:A1993MM10100005 PM 7904823 ER PT J AU ARNOLD, A AF ARNOLD, A TI GENETIC-BASIS OF ENDOCRINE DISEASE .5. MOLECULAR-GENETICS OF PARATHYROID-GLAND NEOPLASIA SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CHROMOSOME-11; TYPE-1; TUMORS; HORMONE; HYPERCALCEMIA; ADENOMA; MAPS C1 HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RP ARNOLD, A (reprint author), MASSACHUSETTS GEN HOSP, ENDOCRINE ONCOL LAB, JACKSON 1021, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA-55909]; NIDDK NIH HHS [DK-11794] NR 15 TC 67 Z9 67 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 NOV PY 1993 VL 77 IS 5 BP 1108 EP 1112 DI 10.1210/jc.77.5.1108 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MG136 UT WOS:A1993MG13600002 PM 8077300 ER PT J AU LAWRENCE, VA GAFNI, A KROENKE, K AF LAWRENCE, VA GAFNI, A KROENKE, K TI PREOPERATIVE HIV TESTING - IS IT LESS EXPENSIVE THAN UNIVERSAL PRECAUTIONS SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE MEDICAL ECONOMICS; PREOPERATIVE CARE; SURGICAL (OPERATIVE); HIV INFECTION, TRANSMISSION, PREVENTION AND CONTROL; OCCUPATIONAL DISEASES; RISK FACTORS ID UNITED-STATES HOSPITALS; HEALTH-CARE WORKERS; GLOVE PERFORATIONS; SURGERY; RISK; AIDS; INFECTION; BLOOD; TRANSMISSION; PHYSICIANS AB Universal precautions are officially recommended to prevent HIV transmission in health care settings but for elective surgery some advocate routine preoperative HIV testing. These strategies have not been tested in clinical trials but universal precautions are very expensive and not cost-effective. Thus, for elective surgery, routine testing might save resources by permitting selective use of additional barrier precautions. We performed an economic evaluation to compare both strategies, using a simple approach to determine if routine testing (RT) is less expensive than universal precautions (UP). Conservatively assuming equal effectiveness in preventing HIV transmission, we compared a minimized estimate for the average cost of RT with a maximized estimate for the average cost of UP per elective operation. The minimized estimate for RT (US$57) was greater than the maximized estimate for UP (US$36) per procedure. Results were stable or strengthened by sensitivity analysis. Routine HIV testing is not a valid economic alternative to UP for elective surgery. The simple methodology used in this study can be a preliminary strategy to review other strategies for preventing HIV transmission. This method is particularly useful when data are inadequate for a formal economic evaluation to determine the utility of collecting the detailed information necessary for a full comparison. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. MCMASTER UNIV,HLTH SCI CTR,CTR HLTH ECON & POLICY ANAL,HAMILTON,ON,CANADA. MCMASTER UNIV,HLTH SCI CTR,DEPT CLIN EPIDEMIOL & BIOSTAT,HAMILTON,ON,CANADA. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. RP LAWRENCE, VA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 40 TC 14 Z9 14 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD NOV PY 1993 VL 46 IS 11 BP 1219 EP 1227 DI 10.1016/0895-4356(93)90084-E PG 9 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA MG589 UT WOS:A1993MG58900001 PM 8229097 ER PT J AU LAWRENCE, VA GAFNI, A KROENKE, K AF LAWRENCE, VA GAFNI, A KROENKE, K TI EVIDENCE-BASED VS EMOTION-BASED MEDICAL DECISION-MAKING - ROUTINE PREOPERATIVE HIV TESTING VS UNIVERSAL PRECAUTIONS SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; RISK; AIDS C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. MCMASTER UNIV,HLTH SCI CTR,DEPT CLIN EPIDEMIOL & BIOSTAT,HAMILTON,ON,CANADA. MCMASTER UNIV,HLTH SCI CTR,CTR HLTH ECON & POLICY ANAL,HAMILTON,ON,CANADA. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. RP LAWRENCE, VA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284, USA. NR 8 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 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD NOV PY 1993 VL 46 IS 11 BP 1233 EP 1236 DI 10.1016/0895-4356(93)90086-G PG 4 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA MG589 UT WOS:A1993MG58900003 PM 8229099 ER PT J AU BARUT, B CHAUHAN, D UCHIYAMA, H ANDERSON, KC AF BARUT, B CHAUHAN, D UCHIYAMA, H ANDERSON, KC TI INTERLEUKIN-6 FUNCTIONS AS AN INTRACELLULAR GROWTH-FACTOR IN HAIRY-CELL LEUKEMIA IN-VITRO SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE B-CELL MALIGNANCY; TUMOR NECROSIS FACTOR; INTERLEUKIN-6 ANTISENSE OLIGONUCLEOTIDE; IL-6 RECEPTORS; AUTOCRINE GROWTH FACTOR ID TUMOR-NECROSIS-FACTOR; CHRONIC LYMPHOCYTIC-LEUKEMIA; HUMAN MULTIPLE-MYELOMA; STIMULATORY FACTOR-II; FACTOR-ALPHA; AUTOCRINE GROWTH; MONOCLONAL-ANTIBODIES; TRANSCRIPTION FACTOR; RESPONSE PATTERNS; INTERFERON-ALPHA AB The role of interleukin-6 (IL-6) in the growth of B cell derived hairy cell leukemia (HCL) was characterized. Purified hairy cells (HCs) did not increase DNA synthesis in vitro in response to exogenous IL-6; however, they expressed IL-6 receptor (IL-6R) mRNA and bound directly fluorochrome labeled IL-6. IL-6 mRNA was not detectable in tumor cells by Northern blotting, but was evident using PCR amplification. Although intracytoplasmic IL-6 protein was not demonstrable, HCs did secrete low levels of IL-6. Neutralizing antibody to IL-6 did not inhibit HC DNA synthesis. Since tumor necrosis factor (TNF) is a growth factor for HCL, we determined whether the TNF effect could be IL-6-mediated. TNF markedly augmented in vitro DNA synthesis by HCs. TNF did not alter IL-6R expression or IL-6 binding; however, IL-6 mRNA and IL-6 protein were detectable after 3-d culture of HCs with TNF. In addition, IL-6 secretion by HCs was markedly augmented by TNF. Finally, although neither IL-6 nor anti-IL-6 antibody altered TNF-induced DNA synthesis by HCs, IL-6 antisense oligonucleotide inhibited TNF-induced DNA synthesis and IL-6 secretion by HCs. Therefore, IL-6 does not directly affect the growth of HCL, but rather mediates TNF-induced DNA synthesis via an intracytoplasmic mechanism. 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 66 TC 43 Z9 43 U1 0 U2 0 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 NOV PY 1993 VL 92 IS 5 BP 2346 EP 2352 DI 10.1172/JCI116839 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MF291 UT WOS:A1993MF29100034 PM 8227350 ER PT J AU BROGI, E WINKLES, JA UNDERWOOD, R CLINTON, SK ALBERTS, GF LIBBY, P AF BROGI, E WINKLES, JA UNDERWOOD, R CLINTON, SK ALBERTS, GF LIBBY, P TI DISTINCT PATTERNS OF EXPRESSION OF FIBROBLAST GROWTH-FACTORS AND THEIR RECEPTORS IN HUMAN ATHEROMA AND NONATHEROSCLEROTIC ARTERIES - ASSOCIATION OF ACIDIC FGF WITH PLAQUE MICROVESSELS AND MACROPHAGES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE BASIC FIBROBLAST GROWTH FACTOR; ATHEROSCLEROSIS; MACROPHAGES; NEOVASCULARIZATION; ANGIOGENESIS ID HUMAN CORONARY-ARTERIES; FACTOR GENE-EXPRESSION; SMOOTH-MUSCLE CELLS; FACTOR FAMILY; VASA VASORUM; SEQUENCE; HEPARIN; PROLIFERATION; CDNA; NEOVASCULARIZATION AB Because fibroblast growth factors (FGFs) modulate important functions of endothelial cells (EC) and smooth muscle cells (SMC), we studied FGF expression in human vascular cells and control or atherosclerotic arteries. All cells and arteries contained acidic (a) FGF and basic (b) FGF mRNA. Northern analysis detected aFGF mRNA only in one of five control arteries but in all five atheroma tested, while levels of bFGF mRNA did not differ among control (n = 3) vs. plaque specimens (n = 6). Immunolocalization revealed abundant bFGF protein in control vessels (n = 10), but little in plaques (n = 14). In contrast, atheroma (n = 14), but not control arteries (n = 10), consistently exhibited immunoreactive aFGF, notably in neovascularized and macrophage-rich regions of plaque. Because macrophages colocalized with aFGF, we tested human monocytoid THP-1 cells and demonstrated accumulation of aFGF mRNA during PMA-induced differentiation. We also examined the expression of mRNA encoding FGF receptors (FGFRs). All cells and arteries contained FGFR-1 mRNA. Only $MC and control vessels had FGFR-2 mRNA, while EC and some arteries contained FGFR-4 mRNA. The relative lack of bFGF in plaques vs. normal arteries suggests that this growth factor may not contribute to cell proliferation in advanced atherosclerosis. However, aFGF produced by plaque macrophages may stimulate the growth of microvessels during human atherogenesis. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,VASC MED & ATHEROSCLEROSIS UNIT,221 LONGWOOD AVE,BOSTON,MA 02115. AMER RED CROSS,HOLLAND LAB,DEPT MOLEC BIOL,ROCKVILLE,MD 20855. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-34636, HL-39727] NR 48 TC 177 Z9 181 U1 1 U2 4 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 NOV PY 1993 VL 92 IS 5 BP 2408 EP 2418 DI 10.1172/JCI116847 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MF291 UT WOS:A1993MF29100042 PM 7693761 ER PT J AU EBBINGHAUS, SW GEE, JE RODU, B MAYFIELD, CA SANDERS, G MILLER, DM AF EBBINGHAUS, SW GEE, JE RODU, B MAYFIELD, CA SANDERS, G MILLER, DM TI TRIPLEX FORMATION INHIBITS HER-2 NEU TRANSCRIPTION IN-VITRO SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE FOOTPRINT; GEL SHIFT; SEQUENCE DNA; ONCOGENE; GENE EXPRESSION ID DIHYDROFOLATE-REDUCTASE PROMOTER; HELIX FORMATION; C-ERBB-2 PROTOONCOGENE; ONCOGENIC ACTIVATION; POINT MUTATION; PROTO-ONCOGENE; HUMAN-BREAST; RECEPTOR; BINDING; DNA AB Triplex-forming oligonucleotides (TFOs) have been shown to bind to target DNA sequences in several human gene promoters such as the c-myc oncogene, the epidermal growth factor receptor, and the dihydrofolate reductase genes. TFOs have been shown to inhibit transcription in vitro and gene expression in cell culture of the c-myc and other genes. The HER-2/neu oncogene, which is overexpressed in breast cancer and other human malignancies, contains a purine-rich sequence in its promoter, which is favorable for purine:purine:pyrimidine (R:R:Y) triplex formation. Although its function in the HER-2/neu promoter is unknown, this purine-rich site is homologous to a protein-binding sequence in the promoter of the epidermal growth factor receptor that is necessary for efficient transcription of this gene. We have shown that this sequence is a site for nuclear protein binding by incubation with a crude nuclear extract. We describe the formation of an interstrand triplex using a purine-rich oligonucleotide antiparallel to this purine-rich target sequence of the HER-2 / neu promoter. Triplex formation by the oligonucleotide prevents protein binding to the target site in the HER-2/neu promoter in vitro. We have shown that this oligonucleotide is a potent and specific inhibitor of HER-2 / neu transcription in an in vitro assay. The triplex target site contains a single pyrimidine base that does not conform to the R:R:Y triplex motif. In an attempt to abrogate the potentially destabilizing effects of this pyrimidine base on triplex formation, we have substituted an abasic linker for the pyrimidine residue in the triplex forming oligonucleotide. Triplex formation with the modified oligonucleotide appears to occur with approximately equivalent binding affinity. Triplex formation in the HER-2/neu oncogene promoter prevents transcription in vitro and may represent a future modality for specific inhibition of this gene in vivo. C1 BIRMINGHAM VET AFFAIRS MED CTR, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT MED, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT ORAL PATHOL, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT BIOCHEM, BIRMINGHAM, AL 35294 USA. FU NCI NIH HHS [R01 CA 42337, CA 09467-08, CA42664] NR 32 TC 75 Z9 75 U1 0 U2 3 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 NOV PY 1993 VL 92 IS 5 BP 2433 EP 2439 DI 10.1172/JCI116850 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MF291 UT WOS:A1993MF29100045 PM 7901237 ER PT J AU TENOVER, FC SWENSON, J FERRARO, MJ HINDLER, J JORGENSEN, J MURRAY, P AF TENOVER, FC SWENSON, J FERRARO, MJ HINDLER, J JORGENSEN, J MURRAY, P TI CEFUROXIME SCREENING-TEST FOR PNEUMOCOCCI SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Letter C1 MASSACHUSETTS GEN HOSP, MICROBIOL LAB, BOSTON, MA 02114 USA. UNIV CALIF LOS ANGELES, MED CTR, MICROBIOL LAB, LOS ANGELES, CA 90024 USA. UNIV TEXAS, HLTH SCI CTR, DEPT PATHOL, SAN ANTONIO, TX 78284 USA. WASHINGTON UNIV, SCH MED, DIV LAB MED, ST LOUIS, MO 63110 USA. RP TENOVER, FC (reprint author), CTR DIS CONTROL & PREVENT, NOSOCOMIAL PATHOGENS LAB BRANCH, ATLANTA, GA 30333 USA. NR 1 TC 4 Z9 4 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD NOV PY 1993 VL 31 IS 11 BP 3078 EP 3080 PG 3 WC Microbiology SC Microbiology GA MC289 UT WOS:A1993MC28900050 PM 8263207 ER PT J AU KORNBLITH, AB HOLLIS, DR ZUCKERMAN, E LYSS, AP CANELLOS, GP COOPER, MR HERNDON, JE PHILLIPS, CA ABRAMS, J AISNER, J NORTON, L HENDERSON, C HOLLAND, JC AF KORNBLITH, AB HOLLIS, DR ZUCKERMAN, E LYSS, AP CANELLOS, GP COOPER, MR HERNDON, JE PHILLIPS, CA ABRAMS, J AISNER, J NORTON, L HENDERSON, C HOLLAND, JC TI EFFECT OF MEGESTROL-ACETATE ON QUALITY-OF-LIFE IN A DOSE-RESPONSE TRIAL IN WOMEN WITH ADVANCED BREAST-CANCER SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID PSYCHOSOCIAL ADAPTATION; TELEPHONE; DISEASE; MASTECTOMY; INTERVIEW; SURVIVORS; PAIN; STRATEGIES; INSTRUMENT; DEPRESSION C1 UNIV MARYLAND,CTR CANC,BALTIMORE,MD 21201. VET ADM MED CTR,FAYETTEVILLE,AR. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. CORNELL UNIV,MED CTR,COLL MED,NEW YORK,NY 10021. DUKE UNIV,MED CTR,CANC & LEUKEMIA GRP,STAT OFF B,DURHAM,NC 27710. MISSOURI BAPTIST MED CTR,ST LOUIS,MO. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC 27103. RP KORNBLITH, AB (reprint author), MEM SLOAN KETTERING CANC CTR,PSYCHIAT SERV,1275 YORK AVE,NEW YORK,NY 10021, USA. FU NCI NIH HHS [CA 03927, CA 32291, CA31946] NR 51 TC 66 Z9 66 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV PY 1993 VL 11 IS 11 BP 2081 EP 2089 PG 9 WC Oncology SC Oncology GA ME932 UT WOS:A1993ME93200005 PM 8229122 ER PT J AU ADELSTEIN, DJ KALISH, LA ADAMS, GL WAGNER, H OKEN, MM REMICK, SC MANSOUR, EG HASELOW, RE AF ADELSTEIN, DJ KALISH, LA ADAMS, GL WAGNER, H OKEN, MM REMICK, SC MANSOUR, EG HASELOW, RE TI CONCURRENT RADIATION-THERAPY AND CHEMOTHERAPY FOR LOCALLY UNRESECTABLE SQUAMOUS-CELL HEAD AND NECK-CANCER - AN EASTERN-COOPERATIVE-ONCOLOGY-GROUP PILOT-STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID INDUCTION CHEMOTHERAPY; RANDOMIZED TRIAL; ORAL CAVITY; RADIOTHERAPY; CARCINOMA; ADJUVANT; 5-FLUOROURACIL; METHOTREXATE; FLUOROURACIL; OROPHARYNX C1 METRO MINNEAPOLIS COMMUNITY CLIN ONCOL PROGRAM,MINNEAPOLIS,MN. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. ALBANY MED COLL,ALBANY,NY 12208. FU NCI NIH HHS [CA 23318, CA 14548, CA 21115] NR 31 TC 61 Z9 62 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV PY 1993 VL 11 IS 11 BP 2136 EP 2142 PG 7 WC Oncology SC Oncology GA ME932 UT WOS:A1993ME93200011 PM 8229127 ER PT J AU TAYLOR, CD ELSON, P TRUMP, DL AF TAYLOR, CD ELSON, P TRUMP, DL TI IMPORTANCE OF CONTINUED TESTICULAR SUPPRESSION IN HORMONE-REFRACTORY PROSTATE-CANCER SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LONG-TERM TREATMENT; PROGNOSTIC FACTORS; CARCINOMA; CHEMOTHERAPY; AGONIST; AMINOGLUTETHIMIDE; SPERMATOGENESIS; TESTOSTERONE; FLUTAMIDE; ANALOG C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI 53706. RP TAYLOR, CD (reprint author), LAWRENCE MEM HOSP MEDFORD,DIV HEMATOL ONCOL,170 GOVERNORS AVE,MEDFORD,MA 02155, USA. FU NCI NIH HHS [CA 21076, CA 21115, CA 23318] NR 33 TC 101 Z9 103 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV PY 1993 VL 11 IS 11 BP 2167 EP 2172 PG 6 WC Oncology SC Oncology GA ME932 UT WOS:A1993ME93200015 PM 8229130 ER PT J AU SCHMAHMANN, JD PANDYA, DN AF SCHMAHMANN, JD PANDYA, DN TI PRELUNATE, OCCIPITOTEMPORAL, AND PARAHIPPOCAMPAL PROJECTIONS TO THE BASIS PONTIS IN RHESUS-MONKEY SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE PRESTRIATE; OCCIPITAL; TEMPORAL; PONS; CEREBELLUM ID SUPERIOR TEMPORAL SULCUS; POSTERIOR PARIETAL CORTEX; CORTICAL CONNECTIONS; VISUAL AREA; CORTICOPONTINE PROJECTIONS; HORSERADISH-PEROXIDASE; INTRINSIC CONNECTIONS; CINGULATE CORTEX; MACAQUE MONKEY; FIBER PATHWAYS AB We used tritiated amino acids to study projections to the basilar pons from prestriate cortices in 18 rhesus monkeys to determine how connectional and functional heterogeneity of these regions are reflected in corticopontine circuitry. Fibers travelled with those from other parasensory associative cortices before terminating in the pontine nuclei. Prelunate projections were derived from area 19 (OA) at the medial convexity (including areas V3 and PO) and from the lateral convexity dorsal to the caudal tip of the Sylvian fissure (including areas DP and the dorsal part of area V4d). Pontine projections also arose from area 19 (OA), and areas TF, TL, and TH in the posterior aspect of the parahippocampal gyrus. No pontine projections arose from the prelunate convexity ventral to the caudal tip of the Sylvian fissure (ventral part of area V4d and area V4v), area TEO, the inferior temporal gyrus, or the lateral ventral temporal region. Terminations in the pons were distributed in the dorsolateral and lateral nuclei, and the lateral part of the peripeduncular nucleus. Medial convexity injections produced more extensive rostrocaudal pontine labeling, as well as terminations in the extreme dorsolateral nucleus and the nucleus reticularis tegmenti pontis. Dorsal prelunate injections had additional terminations in the ventral pontine nucleus. Posterior parahippocampal gyrus injections resulted in discrete label in the lateral and dorsolateral nuclei. Corticopontine projections destined for the cerebellum appear to be derived from extrastriate areas concerned mainly with visual spatial parameters, visual motion, and the peripheral field of vision, but not from areas subserving visual object identification and the central field of vision. Pontine afferents from the posterior parahippocampal gyrus may facilitate a cerebellar contribution to visual spatial memory, particularly when invested with motivational valence. (C) 1993 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,NEUROL UNIT,BOSTON,MA 02215. EDITH NOURSE ROGERS MEM VET HOSP,BEDFORD,MA. RP SCHMAHMANN, JD (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROL SERV,14 FRUIT ST,BOSTON,MA 02114, USA. FU PHS HHS [16841] NR 63 TC 75 Z9 75 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD NOV 1 PY 1993 VL 337 IS 1 BP 94 EP 112 DI 10.1002/cne.903370107 PG 19 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA ME051 UT WOS:A1993ME05100006 PM 8276995 ER PT J AU BOUSSIOTIS, VA FREEMAN, GJ GRAY, G GRIBBEN, J NADLER, LM AF BOUSSIOTIS, VA FREEMAN, GJ GRAY, G GRIBBEN, J NADLER, LM TI B7 BUT NOT INTERCELLULAR-ADHESION MOLECULE-1 COSTIMULATION PREVENTS THE INDUCTION OF HUMAN ALLOANTIGEN-SPECIFIC TOLERANCE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID T-CELL PROLIFERATION; FUNCTION-ASSOCIATED ANTIGEN-3; ACTIVATION ANTIGEN; CLONAL ANERGY; MONOCLONAL-ANTIBODIES; CARDIAC ALLOGRAFT; LYMPHOCYTES-T; CD28; ICAM-1; SIGNAL AB Presentation of antigen by the major histocompatibility complex to T lymphocytes without the requisite costimulatory signals does not induce an immune response but rather results in a state of antigen-specific unresponsiveness, termed anergy. To determine which costimulatory signals are critical for the T cell commitment to activation or anergy, we developed an in vitro model system that isolated the contributions of alloantigen and each candidate costimulatory molecule. Here, we show that transfectants expressing HLA-DR7 and either B7 or intercellular adhesion molecule 1 (ICAM-1) deliver independent costimulatory signals resulting in alloantigen-induced proliferation of CD4-positive T lymphocytes. Although equivalent in their ability to costimulate maximal proliferation of alloreactive T cells, B7 but not ICAM-1 induced detectable interleukin 2 secretion and prevented the induction of alloantigen-specific anergy. These results are consistent with the hypothesis that blockade of the ICAM-1:lymphocyte function-associated 1 pathway results in immunosuppression, whereas blockade of the B7:CD28/CTLA4 pathway results in alloantigen-specific anergy. This approach, using this model system, should facilitate the identification of critical costimulatory pathways which must be inhibited in order to induce alloantigen-specific tolerance before human organ transplantation. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. REPLIGEN INC,CAMBRIDGE,MA 02139. RP BOUSSIOTIS, VA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,MAYER 730,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NCI NIH HHS [CA-40416] NR 48 TC 218 Z9 227 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 NOV 1 PY 1993 VL 178 IS 5 BP 1753 EP 1763 DI 10.1084/jem.178.5.1753 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MD953 UT WOS:A1993MD95300030 PM 7901318 ER PT J AU HAHN, WC BIERER, BE AF HAHN, WC BIERER, BE TI SEPARABLE PORTIONS OF THE CD2 CYTOPLASMIC DOMAIN INVOLVED IN SIGNALING AND LIGAND AVIDITY REGULATION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID T-CELL ACTIVATION; RECEPTOR; ANTIGEN; EXPRESSION; IDENTIFICATION; TRANSDUCTION; PATHWAYS; PROTEIN; EPITOPE; LFA-3 AB Effective T cell immune responses require the molecular interplay between adhesive and signaling events mediated by the T cell receptor for antigen (TCR) and other cell surface coreceptor molecules. In this report, we have distinguished between the role of regulated adhesion and transmembrane signaling in coreceptor function using the T cell glycoprotein CD2. By binding its ligands on antigen-presenting cell (APC), CD2 serves both to initiate signal transduction events and to promote cellular adhesion. Furthermore, the avidity of CD2 for one ligand, CD58 (LFA-3), is regulated by TCR signaling. We have expressed wild type CD2 and a series of mutated CD2 molecules in an antigen-specific murine T cell hybridoma. Structure-function studies using these stably transfected cell lines identify two structurally and functionally distinct regions of the 116 amino acid (aa) cytoplasmic domain. One region is required for CD2-mediated signal transduction, and a separate COOH-terminal 21 aa portion is required for CD2 activity regulation. Cell lines expressing CD2 molecules lacking the cytoplasmic segment required for CD2-initiated IL-2 production retain the ability to upregulate CD2 avidity. Conversely, cell lines expressing CD2 mutants lacking the cytoplasmic segment required for avidity regulation retain the ability to initiate CD2-specific signaling. In antigen-specific T cell responses, basal binding of CD2 to its ligands enhances antigen responsiveness only minimally, whereas regulated avidity and trans-membrane signaling are both required for optimal coreceptor function. Taken together, these studies demonstrate the independent contributions of regulated adhesion and intracellular signaling in CD2 coreceptor function. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,DANA 1710A,44 BINNEY ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIAID NIH HHS [AI-28554] NR 26 TC 38 Z9 39 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 1 PY 1993 VL 178 IS 5 BP 1831 EP 1836 DI 10.1084/jem.178.5.1831 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MD953 UT WOS:A1993MD95300042 PM 7901319 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R AF SILVA, JA LEONG, GB WEINSTOCK, R TI THE PSYCHOTIC PATIENT AS SECURITY GUARD SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; PSYCHOTIC DISORDERS; DANGEROUSNESS; PUBLIC SAFETY; SECURITY GUARDS AB The job of the security guard is generally regarded as stressful because of the potential for violent or other hostile confrontation. Although the public assumes that only mentally healthy individuals who possess the capability to handle stressful situations become employed as security guards, this may not be the case. A series of 15 individuals who suffered from psychotic disorders while working as security guards is studied and discussed in terms of the issues of dangerousness and public safety. One case is described in detail in order to highlight important issues resulting from being psychotic while working as a security guard. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD NOV PY 1993 VL 38 IS 6 BP 1436 EP 1440 PG 5 WC Medicine, Legal SC Legal Medicine GA MH369 UT WOS:A1993MH36900026 PM 8263486 ER PT J AU BISCHOF, JC RUBINSKY, B AF BISCHOF, JC RUBINSKY, B TI MICROSCALE HEAT AND MASS-TRANSFER OF VASCULAR AND INTRACELLULAR FREEZING IN THE LIVER SO JOURNAL OF HEAT TRANSFER-TRANSACTIONS OF THE ASME LA English DT Article DE BIOTECHNOLOGY; CRYOGENICS; PHASE-CHANGE PHENOMENA ID CRYOSURGERY; MECHANISM; TISSUE AB A set of heat and mass transfer equations is developed to predict vascular as well as intracellular ice formation during freezing in liver tissue. A modified Krogh unit with vascular and cellular compartments is used. In the model intracellular ice formation is predicted by a probability integral with functional dependence on cell compartment volume, temperature, and time. Finite difference computer simulations qualitatively predict the amount and location of vascular and intracellular ice, the temperature distribution in the tissue, and the position of the partial and total freezing interfaces at any time. C1 UNIV CALIF BERKELEY,DEPT MECH ENGN,BERKELEY,CA 94720. RP BISCHOF, JC (reprint author), MASSACHUSETTS GEN HOSP,SURG RES LABS,BOSTON,MA 02129, USA. RI Rubinsky, Boris/B-4439-2010 OI Rubinsky, Boris/0000-0002-2794-1543 NR 25 TC 20 Z9 20 U1 0 U2 4 PU ASME-AMER SOC MECHANICAL ENG PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 SN 0022-1481 J9 J HEAT TRANS-T ASME JI J. Heat Transf.-Trans. ASME PD NOV PY 1993 VL 115 IS 4 BP 1029 EP 1035 DI 10.1115/1.2911357 PG 7 WC Thermodynamics; Engineering, Mechanical SC Thermodynamics; Engineering GA MK983 UT WOS:A1993MK98300026 ER PT J AU BIGBY, M MARKOWITZ, JS BLEICHER, PA GRUSBY, MJ SIMHA, S SIEBRECHT, M WAGNER, M NAGLERANDERSON, C GLIMCHER, LH AF BIGBY, M MARKOWITZ, JS BLEICHER, PA GRUSBY, MJ SIMHA, S SIEBRECHT, M WAGNER, M NAGLERANDERSON, C GLIMCHER, LH TI MOST GAMMA-DELTA-T-CELLS DEVELOP NORMALLY IN THE ABSENCE OF MHC CLASS-II MOLECULES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID POSITIVE SELECTION; EPIDERMAL-CELLS; LYMPHOCYTES-T; ANTIGEN RECEPTORS; LANGERHANS CELL; DEFICIENT MICE; THY-1 ANTIGEN; FETAL THYMUS; EXPRESSION; REPERTOIRE AB MHC class I and class II molecules are essential for intrathymic maturation of a normal repertoire of alphabeta T cells. The development of gammadelta T cells may similarly require exposure to conventional MHC or MHC-like molecules for appropriate negative and positive selection. The availability of mice that are devoid of cell surface expression of MHC class II molecules allowed us to test directly the hypothesis that conventional class II molecules play a role in the development of gammadelta T cells. The proportions of gammadelta cells in thymus, lymph nodes, and spleens were indistinguishable between class II-deficient mice and littermate controls by FACS analysis. Gammadelta T cells from class II-deficient mice proliferated normally in response to anti-TCR mAb. Examination of epidermal sheets from ear, torso, and tail skin demonstrated that class II-deficient mice had the same population density and distribution of gammadelta+ dendritic epidermal T cells as that of control littermates. Gammadelta cells in the epidermis of class II-deficient mice expressed Thy-1 and CD3 and were predominantly Vgamma3+. There were no significant differences in the immunophenotype of class II-deficient mice and their normal littermates in two-color immunofluorescence analysis of intestinal intraepithelial lymphocytes. Class II-deficient mice and control mice had 29 to 39% gammadelta bearing intestinal intraepithelial lymphocytes, of which 16 to 21% expressed Vdelta4. Dendritic cells that stained positively for Thy-1, CD3, and gammadelta were identified in the vaginal epithelium of class II-deficient mice and their normal littermates. Our results indicate that MHC class II expression is not essential for the development of most gammadelta T cells. C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,MUCOSAL IMMUNOL LAB,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02129. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP BIGBY, M (reprint author), MASSACHUSETTS GEN HOSP E,CTR CUTANEOUS BIOL RES,3RD FLOOR,BLDG 149,13TH ST,BOSTON,MA 02129, USA. FU PHS HHS [A121569, A131541] NR 47 TC 55 Z9 55 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1993 VL 151 IS 9 BP 4465 EP 4475 PG 11 WC Immunology SC Immunology GA MD349 UT WOS:A1993MD34900005 PM 8409413 ER PT J AU FANGER, GR ERHARDT, P COOPER, GM MAUE, RA AF FANGER, GR ERHARDT, P COOPER, GM MAUE, RA TI RAS-INDEPENDENT INDUCTION OF RAT-BRAIN TYPE-II SODIUM-CHANNEL EXPRESSION IN NERVE GROWTH FACTOR-TREATED PC12-CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE NEURONAL DIFFERENTIATION; NERVE GROWTH FACTOR; SODIUM CHANNELS; RAS; GENE EXPRESSION; PATCH CLAMPING ID PC12 CELLS; NEURONAL DIFFERENTIATION; SIGNAL TRANSDUCTION; FACTOR RECEPTOR; MESSENGER-RNAS; PROTEIN-KINASE; SEQUENCE AB Nerve growth factor (NGF) plays an important role in the development of the nervous system, and there is considerable interest in understanding the molecular mechanisms underlying its effects on neuronal differentiation. To determine if the activity of proteins of the ras gene family is necessary for the NGF-mediated induction of sodium channel expression in pheochromocytoma (PC12) cells, sodium channel expression was analyzed in PC12 sublines stably overexpressing the dominant inhibitory mutant c-Ha-ras(Asn-17). Northern blot analysis, RNase protection assays, and whole-cell patch clamp recordings indicate that the NGF-mediated increase in type 11 sodium channel mRNA and sodium current density can occur independent of ras activity and by doing so provide strong evidence for the importance of ras-independent mechanisms in NGF-mediated neuronal differentiation. C1 DARTMOUTH COLL SCH MED,DEPT PHYSIOL,HANOVER,NH 03755. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT BIOCHEM,HANOVER,NH 03756. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NINDS NIH HHS [NS28767] NR 23 TC 29 Z9 29 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD NOV PY 1993 VL 61 IS 5 BP 1977 EP 1980 DI 10.1111/j.1471-4159.1993.tb09844.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MD350 UT WOS:A1993MD35000053 PM 8229007 ER PT J AU SIMONIAN, NA HYMAN, BT AF SIMONIAN, NA HYMAN, BT TI FUNCTIONAL ALTERATIONS IN ALZHEIMERS-DISEASE - DIMINUTION OF CYTOCHROME-OXIDASE IN THE HIPPOCAMPAL-FORMATION SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ALZHEIMERS DISEASE; CYTOCHROME OXIDASE; DEAFFERENTATION; MITOCHONDRIA ID PERFORANT PATHWAY ZONE; VISUAL-CORTEX; HISTOCHEMISTRY; MONKEY; BRAIN AB In Alzheimer's disease, the relationship between structural alterations such as neurofibrillary tangles and senile plaques and neuronal function is unknown. Cytochrome oxidase, the terminal enzyme of the electron transport, is a marker of neuronal functional activity. Its activity is diminished in experimentally deafferented neurons. Based on evidence that the molecular layer of the dentate gyrus is deafferented in the brains of individuals with Alzheimer's disease, we hypothesized that cytochrome oxidase activity would be diminished in this region secondary to reduced glutamatergic input. Using cytochrome oxidase histochemistry, we found a change in the distribution of cytochrome oxidase in the molecular layer of the dentate gyrus and a decrease in activity in both the dentate gyrus and hippocampal subfields in Alzheimer's disease. In contrast, we found relatively little structural pathology in the dentate gyrus, CA4, and CA3 in these individuals. These results suggest that neurons that remain structurally intact in Alzheimer's disease may nonetheless undergo changes in metabolic function as neural systems fail. RP SIMONIAN, NA (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,WARREN 407,BOSTON,MA 02114, USA. FU NIA NIH HHS [NIA AG08487]; NINDS NIH HHS [NS07009-18] NR 26 TC 74 Z9 74 U1 0 U2 1 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD NOV PY 1993 VL 52 IS 6 BP 580 EP 585 DI 10.1097/00005072-199311000-00004 PG 6 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA MG718 UT WOS:A1993MG71800004 PM 8229076 ER PT J AU HYMAN, BT MARZLOFF, K ARRIAGADA, PV AF HYMAN, BT MARZLOFF, K ARRIAGADA, PV TI THE LACK OF ACCUMULATION OF SENILE PLAQUES OR AMYLOID BURDEN IN ALZHEIMERS-DISEASE SUGGESTS A DYNAMIC BALANCE BETWEEN AMYLOID DEPOSITION AND RESOLUTION SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE 10D5; A-BETA; BETA-A4; ALZHEIMERS DISEASE; AMYLOID BURDEN; SENILE PLAQUES ID NEUROFIBRILLARY TANGLES; PATHOLOGICAL-CHANGES; CORTICAL-NEURONS; SYNAPSE LOSS; DEMENTIA; PROTEIN; BRAIN; IDENTIFICATION; DIAGNOSIS; SEVERITY AB Abeta, a nearly insoluble peptide, is generally assumed to irreversibly deposit and accumulate as senile plaques (SP) during the course of Alzheimer's disease (AD). We have studied temporal neocortex of normal elderly subjects, AD patients, and elderly Down syndrome (DS) patients to determine whether Abeta accumulates with age or with increasing duration of illness. We measured the number, size distribution, and total area (amyloid burden) of Abeta immunoreactive deposits using computerized image analysis techniques. We found far fewer SP in normal control subjects than in AD patients, who in turn have fewer SP than elderly DS patients. No measure of Abeta correlated with age in the control subjects, nor duration of illness in AD or DS patients. These data indicate that Abeta may not continue to accumulate during these disease processes and support the view that the amount of Abeta observed at autopsy may reflect competing processes of deposition and resolution of amyloid. C1 CATHOLIC UNIV CHILE,DEPT NEUROPATHOL,SANTIAGO,CHILE. CATHOLIC UNIV CHILE,DEPT NEUROL,SANTIAGO,CHILE. RP HYMAN, BT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA 01907, USA. FU NIA NIH HHS [AG08487] NR 42 TC 214 Z9 219 U1 2 U2 4 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD NOV PY 1993 VL 52 IS 6 BP 594 EP 600 DI 10.1097/00005072-199311000-00006 PG 7 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA MG718 UT WOS:A1993MG71800006 PM 8229078 ER PT J AU STRASSMAN, AM VOS, BP MINETA, Y NADERI, S BORSOOK, D BURSTEIN, R AF STRASSMAN, AM VOS, BP MINETA, Y NADERI, S BORSOOK, D BURSTEIN, R TI FOS-LIKE IMMUNOREACTIVITY IN THE SUPERFICIAL MEDULLARY DORSAL HORN INDUCED BY NOXIOUS AND INNOCUOUS THERMAL-STIMULATION OF FACIAL SKIN IN THE RAT SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Review ID IMMEDIATE-EARLY GENES; MYELINATED NOCICEPTIVE AFFERENTS; SPINAL TRIGEMINAL NUCLEUS; C-FOS; MONKEYS FACE; RESPONSE PROPERTIES; GLABROUS SKIN; TRIGEMINOTHALAMIC NEURONS; POLYMODAL NOCICEPTORS; SUBSTANTIA GELATINOSA AB 1. To examine further the ability of different classes of nociceptive and nonnociceptive primary afferent neurons to induce c-fos expression in central neurons, fos-like immunoreactivity was examined in the medullary dorsal horn (laminae I-IV) of the rat after facial application of a range of warming and cooling thermal stimuli. Urethan-anesthetized rats received 15 30-s thermal pulses (53, 50, 47, 41, 25, or 10-degrees-C) applied to the vibrissal pad over a period of 30 min and were perfused 2 h after the end of stimulation. 2. Stimulation of 41-degrees-C produced no significant increase in the number of fos-LI-labeled cells in lamina I or II compared with control (35-degrees-C) animals. 3. Stimulation of 47-degrees-C produced a significant increase in the number of fos-LI-labeled cells in both laminae I and II. Stimulation of 50-degrees-C produced a significant increase in labeling, compared with that produced by 47-degrees-C, which was primarily in lamina II. Stimulation of 53-degrees-C produced no further increase in the number of labeled cells, compared with that produced by 50-degrees-C, in lamina I or II. 4. In the cooling direction, 25-degrees-C produced a significant increase in labeling above control levels in both lamina I and II, whereas 10-degrees-C produced a further increase compared with 25-degrees-C, which was restricted to lamina I. 5. None of the stimuli produced a significant increase in labeling in laminae III-IV. 6. The results are interpreted as providing evidence that low-threshold cold receptors, high-threshold cold receptors, and nociceptors are capable of inducing fos expression in dorsal horn neurons, whereas warm receptors are relatively ineffective. The results also provide evidence that neurons that receive input from C poly-modal nociceptors are present in both laminae I and II, as are neurons that receive input from low-threshold cold receptors. Neurons that receive input from high-threshold cold receptors, but not from low-threshold cold receptors, appear to be located preferentially in lamina I. The shape of the curve relating fos-LI labeling to stimulus temperature in the warming direction is consistent with the expected pattern of recruitment of primary afferent nociceptors. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NINDS NIH HHS [NS-24594] NR 109 TC 65 Z9 69 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD NOV PY 1993 VL 70 IS 5 BP 1811 EP 1821 PG 11 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA MG723 UT WOS:A1993MG72300009 PM 8294956 ER PT J AU BABICH, JW SOLOMON, H PIKE, MC KROON, D GRAHAM, W ABRAMS, MJ TOMPKINS, RG RUBIN, RH FISCHMAN, AJ AF BABICH, JW SOLOMON, H PIKE, MC KROON, D GRAHAM, W ABRAMS, MJ TOMPKINS, RG RUBIN, RH FISCHMAN, AJ TI TC-99M-LABELED HYDRAZINO-NICOTINAMIDE DERIVATIZED CHEMOTACTIC PEPTIDE ANALOGS FOR IMAGING FOCAL SITES OF BACTERIAL-INFECTION SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; CHEMOATTRACTANT RECEPTORS; POLYCLONAL IGG; NEUTROPHILS; PROTEIN; CELLS; RATS AB We synthesized and evaluated four hydrazino nicotinamide (HYNIC) derivatized chemotactic peptide analogs: For-NleLFK-HYNIC (HP1), For-MLFK-HYNIC (HP2), For-MLFNH(CH2)6NH-HYNIC (HP3), and For-MLF-(D)-K-HYNIC (HP4), for in vitro bioactivity and receptor binding. The peptides were radiolabeled with Tc-99m via a glucoheptonate co-ligand and their biodistribution determined in rats (n = 6/time point) at 5,30,60 and 120 min after injection. Localization of the peptides at sites of deep thigh Escherichia coli infection was determined by radioactivity measurements on excised tissues in rats (n = 6/time point) and rabbits as well as scintillation camera imaging in rabbits (n = 6). All peptides maintained biological activity (EC50s for O2 production by human PMNs: 12-500 nM) and the ability to bind to the oligopeptide chemoattractant receptor on human PMNs (EC50s for binding: 0.12-40 nM). After incubation with Tc-99m-glucoheptonate, radiolabeled peptides were isolated by HPLC at specific activities of >10,000 mCi/muM. Technetium-99m-labeled peptides retained receptor binding with EC50s < 10 nM. Blood clearance of all four peptides was rapid. Biodistributions of the individual peptides were similar, with low levels of accumulation in most normal tissues. In rats, all of the peptides concentrated at the infection sites (T/B ratio: 2.5-3:1) within 1 hr of injection. In rabbits, outstanding images of the infection sites were obtained, with T/B ratios of >20:1 at 15 hr after injection. This study demonstrates that Tc-99m-labeled chemotactic peptide analogs are effective agents for the external imaging of focal sites of infection. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN INVEST UNIT,MED SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,SURG SERV,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA. RW JOHNSON PHARMACEUT RES INST,RARITAN,NJ. JOHNSON MATTHEY PHARMACEUT RES,W CHESTER,PA. NR 36 TC 117 Z9 120 U1 0 U2 7 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 NOV PY 1993 VL 34 IS 11 BP 1964 EP 1974 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ME930 UT WOS:A1993ME93000026 PM 8229242 ER PT J AU BARROW, SA GRAHAM, W JYAWOOK, S DRAGOTAKES, SC SOLOMON, HF BABICH, JW RUBIN, RH FISCHMAN, AJ AF BARROW, SA GRAHAM, W JYAWOOK, S DRAGOTAKES, SC SOLOMON, HF BABICH, JW RUBIN, RH FISCHMAN, AJ TI LOCALIZATION OF INDIUM-111-IMMUNOGLOBULIN-G, TECHNETIUM-99M-IMMUNOGLOBULIN-G AND INDIUM-111-LABELED WHITE BLOOD-CELLS AT SITES OF ACUTE BACTERIAL-INFECTION IN RABBITS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID TC-99M-HMPAO LABELED LEUKOCYTES; NONSPECIFIC POLYCLONAL IGG; FOCAL SITES; INFLAMMATORY LESIONS; IMMUNOGLOBULIN; IN-111; QUANTITATION AB Biodistribution and infection imaging properties of In-111-DTPA-IgG, Tc-99m-hydrazino nicotinamide-IgG and In-111-WBC were compared in rabbits with E coli infection Groups of six rabbits were injected with 10 mCi of Tc-99m-IgG plus 0.5 mCi of In-111-IgG or 1 mCi of Tc-99m-IgG plus 0.05 mCi of In-111-WBC. At 4 5 and 18-20 hr, dual photon scintigrams were acquired. At both times, the distributions of Tc-99m and In-111-IgG were nearly identical. The sites of infection were well visualized with all three radiopharmaceuticals. In the early images, the target-to-background ratios (T/B) for In-111 and Tc-99m-IgG determined by ROI analysis were 1.95 +/- 0.26 and 2.57 +/- 0.38 (p = NS). In the delayed images, the T/B ratios increased (p < 0.01) to 3.56 +/- 0.49 and 4.90 +/- 0.98. At both times, the T/B ratios for In-111-WBC were higher (p < 0.01); 4.17 +/- 0.78 at 4-5 hr and 8.52 +/- 1.52 at 18-20 hr. These results indicate that all three agents yield excellent images of infection sites. Although In-111-WBC had higher T/B ratios, the ease of preparation of the radiolabeled proteins makes them attractive alternatives for infection imaging. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN INVEST SECT,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RW JOHNSON PHARMACEUT RES INST,SPRING HOUSE,PA. NR 23 TC 24 Z9 24 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 NOV PY 1993 VL 34 IS 11 BP 1975 EP 1979 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ME930 UT WOS:A1993ME93000027 PM 8229243 ER PT J AU HARGENS, AR BOTTE, MJ SWENSON, MR GELBERMAN, RH RHOADES, CE AKESON, WH AF HARGENS, AR BOTTE, MJ SWENSON, MR GELBERMAN, RH RHOADES, CE AKESON, WH TI EFFECTS OF LOCAL COMPRESSION ON PERONEAL NERVE FUNCTION IN HUMANS SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article ID LOWER-EXTREMITY TRAUMA; COMPARTMENT SYNDROME; PRESSURE; CATHETER AB A new apparatus was developed to compress the anterior compartment selectively and reproducibly in humans. Thirty-five normal volunteers were studied to determine short-term thresholds of local tissue pressure that produce significant neuromuscular dysfunction. Local tissue fluid pressure adjacent to the deep peroneal nerve was elevated by the compression apparatus and continuously monitored for 2-3 h by the slit catheter technique. Elevation of tissue fluid pressure to within 35-40 mm Hg of diastolic blood pressure (approximately 40 mm Hg of in situ pressure in our subjects) elicited a consistent progression of neuromuscular deterioration including, in order, (a) gradual loss of sensation, as assessed by Semmes-Weinstein monofilaments, (b) subjective complaints, (c) reduced nerve conduction velocity, (d) decreased action potential amplitude of the extensor digitorum brevis muscle, and (e) motor weakness of muscles within the anterior compartment. Generally, higher intracompartmental pressures caused more rapid deterioration of neuromuscular function. In two subjects, when in situ compression levels were 0 and 30 mm Hg, normal neuromuscular function was maintained for 3 h. Threshold pressures for significant dysfunction were not always the same for each functional parameter studied, and the magnitudes of each functional deficit did not always correlate with compression level. This variable tolerance to elevated pressure emphasizes the need to monitor clinical signs and symptoms carefully in the diagnosis of compartment syndromes. The nature of the present studies was short term; longer term compression of myoneural tissues may result in dysfunction at lower pressure thresholds. C1 VET AFFAIRS MED CTR,DEPT ORTHOPAED,SAN DIEGO,CA. VET AFFAIRS MED CTR,DIV NEUROL,SAN DIEGO,CA. UNIV CALIF SAN DIEGO,MED CTR,LA JOLLA,CA 92093. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA 02114. RP HARGENS, AR (reprint author), NASA,AMES RES CTR,DIV LIFE SCI,MOFFETT FIELD,CA 94035, USA. NR 22 TC 29 Z9 29 U1 1 U2 2 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0736-0266 J9 J ORTHOPAED RES JI J. Orthop. Res. PD NOV PY 1993 VL 11 IS 6 BP 818 EP 827 DI 10.1002/jor.1100110607 PG 10 WC Orthopedics SC Orthopedics GA MR350 UT WOS:A1993MR35000006 PM 8283326 ER PT J AU ESPAT, NJ COPELAND, EM SOUBA, WW AF ESPAT, NJ COPELAND, EM SOUBA, WW TI INFLUENCE OF FASTING ON GLUTAMINE TRANSPORT IN RAT-LIVER SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID PLASMA-MEMBRANE VESICLES; AMINO-ACID-TRANSPORT; METABOLISM; ENDOTOXIN; ALANINE; SYSTEM AB During starvation, the liver switches from an organ of net glutamine uptake to an organ of net glutamine release to help maintain blood glutamine levels. We hypothesized that this shift in hepatic glutamine exchange was regulated at the level of the hepatocyte plasma membrane by adaptive changes in glutamine transport. To test this hypothesis, adult rats (200 g) were allowed to consume regular rat food ad libitum (fed, n = 8) or were fasted for 72 hours (fasted, n = 8, access to water allowed). Livers were excised and hepatocyte plasma membrane vesicles were prepared by differential and Percoll density gradient centrifugation. Vesicle purity and functionality were assessed by marker enzyme measurements, classic ''overshoots,'' and time courses, which showed similar vesicle size. Uptake of H-3-glutamine by hepatocyte plasma membrane vesicles in the presence and absence of sodium was assayed by a rapid mixing/filtration method, which reflects actual transport across the hepatocyte cell membrane in vivo. Fasted rats lost 15 +/- 2% of body weight; fed rats gained weight. Na+-dependent glutamine transport (system ''N,'' mediates uptake into the hepatocyte) fell by 22% in the starved group, indicating a diminished rate of glutamine transport into the hepatocyte. In contrast, carrier-mediated Na+-independent glutamine transport (system ''n,'' mediates the release of glutamine out of the cell) doubled in the starved animals. Diffusion of glutamine across the vesicle membrane was unchanged by starvation. Unlike the activity of system N, which decreased in fasted animals, Na+-dependent transport of the nonmetabolizable system A analog N-methylaminoisobutyric acid was increased in fasted animals. Adaptive changes in both Na+-dependent and Na+-independent hepatic glutamine transport occur during fasting. These changes contribute to the net release of glutamine by the whole organ during starvation and may be designed to provide glutamine for other tissues during starvation. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. UNIV FLORIDA,COLL MED,DEPT SURG,SURG METAB LAB,GAINESVILLE,FL 32611. UNIV FLORIDA,COLL MED,DEPT SURG,NUTR LAB,GAINESVILLE,FL 32611. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA 45327] NR 22 TC 2 Z9 2 U1 0 U2 1 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD NOV-DEC PY 1993 VL 17 IS 6 BP 493 EP 500 DI 10.1177/0148607193017006493 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MH740 UT WOS:A1993MH74000001 PM 8301800 ER PT J AU HARDIN, TC KOELLER, JM KUHN, JG ROODMAN, D VONHOFF, DD AF HARDIN, TC KOELLER, JM KUHN, JG ROODMAN, D VONHOFF, DD TI NUTRITIONAL PARAMETERS OBSERVED DURING 28-DAY INFUSION OF RECOMBINANT HUMAN TUMOR-NECROSIS-FACTOR-ALPHA SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID CACHECTIN; CACHEXIA; METABOLISM; RAT; INTERLEUKIN-1; RABBITS; INJURY AB In conjunction with a Phase I investigation of the antineoplastic activity of recombinant human tumor necrosis factor-alpha (TNF-alpha), administered as a 28-day continuous infusion, selected nutritional parameters were evaluated to identify any effect that might be attributed to the TNF infusion. Seven clinically stable men with a variety of tumor types were studied. None had clinical or laboratory evidence of significant malnutrition before entry into the study. Five patients received 10 mug of recombinant human TNF-alpha per square meter per day and two patients received 25 mug/m2 per day. Indirect calorimetry assessment of resting energy expenditure, body weight, serum TNF concentration, and laboratory analysis of common nutritional markers (albumin, prealbumin, and triglycerides) were performed at baseline, day 14, day 28, and 2 weeks (day 42) after completion of the infusion. There were no statistically significant differences by analysis of variance observed in any parameter during the study period compared with baseline values and values on day 42. Also, there were no differences between any parameters when stratified by dose administered, although the number of patients studied was small. Measured serum TNF concentrations ranged from 0.02 to 1.56 ng/mL and did not correlate with study day or dose of TNF infused. No correlation was observed between serum TNF concentrations and resting energy expenditure. Although others have reported significant metabolic changes associated with acute administration of TNF in humans and animals, our experience does not support a hypermetabolic state in patients receiving low daily dose, long-term (28-day) continuous infusion of recombinant human TNF-alpha, a state that may be consistent with many neoplastic conditions. C1 UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78285. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. RP HARDIN, TC (reprint author), UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT PHARMACOL,PHARM SERV 119,SAN ANTONIO,TX 78284, USA. FU NCI NIH HHS [NCI CM-07305] NR 31 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD NOV-DEC PY 1993 VL 17 IS 6 BP 541 EP 545 DI 10.1177/0148607193017006541 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MH740 UT WOS:A1993MH74000010 PM 8301809 ER PT J AU SHURIN, PA REHMUS, JM JOHNSON, CE MARCHANT, CD CARLIN, SA SUPER, DM VANHARE, GF JONES, PK AMBROSINO, DM SIBER, GR AF SHURIN, PA REHMUS, JM JOHNSON, CE MARCHANT, CD CARLIN, SA SUPER, DM VANHARE, GF JONES, PK AMBROSINO, DM SIBER, GR TI BACTERIAL POLYSACCHARIDE IMMUNE GLOBULIN FOR PROPHYLAXIS OF ACUTE OTITIS-MEDIA IN HIGH-RISK CHILDREN SO JOURNAL OF PEDIATRICS LA English DT Article ID INFLUENZAE TYPE-B; MIDDLE-EAR FLUIDS; HEMOPHILUS-INFLUENZAE; STREPTOCOCCUS-PNEUMONIAE; INTRAVENOUS IMMUNOGLOBULIN; HAEMOPHILUS-INFLUENZAE; PNEUMOCOCCAL VACCINE; INFECTED CHILDREN; EARLY INFANCY; RECURRENT AB We evaluated the prevention of recurrences of acute otitis medio (AOM) by bacterial polysaccharide immune globulin (BPIG), a hyperimmune human immune globulin prepared by immunizing donors with bacterial polysaccharide vaccines. We used a randomized, stratified, double-blind, placebo-controlled design. Children less-than-or-equal-to 24 months of age with 1 to 3 prior episodes of AOM received BPIG, 0.5 ml/kg, or saline placebo intramuscularly at entry and 30 days later. During the 120-day follow-up period, AOM was diagnosed by using clinical criteria and was confirmed with tympanocentesis and culture of the middle ear exudates. Eighty-eight episodes of AOM were observed in 76 patients who completed the study. The incidence of AOM during the entire 120-day study period was similar in BPIG and placebo recipients. Pneumococcal AOM was significantly less frequent in BPIG recipients (0.21 episode per patient) than in placebo recipients (0.45 episode per patient; p = 0.05). Time spent free of AOM was significantly prolonged in recipients of BPIG, in comparison with placebo recipients (51 vs 35 days; p = 0.034). This study demonstrated that circulating antibody, even without stimulation of specific local immunity, may prevent infection of the middle ear. The use of immune globulin preparations for longer periods or at a higher dosage might decrease the incidence of recurrent AOM in otitis-prone children, and deserves further evaluation. C1 CASE WESTERN RESERVE UNIV, SCH MED, CLEVELAND, OH 44106 USA. METROHLTH MED CTR, CLEVELAND, OH USA. TUFTS UNIV, SCH MED, BOSTON, MA 02111 USA. CASE WESTERN RESERVE UNIV, SCH MED, DEPT EPIDEMIOL & BIOSTAT, CLEVELAND, OH 44106 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, INFECT DIS LAB, BOSTON, MA 02115 USA. MASSACHUSETTS DEPT PUBL HLTH, CTR DIS CONTROL, BIOL LABS, BOSTON, MA USA. RP SHURIN, PA (reprint author), COLUMBIA UNIV COLL PHYS & SURG, DEPT PEDIAT, NEW YORK, NY 10032 USA. FU NIAID NIH HHS [AI 18125]; NICHD NIH HHS [1RO1 HD18753 01A1GT] NR 56 TC 69 Z9 69 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD NOV PY 1993 VL 123 IS 5 BP 801 EP 810 DI 10.1016/S0022-3476(05)80865-0 PG 10 WC Pediatrics SC Pediatrics GA MF096 UT WOS:A1993MF09600025 PM 8229496 ER PT J AU SEYMOUR, GJ GEMMELL, E REINHARDT, RA EASTCOTT, J TAUBMAN, MA AF SEYMOUR, GJ GEMMELL, E REINHARDT, RA EASTCOTT, J TAUBMAN, MA TI IMMUNOPATHOGENESIS OF CHRONIC INFLAMMATORY PERIODONTAL-DISEASE - CELLULAR AND MOLECULAR MECHANISMS SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article; Proceedings Paper CT 9TH INTERNATIONAL CONF ON PERIODONTAL RESEARCH CY SEP 23-26, 1992 CL OSAKA, JAPAN DE PERIODONTAL DISEASE; IMMUNOPATHOGENESIS; CELLULAR; MOLECULAR ID TUMOR-NECROSIS-FACTOR; MEMORY T-CELLS; PERIPHERAL-BLOOD; EXPERIMENTAL GINGIVITIS; ADULT PERIODONTITIS; ADHESION MOLECULE; ENDOTHELIAL-CELLS; BACTERIA; LYMPHOCYTES; ACTIVATION AB Recent studies of the cellular mechanisms involved in chronic inflammatory periodontal disease (CIPD) have contributed significantly to our understanding of the pathogenesis of the disease process. Functional studies have demonstrated polymorphonuclear neutrophil (PMN) chemotactic defects in some 70% of subjects with localized juvenile periodontitis while chemiluminescence data have suggested that periphertal blood PMNs from young subjects with adult periodontitis (AP) may be in a metabolically active state. Further studies have shown that stimulation of PMNs with a number of periodontopathic bacteria resulted in the production of an IL-1 inhibitor suggesting a possible regulatory role for PMNs in CIPD in addition to their established protective role. Most work on the immunoregulation of CIPD has, however, concentrated on T-cells. Recent limit dilution analysis has demonstrated the presence of periodontopathic bacteria-specific T cells in peripheral blood and the involvement and homing of these cells to the local lesions of CIPD is currently the focus of many studies. In animal studies, Actinobacillus actinomycetemcomitans (Aa)-specific T-cell clones home to the gingival tissues where they may exert a protective role. Homing and retention of lymphocytes to and in specific sites is dependent upon the expression of adhesion molecules. Recent data indicate however, that while there are increasing levels of ICAM-1, LECAM-1 and PECAM-1 expression with increasing degrees of inflammation, there are no differences between gingivitis and periodontitis lesions. Cytokine profiles may be related to the role of T-cell clones homing to the gingiva in CIPD. In subjects susceptible to periodontal breakdown there may be an increase in the type 2 IL-4 producing T-cells whereas in non-susceptible subjects, type 1 IL-2/IFN-gamma producing T-cells may preferentially home to the gingiva. This hypothesis is generally supported by recent data obtained from human studies but data obtained from animal studies is only partly supportive and may suggest the opposite. Nevertheless, it is now possible to construct a testable framework or model of CIPD based on these cellular and molecular mechanisms. C1 UNIV NEBRASKA,MED CTR,DEPT SURG SPECIALITIES,LINCOLN,NE. FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. RP SEYMOUR, GJ (reprint author), UNIV QUEENSLAND,DEPT DENT,BRISBANE,QLD 4072,AUSTRALIA. OI Seymour, Gregory/0000-0001-7595-5651 FU NIDCR NIH HHS [DE 03420, DE 04881] NR 59 TC 191 Z9 195 U1 1 U2 12 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD NOV PY 1993 VL 28 IS 6 BP 478 EP 486 DI 10.1111/j.1600-0765.1993.tb02108.x PN 2 PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MG593 UT WOS:A1993MG59300008 PM 7505322 ER PT J AU NIEDERMAN, R KENT, R AF NIEDERMAN, R KENT, R TI USE OF SUBGINGIVAL TEMPERATURE IN PERIODONTAL CLINICAL-TRIALS - ASSESSMENT OF ACCURACY AND RELIABILITY SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article; Proceedings Paper CT 9TH INTERNATIONAL CONF ON PERIODONTAL RESEARCH CY SEP 23-26, 1992 CL OSAKA, JAPAN ID GINGIVAL RP NIEDERMAN, R (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE08415, DE04881] NR 17 TC 3 Z9 3 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD NOV PY 1993 VL 28 IS 6 BP 540 EP 542 DI 10.1111/j.1600-0765.1993.tb02120.x PN 2 PG 3 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MG593 UT WOS:A1993MG59300020 PM 8263727 ER PT J AU GOW, DW GORDON, PC AF GOW, DW GORDON, PC TI COMING TO TERMS WITH STRESS - EFFECTS OF STRESS LOCATION IN SENTENCE PROCESSING SO JOURNAL OF PSYCHOLINGUISTIC RESEARCH LA English DT Article ID LEXICAL ACCESS; REACTION-TIME; SPEECH; PHONEME; RHYTHM; SEGMENTATION; PERCEPTION; CONTEXT AB The purpose of this research was to determine the role of syllabic stress in language processing during the early on-line processing of speech and later in the representation of a sentence in memory. Experiment 1 used a syllable monitoring task while Experiment 3 used a probe task in which subjects heard a sentence and then were asked to determine whether a probe syllable had occurred in the sentence. In the monitoring task, stressed syllables were detected more rapidly in word-initial position, but unstressed syllables were detected more rapidly in word-final position. Stress facilitation in initial syllables was strongly related to high relative F0, but not to changes in perceived vowel quality as assessed in Experiment 2. This pattern is interpreted as evidence that lexical stress is used on-line to guide lexical access and/or lexical segmentation. The probe task of Experiment 3 showed stress facilitation in both positions, indicating that stress is independently retained in the postperceptual representation of a sentence. C1 UNIV N CAROLINA,DEPT PSYCHOL,CHAPEL HILL,NC 27599. RP GOW, DW (reprint author), MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,BOSTON,MA 02144, USA. NR 51 TC 13 Z9 13 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0090-6905 J9 J PSYCHOLINGUIST RES JI J. Psycholinguist. Res. PD NOV PY 1993 VL 22 IS 6 BP 545 EP 578 PG 34 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA MJ697 UT WOS:A1993MJ69700001 PM 8295163 ER PT J AU SEARLES, JS ALTERMAN, AI MILLER, SM AF SEARLES, JS ALTERMAN, AI MILLER, SM TI COMPARABILITY OF SELF-REPORT OF FAMILIAL ALCOHOLISM AMONG MALE AND FEMALE COLLEGE-STUDENTS SO JOURNAL OF STUDIES ON ALCOHOL LA English DT Article AB There is a general impression in the literature that women are more accurate reporters of familial psychiatric history. In this regard, this study presents data from a large cohort of young men (n = 427) and women (n = 607) who in answering a questionnaire self-reported alcohol abuse symptoms for various biological relatives. No significant gender differences emerged for any of the family history comparisons including reports for father, mother, either parent, any first- or second-degree relatives, or men or women relatives. The findings are discussed in the context of the existing literature. C1 UNIV VERMONT,DEPT PSYCHIAT,BURLINGTON,VT 05405. UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA. TEMPLE UNIV,DEPT PSYCHOL,PHILADELPHIA,PA 19122. RP SEARLES, JS (reprint author), VERMONT ALCOHOL RES CTR,2000 MT VIEW DR,COLCHESTER,VT 05446, USA. FU NIAAA NIH HHS [5-RO1-AA07361] NR 4 TC 7 Z9 7 U1 0 U2 0 PU ALCOHOL RES DOCUMENTATION INC CENT ALCOHOL STUD RUTGERS UNIV PI PISCATAWAY PA PO BOX 969, PISCATAWAY, NJ 08855-0969 SN 0096-882X J9 J STUD ALCOHOL JI J. Stud. Alcohol PD NOV PY 1993 VL 54 IS 6 BP 730 EP 732 PG 3 WC Substance Abuse; Psychology SC Substance Abuse; Psychology GA ME009 UT WOS:A1993ME00900011 PM 8271809 ER PT J AU FIELD, AE WOLF, AM HERZOG, DB CHEUNG, L COLDITZ, GA AF FIELD, AE WOLF, AM HERZOG, DB CHEUNG, L COLDITZ, GA TI THE RELATIONSHIP OF CALORIC-INTAKE TO FREQUENCY OF DIETING AMONG PREADOLESCENT AND ADOLESCENT GIRLS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article; Proceedings Paper CT 14TH ANNUAL MEETING OF THE SOC-FOR-BEHAVIORAL-MEDICINE CY MAR 13, 1993 CL SAN FRANCISCO, CA SP SOC BEHAV MED DE DIETING; ADOLESCENTS; FEMALE; OBESITY ID PHYSICAL-ACTIVITY; EATING ATTITUDES; BEHAVIOR; OBESITY; WEIGHT; QUESTIONNAIRE; POPULATION; VALIDITY; BULIMIA; NERVOSA AB Objective: To assess the relationships of concern with weight and shape, frequency of dieting, body mass index (weight/height2 ), and energy intake among 431 preadolescent and adolescent girls from a working-class New England suburb. Method: A cross-sectional study design used self-report measures of concern with weight, frequency of dieting, and average dietary intake. Results: Approximately 30% of the girls in each age stratum were above the national age-standardized 85th percentile for body mass index (BMI). Body mass index was positively associated with concern about weight and shape (r = 0.46, p = 0.0001) and frequency of dieting (r = 0.49, p = 0.0001). Extreme concern with weight and shape was most common among the obese preadolescent and adolescent girls; however, dissatisfaction was also present among the underweight females. Fifty percent of the girls who were below the national age-standardized 15th percentile for BMI reported their ideal weight is less than their current weight, implying that among young women thinness is not adequate protection against dissatisfaction with weight and shape. Frequency of dieting was positively associated with concern about weight and shape (r = 0.53, p = 0.001) but not physical activity (r = -0.04, p = 0.36). Overall, we did not find strong evidence that dieters were eating less than their nondieting peers. Only among high school students was there a significant negative association between frequency of dieting and energy intake (r = -0.20, p = 0.01), suggesting that ''dieting'' may have a different meaning to preadolescents and adults. Conclusions: These findings indicate that self-reported frequent dieting in preadolescent and young adolescent girls is more indicative of extreme concern with weight than of decreased energy intake. Furthermore, extreme concern with weight and shape is most common among the obese preadolescent and adolescent girls. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,EATING DISORDER UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,CTR HLTH COMMUN,HARVARD NUTR & FITNESS PROGRAM,BOSTON,MA 02115. RP FIELD, AE (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,CHANNING LAB,180 LONGWOOD AVE,BOSTON,MA 02115, USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NIDDK NIH HHS [P30-DK-46200]; NIMH NIH HHS [2T32 MH 17119] NR 33 TC 44 Z9 45 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD NOV PY 1993 VL 32 IS 6 BP 1246 EP 1252 DI 10.1097/00004583-199311000-00019 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA MD603 UT WOS:A1993MD60300020 PM 8282671 ER PT J AU COHEN, M XIONG, J PARRY, G ADAMS, PC CHAMBERLAIN, D WIECZOREK, I FOX, KAA MCBRIDE, R CHESEBRO, JH FUSTER, V KELLER, C KRONMAL, R STRAIN, J KELLY, A ALI, J LANCASTER, G AF COHEN, M XIONG, J PARRY, G ADAMS, PC CHAMBERLAIN, D WIECZOREK, I FOX, KAA MCBRIDE, R CHESEBRO, JH FUSTER, V KELLER, C KRONMAL, R STRAIN, J KELLY, A ALI, J LANCASTER, G TI PROSPECTIVE COMPARISON OF UNSTABLE ANGINA VERSUS NON-Q-WAVE MYOCARDIAL-INFARCTION DURING ANTITHROMBOTIC THERAPY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID ACUTE CORONARY SYNDROMES; MULTICENTER TRIAL; ASPIRIN; TERM; REINFARCTION; PROGNOSIS; PECTORIS; DEATH AB Objectives. This study was designed to compare the response of unstable angina and non-Q wave myocardial infarction during treatment with antithrombotic therapy. Background. Antithrombotic therapy is beneficial in patients with these two coronary syndromes. Methods. In a multicenter trial of antithrombotic therapy in unstable angina or non-Q wave myocardial infarction, 358 patients admitted within 48 h of chest pain were randomized to antithrombotic therapy with either 1) aspirin alone, or 2) aspirin plus heparin followed by aspirin plus warfarin, and were prospectively followed up for 12 weeks. Admission cardiac enzyme analyses revealed unstable angina in 268 patients and non-Q wave myocardial infarction in 62. Given an event rate of about 25%, this study has a power of 80% to detect a 50% difference between the two groups. Results. Patients with unstable angina and non-Q wave myocardial infarction were similar with regard to age, gender, coronary risk factors and prior antianginal medication. Primary end points at 12 weeks were recurrent ischemia, infarction and death. [GRAPHICS] In the non-Q wave group, all infarctions and death occurred within the 1st week. Conclusions. Patients with unstable angina or non-Q wave myocardial infarction on antithrombotic therapy have a similar total number of ischemic events by 12 weeks. However, despite maximal medical therapy with antianginal and antithrombotic medication, patients with non-Q wave infarction have a significantly higher rate of reinfarction and death. C1 ROYAL SUSSEX CTY HOSP,DEPT CARDIOL,BRIGHTON,E SUSSEX,ENGLAND. ROYAL VICTORIA INFIRM,DEPT CARDIOL,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND. UNIV EDINBURGH,CARDIOVASC RES UNIT,EDINBURGH,MIDLOTHIAN,SCOTLAND. STAT & EPIDEMIOL RES CORP,SEATTLE,WA. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. BIOSTAT CTR,SEATTLE,WA. BETH ISRAEL HOSP,NEW YORK,NY. MT SINAI HOSP,NEW YORK,NY. CITY HOSP ELMHURST,ELMHURST,NY. RP COHEN, M (reprint author), HAHNEMANN UNIV,DEPT MED,LIKOFF CARDIOVASC INST,CARDIOL MS-119,BROAD & VINE,PHILADELPHIA,PA 19102, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 21 TC 27 Z9 27 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD NOV 1 PY 1993 VL 22 IS 5 BP 1338 EP 1343 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ363 UT WOS:A1993MQ36300012 PM 7901254 ER PT J AU CHEN, CG AF CHEN, CG TI DETERMINATION OF MITRAL REGURGITANT FLOW-RATE FROM COLOR-FLOW MAPS OF THE REGURGITANT FLOW CONVERGENCE REGION - REPLY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Letter ID QUANTIFICATION RP CHEN, CG (reprint author), MASSACHUSETTS GEN HOSP,NONINVAS CARDIAC LAB,0 EMERSON PL,2F,BOSTON,MA 02114, USA. NR 9 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 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD NOV 1 PY 1993 VL 22 IS 5 BP 1554 EP 1555 PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ363 UT WOS:A1993MQ36300049 ER PT J AU LEIFER, D KOWALL, NW AF LEIFER, D KOWALL, NW TI IMMUNOHISTOCHEMICAL PATTERNS OF SELECTIVE CELLULAR VULNERABILITY IN HUMAN CEREBRAL-ISCHEMIA SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE CEREBRAL ISCHEMIA; AUTOPSY; HIPPOCAMPUS; CEREBRAL CORTEX; IMMUNOHISTOCHEMISTRY ID TRANSIENT GLOBAL-ISCHEMIA; RAT HIPPOCAMPAL-FORMATION; C-FOS PROTEIN; IMMUNOREACTIVE NEURONS; NEUROFILAMENT PROTEIN; FOREBRAIN ISCHEMIA; ALZHEIMERS-DISEASE; NMDA RECEPTORS; BRAIN INJURY; GLUTAMATE AB Although specific patterns of cellular vulnerability have been identified in experimental models of cerebral ischemia, there is little data on the occurrence of similar abnormalities in human ischemia. We therefore used a variety of histochemical methods to define changes affecting specific classes of cells in post-mortem specimens from seven patients with hippocampal and neocortical ischemic lesions. In acute lesions, staining with SMI-32, an antibody directed against nonphosphorylated neurofilaments that labels pyramidal projection neurons, was prominently depleted even when conventional Nissl staining revealed only mild pyknosis. In contrast, staining for other markers such as microtubule-associated protein 2 (MAP-2), another cytoskeletal protein, or parvalbumin, a calcium-binding protein found in gamma-aminobutyric acid (GABA)-ergic interneurons, were relatively preserved. SMI-32 antibody also labeled dystrophic axons and axonal retraction balls in and around acute ischemic lesions. The pattern of differential changes in immunoreactivity was essentially the same in all acute ischemic injuries, including both diffuse lesions in the CA1 field (Sommer's sector) and discrete infarcts in CA1 and neocortex. In addition, immunoreactivity for the immediate early gene product c-fos was enhanced in and around the acute ischemic lesions that we studied. In some very acute lesions, immunoreactivity for glial fibrillary acidic protein (GFAP) was depleted in areas of severe ischemia and necrosis, but, as expected, GFAP immunoreactivity was increased in lesions more than a few days old. In contrast, the loss of SMI-32 immunoreactivity persisted in chronic lesions. These findings are consistent with those of experimental ischemia in animals and confirm the relevance of these studies for human cerebral ischemia. The pattern of selective changes also resembles that of injuries induced directly by excitatory amino acids, which may play a significant role in the pathogenesis of ischemic damage. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. BEDFORD VET ADM MED CTR,DEPT NEUROL,BEDFORD,MA. BEDFORD VET ADM MED CTR,DEPT PATHOL,BEDFORD,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NICHD NIH HHS [HD00888]; NINDS NIH HHS [NS25588, NS10828] NR 53 TC 44 Z9 47 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD NOV PY 1993 VL 119 IS 2 BP 217 EP 228 DI 10.1016/0022-510X(93)90137-N PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA ME915 UT WOS:A1993ME91500014 PM 8277338 ER PT J AU GAISSERT, HA MATHISEN, DJ GRILLO, HC MALT, RA WAIN, JC MONCURE, AC KIM, JH MUELLER, PR DEANGELIS, R OTTINGER, LW AF GAISSERT, HA MATHISEN, DJ GRILLO, HC MALT, RA WAIN, JC MONCURE, AC KIM, JH MUELLER, PR DEANGELIS, R OTTINGER, LW TI SHORT-SEGMENT INTESTINAL INTERPOSITION OF THE DISTAL ESOPHAGUS SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article AB Esophageal replacement remains a challenge. Colon and jejunum provide alternative conduits to replace the lower esophagus when stomach is not suitable. Between 1971 and 1991, 41 patients underwent short-segment interposition of the esophagus with jejunum or colon. Indications were failed antireflux procedures (n = 21), nondilatable stricture (n = 9), achalasia (n = 2), moniliasis (n = 2), Barrett's esophagus with carcinoma in situ (n = 2), hemorrhagic esophagitis after esophagogastrectomy (n = 1), motility disorder (n = 1), instrumental perforation (n = 1), carcinoma (n = 1), and leiomyosarcoma (n = 1). Thirty-one patients (75.6 %) had prior surgical procedures. Interposition with colon was performed in 22 patients and with jejunum in 19. Major complications occurred in 45 % after colon interposition (10/22) and hospital mortality was 4.5% (1/22). Major complications after jejunal interposition occurred in 31% (6/19) and hospital mortality was 10.5% (2/19). A contained anastomotic leak occurred in 1 patient, perforation of a colon segment in 1, and jejunal graft necrosis in a third. Late functional results in 34 patients with a mean follow-up of 87 months were excellent or good in 26, fair in 5, and poor in 1. Colon interposition failed to improve symptoms in 2 patients with gastrointestinal motility disorders. Six patients underwent manometry and barium food provocation study. Two colon segments and 3 jejunal interpositions were hypoperistaltic or aperistaltic according to manometry. There was 1 case of aperistaltic jejunum with a distended afferent loop. When stomach is not available, successful palliation of swallowing can be accomplished with either jejunum or colon. Surgeons involved in the management of esophageal disease should be familiar with the technical details of both procedures. C1 MASSACHUSETTS GEN HOSP,SURG SERV,WARREN 1109,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 11 TC 29 Z9 29 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD NOV PY 1993 VL 106 IS 5 BP 860 EP 867 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA MF999 UT WOS:A1993MF99900012 PM 8231208 ER PT J AU DRETLER, SP ROSEN, DI AF DRETLER, SP ROSEN, DI TI THE ELECTROMECHANICAL IMPACTOR - THE RESULTS OF DESIGN MODIFICATIONS SO JOURNAL OF UROLOGY LA English DT Article DE CALCULI; LITHOTRIPSY; MEDICAL DEVICES AB The first generation clinical electromechanical impactor was a 5F device that used a 3.0F electrohydraulic probe within a coiled spring with a blunt solder end cap. Clinical trials showed that this device fragmented 70% of the calculi but failed to fragment the harder stones. Applying the principle that impact kinetic energy is most dependent on velocity (KE = 1/2 MV2), 3 major design modifications were made to improve fragmentation efficiency: 1) the spring was changed from an extension to a compression type that captured and used more of each electrical spark, 2) the tip was changed from solder to lightweight titanium and 3) the tip shape was changed from blunt to conical. The result was a 41% increase in impact kinetic energy, a 40% increase in probe longevity and successful in vitro fragmentation of the harder calculi without compromise in tissue safety as determined by membrane perforation studies. C1 PHYS SCI INC,ANDOVER,MA. RP DRETLER, SP (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT SURG UROL,LITHOTRIPTOR UNIT,BOSTON,MA 02115, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD NOV PY 1993 VL 150 IS 5 BP 1399 EP 1401 PN 1 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA MC576 UT WOS:A1993MC57600015 PM 8411408 ER PT J AU DRETLER, SP AF DRETLER, SP TI CLINICAL-EXPERIENCE WITH ELECTROMECHANICAL IMPACTOR SO JOURNAL OF UROLOGY LA English DT Article DE URETERAL CALCULI; LITHOTRIPSY; MEDICAL DEVICES AB The electromechanical impactor is a 3.0F electrohydraulic electrode within a stainless steel sheath attached to a distal compression spring with a conical titanium tip. Eac electrical discharge causes a 2.7 mm. tip extension and a kinetic impact energy of 900 bar. It is 5F, flexible and placed within the straight working port of a 9.5F to 10.OF rigid or semirigid ureteroscope. A clinical trial was performed and 15 patients (16 ureters with calculi) were treated with this device. An upper ureteral stone partially fragmented and migrated cephalad, 1 stone failed to break and was basket extracted, and there was 1 machine failure. The 13 other calculi were successfully broken to fragments less than 5 mm. In 2 patients baskets were also used to remove the larger monohydrate fragments. A secondary procedure was required to basket a 4 mm. calcium oxalate monohydrate fragment in a patient with 3 ureteral calculi. The average size of the calculi was 14 mm. in largest diameter. Excluding the machine failure, the average number of pulses required for fragmentation was 764. The life of each device was 600 to 800 pulses. Of the 15 cases 1 electrode was used in 10, 2 in 3 and 3 in 2. There was no evidence of ureteral wall injury, abrasion or perforation. The electromechanical impactor is a safe and effective method of ureteral stone fragmentation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DRETLER, SP (reprint author), MASSACHUSETTS GEN HOSP,CTR KIDNEY STONE,BOSTON,MA 02114, USA. NR 1 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD NOV PY 1993 VL 150 IS 5 BP 1402 EP 1404 PN 1 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA MC576 UT WOS:A1993MC57600016 PM 8411409 ER PT J AU BARRY, MJ AF BARRY, MJ TI AMERICAN-UROLOGICAL-ASSOCIATION SYMPTOM INDEX FOR WOMEN WITH VOIDING SYMPTOMS - LACK OF INDEX SPECIFICITY FOR BENIGN PROSTATE HYPERPLASIA - COMMENT SO JOURNAL OF UROLOGY LA English DT Editorial Material RP BARRY, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED SERV,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD NOV PY 1993 VL 150 IS 5 BP 1708 EP 1709 PN 2 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA MC578 UT WOS:A1993MC57800029 ER PT J AU MEGERMAN, J HAMILTON, G SCHMITZRIXEN, T ABBOTT, WM AF MEGERMAN, J HAMILTON, G SCHMITZRIXEN, T ABBOTT, WM TI COMPLIANCE OF VASCULAR ANASTOMOSES WITH POLYBUTESTER AND POLYPROPYLENE SUTURES SO JOURNAL OF VASCULAR SURGERY LA English DT Article AB Purpose: Polybutester suture is more easily stretched than other vascular sutures and may produce more compliant anastomoses. The effects of using polybutester and polypropylene sutures were compared acutely in arterial autografts and in chronic implants of cephalic vein grafts into the femoral arteries of dogs. Methods: Paraanastomotic profiles of diameter and compliance were measured with echo-tracked ultrasonography, and profiles of intimal thickening were generated from histologic sections of the vessels harvested after 3 months. Results: Polybutester produced more compliant anastomoses, compared with polypropylene, in arterial autografts (in vitro: 5.9% +/- 2.0% vs 3.3% +/- 0.6% diameter change/100 mm Hg, p < 0.01; in vivo: 3.1% +/- 1.1% vs 1.6% +/- 0.5%, p < 0.05), but this difference was not observed with vein as the graft material, either initially (1.1% +/- 1.2% vs 1.7% +/- 0.5%) or after 3 months (2.1% +/- 1.2% vs 2.4% +/- 0.8%). This dichotomy may reflect a governing influence of the stiffer veingrafts, compared with host artery (2.6% +/- 1.0% vs 5.4% +/- 1.2%), or the use of suboptimal tension on the polybutester suture when creating the anastomosis. Conclusions: Both sutures produced similar compliance and thickness profiles. Polybutester initially produces a more compliant anastomosis when both artery and graft are compliant, reducing anastomotic compliance mismatch. However, this benefit may not apply when the anastomosis includes a vessel of low compliance. C1 UNIV LONDON IMPERIAL COLL SCI TECHNOL & MED,ROYAL FREE HOSP,DEPT SURG,LONDON SW7 2AZ,ENGLAND. UNIV LONDON IMPERIAL COLL SCI TECHNOL & MED,SCH MED,LONDON SW7 2AZ,ENGLAND. MASSACHUSETTS GEN HOSP,DIV VASC SURG,VASC RES LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL29429] NR 11 TC 11 Z9 11 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 NOV PY 1993 VL 18 IS 5 BP 827 EP 834 PG 8 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MG178 UT WOS:A1993MG17800015 PM 8230570 ER PT J AU BERGELSON, JM STJOHN, N KAWAGUCHI, S CHAN, M STUBDAL, H MODLIN, J FINBERG, RW AF BERGELSON, JM STJOHN, N KAWAGUCHI, S CHAN, M STUBDAL, H MODLIN, J FINBERG, RW TI INFECTION BY ECHOVIRUSES-1 AND ECHOVIRUSES-8 DEPENDS ON THE ALPHA-2 SUBUNIT OF HUMAN VLA-2 SO JOURNAL OF VIROLOGY LA English DT Note ID CELLS; RECEPTOR; IDENTIFICATION; ATTACHMENT AB Anti-VLA-2 antibodies protected HeLa cells from infection by echoviruses 1 and 8 but not from infection by other echovirus serotypes. Echoviruses 1 and 8 bound to and infected nonpermissive hamster cells transfected with the alpha2 subunit of human VLA-2. These results indicate that the human alpha2 subunit is critical for infection by echoviruses 1 and 8 but that other echovirus serotypes must bind receptors other than VLA-2. C1 DARTMOUTH HITCHCOCK MED CTR,INFECT DIS SECT,LEBANON,NH 03756. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. RP BERGELSON, JM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NIAID NIH HHS [AI31628] NR 19 TC 78 Z9 82 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1993 VL 67 IS 11 BP 6847 EP 6852 PG 6 WC Virology SC Virology GA MC016 UT WOS:A1993MC01600063 PM 8411387 ER PT J AU BAHRAM, S AF BAHRAM, S TI PEPTIDE TRANSPORTERS AND ANTIGEN PRESENTATION SO M S-MEDECINE SCIENCES LA French DT Review AB Presentation of endogenously derived nonapeptides to the T cell receptor of CD8+ T cells is the central event of the cell mediated immune response. Peptides generated from proteolysis of intracellular proteins must cross the endoplasmic reticulum lipid bilayer in order to associate with major histocompatibility complex class I heavy and light chains. This translocation is dependent on the presence of a putative peptide transporter heterodimer. This paper reviews the recent discovery, inside the major histocompatibility complex class II region, of genes encoding this transporter and two of a cytoplasmic proteolytic system called the proteasome. C1 DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. NR 0 TC 5 Z9 5 U1 0 U2 1 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE SN 0767-0974 J9 M S-MED SCI JI M S-Med. Sci. PD NOV PY 1993 VL 9 IS 11 BP 1204 EP 1213 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MM989 UT WOS:A1993MM98900005 ER PT J AU PFLEIDERER, B ACKERMAN, JL GARRIDO, L AF PFLEIDERER, B ACKERMAN, JL GARRIDO, L TI MIGRATION AND BIODEGRADATION OF FREE SILICONE FROM SILICONE GEL-FILLED IMPLANTS AFTER LONG-TERM IMPLANTATION SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE SILICONE; MIGRATION; DEGRATION; NMR ID BREAST IMPLANTS; SI-29 NMR; PROSTHESES; TISSUE; MODEL AB In vivo H-1 NMR chemical shift imaging (CSI), H-1 NMR localized spectroscopy (STEAM) and multinuclear NMR spectroscopy (Si-29, C-13, H-1) were used to characterize the aging process of silicone gel-filled implants in a rat model after long-term implantation. Although no significant changes could be observed in the implants or surrounding tissue by in vivo H-1 chemical shift imaging, in vivo H-1 localized spectroscopy of the livers from the longer term population revealed the presence of silicone. Ex vivo Si-29 spectroscopy of the liver, spleen, and the capsule formed around the 9 and 12 month implants clearly demonstrated and confirmed for the first time that a significant amount of free silicone migrates from silicone gel-filled implants. Also, these results show that silicones are not metabolically inert, and their biodegradation in tissue and within the implant can be monitored after 9 and 12 months by changes in the Si-29 chemical shifts seen in corresponding ex vivo spectra. The NMR findings are supported by those obtained by atomic absorption spectroscopy. Silicone aging changes not only the chemical composition of the gel, but also its proton T2 relaxation times, which increase with long implantation times. The three dimensional structure of the gel disintegrates (i.e., polymer chain rupture), increasing the molecular mobility of the polymer and, consequently, its protons T2 values. The relaxation data we obtained reflect this in vivo degradation, especially in the case of implant rupture. Additionally, small concentrations of fat in the silicone gel were found within the implants. The presence of these lipophilic substances also might increase the T2 values (plasticizer effect). These findings may assist in evaluating the implant integrity and disease symptoms related to their presence in humans. C1 MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,BLDG 149,13TH ST,BOSTON,MA 02129. HARVARD MED SCH,BOSTON,MA. RI Garrido, Leoncio/K-3092-2014; Ackerman, Jerome/E-2646-2015 OI Garrido, Leoncio/0000-0002-7587-1260; Ackerman, Jerome/0000-0001-5176-7496 NR 24 TC 53 Z9 54 U1 2 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD NOV PY 1993 VL 30 IS 5 BP 534 EP 543 DI 10.1002/mrm.1910300503 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MC689 UT WOS:A1993MC68900002 PM 8259053 ER PT J AU TOMERA, JF FRIEND, KD LILFORD, K AF TOMERA, JF FRIEND, KD LILFORD, K TI MULTIVARIATE INFLUENCE OF PROTEIN-DEFICIENCIES AND SEPSIS ON NEUROMUSCULAR PHARMACODYNAMICS SO METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY LA English DT Article DE ADENOSINE 3'/5'-CYCLIC MONOPHOSPHATE; ENDOTOXICOSIS; GASTROCNEMIUS; MOUSE MODEL; MUSCLE TENSION; PROTEIN-CALORIE DEFICIENCY; PROTEIN DEFICIENCY; SEPSIS ID INTRAPERITONEAL ENDOTOXIN; GASTROCNEMIUS-MUSCLE; RISK FACTOR; INJURY; MODEL; CATECHOLAMINES; METABOLISM; INFECTION; DISEASE; RATS AB The novelty of applying three-dimensional graphic capabilities, utilizing area and vector changes, to understand pathological states broadens the perspective required to formulate therapeutics in treating these conditions. Protein malnutrition and sepsis underlie complications emanating from trauma, burn injury and major elective surgery. This study delineated some of the multiple factors influencing neuromuscular (NM) function (i.e., tension) and d-tubocurarine (dTC) pharmacodynamics influenced by sepsis and malnutrition. Relationships between more than two factors, capable of influencing the dependency of either of rite above parameters, were explored. This study used mouse models of sepsis and malnutrition (via either protein or protein-calorie deficiencies. Sepsis was studied using dosages at 1/4 or 1/3 the LD50 of endotoxin. Diets of 5% protein and 5% protein + 35% fiber achieved protein and protein-calorie deficiencies. When considered simultaneously, some parameters (time (x), weight loss (w) and cAMP (c)) contributed each in part to active tension (y). Also, some of the same parameters determined the dependency of dTC-ED(50) (t) (time (x), active tension (y) and total body weight (z)). These findings indicate that multiple factors are responsible for the muscle weakness (tension dysfunction) and dTC hyposensitivity observed in endotoxicosis and protein malnutrition. Consideration of these multiple factors involving nutrient deprivation and septic stress would prove beneficial in improving the quality of rehabilitative trauma care. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIOL,BOSTON,MA. RP TOMERA, JF (reprint author), SHRINERS BURNS INST,RES CTR,ANESTHESIA SERV,CLIN PHARMACOL LAB,1 KENDALL SQ,BLDG 1400W,CAMBRIDGE,MA 02142, USA. NR 44 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 NOV PY 1993 VL 15 IS 9 BP 571 EP 586 PG 16 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MP819 UT WOS:A1993MP81900001 ER PT J AU CHUANG, LM MYERS, MG BACKER, JM SHOELSON, SE WHITE, MF BIRNBAUM, MJ KAHN, CR AF CHUANG, LM MYERS, MG BACKER, JM SHOELSON, SE WHITE, MF BIRNBAUM, MJ KAHN, CR TI INSULIN-STIMULATED OOCYTE MATURATION REQUIRES INSULIN-RECEPTOR SUBSTRATE-1 AND INTERACTION WITH THE SH2 DOMAINS OF PHOSPHATIDYLINOSITOL 3-KINASE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID XENOPUS-LAEVIS OOCYTES; TYROSINE KINASE-ACTIVITY; GERMINAL VESICLE BREAKDOWN; RIBOSOMAL-PROTEIN S6; SIGNAL TRANSDUCTION; 3T3-L1 ADIPOCYTES; IGF-I; PHOSPHORYLATION; ASSOCIATION; EXPRESSION AB Xenopus oocytes from unprimed frogs possess insulin-like growth factor I (IGF-I) receptors but lack insulin and IGF-I receptor substrate 1 (IRS-1), the endogenous substrate of this kinase, and fail to show downstream responses to hormonal stimulation. Microinjection of recombinant IRS-1 protein enhances insulin-stimulated phosphatidylinositol (PtdIns) 3-kinase activity and restores the germinal vesicle breakdown response. Activation of PtdIns 3-kinase results from formation of a complex between phosphorylated IRS-1 and the p85 subunit of PtdIns 3-kinase. Microinjection of a phosphonopeptide containing a pYMXM motif with high affinity for the src homology 2 (SH2) domain of PtdIns 3-kinase p85 inhibits IRS-1 association with and activation of the PtdIns 3-kinase. Formation of the IRS-1-PtdIns 3-kinase complex and insulin-stimulated PtdIns 3-kinase activation are also inhibited by microinjection of a glutathione S-transferase fusion protein containing the SH2 domain of p85. This effect occurs in a concentration-dependent fashion and results in a parallel loss of hormone-stimulated oocyte maturation. These inhibitory effects are specific and are not mimicked by glutathione S-transferase fusion proteins expressing the SH2 domains of ras-GAP or phospholipase Cgamma. Moreover, injection of the SH2 domains of p85, ras-GAP, and phospholipase Cgamma do not interfere with progesterone-induced oocyte maturation. These data demonstrate that phosphorylation of IRS-1 plays an essential role in IGF-I and insulin signaling in oocyte maturation and that this effect occurs through interactions of the phosphorylated YMXM/YXXM motifs of IRS-1 with SH2 domains of PtdIns 3-kinase or some related molecules. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,PROGRAM CELL & DEV BIOL,BOSTON,MA 02215. OI CHUANG, LEE-MING/0000-0003-0978-2662; Birnbaum, Morris/0000-0001-9972-8680 FU NIDDK NIH HHS [DK 33201, DK 39519, DK 43808] NR 66 TC 66 Z9 67 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD NOV PY 1993 VL 13 IS 11 BP 6653 EP 6660 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MC844 UT WOS:A1993MC84400005 PM 8413261 ER PT J AU BOUBNOV, NV WILLS, ZP WEAVER, DT AF BOUBNOV, NV WILLS, ZP WEAVER, DT TI V(D)J RECOMBINATION CODING JUNCTION FORMATION WITHOUT DNA HOMOLOGY - PROCESSING OF CODING TERMINI SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID COMBINED IMMUNE-DEFICIENCY; PRE-B CELLS; SCID MUTATION; GENE REARRANGEMENT; SEQUENCE HOMOLOGIES; JOINING SIGNALS; RECEPTOR GENES; DEFECT; MICE; DIVERSITY AB Coding junction formation in V(D)J recombination generates diversity in the antigen recognition structures of immunoglobulin and T-cell receptor molecules by combining processes of deletion of terminal coding sequences and addition of nucleotides prior to joining. We have examined the role of coding end DNA composition in junction formation with plasmid substrates containing defined homopolymers flanking the recombination signal sequence elements. We found that coding junctions formed efficiently with or without terminal DNA homology. The extent of junctional deletion was conserved independent of coding ends with increased, partial, or no DNA homology. Interestingly, G/C homopolymer coding ends showed reduced deletion regardless of DNA homology. Therefore, DNA homology cannot be the primary determinant that stabilizes coding end structures for processing and joining. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NIGMS NIH HHS [GM39312] NR 41 TC 34 Z9 34 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD NOV PY 1993 VL 13 IS 11 BP 6957 EP 6968 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MC844 UT WOS:A1993MC84400034 PM 8413286 ER PT J AU MILLER, CP LIN, JC HABENER, JF AF MILLER, CP LIN, JC HABENER, JF TI TRANSCRIPTION OF THE RAT GLUCAGON GENE BY THE CYCLIC-AMP RESPONSE ELEMENT-BINDING PROTEIN CREB IS MODULATED BY ADJACENT CREB-ASSOCIATED PROTEINS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CELL-SPECIFIC EXPRESSION; PANCREATIC-ISLET CELLS; DNA-BINDING; SOMATOSTATIN GENE; CCAAT BOX; GLUCOCORTICOID RECEPTOR; NEGATIVE REGULATION; C-JUN; CAMP; ENHANCER AB The cyclic AMP (cAMP) response element (CRE) of the rat glucagon gene (Glu-CRE, 5'-TGACGTCA-3') mediates transcriptional responses to 8-bromo-cAMP and protein kinase A (PKA) in a glucagon-producing hamster islet cell line (InR1G9). By several different DNA-protein binding assays, we show that the transcription factor CREB binds to the CRE octamer and that additional nuclear proteins bind to sequences adjacent to the CRE. Mutation of the Glu-CRE octamer attenuates both the binding of CREB and cAMP-dependent PKA-stimulated transcriptional activity in transient transfection experiments but does not affect the binding of adjacent CR-EB-associated proteins. Progressive deletions and clustered point mutations of the sequences flanking the Glu-CRE identify sequences (5'-TCATT-3') located both 5' and 3' to the core CRE octamer that bind several proteins. Two proteins with molecular masses of 80 and 100 kDa bind to each of the 5' and 3' TCATT sites. Formation of additional protein-DNA complexes containing 45- and 20-kDa proteins depends upon the integrity of both TCATT sequences. Deletion or point mutation of the TCATT motif located on the 3' side of the CRE octamer results in enhanced transcriptional responses to PKA, suggesting that the CREB-associated proteins decrease the ability of CREB to mediate PKA-stimulated transcription. Results from these studies demonstrate that nucleotides flanking the core CRE octamer can influence the activity of the CRE by serving as binding sites for proteins that modulate the function of CREB and suggest a mechanism to explain why some consensus palindromic CREs are less responsive to cAMP stimulation than others. C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. RP MILLER, CP (reprint author), MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK30834] NR 44 TC 38 Z9 38 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD NOV PY 1993 VL 13 IS 11 BP 7080 EP 7090 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MC844 UT WOS:A1993MC84400046 PM 8413297 ER PT J AU SLANSKY, JE LI, Y KAELIN, WG FARNHAM, PJ AF SLANSKY, JE LI, Y KAELIN, WG FARNHAM, PJ TI A PROTEIN SYNTHESIS-DEPENDENT INCREASE IN E2F1 MESSENGER-RNA CORRELATES WITH GROWTH-REGULATION OF THE DIHYDROFOLATE-REDUCTASE PROMOTER, (VOL 13, PG 1613, 1993) SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Correction, Addition C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SLANSKY, JE (reprint author), UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706, USA. NR 1 TC 20 Z9 20 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD NOV PY 1993 VL 13 IS 11 BP 7201 EP 7201 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MC844 UT WOS:A1993MC84400061 ER PT J AU MORBECK, DE ROCHE, PC KEUTMANN, HT MCCORMICK, DJ AF MORBECK, DE ROCHE, PC KEUTMANN, HT MCCORMICK, DJ TI A RECEPTOR-BINDING SITE IDENTIFIED IN THE REGION 81-95 OF THE BETA-SUBUNIT OF HUMAN LUTEINIZING-HORMONE (LH) AND CHORIONIC-GONADOTROPIN (HCG) SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE GONADOTROPIN; LH; HCG; RECEPTOR BINDING; HORMONE PEPTIDE ID HUMAN CHORIOGONADOTROPIN-BETA; BIOLOGICAL-ACTIVITY; PEPTIDES; MUTAGENESIS; INHIBITION; SEQUENCE AB Two series of overlapping peptides comprising the entire sequence of the beta-subunits of human lutropin (LH) and choriogonadotropin (hCG) were prepared by a comprehensive synthetic strategy in order to identify all linear regions of the subunit that may participate in binding of the hormone to its receptor. Each series of peptides (15 residues in length) spanned the entire amino acid sequences of the two beta-subunits. The peptides were tested for their ability to inhibit the binding of I-125-labeled hCG or LH to rat ovarian membranes and for their ability to inhibit hCG-stimulated progesterone production in a Leydig cell bioassay. The most potent inhibitor of LH/hCG binding was a peptide containing the sequence beta 81-95, a receptor binding site of the LH/hCG beta subunit not previously described. The concentration at which LH/hCG binding was inhibited at 50% (IC50) was 20 mu M and 30 mu M for hCG beta 81-95 and LH beta 81-95, respectively. These peptides also inhibited the stimulation of progesterone production by hCG in Leydig cell bioassays. In order to determine important residues that inhibit binding within this region, a third set of peptides was synthesized in which each residue of hCG beta 81-95 was sequentially replaced with the residue L-alanine. Five residues (Leu-86, Cys-88, Cys-90, Arg-94, and Arg-95) were critical for maximal inhibition of hCG binding by CG beta 81-95. In addition to site beta 81-95, other sites that inhibited hCG/LH binding but with significantly lower potencies included hCG beta 1-15, LH beta 41-55, and LH beta 91-105. These results affirm the presence of several binding regions in the LH/hCG beta-subunit prominent among which is the sequence beta 81-95. This region represents a previously unidentified binding site of high inhibitory activity and contains at least 5 residues important for maximal interaction with the LH/hCG receptor. C1 MAYO CLIN,DEPT LAB MED PATHOL,ROCHESTER,MN 55905. MASSACHUSETTS GEN HOSP,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP MORBECK, DE (reprint author), MAYO CLIN,DEPT BIOCHEM & MOLEC BIOL,GUGGENHEIM 1621C,ROCHESTER,MN 55905, USA. FU NICHD NIH HHS [HD-07108, HD-09140] NR 22 TC 37 Z9 37 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD NOV PY 1993 VL 97 IS 1-2 BP 173 EP 181 DI 10.1016/0303-7207(93)90225-9 PG 9 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA MU125 UT WOS:A1993MU12500022 PM 8143901 ER PT J AU BALLARD, J SOKOLOV, Y YUAN, WL KAGAN, BL TWETEN, RK AF BALLARD, J SOKOLOV, Y YUAN, WL KAGAN, BL TWETEN, RK TI ACTIVATION AND MECHANISM OF CLOSTRIDIUM-SEPTICUM ALPHA-TOXIN SO MOLECULAR MICROBIOLOGY LA English DT Article ID PHOSPHOLIPID-BILAYER MEMBRANES; ESCHERICHIA-COLI HEMOLYSIN; PERFRINGENS THETA-TOXIN; FORMING TOXIN; AEROLYSIN; AGGREGATION; CHANNELS; ERYTHROCYTES; FRAGMENT; DIVALENT AB Clostridium septicum produces a single lethal factor, alpha toxin (AT), which is a cytolytic protein with a molecular mass of approximately 48 kDa. The 48 kDa toxin was found to be an inactive protoxin (AT(pro)) which could be activated via a carboxy-terminal cleavage with trypsin. The cleavage site was located approximately 4 kDa from the carboxy-terminus. Proteolytically activated AT(pro) had a specific activity of approximately 1.5 x 10(6) haemolytic units mg-1. The trypsin-activated toxin (AT(act)) was haemolytic, stimulated a prelytic release of potassium ions from erythrocytes which was followed by haemoglobin release, induced channel formation in planar membranes and aggregated into a complex of M(r) > 210 000 on erythrocyte membranes. AT(pro) did not exhibit these properties. AT(act) formed pores with a diameter of at least 1.3-1.6 nm. We suggest that pore formation on target cell membranes is responsible for the cytolytic activity of alpha toxin. C1 UNIV OKLAHOMA HLTH SCI CTR, HLTH SCI CTR, DEPT MICROBIOL & IMMUNOL, OKLAHOMA CITY, OK 73190 USA. UNIV CALIF LOS ANGELES, INST NEUROPSYCHIAT, DEPT PSYCHIAT, LOS ANGELES, CA 90024 USA. W LOS ANGELES DEPT VET AFFAIRS MED CTR, LOS ANGELES, CA 90024 USA. FU NIAID NIH HHS [AI28697, AI32097]; NIMH NIH HHS [MH43433] NR 26 TC 62 Z9 63 U1 0 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD NOV PY 1993 VL 10 IS 3 BP 627 EP 634 DI 10.1111/j.1365-2958.1993.tb00934.x PG 8 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA MF565 UT WOS:A1993MF56500018 PM 7968539 ER PT J AU MYERS, RH MACDONALD, ME GUSELLA, JF AF MYERS, RH MACDONALD, ME GUSELLA, JF TI DISCREPANCY RESOLVED SO NATURE GENETICS LA English DT Letter RP MYERS, RH (reprint author), MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA 02129, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD NOV PY 1993 VL 5 IS 3 BP 215 EP 215 DI 10.1038/ng1193-215b PG 1 WC Genetics & Heredity SC Genetics & Heredity GA MF122 UT WOS:A1993MF12200008 PM 8110292 ER PT J AU ALBERT, M AF ALBERT, M TI NEUROPSYCHOLOGICAL AND NEUROPHYSIOLOGICAL CHANGES IN HEALTHY ADULT HUMANS ACROSS THE AGE RANGE SO NEUROBIOLOGY OF AGING LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RP ALBERT, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114, USA. NR 4 TC 103 Z9 110 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD NOV-DEC PY 1993 VL 14 IS 6 BP 623 EP 625 DI 10.1016/0197-4580(93)90049-H PG 3 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA MH158 UT WOS:A1993MH15800017 PM 8295666 ER PT J AU BEAL, MF AF BEAL, MF TI NEUROCHEMICAL ASPECTS OF AGING IN PRIMATES SO NEUROBIOLOGY OF AGING LA English DT Article ID RHESUS-MONKEYS RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. NR 3 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD NOV-DEC PY 1993 VL 14 IS 6 BP 707 EP 709 DI 10.1016/0197-4580(93)90080-U PG 3 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA MH158 UT WOS:A1993MH15800048 PM 7905191 ER PT J AU ROGAEV, EI LUKIW, WJ VAULA, G HAINES, JL ROGAEVA, EA TSUDA, T ALEXANDROVA, N LIANG, Y MORTILLA, M AMADUCCI, L BERGAMINI, L BRUNI, AC FONCIN, JF MACCIARDI, F MONTTESI, MP SORBI, S RAINERO, I PINESSI, L POLINSKY, RJ FROMMELT, P DUARA, R LOPEZ, R POLLEN, D GUSELLA, JF TANZI, R MACLACHLAN, DC STGEORGEHYSLOP, PH AF ROGAEV, EI LUKIW, WJ VAULA, G HAINES, JL ROGAEVA, EA TSUDA, T ALEXANDROVA, N LIANG, Y MORTILLA, M AMADUCCI, L BERGAMINI, L BRUNI, AC FONCIN, JF MACCIARDI, F MONTTESI, MP SORBI, S RAINERO, I PINESSI, L POLINSKY, RJ FROMMELT, P DUARA, R LOPEZ, R POLLEN, D GUSELLA, JF TANZI, R MACLACHLAN, DC STGEORGEHYSLOP, PH TI ANALYSIS OF THE C-FOS GENE ON CHROMOSOME-14 AND THE PROMOTER OF THE AMYLOID PRECURSOR PROTEIN GENE IN FAMILIAL ALZHEIMERS-DISEASE SO NEUROLOGY LA English DT Article ID APP GENE; MUTATIONS; LOCUS; POLYMORPHISM; DIAGNOSIS; MISSENSE; LINKAGE; REGION; BRAIN AB The c-FOS gene product, a putative transacting transcriptional regulator of the amyloid precursor protein (APP) gene, is a candidate locus for the familial Alzheimer's disease (FAD) mutation on chromosome 14 (FAD14). In light of this functional relationship, we investigated the nucleotide sequence and segregation of c-FOS and the nucleotide sequence of the 5' APP promoter. Single-stranded conformational polymorphisms (SSCPs) in the c-FOS gene revealed that c-FOS closely cosegregates with the FAD14 gene but does not show allelic association with FAD. A conservative third-position T-->C mutation was demonstrated in exon 2 (codon 84) of c-FOS, and a C-->G substitution was detected at -209 bp in the 5' promoter of APP. Neither were unique to FAD and are unlikely to be pathogenic or secondary modifiers of the FAD phenotype. We conclude that the c-FOS open reading frame is probably not the site of the FAD14 locus, but we cannot exclude the existence of modifier loci on chromosome 21. C1 UNIV TORONTO, CTR RES NEURODEGENERAT DIS, DIV NEUROL, TORONTO M5S 1A8, ONTARIO, CANADA. ACAD MED SCI, NATL RES CTR MENTAL HLTH, MOLEC BRAIN GENET LAB, MOSCOW, RUSSIA. UNIV TURIN, DEPT NEUROL, I-10124 TURIN, ITALY. MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET LAB, BOSTON, MA USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. UNIV FLORENCE, DEPT NEUROL, I-50121 FLORENCE, ITALY. SERV NEUROL, LAMEZIA TERME, ITALY. ECOLE PRAT HAUTES ETUD, NEUROHISTOL LAB, F-75231 PARIS 05, FRANCE. INSERM, U106, F-75005 PARIS, FRANCE. UNIV MILAN, SCH MED, DEPT NEUROSCI, I-20122 MILAN, ITALY. SANDOZ PHARMACEUT CORP, SANDOZ RES INST, E HANOVER, NJ USA. KLIN BAVARIA, DEPT NEUROL, DEGGENDORF, GERMANY. MT SINAI MED CTR, WIEN CTR ALZHEIMERS DIS, MIAMI BEACH, FL 33140 USA. UNIV MASSACHUSETTS, MED CTR, DEPT NEUROL, WORCESTER, MA 01605 USA. RI Haines, Jonathan/C-3374-2012; Macciardi, Fabio/N-3768-2014; OI Macciardi, Fabio/0000-0003-0537-4266; sorbi, sandro/0000-0002-0380-6670; Lopez, Ramon/0000-0001-5881-1365 NR 40 TC 33 Z9 33 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 EI 1526-632X J9 NEUROLOGY JI Neurology PD NOV PY 1993 VL 43 IS 11 BP 2275 EP 2279 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA MH652 UT WOS:A1993MH65200023 PM 8232942 ER PT J AU BASHIR, R LUKA, J CHELOHA, K CHAMBERLAIN, M HOCHBERG, F AF BASHIR, R LUKA, J CHELOHA, K CHAMBERLAIN, M HOCHBERG, F TI EXPRESSION OF EPSTEIN-BARR-VIRUS PROTEINS IN PRIMARY CNS LYMPHOMA IN AIDS PATIENTS SO NEUROLOGY LA English DT Article ID NERVOUS-SYSTEM LYMPHOMA; IMMUNE-DEFICIENCY-SYNDROME; LYMPHOPROLIFERATIVE DISEASE; INSITU HYBRIDIZATION; GENE-EXPRESSION; MOUSE MODEL; LATENT; CELLS; ASSOCIATION; INFECTION AB We examined the expression of the Epstein-Barr virus (EBV)-induced proteins (LMP [latent membrane protein], EBNA-2, and CD23) and a lytic protein, viral capsid antigen (VCA), in five acquired immune deficiency syndrome (AIDS)-related primary CNS lymphomas (PCNSLs). We compared that expression with the expression of the same proteins in PCNSL from six immunocompetent patients and severe combined immune deficiency (SCID) mouse brains injected with EBV-infected lymphoblastoid cell lines (LCLs). Brain biopsy tissue from an AIDS patient with progressive multifocal leukoencephalopathy (PML) and a normal brain was also studied. Three of the AIDS PCNSLs expressed both human immunoglobulin kappa and lambda light chains and two expressed lambda light chain only. All non-AIDS-related PCNSLs expressed a single light-chain isotype. All five AIDS-related PCNSLs expressed LMP-1 (>40%), EBNA-2 (>60%), and VCA (1 to 5%) of tumor cells. These proteins were similarly expressed in the SCID/human chimeras. None of the PCNSLs from immunocompetent subjects, the normal brain, or the brain of the patient with PML expressed these proteins. PCNSL in AIDS patients bears greater similarity to EBV-infected LCLs than to PCNSL from immunocompetent patients. C1 UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. UNIV NEBRASKA,MED CTR,DEPT PATHOLOGY,OMAHA,NE 68198. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP BASHIR, R (reprint author), UNIV NEBRASKA,MED CTR,DEPT INTERNAL MED,DIV NEUROL,600 S 42ND ST,OMAHA,NE 68198, USA. NR 34 TC 45 Z9 45 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1993 VL 43 IS 11 BP 2358 EP 2362 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA MH652 UT WOS:A1993MH65200039 PM 8232956 ER PT J AU VANDENBARK, AA BOURDETTE, DN WHITHAM, R CHOU, YK HASHIM, GA OFFNER, H AF VANDENBARK, AA BOURDETTE, DN WHITHAM, R CHOU, YK HASHIM, GA OFFNER, H TI EPISODIC CHANGES IN T-CELL FREQUENCIES TO MYELIN BASIC-PROTEIN IN PATIENTS WITH MULTIPLE-SCLEROSIS SO NEUROLOGY LA English DT Note C1 OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MICROBIOL & IMMUNOL,PORTLAND,OR 97201. COUNCIL TOBACCO RES,NEW YORK,NY. RP VANDENBARK, AA (reprint author), PORTLAND VET AFFAIRS MED CTR,NEUROIMMUNOL RES 151-D,3710 SW US VET HOSP RD,PORTLAND,OR 97201, USA. FU NINDS NIH HHS [NS23444, NS23221] NR 7 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1993 VL 43 IS 11 BP 2416 EP 2417 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA MH652 UT WOS:A1993MH65200059 PM 7694188 ER PT J AU MANZO, CB DICKERSON, RN SETTLE, RG RAJTER, JJ AF MANZO, CB DICKERSON, RN SETTLE, RG RAJTER, JJ TI INSULIN-LIKE GROWTH FACTOR-I AND ENDOTOXIN-MEDIATED KIDNEY DYSFUNCTION IN CRITICALLY ILL, PARENTERALLY FED RATS SO NUTRITION LA English DT Article DE INSULIN-LIKE GROWTH FACTOR-I; ACUTE KIDNEY FAILURE; LIPOPOLYSACCHARIDE; GLOMERULAR FILTRATION RATE; SOMATOMEDIN-C; CREATININE CLEARANCE ID PLATELET-ACTIVATING FACTOR; GLOMERULAR-FILTRATION RATE; ACUTE RENAL-FAILURE; FACTOR-I; PLASMA-FLOW; NECROSIS; HORMONE; HUMANS AB Endotoxemia is an important contributor to the pathogenesis of acute kidney failure in sepsis. Data suggest insulinlike growth factor 1 (IGF-1) can increase creatinine clearance in healthy humans. The influence of recombinant human IGF-1 on kidney function in endotoxemia was investigated in 34 male Sprague-Dawley rats. After venous cannulation and postoperative parenteral nutrition (PN), the animals were randomly assigned to receive PN only, PN plus Escherichia coli lipopolysaccharide (LPS), or PN plus LPS plus IGF-1. Urine output was significantly higher for the IGF-1 and control groups compared with the LPS group (18.9 +/- 5.7, 13.0 +/- 3.8, and 17.7 +/- 3.1 ml/day for control, LPS, and IGF-1 groups, respectively, analysis of variance, p < 0.05). Creatinine clearance was significantly higher in the IGF-1 group than the LPS group and exceeded the control group (0.49 +/- 0.27, 0.36 +/- 0.14, and 0.65 +/- 0.27 ml min-1 100(-1) g body wt) for control, LPS, and IGF-1, respectively (analysis of variance, p < 0.05). IGF-1 ameliorates the effects of endotoxin on kidney function as measured by creatinine clearance and urine output in endotoxemic parenterally fed rats. C1 UNIV TENNESSEE CTR HLTH SCI,DEPT CLIN PHARM,MEMPHIS,TN 38163. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. PHILADELPHIA COLL PHARM & SCI,PHILADELPHIA,PA 19104. RI Dickerson, Roland/C-5185-2008 FU NIDDK NIH HHS [1R15DK46545-01] NR 26 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0899-9007 J9 NUTRITION JI Nutrition PD NOV-DEC PY 1993 VL 9 IS 6 BP 528 EP 531 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MM144 UT WOS:A1993MM14400007 PM 8111143 ER PT J AU PRICE, BD CALDERWOOD, SK AF PRICE, BD CALDERWOOD, SK TI INCREASED SEQUENCE-SPECIFIC P53 DNA-BINDING ACTIVITY AFTER DNA-DAMAGE IS ATTENUATED BY PHORBOL ESTERS SO ONCOGENE LA English DT Article ID PROTEIN KINASE-C; WILD-TYPE P53; TUMOR SUPPRESSOR PROTEIN; CELL-CYCLE; GROWTH-REGULATION; MUTANT P53; MONOCLONAL-ANTIBODY; IONIZING-RADIATION; GENE-PRODUCT; 3T3 CELLS AB Damage to cellular DNA greatly increases the levels of the tumor-suppressor gene p53 and induces cell cycle arrest in G1. A critical function of wild-type p53 is its ability to bind to specific DNA sequences. The effect of DNA damage on the sequence-specific DNA-binding properties of cellular p53 was investigated using DNA gel mobility-shift assays with nuclear extracts from NIH-3T3 cells. DNA damage (initiated by radiation) induced a rapid, cycloheximide-sensitive increase in the levels of nuclear p53-DNA binding activity and an increase in the half-life of the p53 protein. Increased p53-DNA binding activity could be detected at low (0.2 Gy), non-lethal doses of radiation. The tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA) attenuated the DNA damage-induced increase in p53-DNA binding activity by decreasing the half-life of the p53 protein. The tumor promoter properties of TPA may therefore be mediated by interfering with the cellular p53 response to DNA damage. The increased levels of p53 bound to specific DNA sequences following DNA damage may induce cell cycle arrest. p53-mediated growth arrest could occur by inhibition of DNA replication and/or alterations in transcription of cell cycle genes. RP PRICE, BD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,STRESS PROT GRP RM JF209,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R29CA44940]; PHS HHS [R01 47407] NR 54 TC 64 Z9 64 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD NOV PY 1993 VL 8 IS 11 BP 3055 EP 3062 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA MC093 UT WOS:A1993MC09300021 PM 8414506 ER PT J AU FATTAEY, AR HELIN, K DEMBSKI, MS DYSON, N HARLOW, E VUOCOLO, GA HANOBIK, MG HASKELL, KM OLIFF, A DEFEOJONES, D JONES, RE AF FATTAEY, AR HELIN, K DEMBSKI, MS DYSON, N HARLOW, E VUOCOLO, GA HANOBIK, MG HASKELL, KM OLIFF, A DEFEOJONES, D JONES, RE TI CHARACTERIZATION OF THE RETINOBLASTOMA BINDING-PROTEINS RBP1 AND RBP2 SO ONCOGENE LA English DT Note ID CELLULAR TRANSCRIPTION FACTOR; ADENOVIRUS E1A PROTEINS; LARGE T-ANTIGEN; GENE-PRODUCT; TUMOR SUPPRESSOR; CARCINOMA-CELLS; DNA-BINDING; 2 DISTINCT; FACTOR E2F; IDENTIFICATION AB The retinoblastoma gene product, pRB, regulates cell proliferation by binding to and inhibiting the activity of key growth promoting proteins. Several cellular proteins have been shown to bind directly to pRB and the genes encoding a number of them have been isolated. The protein product of one of these genes is the transcription factor E2F. We have now isolated cDNA clones that contain the full-length coding sequence of two other proteins, RBP1 and RBP2, cloned originally by their interaction with pRB. The products of the RBP1 and RBP2 genes are ubiquotosly expressed, large (200 kDa for RBP1 and 195 kDa for RBP2) nuclear phosphoproteins with structural motifs that suggest a role in transcriptional regulation. In addition we have been able to identify complexes of pRB and RBP1 in vivo that are dissociated in the presence of purified human papillomavirus E7 protein. C1 MERCK & CO INC,RES LABS,DEPT CANC RES,W POINT,PA 19486. RP FATTAEY, AR (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 48 TC 146 Z9 149 U1 0 U2 4 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD NOV PY 1993 VL 8 IS 11 BP 3149 EP 3156 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA MC093 UT WOS:A1993MC09300032 PM 8414517 ER PT J AU TSUBOTA, K YOSHIDA, M TODA, T ONO, M KAJIWARA, K CHENG, HM AF TSUBOTA, K YOSHIDA, M TODA, T ONO, M KAJIWARA, K CHENG, HM TI ALDOSE REDUCTASE INHIBITION AND THE P-31 PROFILE OF THE INTACT DIABETIC RAT LENS SO OPHTHALMIC RESEARCH LA English DT Article DE DIABETIC RAT LENS; WISTAR RAT; ALDOSE REDUCTASE INHIBITOR; SORBITOL PATHWAY; ADENOSINE 5'-TRIPHOSPHATE; SORBITOL-3-PHOSPHATE; FRUCTOSE-3-PHOSPHATE; P-31 NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY ID PHOSPHATE-METABOLISM; HIGH GLUCOSE; IDENTIFICATION; 3-PHOSPHATE AB Diabetic metabolic change and response to aldose reductase inhibition in the Wistar rat lens were examined with phosphorus-31 (P-31) nuclear magnetic resonance (NMR) spectroscopy. To avoid artifacts in sample preparation, we used freshly excised lenses and acquired Nh IR data for 20 min immediately after lens extraction. The results showed a diabetes-induced time-dependent loss of ATP and phosphorylcholine (PC), an increase in alpha-glycerophosphate (alpha-GP) and inorganic phosphate and the appearance of sorbitol-3-phosphate (S-3-P) and fructose-3-phosphate (F-3-P). Oral but not topical dosing of an aldose reductase inhibitor, 5-(3-ethoxy-4-pentyloxyphenyl)-2,4-thiazolidinedione, resulted in a positive dose-response correlation characterized by a restoration of PC, S-3-P and F-3-P to the prediabetic level, however, alpha-GP and ATP were only partially normalized. The significance of the P-31 change was further discussed. C1 HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. TOKYO DENT COLL,ICHIKAWA GEN HOSP,DEPT OPHTHALMOL,CHIBA,CHIBA,JAPAN. KEIO UNIV,SCH MED,DEPT OPHTHALMOL,TOKYO,TOKYO,JAPAN. UTSUNOMIYA UNIV,SCH TECHNOL,UTSUNOMIYA,TOCHIGI,JAPAN. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA. FU NEI NIH HHS [EY04424] NR 11 TC 3 Z9 3 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0030-3747 J9 OPHTHALMIC RES JI Ophthalmic Res. PD NOV-DEC PY 1993 VL 25 IS 6 BP 393 EP 399 PG 7 WC Ophthalmology SC Ophthalmology GA MM874 UT WOS:A1993MM87400008 PM 8309679 ER PT J AU NETLAND, PA WALTON, DS AF NETLAND, PA WALTON, DS TI GLAUCOMA DRAINAGE IMPLANTS IN PEDIATRIC-PATIENTS SO OPHTHALMIC SURGERY AND LASERS LA English DT Article ID REFRACTORY GLAUCOMA; CONGENITAL GLAUCOMA; MOLTENO IMPLANT; TRABECULECTOMY; SURGERY; ENDOPHTHALMITIS AB To assess the use of drainage implants in pediatric patients with glaucoma refractory to conventional medical and surgical therapy, we retrospectively reviewed 20 consecutive eyes in children 10 years of age or younger treated with 16 Molteno (three of which were removed and replaced with second Molteno shunts) and seven Baerveldt implants. The age of the patients ranged from 1 month to 10 years (mean, 3 years). The patients had undergone a mean of two previous failed glaucoma procedures (range, one to six). The mean intraocular pressure (IOP) prior to drainage tube implantation was 37 +/- 4 mm Hg, compared with a mean of 18 +/- 6 mm Hg following surgery, with average postoperative follow up of 25 months (range, 8 to 41 months). The overall success, defined as IOP less-than-or-equal-to 21 mm Hg without further surgical therapy, was 80%. Postoperative glaucoma medications were required in 75% of patients. There were 23 complications, one of which resulted in decreased visual acuity. These findings demonstrate that drainage tube implants can be effective in lowering IOP in uncontrolled pediatric glaucomas. Patients often require postoperative glaucoma medications and close monitoring for complications. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 31 TC 81 Z9 81 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD NOV PY 1993 VL 24 IS 11 BP 723 EP 729 PG 7 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA MH638 UT WOS:A1993MH63800002 PM 8290209 ER PT J AU KASSOFF, A RAY, GS KREPOSTMAN, J CHANG, MM GARZA, D BUEHLER, J DYLONG, K BERGER, BB BRITT, M MURPHY, RP TURCOTTE, P ELMAN, M FERRIS, FL LERNER, BC SCHENNING, S SACKETT, C CHEW, EY OPTICAN, D SHARUK, G AIELLO, L SHAH, S RAND, L KORETZ, D RUDICH, R WEISS, J CONWAY, BP CAMPOCHAIRO, P CASADA, R JOHNSTON, R KAMINSKI, F ORTH, D FLOOD, TP PACKO, K ARREDONDO, L BRYANT, D SINGERMAN, LJ RICE, TA NOVAK, MA TEICHER, P PRESEREN, D SCHWARTZ, PL FASTENBURG, D ROSEN, D GRIFFITH, C DROUILHET, JH NOBLER, D GARCIA, CA BLOOME, MA RUIZ, RS RUIZ, NJ WEINGEIST, T SNEED, S FOUNTAIN, C CHANDRA, SR MYERS, FL BRESNICK, GH STEWART, L JABBOUR, N TAYLOR, N LIANG, JC BENNETT, TA ZIEBA, K SUMMERSON, L YANNUZZI, L DALY, J DEROSA, JT SISCO, L KINGSLEY, RM WILKINSON, CP CONNER, B ADAMS, C BRUCKER, J SANDBURG, E DOFT, BH LOBES, LA RINKOFF, J MELLINGER, K HOFFMAN, ME SORR, EM FELLER, A HANDELMAN, IL CHENOWETH, RG ROYCE, B MINCEY, GJ FLEMING, J SINGERMAN, LJ MOWERY, RP REMALEY, NA LERNER, B LUSTBADER, J KIVITZ, I FINKELSTEIN, D MAGUIRE, MG NUSSENBLATT, R PODGOR, M SEIGEL, D AF KASSOFF, A RAY, GS KREPOSTMAN, J CHANG, MM GARZA, D BUEHLER, J DYLONG, K BERGER, BB BRITT, M MURPHY, RP TURCOTTE, P ELMAN, M FERRIS, FL LERNER, BC SCHENNING, S SACKETT, C CHEW, EY OPTICAN, D SHARUK, G AIELLO, L SHAH, S RAND, L KORETZ, D RUDICH, R WEISS, J CONWAY, BP CAMPOCHAIRO, P CASADA, R JOHNSTON, R KAMINSKI, F ORTH, D FLOOD, TP PACKO, K ARREDONDO, L BRYANT, D SINGERMAN, LJ RICE, TA NOVAK, MA TEICHER, P PRESEREN, D SCHWARTZ, PL FASTENBURG, D ROSEN, D GRIFFITH, C DROUILHET, JH NOBLER, D GARCIA, CA BLOOME, MA RUIZ, RS RUIZ, NJ WEINGEIST, T SNEED, S FOUNTAIN, C CHANDRA, SR MYERS, FL BRESNICK, GH STEWART, L JABBOUR, N TAYLOR, N LIANG, JC BENNETT, TA ZIEBA, K SUMMERSON, L YANNUZZI, L DALY, J DEROSA, JT SISCO, L KINGSLEY, RM WILKINSON, CP CONNER, B ADAMS, C BRUCKER, J SANDBURG, E DOFT, BH LOBES, LA RINKOFF, J MELLINGER, K HOFFMAN, ME SORR, EM FELLER, A HANDELMAN, IL CHENOWETH, RG ROYCE, B MINCEY, GJ FLEMING, J SINGERMAN, LJ MOWERY, RP REMALEY, NA LERNER, B LUSTBADER, J KIVITZ, I FINKELSTEIN, D MAGUIRE, MG NUSSENBLATT, R PODGOR, M SEIGEL, D TI RANDOMIZED COMPARISON OF KRYPTON VERSUS ARGON SCATTER PHOTOCOAGULATION FOR DIABETIC DISC NEOVASCULARIZATION - THE KRYPTON ARGON REGRESSION NEOVASCULARIZATION STUDY REPORT NUMBER 1 SO OPHTHALMOLOGY LA English DT Article ID LASER; RETINOPATHY; FUNDUS AB Background: The Krypton Argon Regression of Neovascularization Study (KARNS) was designed to compare the efficacy of red krypton versus blue-green argon laser photocoagulation for the management of high-risk proliferative diabetic retinopathy. Methods: A prospective, randomized clinical trial was performed in 24 clinical centers. Patients (n = 696, 907 eyes) with diabetes and neovascularization of the disc (NVD) of one-third disc area or greater in extent were assigned at random to either argon or krypton laser scatter (panretinal) photocoagulation. The major endpoint of the regression of NVD to less than one-third disc area in extent at 3 months was evaluated by comparisons of gradings of the fundus photographs obtained at baseline and follow-up. Results: At 3 months' follow-up, the proportion of eyes with regression of NVD to less than or equal to one-third disc area in extent were 41.1% in the argon-treated group and 41.8% in the krypton-treated group (P = 0.92). The odds of regressing to this extent of NVD at 3 months for argon-treated eyes versus krypton-treated eyes was 0.98 (95% confidence interval, 0.74-1.31). Conclusion: Scatter laser photocoagulation with either krypton red or argon appears to be equally effective in the treatment of proliferative diabetic retinopathy with NVD. C1 NEI, BLDG 31, RM 6A52, BETHESDA, MD 20892 USA. ALBANY MED COLL, ALBANY, NY 12208 USA. JOHNS HOPKINS UNIV, BALTIMORE, MD 21218 USA. JOSLIN DIABET CTR, BOSTON, MA USA. UNIV VIRGINIA, MED CTR, CHARLOTTESVILLE, VA 22903 USA. JOHNSTON EYE CLIN, CHEYENNE, WY USA. INGALLS MEM HOSP, ILLINOIS RETINA ASSOCIATES, CHICAGO, IL USA. LONG ISL JENISH MED CTR, GREAT NECK, NY USA. HERMANN EYE CTR, HOUSTON, TX USA. UNIV IOWA, IOWA CITY, IA 52242 USA. UNIV WISCONSIN, MADISON, WI 53706 USA. W VIRGINIA UNIV, MED CTR, MORGANTOWN, WV 26506 USA. MANHATTAN EYE EAR & THROAT HOSP, NEW YORK, NY 10021 USA. DEAN MCGEE EYE INST, OKLAHOMA CITY, OK USA. UNIV PENN, SCHEIE EYE INST, PHILADELPHIA, PA 19104 USA. RETINA VITREOUS PA, PITTSBURGH, PA USA. EVERETT & HURITE, PITTSBURGH, PA USA. OREGON LIONS SIGHT & HEARING INST, PORTLAND, OR USA. CAROLINA EYE ASSOC, SOUTHERN PINES, NC USA. NR 25 TC 13 Z9 14 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0161-6420 EI 1549-4713 J9 OPHTHALMOLOGY JI Ophthalmology PD NOV PY 1993 VL 100 IS 11 BP 1655 EP 1664 PG 10 WC Ophthalmology SC Ophthalmology GA MF323 UT WOS:A1993MF32300029 ER PT J AU EAVEY, RD SANTOS, JI ARRIAGA, MA GLIKLICH, R ODIO, C DESMOND, MS VILLASENOR, A BELTRAN, S ORLOFF, L STOOL, SE AF EAVEY, RD SANTOS, JI ARRIAGA, MA GLIKLICH, R ODIO, C DESMOND, MS VILLASENOR, A BELTRAN, S ORLOFF, L STOOL, SE TI AN EDUCATION MODEL FOR OTITIS-MEDIA CARE FIELD-TESTED IN LATIN-AMERICA SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID SUPPORT AB The World Health Organization has designated the teaching of otitis media management skills a ''priority'' status. Effective treatment of ear disease requires that the physician be both informationally educated as well as physically trained to use otoscopy. Little is known about how well this education can be provided in a short time and in a foreign country. To more objectively assess teaching effect, results of an education session for rural Mexican pediatric primary-care providers who were given an intensive otitis media lecture and otoscopy skills workshop in 1990 were evaluated. To test immediate cognitive impact, an anonymous written examination was given both before and after the teaching session. Average test scores after the educational sessions improved 24% (p <0.001) over baseline scores before the sessions. To evaluate long-term impact on clinical practice, a follow-up telephone survey 2 years later was conducted. The use of an otoscope to diagnose otitis media had increased from 40% to 93% of respondents. We conclude that pediatric primary-care providers in rural Mexico possess a baseline level of knowledge about otitis media that can be significantly enhanced with one educational session. Further, this teaching effort produces an impact on practice pattern that lasts of least 2 years. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA. HOSP INFANTIL MEXICO FREDERICO GOMEZ,DIV INVEST,MEXICO CITY,DF,MEXICO. HOSP INFANTIL MEXICO FREDERICO GOMEZ,DEPT ENGERMEDADES INFECCIOSAS,MEXICO CITY,DF,MEXICO. UNIV PITTSBURGH,SCH MED,INST EYE & EAR,DEPT OTOLARYNGOL,PITTSBURGH,PA. UNIV COSTA RICA,HOSP NACL NINOS,SAN JOSE,COSTA RICA. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. UNIV WASHINGTON,DEPT OTOLARYNGOL,SEATTLE,WA. UNIV PITTSBURGH,CHILDRENS HOSP PITTSBURGH,SCH MED,DEPT PEDIAT OTOLARYNGOL,PITTSBURGH,PA. RP EAVEY, RD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 11 TC 9 Z9 10 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD NOV PY 1993 VL 109 IS 5 BP 895 EP 898 PG 4 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA MJ891 UT WOS:A1993MJ89100019 PM 8247571 ER PT J AU GUIDA, RA COHEN, JI COOK, TA SWANSON, NA BURGESON, R JOHNSON, TM AF GUIDA, RA COHEN, JI COOK, TA SWANSON, NA BURGESON, R JOHNSON, TM TI ASSESSMENT OF SURVIVAL AND MICROSCOPIC CHANGES IN PORCINE SKIN FLAPS UNDERGOING IMMEDIATE INTRAOPERATIVE TISSUE EXPANSION SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID PIG SKIN; RECONSTRUCTION; PHYSIOLOGY AB The technique of rapid intraoperative tissue expansion has been used with increasing frequency in the clinical setting over the last several years. This technique takes advantage of the skin's ability to immediately stretch and increase in surface area when expanded under a constant load. Sixteen random-pattern, rapidly expanded skin flaps on 10 domestic male pigs were studied to assess the predictive value of the fluorescein test for flap viability after rapid intraoperative tissue expansion. Partial fluorescence was found to be a more accurate predictor of flap survival in the experimental rapidly expanded flaps when compared to full fluorescence. Partial fluorescence was found to under-predict flap survival by 0.3 to 0.5 cm, whereas full fluorescence was found to under-predict flap survival by 2.5 cm. Additionally, histologic and ultrastructural changes were examined in rapidly expanded skin from the hip region in three pigs. The only microscopic change noted between control and experimental flaps was dilated capillaries in the dermis of expanded skin, which was noted by electron microscopy. Collagen and elastic tissue changes were not demonstrated in rapidly expanded pig skin by electron microscopy, direct immunoflurescence, collagen, and elastic tissue stains. C1 OREGON HLTH SCI UNIV,DEPT OTOLARYNGOL,PORTLAND,OR. OREGON HLTH SCI UNIV,DEPT DERMATOL,PORTLAND,OR 97201. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA. UNIV MICHIGAN,MED CTR,DEPT DERMATOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT OTOLARYNGOL,ANN ARBOR,MI. UNIV MICHIGAN,MED CTR,DEPT SURG,ANN ARBOR,MI 48109. RP GUIDA, RA (reprint author), NEW YORK HOSP,CORNELL MED COLL,DEPT OTOLARYNGOL,DIV FACIAL PLAST & RECONSTRUCT SURG,NEW YORK,NY 10021, USA. NR 22 TC 7 Z9 7 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD NOV PY 1993 VL 109 IS 5 BP 926 EP 932 PG 7 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA MJ891 UT WOS:A1993MJ89100023 PM 8247574 ER PT J AU SOTERO, M AF SOTERO, M TI QUESTIONS ABOUT ELECTROGRAPHIC SEIZURES IN NEWBORNS SO PEDIATRICS LA English DT Letter RP SOTERO, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,KENNEDY BLDG,7TH FLOOR,FRUIT ST,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD NOV PY 1993 VL 92 IS 5 BP 736 EP 736 PG 1 WC Pediatrics SC Pediatrics GA ME773 UT WOS:A1993ME77300025 PM 8292171 ER PT J AU SCHYDLOWER, M PERRIN, J AF SCHYDLOWER, M PERRIN, J TI PREVENTION OF FETAL ALCOHOL SYNDROME - REPLY SO PEDIATRICS LA English DT Letter C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,AAP COMM CHILDREN DISABIL,BOSTON,MA 02114. RP SCHYDLOWER, M (reprint author), WILLIAM BEAUMONT ARMY MED CTR,ADOLESCENT MED PROGRAM,AAP COMM SUBST ABUSE,EL PASO,TX 79920, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD NOV PY 1993 VL 92 IS 5 BP 739 EP 739 PG 1 WC Pediatrics SC Pediatrics GA ME773 UT WOS:A1993ME77300032 ER PT J AU NUSS, RC EAVEY, RD EVANS, G AF NUSS, RC EAVEY, RD EVANS, G TI HEARING-LOSS NOT ASSOCIATED WITH DTP VACCINATION OR FEVER SO PEDIATRICS LA English DT Letter C1 DIV VACCINE INJURY COMPENSAT,ROCKVILLE,MD. RP NUSS, RC (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. NR 18 TC 1 Z9 1 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD NOV PY 1993 VL 92 IS 5 BP 740 EP 740 PG 1 WC Pediatrics SC Pediatrics GA ME773 UT WOS:A1993ME77300033 PM 8414874 ER PT J AU CHAUDHRY, H LYNCH, M SCHOMACKER, K BIRNGRUBER, R GREGORY, K KOCHEVAR, I AF CHAUDHRY, H LYNCH, M SCHOMACKER, K BIRNGRUBER, R GREGORY, K KOCHEVAR, I TI RELAXATION OF VASCULAR SMOOTH-MUSCLE INDUCED BY LOW-POWER LASER-RADIATION SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID SOLUBLE GUANYLATE-CYCLASE; PULSED-DYE LASER; NITRIC-OXIDE; CYCLIC-GMP; ULTRAVIOLET-RADIATION; CARBON-MONOXIDE; RAT AORTA; CELLS; IRRADIATION; LIGHT AB The relaxation of rabbit aorta rings induced by low-power laser radiation was investigated in vitro to determine the location of the chromophore(s) responsible for this response and evaluate possible mechanisms. An action spectrum for relaxation was measured on rabbit thoracic aorta rings precontracted with norepinephrine. The decrease in isometric tension was measured during exposure to laser light (351-625 nm) delivered via a fiber optic to a small spot on the adventitial surface. The shortest UV wavelength (351 nm) was 35-fold more effective than 390 nm and 1700-fold more effective than 460 nm. Ultraviolet wavelengths also produced greater maximum relaxation (0.40-0.45) than visible wavelengths (0.20-0.25), suggesting that photovasorelaxation involves more than one chromophore. The adventitial layer was not necessary for photovasorelaxation, indicating that the light is absorbed by a chromophore in the medial layer. The same degree of relaxation was obtained on rings without adventitia when either one-half of the ring, or a small spot was irradiated indicating that communication between smooth muscle cells spreads a signal from the area illuminated to the entire ring. The mechanism for photovasorelaxation was investigated using potential inhibitors. N-monomethyl-L-arginine and N-amino-L-arginine, inhibitors of nitric oxide synthase, did not alter photovasorelaxation nor did indomethacin, an inhibitor of cyclooxygenase, and zinc protoporphyrin, an inhibitor of heme oxygenase. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RI Birngruber, Reginald/Q-2342-2016 NR 27 TC 35 Z9 36 U1 0 U2 1 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD NOV PY 1993 VL 58 IS 5 BP 661 EP 669 DI 10.1111/j.1751-1097.1993.tb04949.x PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA ML057 UT WOS:A1993ML05700007 PM 8284321 ER PT J AU FIALA, TGS WRIGHTSON, DM YAREMCHUK, MJ AF FIALA, TGS WRIGHTSON, DM YAREMCHUK, MJ TI AN ELECTRONIC DEVICE FOR SURGICAL GLOVE TESTING SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Note ID PERFORATION; SURGERY; SINGLE C1 MASSACHUSETTS GEN HOSP,WANG AMBULATORY CARE CTR,DEPT SURG,DIV PLAST SURG,SUITE 453,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT BIOMED ENGN,DESIGN & DEV GRP,BOSTON,MA 02114. NR 15 TC 2 Z9 2 U1 1 U2 2 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 NOV PY 1993 VL 92 IS 6 BP 1192 EP 1194 DI 10.1097/00006534-199311000-00033 PG 3 WC Surgery SC Surgery GA ME590 UT WOS:A1993ME59000033 PM 8234519 ER PT J AU ZHEN, L KING, AAJ XIAO, YH CHANOCK, SJ ORKIN, SH DINAUER, MC AF ZHEN, L KING, AAJ XIAO, YH CHANOCK, SJ ORKIN, SH DINAUER, MC TI GENE TARGETING OF X-CHROMOSOME-LINKED CHRONIC GRANULOMATOUS-DISEASE LOCUS IN A HUMAN MYELOID-LEUKEMIA CELL-LINE AND RESCUE BY EXPRESSION OF RECOMBINANT GP91(PHOX) SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE NADPH OXIDASE; SUPEROXIDE; RESPIRATORY BURST; CYTOCHROME-B; NEUTROPHIL ID NEUTROPHIL CYTOCHROME-B; 2 CYTOSOLIC COMPONENTS; NADPH OXIDASE; PLASMA-MEMBRANE; LIGHT CHAIN; STEM-CELLS; G-PROTEIN; MUTATIONS; SUBUNIT; SYSTEM AB The X chromosome-linked chronic granulomatous disease (X-CGD) locus, which encodes the gp91phox subunit of the phagocyte respiratory-burst oxidase cytochrome b, was disrupted by homologous recombination in the PLB-985 human myeloid cell line to develop an in vitro model of X-CGD. Superoxide formation was absent in targeted cells after differentiation to granulocytes but was rescued by stable transfection and expression of wild-type gp91phox cDNA. The targeted cell line should be useful in experiments aimed at defining functional regions within gp91phox by expression of mutant gp91phox cDNAs, complementing studies of naturally occurring mutations in X-CGD. In addition, the mutant line provides a model system in which to establish an experimental basis for the treatment of X-CGD patients with gene replacement therapy. Rescued clones containing even modest amounts of recombinant gp91phox had respiratory-burst activity comparable to the wild-type PLB-985 tine, suggesting that functional correction of X-CGD neutrophils may not require high-level expression of gp91phox. C1 INDIANA UNIV,JAMES WHITCOMB RILEY HOSP CHILDREN,MED CTR,HERMAN B WELLS CTR,INDIANAPOLIS,IN 46202. INDIANA UNIV,JAMES WHITCOMB RILEY HOSP CHILDREN,MED CTR,DEPT MED & MOLEC GENET,INDIANAPOLIS,IN 46202. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. NR 39 TC 166 Z9 169 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 1 PY 1993 VL 90 IS 21 BP 9832 EP 9836 DI 10.1073/pnas.90.21.9832 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MF296 UT WOS:A1993MF29600019 PM 8234321 ER PT J AU JEFFREY, PD STRONG, RK SIEKER, LC CHANG, CYY CAMPBELL, RL PETSKO, GA HABER, E MARGOLIES, MN SHERIFF, S AF JEFFREY, PD STRONG, RK SIEKER, LC CHANG, CYY CAMPBELL, RL PETSKO, GA HABER, E MARGOLIES, MN SHERIFF, S TI 26-10 FAB-DIGOXIN COMPLEX - AFFINITY AND SPECIFICITY DUE TO SURFACE COMPLEMENTARITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE X-RAY CRYSTALLOGRAPHY; ANTIBODY ANTIGEN COMPLEX; ANTIBODIES; ANTIDIGOXIN ID ANTIBODIES; FRAGMENTS; REVERSAL; CRYSTALS; BINDING; PROGRAM; PROTEIN; CHAIN AB We have determined the three-dimensional structures of the antigen-binding fragment of the anti-digoxin monoclonal antibody 26-10 in the uncomplexed state at 2.7 angstrom resolution and as a complex with digoxin at 2.5 angstrom resolution. Neither the antibody nor digoxin undergoes any significant conformational changes upon forming the complex. Digoxin interacts primarily with the antibody heavy chain and is oriented such that the carbohydrate groups are exposed to solvent and the lactone ring is buried in a deep pocket at the bottom of the combining site. Despite extensive interactions between antibody and antigen, no hydrogen bonds or salt links are formed between 26-10 and digoxin. Thus the 26-10-digoxin complex is unique among the known three-dimensional structures of antibody-antigen complexes in that specificity and high affinity arise primarily from shape complementarity. C1 BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,POB 4000,PRINCETON,NJ 08543. MIT,DEPT CHEM,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. OI Campbell, Robert/0000-0002-5473-5876 FU NHLBI NIH HHS [R01-HL47415, P01-HL19259] NR 27 TC 129 Z9 129 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 1 PY 1993 VL 90 IS 21 BP 10310 EP 10314 DI 10.1073/pnas.90.21.10310 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MF296 UT WOS:A1993MF29600117 PM 8234291 ER PT J AU TROUTON, TG POWELL, AC GARAN, H RUSKIN, JN AF TROUTON, TG POWELL, AC GARAN, H RUSKIN, JN TI RISK IDENTIFICATION FOR SUDDEN CARDIAC DEATH - IMPLICATIONS FOR IMPLANTABLE CARDIOVERTER-DEFIBRILLLATOR USE SO PROGRESS IN CARDIOVASCULAR DISEASES LA English DT Review ID ACUTE MYOCARDIAL-INFARCTION; SUSTAINED VENTRICULAR-TACHYCARDIA; LONG QT SYNDROME; PROGRAMMED ELECTRICAL-STIMULATION; CORONARY-ARTERY DISEASE; TERM FOLLOW-UP; IDIOPATHIC DILATED CARDIOMYOPATHY; SIGNAL-AVERAGED ELECTROCARDIOGRAM; HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY; RECURRENT UNEXPLAINED SYNCOPE C1 MASSACHUSETTS GEN HOSP,CARDIAC ARRHYTHMIA SERV,BOSTON,MA 02114. NR 145 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 0033-0620 J9 PROG CARDIOVASC DIS JI Prog. Cardiovasc. Dis. PD NOV-DEC PY 1993 VL 36 IS 3 BP 195 EP 208 DI 10.1016/0033-0620(93)90013-4 PG 14 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MH131 UT WOS:A1993MH13100002 PM 8234773 ER PT J AU ABE, K KAKIUCHI, M SHIMADA, Y AF ABE, K KAKIUCHI, M SHIMADA, Y TI EPIDURAL BLOOD-FLOW DURING PROSTAGLANDIN-E(1) OR TRIMETHAPHAN INDUCED HYPOTENSION SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID SPINAL-CORD; ANESTHESIA; FUSION AB To evaluate the effect of prostaglandin E1 (PGE1) or trimethaphan (TMP) induced hypotension on epidural blood flow (EBF) during spinal surgery, EBF was measured using the heat clearance method in 30 patients who underwent postero-lateral interbody fusion under isoflurane anaesthesia. An initial dose of 0.1 mug.kg-1.min-1 of PGE1 (15 patients), or 10 mug.kg-1.min-1 of TMP (15 patients) was administered intravenously after the dural opening and the dose was adjusted to maintain the mean arterial blood pressure (MAP) at about 60 mmHg. The hypotensive drug was discontinued at the completion of the operative procedure. After starting PGE1 or TMP, MAP and rate pressure product (RPP) decreased significantly compared with preinfusion values (P < 0.01), and the degree of hypotension due to PGE1 remained constant until 60 min after its discontinuation. Heart rate (HR) did not change in either group. EBF did not change during PGE1 infusion whereas in the TMP group, EBF decreased significantly at 30 and 60 min after the start of TMP (preinfusion: 45.9 +/- 13.9 ml/100 g/min. 30 min: 32.3 +/- 9.9 ml/100 g/min (P < 0.05). 60 min: 30 +/- 7.5 ml/100 g/min (P < 0.05)). These results suggest that PGE1 may be preferable to TMP for hypotensive anaesthesia in spinal surgery because TMP decreased EBF. C1 OSAKA POLICE HOSP,DEPT ORTHOPAED,OSAKA,JAPAN. NAGOYA UNIV,SCH MED,DEPT ANAESTHESIA,NAGOYA,AICHI 466,JAPAN. RP ABE, K (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. NR 23 TC 1 Z9 1 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD NOV PY 1993 VL 49 IS 5 BP 873 EP 876 DI 10.1016/0952-3278(93)90213-G PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA MF247 UT WOS:A1993MF24700010 PM 8302922 ER PT J AU WEISMAN, AD AF WEISMAN, AD TI AVOIDING RESEARCH IN CONSULTATION-LIAISON PSYCHIATRY SO PSYCHOSOMATICS LA English DT Article ID WRITING BLOCK C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,AVERY D WEISMAN PSYCHIAT CONSULTAT SERV,BOSTON,MA 02114. NR 10 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 NOV-DEC PY 1993 VL 34 IS 6 BP 469 EP 477 PG 9 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MD779 UT WOS:A1993MD77900001 PM 8284336 ER PT J AU STERN, TA GLICK, RL AF STERN, TA GLICK, RL TI SIGNIFICANCE OF STUFFED ANIMALS AT THE BEDSIDE AND WHAT THEY CAN REVEAL ABOUT PATIENTS SO PSYCHOSOMATICS LA English DT Note C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP STERN, TA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,RESIDENT PSYCHIAT CONSULTAT SERV,WARREN BLDG 605,BOSTON,MA 02114, USA. NR 9 TC 6 Z9 6 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 NOV-DEC PY 1993 VL 34 IS 6 BP 519 EP 521 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MD779 UT WOS:A1993MD77900008 PM 8284343 ER PT J AU OSULLIVAN, RL GREENBERG, DB AF OSULLIVAN, RL GREENBERG, DB TI H2 ANTAGONISTS, RESTLESS LEG SYNDROME, AND MOVEMENT-DISORDERS SO PSYCHOSOMATICS LA English DT Note ID CIMETIDINE; OPIOIDS C1 MASSACHUSETTS GEN HOSP,HOSP CANC CTR,HEMATOL ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP OSULLIVAN, RL (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,ACC815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 17 TC 15 Z9 15 U1 2 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD NOV-DEC PY 1993 VL 34 IS 6 BP 530 EP 532 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MD779 UT WOS:A1993MD77900011 PM 7904357 ER PT J AU HALMAN, MH AF HALMAN, MH TI AIDS HEALTH AND MENTAL-HEALTH - A PRIMARY SOURCEBOOK - LANDAUSTANTON,J, CLEMENTS,CD SO PSYCHOSOMATICS LA English DT Book Review RP HALMAN, MH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,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 NOV-DEC PY 1993 VL 34 IS 6 BP 533 EP 534 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MD779 UT WOS:A1993MD77900012 ER PT J AU LEITER, F AF LEITER, F TI MEDICAL ISSUES AND THE EATING DISORDERS - THE INTERFACE - KAPLAN,AS, GARFINKEL,PE SO PSYCHOSOMATICS LA English DT Book Review RP LEITER, F (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 NOV-DEC PY 1993 VL 34 IS 6 BP 534 EP 535 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MD779 UT WOS:A1993MD77900013 ER PT J AU SCHOUTEN, R AF SCHOUTEN, R TI INTERVIEWING - A FORENSIC GUIDE TO INTERROGATION, 2ND EDITION - YESCHKE,CL SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SCHOUTEN, R (reprint author), MASSACHUSETTS GEN HOSP,LAW SERV,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 2 U2 3 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD NOV-DEC PY 1993 VL 34 IS 6 BP 535 EP 535 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MD779 UT WOS:A1993MD77900014 ER PT J AU LEE, MJ DAWSON, SL MUELLER, PR SAINI, S HAHN, PF GOLDBERG, MA LU, DSK MAYOSMITH, WW AF LEE, MJ DAWSON, SL MUELLER, PR SAINI, S HAHN, PF GOLDBERG, MA LU, DSK MAYOSMITH, WW TI PERCUTANEOUS MANAGEMENT OF HILAR BILIARY MALIGNANCIES WITH METALLIC ENDOPROSTHESES - RESULTS, TECHNICAL PROBLEMS, AND CAUSES OF FAILURE SO RADIOGRAPHICS LA English DT Article DE BILE DUCTS, INTERVENTIONAL PROCEDURE; BILE DUCTS, NEOPLASMS; BILE DUCTS, PROSTHESES; BILE DUCTS, STENOSIS OR OBSTRUCTION; CHOLANGITIS ID OBSTRUCTION; DRAINAGE; STENTS AB Malignant obstruction at the biliary hilum is a challenging problem for percutaneous management because of the anatomy of the biliary hilum, which facilitates spread of tumor into multiple biliary radicles. Metallic self-expanding stents were used in 22 patients with hilar malignancies. Sixteen patients had focal common hepatic duct strictures, and six had multisegmental disease. Stents were placed in the biliary system with a single transhepatic approach in 16 patients with common hepatic duct strictures; stent placement in the right and left biliary ducts was performed with a bilateral transhepatic approach in five patients and with a single transhepatic approach in one patient. Metal stent occlusion occurred in six patients (27%) at a mean of 2.5 months after initial insertion. Stent occlusion was due to inspissated debris in two of these patients and to tumor overgrowth in four. The key to successful long-term treatment is to ''overstent'' to ensure adequate purchase above hilar tumors and insertion in a balanced position. Thus, the prevalence of tumor overgrowth is decreased. RP LEE, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 11 TC 35 Z9 36 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0271-5333 J9 RADIOGRAPHICS JI Radiographics PD NOV PY 1993 VL 13 IS 6 BP 1249 EP 1263 PG 15 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG623 UT WOS:A1993MG62300013 PM 8290722 ER PT J AU NIEMIERKO, A GOITEIN, M AF NIEMIERKO, A GOITEIN, M TI IMPLEMENTATION OF A MODEL FOR ESTIMATING TUMOR-CONTROL PROBABILITY FOR AN INHOMOGENEOUSLY IRRADIATED TUMOR SO RADIOTHERAPY AND ONCOLOGY LA English DT Article; Proceedings Paper CT 10th Anniversary Meeting of the European-Organization-for-Research-on-the-Treatment-of-Cancer, Radiotherapy-Cooperative-Group: High Dose High Precision in Radiotherapy CY JAN 15-16, 1993 CL GENEVA, SWITZERLAND SP EUROPEAN ORG RES TREATMENT CANC, RADIOTHERAPY COOPERAT GRP DE TUMOR CONTROL PROBABILITY; TCP; BIOLOGICAL MODEL; MODELING; TREATMENT PLANNING; OPTIMIZATION AB This paper presents the details of a practical implementation of a model for the prediction of the tumor control probability (TCP) when a tumor is irradiated non-uniformly. The implementation is based on a previously published model and represents a simplified version of the model with a limited number (five) of parameters. We show how to derive the model parameters from clinically available data and offer pseudocode for computer implementation. The model should be a useful tool for evaluating and optimizing 3D dose distributions. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NIEMIERKO, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 21239, CA 50628] NR 3 TC 129 Z9 130 U1 0 U2 7 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD NOV PY 1993 VL 29 IS 2 BP 140 EP 147 DI 10.1016/0167-8140(93)90239-5 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA MU124 UT WOS:A1993MU12400012 PM 8310139 ER PT J AU WOLFSON, M AF WOLFSON, M TI SEVERE MALNUTRITION .1. SO SEMINARS IN DIALYSIS LA English DT Article AB A.Y. is a 56-year-old retired male airline pilot who presented with rapidly progressive renal failure in a single functioning (right) kidney. His left kidney had been obstructed by stones for several years and at presentation he had a left kidney double-J stent. His creatinine had. increased from 1.9 to 7.0 over the previous eight months. Physical examination revealed a well-developed, well-nourished male who had a blood pressure of 150/95, pulse 80 and regular, and respirations of 12/min. The rest of the physical exam was within normal limits. Laboratory studies revealed a blood urea nitrogen (BUN) of 70 mg/dl, creatinine of 7.2 mg/dl, glucose of 95 mg/dl, and normal liver function tests with a normal serum albumin. His complete blood count (CBC) was remarkable for a hematocrit of 33%. Serum iron and total iron binding capacity (TIBC) were also normal. The underlying cause of his renal insufficiency was never delineated. He was initially begun on hemodialysis, but underwent placement of a continuous ambulatory peritoneal dialysis (CAPD) catheter and was to begin training in this procedure. He was given 1 g of ceftriaxone at the time of catheter placement to prevent catheter infection and subsequently developed severe diarrhea, secondary to C. dificil infection. Despite this, the patient completed his dialysis training and hemodialysis was discontinued. Soon after he began CAPD, he also developed severe nausea and vomiting and was unable to eat. He was hospitalized and treated with intravenous fluids. His diarrhea resolved as did his nausea and vomiting. He was discharged from the hospital. At home he began vomiting again. He refused initially to be hospitalized, but awoke 72 hr after discharge with sudden blindness in both eyes. At presentation to the emergency room he was diagnosed with bilateral retinal artery emboli or thromboses. Vasculitis was ruled out, although he was given a short course of high dose prednisone therapy. The patient also was begun on subcutaneous heparin therapy. Hemodialysis was again instituted and CAPD discontinued. He continued to have severe nausea whenever food was offered. Complete gastroenterologic evaluation failed to reveal an anatomical cause for the vomiting. His course was also complicated by the development of pericarditis, refractory to treatment, and the patient underwent surgery for a pericardial window. The patient developed severe malnutrition over the course of these events with marked weight loss, serum albumin of 2.1, and serum prealbumin of 7.0. While initially reluctant, he subsequently agreed to placement of a nasoenteric feeding tube and was started on tube feedings daily. During his hemodialysis procedures, an attempt was made to provide intradialytic parenteral nutrition (IDPN). However, this resulted in severe hypophosphatemia. He initially did well with the nasoenteral tube feedings and was able to return home. However, he developed severe esophagitis and the tube was removed. Since he was still unable to eat because of continued nausea and vomiting, a feeding jejunostomy tube was placed. The patient did very well. His esophagitis improved, his albumin increased over three to four months to 3.9 g/dl and his prealbumin increased to 37. His appetite gradually improved and he began eating while continuing the jejunal feedings. After approximately one year, the jejunostomy tube was successfully removed:The patient is able to eat normally and his malnutrition is now resolved. RP WOLFSON, M (reprint author), PORTLAND VET AFFAIRS MED CTR,NEPHROL SECT 111C,3710 SW US VET HOSP RD,POB 1034,PORTLAND,OR 97201, USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0894-0959 J9 SEMIN DIALYSIS JI Semin. Dial. PD NOV-DEC PY 1993 VL 6 IS 6 BP 361 EP 362 DI 10.1111/j.1525-139X.1993.tb00175.x PG 2 WC Urology & Nephrology SC Urology & Nephrology GA MH463 UT WOS:A1993MH46300010 ER PT J AU DISLER, DG ROSENBERG, AE SPRINGFIELD, D OCONNELL, JX ROSENTHAL, DI KATTAPURAM, SV AF DISLER, DG ROSENBERG, AE SPRINGFIELD, D OCONNELL, JX ROSENTHAL, DI KATTAPURAM, SV TI EXTENSIVE SKELETAL METASTASES FROM CHONDROSARCOMA WITHOUT PULMONARY INVOLVEMENT SO SKELETAL RADIOLOGY LA English DT Article DE CHONDROSARCOMA; BONE METASTASIS; MULTICENTRIC; SARCOMA ID TUMOR AB Among 251 patients who presented to our orthopedic oncology unit over the last 20 years with chondrosarcoma, we identified two patients with low to intermediate grade conventional chondrosarcoma who developed multifocal bone metastases in the absence of pulmonary spread. The metastatic lesions were of a similar histologic grade to the primary site. One of the patients had synchronous foci, while the other developed the bone lesions 3 years after initial presentation. The unusual behavior of these cases, as well as the possibility that they may represent instances of multicentric chondrosarcoma, is discussed. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. RP DISLER, DG (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,15 PARKMAN ST,SUITE 515,BOSTON,MA 02114, USA. NR 23 TC 7 Z9 7 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 NOV PY 1993 VL 22 IS 8 BP 595 EP 599 PG 5 WC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging SC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging GA MK473 UT WOS:A1993MK47300007 PM 8291012 ER PT J AU MAYOSMITH, W ROSENTHAL, DI ROSENBERG, AE HARRIS, WH AF MAYOSMITH, W ROSENTHAL, DI ROSENBERG, AE HARRIS, WH TI CASE-REPORT 816 - DIAGNOSIS - RAPID ACCELERATION OF OSTEOLYSIS FROM LOOSE CEMENTED TOTAL HIP-REPLACEMENT SO SKELETAL RADIOLOGY LA English DT Note ID SYNOVIAL-LIKE MEMBRANE; FOREIGN-BODY REACTION; BONE-RESORPTION; ARTHROPLASTY; INTERFACE C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,WANG AMBULATORY CARE CTR,SUITE 515,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED,BOSTON,MA 02114. NR 14 TC 2 Z9 2 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 NOV PY 1993 VL 22 IS 8 BP 619 EP 621 PG 3 WC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging SC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging GA MK473 UT WOS:A1993MK47300012 PM 8291017 ER PT J AU DRINKA, PJ VOEKS, S BAUWENS, S BINKLEY, N AF DRINKA, PJ VOEKS, S BAUWENS, S BINKLEY, N TI SENSITIVITY AND POSITIVE PREDICTIVE VALUE OF CLINICAL SIGNS OF HYPOGONADISM IN ELDERLY MEN SO SOUTHERN MEDICAL JOURNAL LA English DT Article AB One hundred three ambulatory elderly men had serum free testosterone (FT) assessed as part of a study of bone loss. The FT was analyzed using radioimmunoassay. Each participant was questioned regarding the presence of erections adequate for sexual activity and the presence of sexual desire. Each was examined for decreased axillary and pubic hair. h FT of less than 9.0 pg/mL was found in eight subjects. The sensitivity of the clinical predictors as an indicator of a low FT value ranged from 4.3% to 86%, while positive predictive value ranged from 12% to 19%. The abnormal clinical signs and symptoms investigated in this study obviously have mechanisms in addition to hypogonadism. A history of adequate erections ruled out a low FT value in all but 1 of 44 cases. C1 MANAGED CARE RESOURCES INC,CHESAPEAKE,VA. WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIATR SECT,MADISON,WI 53705. RP DRINKA, PJ (reprint author), WISCONSIN VET HOME,KING,WI 54946, USA. NR 7 TC 6 Z9 6 U1 0 U2 0 PU SOUTHERN MEDICAL ASSN PI BIRMINGHAM PA 35 LAKESHORE DR PO BOX 190088, BIRMINGHAM, AL 35219 SN 0038-4348 J9 SOUTHERN MED J JI South.Med.J. PD NOV PY 1993 VL 86 IS 11 BP 1264 EP 1265 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MH676 UT WOS:A1993MH67600017 PM 8235781 ER PT J AU MOSKOWITZ, MA AF MOSKOWITZ, MA TI NITRIC-OXIDE PRODUCTION DURING FOCAL CEREBRAL-ISCHEMIA IN RATS - COMMENT SO STROKE LA English DT Editorial Material RP MOSKOWITZ, MA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. RI Moskowitz, Michael/D-9916-2011 NR 6 TC 1 Z9 1 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 NOV PY 1993 VL 24 IS 11 BP 1716 EP 1716 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA ME789 UT WOS:A1993ME78900019 ER PT J AU MOSKOWITZ, MA AF MOSKOWITZ, MA TI EFFECT OF NITRIC-OXIDE SYNTHASE INHIBITION ON CEREBRAL BLOOD-FLOW AND INJURY VOLUME DURING FOCAL ISCHEMIA IN CATS - COMMENT SO STROKE LA English DT Editorial Material RP MOSKOWITZ, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD NOV PY 1993 VL 24 IS 11 BP 1724 EP 1724 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA ME789 UT WOS:A1993ME78900021 ER PT J AU BUSAM, KJ ROBERTS, DJ GOLDEN, JA AF BUSAM, KJ ROBERTS, DJ GOLDEN, JA TI CLINICAL TERATOLOGY COUNSELING AND CONSULTATION CASE-REPORT - 2 DISTINCT ANTERIOR NEURAL-TUBE DEFECTS IN A HUMAN FETUS - EVIDENCE FOR AN INTERMITTENT PATTERN OF NEURAL-TUBE CLOSURE SO TERATOLOGY LA English DT Note ID AMNIOTIC BAND SYNDROME; MOUSE EMBRYO; NEURULATION; BRAIN AB Human neural tube closure is believed to be a continuous process that begins in the cervical region and progresses both rostrally and caudally. In contrast, an intermittent pattern of anterior neural tube closure has been demonstrated in rodents. Based on individual case photographs, a similar pattern of anterior neural tube closure, with multiple sites of closure, may also exist in humans. We report a human fetus with two distinct anterior neural tube defects separated by a cutaneous and mesenchymal bridge. The two defects occurred within distinct closure sites predicted by the murine model, one falling within closure II and the second within closure IV. Although one defect had adherent amniotic bands, evidence is presented to support a primary dysraphy rather than disruption from an amniotic band. This case provides further evidence supporting an intermittent pattern of anterior neural tube closure in human embryogenesis. (C) 1993 Wiley-Liss, Inc. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV NEUROPATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT NEUROPATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT WOMENS & PERINATAL PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,CHARLES S KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 30 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0040-3709 J9 TERATOLOGY JI Teratology PD NOV PY 1993 VL 48 IS 5 BP 399 EP 403 DI 10.1002/tera.1420480503 PG 5 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA MK528 UT WOS:A1993MK52800001 PM 7508150 ER PT J AU LEE, JC PILLAI, S AF LEE, JC PILLAI, S TI COMPLETE NUCLEOTIDE-SEQUENCE OF MHC CLASS-I ALLELES IN THE HT29 COLON-CANCER CELL-LINE SO TISSUE ANTIGENS LA English DT Note ID REGION; TRANSPORTERS; ANTIGENS; FAMILY; GENE RP LEE, JC (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST CHARLESTOWN NAVY YARD,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI 27835] NR 18 TC 0 Z9 3 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 NOV PY 1993 VL 42 IS 5 BP 530 EP 532 DI 10.1111/j.1399-0039.1993.tb02199.x PG 3 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA MN115 UT WOS:A1993MN11500010 PM 8146863 ER PT J AU GOODNOUGH, LT ANDERSON, KC KURTZ, S LANE, TA PISCIOTTO, PT SAYERS, MH SILBERSTEIN, LE AF GOODNOUGH, LT ANDERSON, KC KURTZ, S LANE, TA PISCIOTTO, PT SAYERS, MH SILBERSTEIN, LE TI INDICATIONS AND GUIDELINES FOR THE USE OF HEMATOPOIETIC GROWTH-FACTORS SO TRANSFUSION LA English DT Review ID COLONY-STIMULATING FACTOR; RECOMBINANT-HUMAN-ERYTHROPOIETIN; BONE-MARROW TRANSPLANTATION; SERUM IMMUNOREACTIVE ERYTHROPOIETIN; AUTOLOGOUS BLOOD DONATION; FACTOR GM-CSF; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; TRANSITIONAL-CELL-CARCINOMA; PLACEBO-CONTROLLED TRIAL; AIDS-RELATED COMPLEX C1 HARVARD UNIV,SCH MED,BOSTON,MA 02125. DANA FARBER CANC INST,BLOOD COMPONENT LAB,BOSTON,MA 02125. LAHEY CLIN FDN,DEPT LAB MED,BURLINGTON,MA 01805. UNIV CALIF SAN DIEGO,SCH MED,DEPT PATHOL,LA JOLLA,CA 92093. UNIV CONNECTICUT,CTR HLTH,MED LAB,FARMINGTON,CT 06030. UNIV CONNECTICUT,CTR HLTH,BLOOD BANK HEMATOL,FARMINGTON,CT 06030. UNIV WASHINGTON,SCH MED,DEPT MED,DIV HEMATOL,SEATTLE,WA 98104. PUGET SOUND BLOOD CTR,SEATTLE,WA 98104. UNIV PENN,BLOOD BANK,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. RP GOODNOUGH, LT (reprint author), WASHINGTON UNIV,SCH MED,DIV LAB MED,TRANSFUS SERV,BOX 8118,660 S EUCLID AVE,ST LOUIS,MO 63110, USA. NR 135 TC 36 Z9 37 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD NOV-DEC PY 1993 VL 33 IS 11 BP 944 EP 959 DI 10.1046/j.1537-2995.1993.331194082388.x PG 16 WC Hematology SC Hematology GA MM278 UT WOS:A1993MM27800013 PM 7505068 ER PT J AU DUKECOHAN, JS MORIMOTO, C SCHLOSSMAN, SF AF DUKECOHAN, JS MORIMOTO, C SCHLOSSMAN, SF TI DEPLETION OF THE HELPER/INDUCER (MEMORY) T-CELL SUBSET USING A BISPECIFIC ANTIBODY-TOXIN CONJUGATE DIRECTED AGAINST CD4 AND CD29 SO TRANSPLANTATION LA English DT Article ID MONOCLONAL-ANTIBODIES; ORGAN-TRANSPLANTATION; HELPER-INDUCER; RICIN; CYCLOSPORINE; CYTOTOXICITY; MAINTENANCE; IMMUNOTOXIN; ENDOCYTOSIS; DIAGNOSIS AB We have developed a bispecific antibody that recognizes the CD4 and CD29 antigens simultaneously and that was examined for its ability to target CD4(+)CD29(bright) T cells. The premise for using bispecific antibody-toxin conjugates was that monovalent binding to one antigen would not result in internalization while binding through both antigens would predispose toward endocytosis and delivery of the toxin to the cell interior. In this study, we show that the bispecific antibody binds monovalently to CD4 and CD29 and bivalently to both antigens. Both monovalent and bivalent binding rendered the target cells sensitive to complement-mediated lysis, demonstrating that this effector modality cannot take advantage of the dual specificity of the antibody. Bivalent binding, however, allowed modulation of more than 60% of the bound antibody off the surface of CD4(+)CD29(bright) cells, which we further exploited to deliver a toxin moiety preferentially to CD4(+)CD29(bright) cells. Immunoconjugates incorporating blocked ricin (a ricin holotoxin that has its intrinsic galactose-binding sites blocked by chemically linked affinity ligands) preferentially killed CD4(+)CD29(bright) cells in vitro by a factor of 25 in comparison with killing of total CD4(+) cells in functional assays. Assays on resting PBL demonstrated a similar specificity of the bispecific immunotoxin for CD4(+)CD29(bright) cells with a concomitant relative survival of CD4(+)CD29(dim) (CD45RA(+)). We demonstrated that the potency of the immunotoxin is not only a function of its affinity but also of its propensity to internalize, and that this property is influenced by the degree of bivalent binding. These results open up the possibility of engineering bispecific antibody toxin conjugates for use as therapeutic immunotoxins for selective removal of restricted T cell subsets. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP DUKECOHAN, JS (reprint author), DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Duke-Cohan, Jonathan/A-5812-2010 OI Duke-Cohan, Jonathan/0000-0002-9478-9609 FU NIAID NIH HHS [AI-23360-08, AI-29530] NR 39 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 NOV PY 1993 VL 56 IS 5 BP 1188 EP 1196 DI 10.1097/00007890-199311000-00027 PG 9 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA MH951 UT WOS:A1993MH95100027 PM 7504344 ER PT J AU KUNZENDORF, U NOTTER, M HOCK, H DISTLER, A DIAMANTSTEIN, T WALZ, G AF KUNZENDORF, U NOTTER, M HOCK, H DISTLER, A DIAMANTSTEIN, T WALZ, G TI T-CELLS BIND TO THE ENDOTHELIAL ADHESION MOLECULE GMP-140 (P-SELECTIN) SO TRANSPLANTATION LA English DT Article ID NEUTROPHIL ADHESION; ACTIVATED PLATELETS; PROTEIN; RECEPTOR; ANTIGEN; ICAM-1; ELAM-1; LYMPHOCYTES; RECOGNITION; SECRETION AB A crucial step in an effective immune response is the adhesion of circulating lymphocytes. Lymphocytes must attach to endothelial cells before they can migrate into the graft. It has been shown that T cells bind to ICAM-1 and VCAM-1. Additionally, certain T cell subsets bind to ELAM-1. We now report that resting CD4(+) and CD8(+) T cells as well as individual CD4(+) T cell clones and CD8(+) T cell lines bind to GMP-140 in an adhesion assay using protein chimeras consisting of the extracellular domain of GMP-140 linked to the hinge domain of human IgG1. Whereas resting T cells bound similarly to ELAM-1 IgG and GMP-140 IgG, activated T cells represented by CD4(+) T cell clones and CD8(+) T cell lines bound to GMP-140 IgG, but not to ELAM-1 IgG. Neither the binding to immobilized GMP-140 IgG, nor to immobilized ELAM-1 IgG could provide T cells with costimulatory signals for proliferation in the presence of submitogenic concentrations of anti-CD3 antibodies. The binding of T cells to the endothelial adhesion receptor GMP-140 might be important during the initial adhesion process of lymphocytes in rejecting grafts. C1 UNIV BERLIN,KLINIKUM STEGLITZ,INST IMMUNOL,W-1000 BERLIN 45,GERMANY. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA. RP KUNZENDORF, U (reprint author), UNIV BERLIN,KLINIKUM STEGLITZ,DEPT INTERNAL MED,HINDENBURGDAMM 30,W-1000 BERLIN 45,GERMANY. RI Kunzendorf, Ulrich/A-8257-2010 NR 29 TC 14 Z9 14 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 NOV PY 1993 VL 56 IS 5 BP 1213 EP 1217 DI 10.1097/00007890-199311000-00031 PG 5 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA MH951 UT WOS:A1993MH95100031 PM 7504345 ER PT J AU ROSS, DS AF ROSS, DS TI CURRENT THERAPEUTIC APPROACHES TO HYPERTHYROIDISM SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID LOW-DOSE I-131; GRAVES-DISEASE; POTASSIUM-IODIDE; RISK; OPHTHALMOPATHY; THYROTOXICOSIS; HYPOTHYROIDISM; PROPRANOLOL; METHIMAZOLE; ANTIBODIES AB Treatment of hyperthyroidism varies, depending upon the underlying etiology of thyrotoxicosis. Antithyroid drugs may be administered to patients with Graves' hyperthyroidism for prolonged periods in an attempt to obtain a remission. Alternatively, a short course of antithyroid drugs may be administered to patients with Graves' disease or toxic adenoma to achieve euthyroidism prior to definitive therapy with radioiodine or surgery. Radioiodine is the preferred therapy for most adult patients; however, large goiters, especially if obstructive symptoms are present, are best treated with surgery. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROSS, DS (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,THYROID UNIT,BOSTON,MA 02114, USA. NR 27 TC 4 Z9 5 U1 0 U2 1 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 NOV PY 1993 VL 4 IS 9 BP 281 EP 285 DI 10.1016/1043-2760(93)90046-H PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ML257 UT WOS:A1993ML25700002 PM 18407170 ER PT J AU JAKLITSCH, MT STRAUSS, GM SUGARBAKER, DJ AF JAKLITSCH, MT STRAUSS, GM SUGARBAKER, DJ TI NEOADJUVANT AND ADJUVANT THERAPY IN THE MANAGEMENT OF LOCALLY ADVANCED NON-SMALL-CELL LUNG-CANCER SO WORLD JOURNAL OF SURGERY LA English DT Article ID RADIATION-THERAPY; PHASE-II; PREOPERATIVE CHEMOTHERAPY; STAGE-II; CARCINOMA; SURGERY; CISPLATIN; SURVIVAL; EXTENT; TRIAL AB The role of adjuvant therapy in non-small-cell lung cancer continues to be defined. We review the most recent major reports of adjuvant trials. Three large randomized trials of postoperative chemotherapy and/or radiation therapy for stage I and II patients have noted improvement trends in median and long-term survival. Two large preoperative phase II trials for stage IIIA patients have reported high response and surgical resectability rates for preoperative combinations of radiation and chemotherapy, but without significant improvement in survival. In general, most of these protocols require months to complete, and not all patients are able to withstand the associated toxicity. The field of adjuvant therapy is continuing to develop; some of the strategies of ongoing protocols are reviewed. C1 BRIGHAM & WOMENS HOSP,DIV THORAC SURG,75 FRANCIS ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 31 TC 3 Z9 3 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2313 J9 WORLD J SURG JI World J.Surg. PD NOV-DEC PY 1993 VL 17 IS 6 BP 729 EP 734 PG 6 WC Surgery SC Surgery GA MN658 UT WOS:A1993MN65800008 PM 8109109 ER PT J AU OGUCHI, S WALKER, WA SANDERSON, IR AF OGUCHI, S WALKER, WA SANDERSON, IR TI INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEIN PROFILE SECRETED BY HUMAN INTESTINAL EPITHELIAL-CELLS VARIES WITH POLARITY SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID FACTOR-I; IGF-I; SOMATOMEDIN-C; HUMAN-MILK; RECEPTOR; PLASMA RP OGUCHI, S (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114, USA. FU NICHD NIH HHS [HD 12437]; NIDDK NIH HHS [DK33506] NR 22 TC 21 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 29 PY 1993 VL 196 IS 2 BP 789 EP 793 DI 10.1006/bbrc.1993.2318 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MG114 UT WOS:A1993MG11400041 PM 7694578 ER PT J AU LEE, WS MOSKOWITZ, MA AF LEE, WS MOSKOWITZ, MA TI CONFORMATIONALLY RESTRICTED SUMATRIPTAN ANALOGS, CP-122,288 AND CP-122,638 EXHIBIT ENHANCED POTENCY AGAINST NEUROGENIC INFLAMMATION IN DURA-MATER SO BRAIN RESEARCH LA English DT Note DE SUMATRIPTAN; MIGRAINE; NEUROGENIC INFLAMMATION; TACHYKININ; TRIGEMINAL GANGLIA; SEROTONIN; CP-122,288; CP-122,638 ID PLASMA EXTRAVASATION; ERGOT ALKALOIDS; RECEPTOR; RAT AB CP-122,288 and CP-122,638 blocked plasma protein extravasation response within dura mater following trigeminal ganglion stimulation. The threshold (1 and 0.1 pmol/kg, respectively) was remarkably lower than for sumatriptan (7 nmol/kg), as was the dose at maximum response. As with sumatriptan, substance P-induced plasma leakage was unaffected by either compound, and metergoline only partially (27%) reversed the effects of CP-122,288. The data suggest the importance of modifications at the aminoethyl side chain to the actions of sumatriptan and possibly to the treatment of migraine headache. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,STROKE RES LAB,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA 02114. FU NINDS NIH HHS [NS 21558] NR 9 TC 75 Z9 76 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 29 PY 1993 VL 626 IS 1-2 BP 303 EP 305 PG 3 WC Neurosciences SC Neurosciences & Neurology GA MC801 UT WOS:A1993MC80100036 PM 8281439 ER PT J AU NITSCH, RM BLUSZTAJN, JK DOYLE, FM ROBITAILLE, Y WURTMAN, RJ GROWDON, JH KISH, SJ AF NITSCH, RM BLUSZTAJN, JK DOYLE, FM ROBITAILLE, Y WURTMAN, RJ GROWDON, JH KISH, SJ TI PHOSPHOLIPID METABOLITE LEVELS ARE ALTERED IN CEREBRAL-CORTEX OF PATIENTS WITH DOMINANTLY INHERITED OLIVOPONTOCEREBELLAR ATROPHY SO NEUROSCIENCE LETTERS LA English DT Article DE GLYCEROPHOSPHOCHOLINE; GLYCEROPHOSPHOETHANOLAMINE; CHOLINE; ETHANOLAMINE; SERINE; PHOSPHATIDYLCHOLINE; PHOSPHATIDYLETHANOLAMINE; ALZHEIMERS DISEASE ID ALZHEIMERS-DISEASE; CHOLINE; BRAIN; ACETYLCHOLINE; GLYCEROPHOSPHOETHANOLAMINE; STIMULATION; STRIATUM; RELEASE AB We measured metabolic precursors and breakdown products of phosphatidylcholine (choline, glycerophosphocholine (GPC)) and phosphatidyl-ethanolamine (ethanolamine, glycerophosphoethanolamine (GPE)) as well as the amino acid serine, a precursor of phosphatidylserine, in four morphologically unaffected cerebral cortical areas obtained at autopsy from 14 patients with dominantly inherited olivopontocerebellar atrophy (OPCA) and 13 controls matched for age and postmortem interval. As compared with the controls, mean GPE levels were elevated by 49-57% in frontal and parietal cortices of OPCA brains whereas concentrations of ethanolamine were significantly reduced in temporal, occipital and parietal cortex (-40 to -54%). This resulted in increased GPE/ethanolamine ratios (+80 to +146%). GPC levels were significantly increased (by 53%) in the frontal cortex of OPCA patients relative to controls. Free serine levels were reduced by 20 to 28% in frontal, parietal, temporal, and occipital cortices. These abnormalities in phospholipid metabolite levels in OPCA resemble those seen in Alzheimer's disease, although the changes in GPC are less pronounced. These changes in phospholipid metabolism in OPCA cerebral cortex, a brain area spared from neurodegenerative changes, points to generalized disturbances in cellular membrane function in this disease. C1 MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. BOSTON UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02118 USA. BOSTON UNIV, SCH MED, DEPT PSYCHIAT, BOSTON, MA 02118 USA. MONTREAL NEUROL HOSP & INST, MONTREAL H3A 2B4, QUEBEC, CANADA. CLARKE INST PSYCHIAT, TORONTO M5T 1R8, ONTARIO, CANADA. RP NITSCH, RM (reprint author), MIT, DEPT BRAIN & COGNIT SCI, E25-604, CAMBRIDGE, MA 02139 USA. FU NIA NIH HHS [AG05134]; NIMH NIH HHS [MH28783]; NINDS NIH HHS [NS26034] NR 23 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0304-3940 EI 1872-7972 J9 NEUROSCI LETT JI Neurosci. Lett. PD OCT 29 PY 1993 VL 161 IS 2 BP 191 EP 194 DI 10.1016/0304-3940(93)90291-R PG 4 WC Neurosciences SC Neurosciences & Neurology GA MC332 UT WOS:A1993MC33200018 PM 8272265 ER PT J AU VIGNALI, DAA DOYLE, C KINCH, MS SHIN, JY STROMINGER, JL AF VIGNALI, DAA DOYLE, C KINCH, MS SHIN, JY STROMINGER, JL TI INTERACTIONS OF CD4 WITH MHC CLASS-II MOLECULES, T-CELL RECEPTORS AND P56(LCK) SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article ID TYROSINE-PROTEIN-KINASE; AMINO-TERMINAL DOMAIN; TOXIC LYMPHOCYTES-T; ANTIGEN RECEPTOR; BINDING-SITE; PHYSICAL ASSOCIATION; CROSS-LINKING; HISTOCOMPATIBILITY MOLECULES; IMMUNOGENIC PEPTIDES; SIGNAL TRANSDUCTION AB CD4 and CD8 are members of the immunoglobulin supergene family of proteins, and function as coreceptors with the T cell receptor (TCR) in binding MHC class II or class I molecules, respectively. Within this multimeric complex, CD4 interacts with three distinct ligands. CD4 interacts through its D1 and D2 domains with MHC class II proteins, through its D3 and D4 domains with T cell receptors, and through its cytoplasmic tail with p56lck, a src-related, protein tyrosine kinase. Each of these interactions is important in the function of CD4 and will be discussed in turn. C1 DUKE UNIV,MED CTR,DEPT IMMUNOL,DURHAM,NC 27710. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. RP VIGNALI, DAA (reprint author), HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138, USA. OI Kinch, Michael/0000-0003-3939-3756 NR 86 TC 13 Z9 13 U1 0 U2 1 PU ROYAL SOC LONDON PI LONDON PA 6 CARLTON HOUSE TERRACE, LONDON, ENGLAND SW1Y 5AG SN 0962-8436 J9 PHILOS T ROY SOC B JI Philos. Trans. R. Soc. Lond. Ser. B-Biol. Sci. PD OCT 29 PY 1993 VL 342 IS 1299 BP 13 EP 24 DI 10.1098/rstb.1993.0130 PG 12 WC Biology SC Life Sciences & Biomedicine - Other Topics GA MH277 UT WOS:A1993MH27700003 PM 7506833 ER PT J AU PRASAD, KVS KAPELLER, R JANSSEN, O DUKECOHAN, JS REPKE, H CANTLEY, LC RUDD, CE AF PRASAD, KVS KAPELLER, R JANSSEN, O DUKECOHAN, JS REPKE, H CANTLEY, LC RUDD, CE TI REGULATION OF CD4-P56(LCK)-ASSOCIATED PHOSPHATIDYLINOSITOL 3-KINASE (PI 3-KINASE) AND PHOSPHATIDYLINOSITOL 4-KINASE (PI 4-KINASE) SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYROSINE-PROTEIN-KINASE; T-CELL RECEPTOR; GROWTH-FACTOR RECEPTOR; HUMAN LYMPHOCYTES-T; SIGNAL TRANSDUCTION; ANTIGEN RECEPTOR; CROSS-LINKING; CD3 COMPLEX; MIDDLE-T AB CD4 serves as a receptor for MHC class II antigens and as a receptor for the human immunodeficiency virus (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. Although anti-CD4 crosslinking may increase lck activity, the effects of HIV-1 gp120 have been controversial. Activated protein-tyrosine kinases are known to associate with certain intracellular proteins possessing src-homology regions (SH-2 domains) such as phosphatidylinositol 3-kinase (PI 3-kinase). In this paper, we demonstrate that the CD4: p56lck complex associates with significant amounts of phosphatidylinositol (PI) kinase activity. High pressure liquid chromatographic (HPLC) analysis of the reaction products demonstrated the presence of phosphatidylinositol 3-phosphate (PI 3-P) and phosphatidylinositol 4-phosphate (PI 4-P), thus indicating that PI 3 and PI 4 kinases associate with CD4-p56lck. The p85 subunit of PI 3-kinase was also detected in anti-CD4 immunoprecipitates by immunoblotting with anti-p85 antiserum. Significantly, p56lck binding to CD4 appears to be necessary for the detection of lipid kinase activity associated with p56lck . Also, anti-HIV gp120 and anti-CD4 crosslinking induced a 10-15-fold increase in levels of both PI 3- and PI 4-kinase activity in anti-CD4 precipitates. Stimulation of CD4-p56lck-linked PI kinases by crosslinked HIV-1 gp120 may play a role in HIV-1-induced immune defects. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV RETROVIROL,BOSTON,MA 02115. BETH ISRAEL HOSP,DIV SIGNAL TRANSDUCT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. RP PRASAD, KVS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. RI Janssen, Ottmar/E-9735-2010; Cantley, Lewis/D-1800-2014; OI Cantley, Lewis/0000-0002-1298-7653; Duke-Cohan, Jonathan/0000-0002-9478-9609 FU NIGMS NIH HHS [R01 GM041890] NR 53 TC 4 Z9 4 U1 0 U2 0 PU ROYAL SOC LONDON PI LONDON PA 6 CARLTON HOUSE TERRACE, LONDON, ENGLAND SW1Y 5AG SN 0962-8436 J9 PHILOS T ROY SOC B JI Philos. Trans. R. Soc. Lond. Ser. B-Biol. Sci. PD OCT 29 PY 1993 VL 342 IS 1299 BP 35 EP 42 DI 10.1098/rstb.1993.0132 PG 8 WC Biology SC Life Sciences & Biomedicine - Other Topics GA MH277 UT WOS:A1993MH27700005 PM 7904344 ER PT J AU MOORE, JP JAMESON, BA SATTENTAU, QJ WILLEY, R SODROSKI, J AF MOORE, JP JAMESON, BA SATTENTAU, QJ WILLEY, R SODROSKI, J TI TOWARDS A STRUCTURE OF THE HIV-1 ENVELOPE GLYCOPROTEIN GP120 - AN IMMUNOCHEMICAL APPROACH SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article ID VIRUS TYPE-1 GP120; T4 MOLECULE; HUMAN CD4; RECEPTOR; BINDING; RETROVIRUS; COMPONENT; FRAGMENT; ANTIGEN; DOMAINS AB The HIV-1 surface glycoprotein gp120 binds CD4 in the initial state of virus-cell fusion. The extensive glycosylation of gp120 has thus far precluded definition of its structure by crystallographic methods. As an initial approach to a gp120 structure, the surface topology was mapped using antibodies. First, the regions of gp120 that are accessible on the surface of the native molecule, and those that are internal but exposed after denaturation, are identified. Second, epitopes for antibodies that recognize complex surface strutures comprising segments of different domains are identified. Third, we define how mutations in one domain of gp120 influence the binding of antibodies to defined epitopes on other domains. These latter approaches enable us to start to understand the inter-domain interactions that contribute to the overall structure of the gp 120 molecule. Information from these studies is being used to model the structures of individual gp120 domains, and the way in which these interact in the folded protein. C1 JEFFERSON CANC INST,PHILADELPHIA,PA 19107. CTR IMMUNOL MARSEILLE LUMINY,F-13288 MARSEILLE 9,FRANCE. NIAID,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. RP MOORE, JP (reprint author), NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10016, USA. NR 21 TC 8 Z9 8 U1 1 U2 1 PU ROYAL SOC LONDON PI LONDON PA 6 CARLTON HOUSE TERRACE, LONDON, ENGLAND SW1Y 5AG SN 0962-8436 J9 PHILOS T ROY SOC B JI Philos. Trans. R. Soc. Lond. Ser. B-Biol. Sci. PD OCT 29 PY 1993 VL 342 IS 1299 BP 83 EP 88 DI 10.1098/rstb.1993.0139 PG 6 WC Biology SC Life Sciences & Biomedicine - Other Topics GA MH277 UT WOS:A1993MH27700012 PM 7904352 ER PT J AU MCCAFFREY, PG LUO, C KERPPOLA, TK JAIN, J BADALIAN, TM HO, AM BURGEON, E LANE, WS LAMBERT, JN CURRAN, T VERDINE, GL RAO, A HOGAN, PG AF MCCAFFREY, PG LUO, C KERPPOLA, TK JAIN, J BADALIAN, TM HO, AM BURGEON, E LANE, WS LAMBERT, JN CURRAN, T VERDINE, GL RAO, A HOGAN, PG TI ISOLATION OF THE CYCLOSPORINE-SENSITIVE T-CELL TRANSCRIPTION FACTOR NFATP SO SCIENCE LA English DT Article ID LYMPHOCYTES-T; INTERLEUKIN-2 ENHANCER; NUCLEAR FACTOR; ACTIVATION; BINDING; FOS; CALCINEURIN; SEQUENCE; PROTEIN; FK-506 AB Nuclear factor of activated T cells (NFAT) is a transcription factor that regulates expression of the cytokine interleukin-2 (IL-2) in activated T cells. The DNA-binding specificity of NFAT is conferred by NFATp, a phosphoprotein that is a target for the immunosuppressive compounds cyclosporin A and FK506. Here, the purification of NFATp from murine T cells and the isolation of a complementary DNA clone encoding NFATp are reported. A truncated form of NFATp, expressed as a recombinant protein in bacteria, binds specifically to the NFAT site of the murine IL-2 promoter and forms a transcriptionally active complex with recombinant c-Fos and c-Jun. Antisera to tryptic peptides of the purified protein or to the recombinant protein fragment react with T cell NFATp. The molecular cloning of NFATp should allow detailed analysis of a T cell transcription factor that is central to initiation of the immune response. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. ROCHE INST MOLEC BIOL,ROCHE RES CTR,DEPT MOLEC ONCOL & VIROL,NUTLEY,NJ 07110. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. HARVARD UNIV,MICROCHEM FACIL,CAMBRIDGE,MA 02138. HARVARD UNIV,DEPT CHEM,CAMBRIDGE,MA 02138. RI Curran, Tom/C-1164-2008; Curran, Tom/D-7515-2011; OI Curran, Tom/0000-0003-1444-7551; Kerppola, Tom/0000-0002-0611-9446 FU NCI NIH HHS [CA42471]; NIGMS NIH HHS [GM46227]; NINDS NIH HHS [NS25078] NR 32 TC 395 Z9 398 U1 0 U2 4 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 29 PY 1993 VL 262 IS 5134 BP 750 EP 754 DI 10.1126/science.8235597 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MD952 UT WOS:A1993MD95200045 PM 8235597 ER PT J AU HENSON, JW FERRARO, MJ HUNTER, JV HEDLEYWHYTE, ET RUBIN, EJ AF HENSON, JW FERRARO, MJ HUNTER, JV HEDLEYWHYTE, ET RUBIN, EJ TI A 71-YEAR-OLD WOMAN WITH CONFUSION, HEMIANOPIA, AND AN OCCIPITAL MASS - BRAIN-ABSCESS, CEREBRAL, DUE TO FUSOBACTERIUM-NUCLEATUM AND PEPTOSTREPTOCOCCUS-MICROS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID FOLLOW-UP; METASTASES; MANAGEMENT; NEOPLASMS; DIAGNOSIS; SURVIVAL; GLIOMAS; LESIONS; TUMOR C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HENSON, JW (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 35 TC 6 Z9 6 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 OCT 28 PY 1993 VL 329 IS 18 BP 1335 EP 1341 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA MD557 UT WOS:A1993MD55700009 ER PT J AU WILLIAMS, KP SHOELSON, SE AF WILLIAMS, KP SHOELSON, SE TI COOPERATIVE SELF-ASSEMBLY OF SH2 DOMAIN FRAGMENTS RESTORES PHOSPHOPEPTIDE BINDING SO BIOCHEMISTRY LA English DT Article ID GROWTH-FACTOR RECEPTORS; PROTEINS; SRC; ASSOCIATION; BARNASE; KINASE; SITE; GAP; ABL AB Multifunctional proteins frequently can be subdivided into discrete functional domains. Selected cytoplasmic proteins involved in signal transduction contain catalytic domains in addition to protein binding modules termed Src homology (SH) domains; SH2 domains bind phosphotyrosyl peptide sequences. Even as isolated modules, SH2 domains have the intrinsic capacity to fold properly and retain sequence selectivity for binding. Following limited digestion with trypsin, the 14-kDa SH2 domains of Src and PI 3-kinase p85 were split at a lysine within the flexible, phosphotyrosine-binding (BC) loop into 5- and 9-kDa fragments. Whereas the purified fragments did not exhibit cooperative unfolding or phosphopeptide binding, when combined they spontaneously reassembled to restore specific phosphopeptide binding and the unique spectroscopic signatures of bound and free intact SH2 domains. Like fragments of intact proteins, we now show that fragments of SH2 domains, and therefore protein modules, possess the intrinsic capacity for self-assembly with restoration of function. Analyses of fragment structures may provide insights into pathways of module folding, which will facilitate a more global understanding of how complex, multifunctional proteins fold. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. FU NIDDK NIH HHS [DK36836] NR 41 TC 18 Z9 18 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 26 PY 1993 VL 32 IS 42 BP 11279 EP 11284 DI 10.1021/bi00093a003 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MD710 UT WOS:A1993MD71000003 PM 7692962 ER PT J AU SUCHER, NJ BROSE, N DEITCHER, DL AWOBULUYI, M GASIC, GP BADING, H CEPKO, CL GREENBERG, ME JAHN, R HEINEMANN, SF LIPTON, SA AF SUCHER, NJ BROSE, N DEITCHER, DL AWOBULUYI, M GASIC, GP BADING, H CEPKO, CL GREENBERG, ME JAHN, R HEINEMANN, SF LIPTON, SA TI EXPRESSION OF ENDOGENOUS NMDAR1 TRANSCRIPTS WITHOUT RECEPTOR PROTEIN SUGGESTS POST-TRANSCRIPTION CONTROL IN PC12-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHEOCHROMOCYTOMA PC12 CELLS; RETINAL GANGLION-CELLS; EXCITATORY AMINO-ACIDS; NERVE GROWTH-FACTOR; MESSENGER-RNA; RAT-BRAIN; FUNCTIONAL EXPRESSION; MOLECULAR-CLONING; PURKINJE-CELLS; IONIC CURRENTS AB Expression of RNA for the NMDAR1 subunit of the N-methyl-D-aspartate receptor was detected by Northern hybridization in both nerve growth factor-differentiated and undifferentiated rat pheochromocytoma (PC12) cells. The NMDA receptor type 1 (NMDAR1) message in PC12 cells was similar in size to that expressed in hippocampal neurons. PC12 cell cDNAs that were amplified by polymerase chain reaction with primers flanking the coding region of NMDAR1 corresponded to the NMDAR1 splice variant NMDA receptor type 1 isoform C (NMDAR1C). Using calcium imaging or patch-clamp recording, no functional NMDA-gated ion channels were found in PC12 cells. A monoclonal antibody against NMDAR1 was developed in order to investigate whether or not NMDAR1 protein was present in PC12 cells. Only trace amounts of NMDAR1 protein were found in native PC 12 cells. However, expression of NMDAR1 protein was detected in PC12 cells that were transfected with an expression vector containing an NMDAR1C clone under control of a cytomegalovirus promoter. These findings suggest that the expression of NMDAR1 protein in PC12 cells may be controlled by post-transcriptional mechanisms. The PC12 cell line may serve as a model system for the study of the transcriptional, post-transcriptional, and translational regulation of NMDAR1. Furthermore, the presence of NMDAR1 RNA in a particular cell type may not necessarily indicate expression of NMDAR1 protein. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. SALK INST BIOL STUDIES,MOLEC NEUROBIOL LAB,LA JOLLA,CA 92037. YALE UNIV,SCH MED,BOYER CTR MOLEC MED,HOWARD HUGHES MED INST,NEW HAVEN,CT 06510. RP SUCHER, NJ (reprint author), HARVARD UNIV,CHILDRENS HOSP,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115, USA. OI Sucher, Nikolaus/0000-0001-6233-1612 FU NEI NIH HHS [T32 EY07110]; NICHD NIH HHS [P01 HD29587]; NINDS NIH HHS [R01 NS23021] NR 59 TC 145 Z9 145 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 OCT 25 PY 1993 VL 268 IS 30 BP 22299 EP 22304 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MD348 UT WOS:A1993MD34800020 PM 8226739 ER PT J AU LI, CJ AVERBOUKH, L PARDEE, AB AF LI, CJ AVERBOUKH, L PARDEE, AB TI BETA-LAPACHONE, A NOVEL DNA TOPOISOMERASE-I INHIBITOR WITH A MODE OF ACTION DIFFERENT FROM CAMPTOTHECIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BREAKAGE-REUNION REACTION; CELL LUNG-CANCER; ANTITUMOR DRUGS; CLEAVAGE; MECHANISM; BINDING; COVALENT; PROTEIN; COMPLEX; DAMAGE AB Beta-lapachone is a plant product that has been found to have many pharmacological effects. To date, very little is known about its biochemical target. In this study, we found that beta-lapachone inhibits the catalytic activity of topoisomerase I from calf thymus and human cells. But, unlike camptothecin, beta-lapachone does not stabilize the cleavable complex, indicating a different mechanism of action. Beta-lapachone inhibits topoisomerase I-mediated DNA cleavage induced by camptothecin. Incubation of topoisomerase I with beta-lapachone before adding DNA substrate dramatically increases this inhibition. Incubation of topoisomerase I with DNA prior to beta-lapachone makes the enzyme refractory, and treatment of DNA with beta-lapachone before topoisomerase has no effect. These results suggest a direct interaction of beta-lapachone with topoisomerase I rather than DNA substrate. Beta-lapachone does not inhibit binding of enzyme to DNA substrate. In cells, beta-lapachone itself does not induce a SDS-K+-precipitable complex, but it inhibits complex formation with camptothecin. We propose that the direct interaction of beta-lapachone with topoisomerase I does not affect the assembly of the enzyme-DNA complex but does inhibit the formation of cleavable complex. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP LI, CJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA50608] NR 47 TC 192 Z9 196 U1 3 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 25 PY 1993 VL 268 IS 30 BP 22463 EP 22468 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MD348 UT WOS:A1993MD34800044 PM 8226754 ER PT J AU MA, TH FRIGERI, A TSAI, ST VERBAVATZ, JM VERKMAN, AS AF MA, TH FRIGERI, A TSAI, ST VERBAVATZ, JM VERKMAN, AS TI LOCALIZATION AND FUNCTIONAL-ANALYSIS OF CHIP28K WATER CHANNELS IN STABLY TRANSFECTED CHINESE-HAMSTER OVARY CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INTEGRAL MEMBRANE-PROTEIN; KIDNEY PROXIMAL TUBULE; BRUSH-BORDER; ENDOSOMES; TRANSPORT; RECONSTITUTION; EXPRESSION; VESICLES; PERMEABILITY; PURIFICATION AB CHIP28 is a major water transporting protein in erythrocytes and plasma membranes in kidney proximal tubule and thin descending limb of Henle. Chinese hamster ovary cells were stably transfected with the coding sequence of cloned rat kidney CHIP28k using expression vectors containing cytomegalovirus or Rous sarcoma virus promoters. Clonal cell populations expressed a 1.3-kilobase mRNA on Northern blot probed by CHIP28k cDNA and a 28-kDa protein on immunoblot probed by a polyclonal CHIP28 antibody. The clone with greatest expression produced approximately 8 x 10(6) copies of CHIP28k protein/cell. Plasma membrane osmotic water permeability (P(f)), measured by stopped-flow light scattering, was 0.004 cm/s in control (vector-transfected) cells (10-degrees-C) and 0.014 cm/s in the CHIP28k-transfected cells. P(f) in CHIP28k-transfected cells had an activation energy of 4.9 kcal/mol and was reversibly inhibited by HgCl2. CHIP28k expression did not affect the transport of protons and the small polar non-electrolytes urea and formamide. CHIP28k immunoreactivity and function was then determined in subcellular fractions. P(f) in 6-carboxyfluorescein-labeled endocytic vesicles, measured by a stopped-flow fluorescence quenching assay, was 0.002 cm/s (control cells) and 0.011 cm/s (CHIP28k-transfected cells); P(f) in transfected cells was inhibited by HgCl2. Immunoblotting of fractionated endoplasmic reticulum, Golgi, and plasma membranes revealed high densities of CHIP28k (approximately 5000 monomers/mum2 in plasma membrane) with different glycosylation patterns; functional water transport activity was present only in Golgi and plasma membrane vesicles. Antibody detection of CHIP28k by confocal fluorescence microscopy and immunogold electron microscopy revealed localization to plasma membrane and intracellular vesicles. These studies establish a stably transfected somatic cell line that strongly expresses functional CHIP28k water channels. As in the original proximal tubule cells, the expressed CHIP28k protein is a selective water channel that is functional in endocytic vesicles and the cell plasma membrane. C1 UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,DEPT MED & PHYSIOL,1065 HLTH SCI E TOWER,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,DEPT MED & PHYSIOL,RENAL UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL42368]; NIDDK NIH HHS [DK35124] NR 43 TC 74 Z9 74 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 OCT 25 PY 1993 VL 268 IS 30 BP 22756 EP 22764 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MD348 UT WOS:A1993MD34800083 PM 8226786 ER PT J AU SUGIMOTO, S LECHLEIDER, RJ SHOELSON, SE NEEL, BG WALSH, CT AF SUGIMOTO, S LECHLEIDER, RJ SHOELSON, SE NEEL, BG WALSH, CT TI EXPRESSION, PURIFICATION, AND CHARACTERIZATION OF SH2-CONTAINING PROTEIN-TYROSINE-PHOSPHATASE, SH-PTP2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH-FACTOR RECEPTORS; BINDING-SITE; SH2 DOMAINS; PHOSPHATIDYLINOSITOL-3 KINASE; SEQUENCE SIMILARITY; HUMAN-PLACENTA; EGF RECEPTOR; BETA-SUBUNIT; DROSOPHILA; TORSO AB A human protein tyrosine phosphatase containing two src homology 2 (SH2) domains (SH-PTP2) was expressed in Escherichia coli under T7 promoter control and purified to near homogeneity. The purified protein, with molecular mass of 68 kDa on SDS-polyacrylamide gel electrophoresis, was identified as SH-PTP2 by its protein tyrosine phosphatase activity and N-terminal amino acid sequence analysis. Its protein tyrosine phosphatase activity was sensitive to pH and salt concentration. Whereas its optimum pH for the low molecular weight substrate para-nitrophenyl phosphate is 5.6, the pH optima for peptide substrates were shifted toward neutral. With the artificial protein substrate reduced, carboxy-amidomethylated, and maleylated lysozyme, it displays 2000-fold lower K(m) (1.7 muM) and 2.4-fold higher k(cat) (0.11 s-1) than with para-nitrophenyl phosphate. Among the phosphopeptides from autophosphorylation sites of receptors for epidermal growth factor and platelet-derived growth factor, SH-PTP2 displayed high activity toward phosphopeptides corresponding to pY992 of the epidermal growth factor receptor and pY1009 and pY1021 of the platelet-derived growth factor receptor. In further enzymatic studies with phosphopeptides corresponding to pY1009, SH-PTP2 showed nonlinear Line-weaver-Burk double-reciprocal plots, suggesting that the phosphopeptide corresponding to pY1009 may have a substrate and allosteric effect. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,240 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. BETH ISRAEL HOSP,MOLEC MED UNIT,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DIV PULM MED,BOSTON,MA 02115. FU NIDCR NIH HHS [DERC 36836]; NIGMS NIH HHS [GM20011]; PHS HHS [49152] NR 58 TC 72 Z9 73 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 OCT 25 PY 1993 VL 268 IS 30 BP 22771 EP 22776 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MD348 UT WOS:A1993MD34800085 PM 8226787 ER PT J AU MOMBAERTS, P MIZOGUCHI, E GRUSBY, MJ GLIMCHER, LH BHAN, AK TONEGAWA, S AF MOMBAERTS, P MIZOGUCHI, E GRUSBY, MJ GLIMCHER, LH BHAN, AK TONEGAWA, S TI SPONTANEOUS DEVELOPMENT OF INFLAMMATORY BOWEL-DISEASE IN T-CELL RECEPTOR MUTANT MICE SO CELL LA English DT Article ID MONOCLONAL-ANTIBODIES; TARGETED DISRUPTION; GENE; MOUSE; LYMPHOCYTES AB We describe the spontaneous development of inflammatory bowel disease (IBD) in several immunodeficient mouse strains created via gene targeting in embryonic stem cells. Chronic colitis was observed in T cell receptor (TCR) alpha mutant, TCR beta mutant, TCR beta x delta double mutant, or class II major histocompatibility complex (MHC) mutant mice, but not in recombination-activating gene RAG-1 mutant mice or nude mice kept in the same specific pathogen-free animal facility. This clinical pattern suggests that the disease requires the presence of B lymphocytes and the absence of class II HC-restricted CD4+ alphabeta T cells. IBD in the mutant mice has some of the features of the human disease ulcerative colitis. Based on these results, we suggest that dysfunction of the mucosal immune system may underly the pathogenesis of some types of IBD in humans. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR STUDY INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. NEW ENGLAND REG PRIMATE RES CTR,BOSTON,MA 02114. RP MOMBAERTS, P (reprint author), MIT,HOWARD HUGHES MED INST,CTR CANC RES,DEPT BIOL,CAMBRIDGE,MA 02139, USA. NR 24 TC 288 Z9 292 U1 1 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 22 PY 1993 VL 75 IS 2 BP 275 EP 282 DI 10.1016/0092-8674(93)80069-Q PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MD885 UT WOS:A1993MD88500009 ER PT J AU BRUNNER, HG NELEN, M BREAKEFIELD, XO ROPERS, HH VANOOST, BA AF BRUNNER, HG NELEN, M BREAKEFIELD, XO ROPERS, HH VANOOST, BA TI ABNORMAL-BEHAVIOR ASSOCIATED WITH A POINT MUTATION IN THE STRUCTURAL GENE FOR MONOAMINE OXIDASE-A SO SCIENCE LA English DT Article ID CEREBROSPINAL-FLUID MONOAMINE; HUMAN-SKIN FIBROBLASTS; NORRIE DISEASE; PRENATAL-DIAGNOSIS; X-CHROMOSOME; NORWAY RATS; AGGRESSION; INHIBITORS; DELETION; ACID AB Genetic and metabolic studies have been done on a large kindred in which several males are affected by a syndrome of borderline mental retardation and abnormal behavior. The types of behavior that occurred include impulsive aggression, arson, attempted rape, and exhibitionism. Analysis of 24-hour urine samples indicated markedly disturbed monoamine metabolism. This syndrome was associated with a complete and selective deficiency of enzymatic activity of monoamine oxidase A (MAOA). In each of five affected males, a point mutation was identified in the eighth exon of the MAOA structural gene, which changes a glutamine to a termination codon. Thus, isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression. C1 UNIV HOSP NIJMEGEN,DEPT HUMAN GENET,6500 HB NIJMEGEN,NETHERLANDS. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA 02129. RP BRUNNER, HG (reprint author), UNIV HOSP NIJMEGEN,DEPT HUMAN GENET,GEERT GROOTEPLEIN 20,6525 GA NIJMEGEN,NETHERLANDS. RI Brunner, Han/C-9928-2013; Nelen, Marcel/L-4542-2015 FU NINDS NIH HHS [NS 21921] NR 43 TC 888 Z9 914 U1 10 U2 98 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 22 PY 1993 VL 262 IS 5133 BP 578 EP 580 DI 10.1126/science.8211186 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MC935 UT WOS:A1993MC93500044 PM 8211186 ER PT J AU CASTRESANA, JS RUBIO, MP VAZQUEZ, JJ IDOATE, M SOBER, AJ SEIZINGER, BR BARNHILL, RL AF CASTRESANA, JS RUBIO, MP VAZQUEZ, JJ IDOATE, M SOBER, AJ SEIZINGER, BR BARNHILL, RL TI LACK OF ALLELIC DELETION AND POINT MUTATION AS MECHANISMS OF P53 ACTIVATION IN HUMAN-MALIGNANT MELANOMA SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID POLYMERASE CHAIN-REACTION; DNA POLYMORPHISMS; EXPRESSION; CANCERS; GENE AB To investigate the role of the p53 tumor-suppressor gene in the development of human melanoma, loss of heterozygosity (LOH) of p53 was studied in 46 cases of melanoma by a polymerase-chain-reaction/restriction-fragment-length polymorphism (PCR/RFLP) analysis, and p53 mutations were assessed in 51 cases of melanoma by a polymerase-chain-reaction/ single-strand-conformation polymorphism (PCR/SSCP) analysis. Frozen tumors and paraffin samples were used in the study. We were not able to detect any allelic loss in 12 BstUI informative cases or any single mutation in exons 5 to 8 of the p53 gene. Our results, together with other findings at the DNA level, suggest that the p53 gene appears not to be commonly involved in the development of melanoma, at least by its most frequent mechanisms of deletion of one allele and/or mutation in the other. (C) 1993 Wiley-Liss, Inc. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. UNIV NAVARRA,DEPT HISTOL & ANAT PATHOL,PAMPLONA,SPAIN. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL DERMATOPATHOL,BOSTON,MA 02115. RI Rubio, Mari-Paz/K-4364-2014; OI Rubio, Mari-Paz/0000-0003-3963-5903; Castresana, Javier S./0000-0002-2373-482X NR 17 TC 96 Z9 96 U1 2 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 21 PY 1993 VL 55 IS 4 BP 562 EP 565 DI 10.1002/ijc.2910550407 PG 4 WC Oncology SC Oncology GA ME125 UT WOS:A1993ME12500006 PM 8104906 ER PT J AU SMITH, DB STOWELL, CP HARRIS, NL HAHN, PF ELLMAN, L SCULLY, RE LEINBACH, RC AF SMITH, DB STOWELL, CP HARRIS, NL HAHN, PF ELLMAN, L SCULLY, RE LEINBACH, RC TI JAUNDICE AND ANEMIA 2 WEEKS AFTER AN AORTIC VALVULOPLASTY IN A 62-YEAR-OLD WOMAN WITH SPLENOMEGALY - DELAYED TRANSFUSION REACTION - SPLENOMEGALY OF UNKNOWN CAUSE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID T-CELL LYMPHOCYTOSIS; MALIGNANT-LYMPHOMA; UREA TRANSPORT; SPLENECTOMY; SPLEEN; HISTIOCYTOSIS; NEUTROPENIA; LEUKEMIA; ANTIBODY C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SMITH, DB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 48 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 OCT 21 PY 1993 VL 329 IS 17 BP 1254 EP 1261 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA MB988 UT WOS:A1993MB98800009 ER PT J AU MACKLIS, RM BERESFORD, BA PALAYOOR, S SWEENEY, S HUMM, JL AF MACKLIS, RM BERESFORD, BA PALAYOOR, S SWEENEY, S HUMM, JL TI CELL-CYCLE ALTERATIONS, APOPTOSIS, AND RESPONSE TO LOW-DOSE-RATE RADIOIMMUNOTHERAPY IN LYMPHOMA-CELLS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 34TH ANNUAL MEETING OF THE AMERICAN-SOC-FOR-THERAPEUTIC-RADIOLOGY-AND-ONCOLOGY CY NOV 09-13, 1992 CL SAN DIEGO, CA SP AMER SOC THERAPEUT RADIOL & ONCOL DE RADIOIMMUNOTHERAPY; RADIOBIOLOGY; LOW-DOSE-RATE EFFECTS; MALIGNANT LYMPHOMA; APOPTOSIS; Y-90 ID MONOCLONAL-ANTIBODY; RADIATION; TUMOR; DEATH; INDUCTION; RADIOBIOLOGY; IRRADIATION; REPAIR; DAMAGE; LINE AB Purpose: In an attempt to elucidate some aspects of the radiobiological basis of radioimmunotherapy, we have evaluated the in vitro cellular response patterns for malignant lymphoma cell lines exposed to high- and low-dose-rate radiation administered within the physiological context of antibody cell-surface binding. Methods and Materials: We used two different malignant lymphoma cell lines, a Thy1.2+ murine T-lymphoma line called EL-4 and a CD20+ human B-lymphoma line called Raji. Cells were grown in suspension cultures and exposed to high-dose-rate gamma radiation from an external 137Cs source or low-dose-rate beta radiation from DTPA-solubilized 90Y in solution. In some experiments, cells were pre-incubated with an excess of nonradioactive antibody in order to assess the effects of immunoglobulin surface binding during radiation exposure. Irradiated cells were evaluated for viability, cell-cycle changes, patterns of post-radiation morphologic changes, and biochemical hallmarks of radiation-associated necrosis and programmed cell death. Results: The EL-4 line was sensitive to both high-dose-rate and low-dose-rate irradiation, while the Raji showed efficient cell kill only after high-dose-rate irradiation. Studies of radiation-induced cell cycle changes demonstrated that both cell lines were efficiently blocked at the G2/M interface by high-dose-rate irradiation, with the Raji cells appearing somewhat more susceptible than the EL-4 cells to low-dose-rate radiation-induced G2/M block. Electron microscopy and DNA gel electrophoresis studies showed that a significant proportion of the EL-4 cells appeared to be dying by radiation-induced programmed cell death (apoptosis) while the Raji cells appeared to be dying primarily by classical radiation-induced cellular necrosis. Conclusion: We propose that the unusual clinical responsiveness of some high and low grade lymphomas to modest doses of low-dose-rate radioimmunotherapy may be explained in part by the induction of apoptosis. The unusual dose-response characteristics observed in some experimental models of radiation-induced apoptosis may require a reappraisal of standard linear quadratic and alpha/beta algorithms used to predict target tissue cytoreduction after radioimmunotherapy. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MACKLIS, RM (reprint author), HARVARD JOINT CTR RADIAT THERAPY,50 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [NCI CA-50886, NCI CA-49017] NR 34 TC 52 Z9 52 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 20 PY 1993 VL 27 IS 3 BP 643 EP 650 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA MF620 UT WOS:A1993MF62000021 PM 8226159 ER PT J AU SICKLES, EA KOPANS, DB AF SICKLES, EA KOPANS, DB TI DEFICIENCIES IN THE ANALYSIS OF BREAST-CANCER SCREENING DATA SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID QUALITY ASSURANCE; DEATH RATES; MAMMOGRAPHY; WOMEN; TRIAL C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SICKLES, EA (reprint author), UNIV CALIF SAN FRANCISCO,SCH MED,DEPT RADIOL,BOX 0628,SAN FRANCISCO,CA 94143, USA. NR 18 TC 67 Z9 69 U1 1 U2 1 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 OCT 20 PY 1993 VL 85 IS 20 BP 1621 EP 1624 DI 10.1093/jnci/85.20.1621 PG 4 WC Oncology SC Oncology GA MB670 UT WOS:A1993MB67000003 PM 8179650 ER PT J AU OHASHI, H ROSEN, KM SMITH, FE VILLAKOMAROFF, L NAYAK, RC KING, GL AF OHASHI, H ROSEN, KM SMITH, FE VILLAKOMAROFF, L NAYAK, RC KING, GL TI CHARACTERIZATION OF TYPE-I IGF RECEPTOR AND IGF-I MESSENGER-RNA EXPRESSION IN CULTURED HUMAN AND BOVINE GLOMERULAR CELLS SO REGULATORY PEPTIDES LA English DT Article DE IGF-I; MESSENGER RNA EXPRESSION; CHARACTERIZATION; GLOMERULAR CELL; HUMAN; BOVINE ID GROWTH FACTOR-I; RENAL PLASMA-FLOW; MESANGIAL CELLS; FILTRATION-RATE; SOMATOMEDIN-C; INSULIN; BINDING; HORMONE; PURIFICATION; HYPERTROPHY AB Glomerular hypertrophy is reported in several endocrine disorders such as acromegaly and diabetes mellitus, where abnormalities of growth hormone and insulin-like growth factor (IGF-I) have been reported. In the present report, we have cultured bovine and human glomerular endothelial cells, and bovine glomerular epithelial and mesangial cells, and characterized the expression of IGF-I mRNA and its receptor in these cells. High affinity, specific receptors for IGF-I were identified in all three types of cells by radioreceptor assays. Receptor number (R(o)) derived by Scatchard analysis revealed an unusually high number of Type I IGF receptors, approx. 1.2-105 receptors/cell in glomerular endothelial cells. Affinity crosslinking studies and immunoprecipitation with antibodies against the Type I IGF receptor identified the alpha-subunit of the IGF-I receptor as having a molecular mass of 140 kDa. Biologically, IGF-I was more potent than insulin or IGF-II in stimulating DNA synthesis in glomerular endothelial cells. Northern blot analysis showed that glomerular and aortic endothelial cells expressed IGF-I mRNA of 1.7 kb. In contrast, renal glomeruli showed several IGF-I mRNAs of 7.5, 1.7 and 1.2 kb. Thus, the demonstration of both a prepondence of Type I IGF receptors coupled with the growth promoting effects of IGF-I in glomerular endothelial and epithelial cells, as well as the local production of IGF-I mRNA suggests that IGF-I serves an important role as an autocrine or paracrine regulator of the growth of renal glomeruli. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,BOSTON,MA 02115. FU NEI NIH HHS [EY05110]; NIDDK NIH HHS [NIDDK 39783-03]; NINDS NIH HHS [NS27832] NR 34 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD OCT 20 PY 1993 VL 48 IS 1-2 BP 9 EP 20 DI 10.1016/0167-0115(93)90331-2 PG 12 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA MD637 UT WOS:A1993MD63700003 PM 8265820 ER PT J AU BASKIN, DG SIPOLS, AJ SCHWARTZ, MW WHITE, MF AF BASKIN, DG SIPOLS, AJ SCHWARTZ, MW WHITE, MF TI IMMUNOCYTOCHEMICAL DETECTION OF INSULIN-RECEPTOR SUBSTRATE-1 (IRS-1) IN RAT-BRAIN - COLOCALIZATION WITH PHOSPHOTYROSINE SO REGULATORY PEPTIDES LA English DT Article DE HYPOTHALAMUS; SIGNAL TRANSDUCTION; PHOSPHOTYROSINE; CHOROID PLEXUS; PP185 ID GROWTH FACTOR-I; QUANTITATIVE AUTORADIOGRAPHY; MESSENGER-RNA; PHOSPHATIDYLINOSITOL 3'-KINASE; INSITU HYBRIDIZATION; ARCUATE NUCLEUS; BINDING-SITES; ZUCKER RATS; INTACT RAT; LOCALIZATION AB In peripheral insulin-sensitive tissues, insulin receptor substrate (IRS-1) undergoes tyrosine phosphorylation immediately after cells are stimulated by insulin or insulin-like growth factor-I (IGF-1), and may function as a molecular link between insulin/IGF-1 receptor tyrosine kinases and enzymes regulating cell growth and metabolism. A fundamental question pertaining to insulin/IGF-1 action in the brain is whether IRS-1 is expressed by neurons. In this study, the distribution of cells containing immunoreactivity to IRS-1 in the brain was determined by immunocytochemistry with polyclonal IRS-1 antiserum, and compared to the localization of immunostaining for phosphotyrosine using polyclonal phosphotyrosine antiserum. The immunostaining results with ABC-peroxidase method and cryostat sections showed the presence of IRS-1 immunoreactivity in many neuron cell bodies throughout the rat forebrain, particularly in the habenula, cerebral cortex and piriform cortex. In the hypothalamus, IRS-1 immunostaining was present in neurons of the paraventricular nucleus, supraoptic nucleus, and arcuate nucleus. The choroid plexus stained intensely for IRS-1. The populations of cells that stained for IRS-1 also showed strong immunostaining for phosphotyrosine. Studies at the cellular level are needed to verify coexpression of IRS-1 and receptors for insulin or IGF-1 by the same neurons, as well as in cells of the choroid plexus. The present results are the first demonstration of IRS-1 expression by neurons in adult mammalian brain. These findings are consistent with the hypothesis that insulin and IGF-I actions in the brain involve signal transduction mechanisms common to those found in peripheral tissues. C1 UNIV WASHINGTON,SCH MED,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT BIOL STRUCT,SEATTLE,WA 98195. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. RP BASKIN, DG (reprint author), UNIV WASHINGTON,SCH MED,VET AFFAIRS MED CTR,DIV ENDOCRINOL METAB,GEN MED RES SERV,SEATTLE,WA 98195, USA. RI Schwartz, Michael/H-9950-2012 FU NIDDK NIH HHS [DK-17047, DK-12829] NR 31 TC 45 Z9 47 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD OCT 20 PY 1993 VL 48 IS 1-2 BP 257 EP 266 DI 10.1016/0167-0115(93)90355-C PG 10 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA MD637 UT WOS:A1993MD63700027 PM 7505468 ER PT J AU ALEXANDRIDES, TK CHEN, JH BUENO, R GIORGINO, F SMITH, RJ AF ALEXANDRIDES, TK CHEN, JH BUENO, R GIORGINO, F SMITH, RJ TI EVIDENCE FOR 2 INSULIN-LIKE GROWTH FACTOR-I RECEPTORS WITH DISTINCT PRIMARY STRUCTURE THAT ARE DIFFERENTIALLY EXPRESSED DURING DEVELOPMENT SO REGULATORY PEPTIDES LA English DT Article DE IGF-I RECEPTOR ANTIBODY; INSULIN RECEPTOR; SKELETAL MUSCLE; TYROSINE KINASE; TYROSINE PHOSPHORYLATION ID STIMULATES TYROSINE PHOSPHORYLATION; NEURO-BLASTOMA CELLS; RAT SKELETAL-MUSCLE; BETA-SUBUNIT; IGF-I; MONOCLONAL-ANTIBODY; KINASE-ACTIVITY; HEPATOMA-CELLS; SOMATOMEDIN-C; INTACT-CELLS AB We have previously presented evidence for two IGF I receptor species in rat skeletal muscle. One form of IGF I receptor is selectively expressed in fetal and early postnatal life, and the second is present in both fetal and adult animals. These two IGF I receptors were shown to have similar tryptic phosphopeptide maps but to differ in beta subunit molecular weight (105,000 for the fetal vs. 95,000 for the adult type receptor). In this study, we have used specific antibodies to investigate the structural relationships between the two IGF I receptors. Anti-IGF I receptor beta subunit antibodies were generated against synthetic peptides corresponding to residues 1284-1293 and 1308-1318 of the cloned human IGF I receptor, and the capacity of these antibodies to interact with the two IGF I receptors was investigated. Both anti-peptide antibodies selectively immunoprecipitated the higher molecular weight fetal receptor and not the adult receptor from rat muscle. Human placenta and muscle were shown to contain two receptors similar to those observed in rat muscle. In human muscle, the anti-peptide antibodies and the human-specific monoclonal alpha subunit antibody alpha-IR3 also selectively immunoprecipitated the fetal type receptor. The presence of a 95,000 M(r) IGF I receptor beta subunit distinct from the insulin receptor beta subunit in human muscle was confirmed by the demonstration of an IGF I sensitive receptor with a beta subunit of this size after insulin receptor immunodepletion. These data strongly support the conclusion that the fetal and adult type IGF I receptors differ in primary structure. The fetal receptor corresponds to the cloned and sequenced IGF I receptor, and the primary structure of the adult type receptor has not yet been established. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,DEPT MED,DIV RES,JOSLIN DIABET CTR,ELLIOT P JOSLIN RES LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Giorgino, Francesco/K-7262-2016 OI Giorgino, Francesco/0000-0001-7372-2678 FU NIDDK NIH HHS [DK39077, DK43038]; NIGMS NIH HHS [GM36428] NR 46 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD OCT 20 PY 1993 VL 48 IS 1-2 BP 279 EP 290 DI 10.1016/0167-0115(93)90357-E PG 12 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA MD637 UT WOS:A1993MD63700029 PM 8265815 ER PT J AU PUDER, M BARNARD, GF STANIUNAS, RJ STEELE, GD CHEN, LB AF PUDER, M BARNARD, GF STANIUNAS, RJ STEELE, GD CHEN, LB TI NUCLEOTIDE AND DEDUCED AMINO-ACID-SEQUENCE OF HUMAN RIBOSOMAL PROTEIN-L18 SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Note DE RIBOSOMAL PROTEIN; L18; CDNA; (HUMAN) ID TRANSLATIONAL CONTROL; INCREASED EXPRESSION; MESSENGER-RNAS; TUMORS; GENE AB Ribosomal protein L18 mRNA is overexpressed in human colorectal cancer compared to normal colon tissue. We report the nucleotide sequence of human L18 cDNA derived from a normal colon source. There were no mutational changes in segments of L18 cDNA derived from two tumor sources. The L18 cDNA was 690 base pairs long and predicts a single open reading frame of 564 nucleotides, encoding 188 amino acids with a M(r) = 21 621, it is homologous to rat L18 and Xenopus laevis L14. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02215. UNIV MASSACHUSETTS,MED CTR,DEPT MED,WORCESTER,MA 01605. FU NCI NIH HHS [NCI 5F32CA-0900, CA44704]; NIDDK NIH HHS [DK07533] NR 17 TC 9 Z9 11 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD OCT 19 PY 1993 VL 1216 IS 1 BP 134 EP 136 DI 10.1016/0167-4781(93)90050-N PG 3 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MF888 UT WOS:A1993MF88800021 PM 8218404 ER PT J AU LI, XQ GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ AF LI, XQ GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ TI DNA-PLOIDY AS A PREDICTIVE FACTOR FOR METASTATIC RISK IN PATIENTS WITH SOFT-TISSUE SARCOMAS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD OCT 15 PY 1993 VL 138 IS 8 BP 670 EP 670 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MH147 UT WOS:A1993MH14700313 ER PT J AU HAMMOND, TG MORRE, DJ HARRIS, HW ZEIDEL, ML AF HAMMOND, TG MORRE, DJ HARRIS, HW ZEIDEL, ML TI ISOLATION OF HIGHLY PURIFIED, FUNCTIONAL ENDOSOMES FROM TOAD URINARY-BLADDER SO BIOCHEMICAL JOURNAL LA English DT Article ID ANTIDIURETIC-HORMONE; MEMBRANE-VESICLES; WATER; TRANSPORT; PROTON AB Endosomes are difficult to isolate as they share size and density properties with much more abundant cellular organelles such as mitochondria. In cultured cell lines the tandem use of charge-dependent isolation techniques and differential centrifugation is necessary to isolate endosomes. Endosomal populations of the toad urinary bladder are of special interest because they are thought to contain a water channel. Understanding of the molecular structure of the water channel has been constrained. as there is currently no practical method to isolate functional water-channel-containing vesicles. This study reports the tandem use of charge-dependent techniques and centrifugation to isolate populations of endosomes from the toad urinary bladder. To purify water-channel-containing vesicles aqueous two-phase partition was utilized to fractionate a preparation partially purified by differential centrifugation. Populations of endosomes were analysed by small-particle flow cytometry techniques. A 5-fold enrichment in endosomes, achieved with aqueous two-phase partition, allowed us to identify two populations of endosomes of diverse size in a toad bladder endosomal fraction. Pre-enrichment also improved the efficiency of flow cytometry sorting, allowing isolation of the two endosomal populations in sufficient quantities for secondary analysis. A population of larger endosomes had very high water permeability. indicating the presence of water channels. The two populations had different SDS/PAGE fingerprints. Electron micrographs of the flow-sorted material shows a uniform population of membrane vesicles devoid of mitochondria and other identifiable cellular organelles. Hence. aqueous two-phase partition and flow cytometry allow identification of two populations of endosomes in the toad urinary bladder which have diverse structural and functional properties. Isolation of functional water-channel-containing vesicles allows co-localization of water-channel function with candidate water-channel proteins. C1 BROCKTON W ROXBURY DEPT VET AFFAIRS MED CTR,MED SERV,RENAL SECT,BOSTON,MA. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. PURDUE UNIV,DEPT MED CHEM & PHARMACOGNOSY,W LAFAYETTE,IN 47907. CHILDRENS HOSP MED CTR,DIV RENAL,BOSTON,MA 02115. RP HAMMOND, TG (reprint author), UNIV WISCONSIN HOSP & CLIN,MADISON,WI, USA. FU NIDDK NIH HHS [R01 DK43955, DK46117, DK38744] NR 20 TC 7 Z9 7 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD OCT 15 PY 1993 VL 295 BP 471 EP 476 PN 2 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA ME516 UT WOS:A1993ME51600019 PM 8240245 ER PT J AU DEMETRI, GD AF DEMETRI, GD TI BEYOND SUPPORTIVE CARE - WHAT ARE THE NEXT QUESTIONS IN THE USE OF HEMATOPOIETIC CYTOKINES WITH CYTOTOXIC CHEMOTHERAPY SO BLOOD LA English DT Editorial Material ID COLONY-STIMULATING FACTOR; CELL LUNG-CANCER; NEUTROPENIA; CARCINOMA; DISEASE RP DEMETRI, GD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 18 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1993 VL 82 IS 8 BP 2278 EP 2280 PG 3 WC Hematology SC Hematology GA MC276 UT WOS:A1993MC27600003 PM 7691255 ER PT J AU KATAYAMA, N SHIH, JP NISHIKAWA, S KINA, T CLARK, SC OGAWA, M AF KATAYAMA, N SHIH, JP NISHIKAWA, S KINA, T CLARK, SC OGAWA, M TI STAGE-SPECIFIC EXPRESSION OF C-KIT PROTEIN BY MURINE HEMATOPOIETIC PROGENITORS SO BLOOD LA English DT Article ID STEM-CELL FACTOR; COLONY FORMATION; GROWTH-FACTOR; W-LOCUS; MONOCLONAL-ANTIBODY; MARROW-CELLS; LIGAND; MOUSE; DIFFERENTIATION; CULTURE C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. KUMAMOTO UNIV,SCH MED,INST MOLEC EMBRYOL & GENET,KUMAMOTO 860,JAPAN. KYOTO UNIV,CHEST DIS RES INST,DEPT MOLEC PATHOL,KYOTO 606,JAPAN. GENET INST INC,CAMBRIDGE,MA. FU NIDDK NIH HHS [DK32294] NR 34 TC 115 Z9 116 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 OCT 15 PY 1993 VL 82 IS 8 BP 2353 EP 2360 PG 8 WC Hematology SC Hematology GA MC276 UT WOS:A1993MC27600013 PM 7691257 ER PT J AU ANDERSON, KC ANDERSEN, J SOIFFER, R FREEDMAN, AS RABINOWE, SN ROBERTSON, MJ SPECTOR, N BLAKE, K MURRAY, C FREEMAN, A CORAL, F MARCUS, KC MAUCH, P NADLER, LM RITZ, J AF ANDERSON, KC ANDERSEN, J SOIFFER, R FREEDMAN, AS RABINOWE, SN ROBERTSON, MJ SPECTOR, N BLAKE, K MURRAY, C FREEMAN, A CORAL, F MARCUS, KC MAUCH, P NADLER, LM RITZ, J TI MONOCLONAL ANTIBODY-PURGED BONE-MARROW TRANSPLANTATION THERAPY FOR MULTIPLE-MYELOMA SO BLOOD LA English DT Article ID HIGH-DOSE MELPHALAN; SOUTHWEST-ONCOLOGY-GROUP; NON-HODGKINS-LYMPHOMA; COMBINATION CHEMOTHERAPY; REFRACTORY MYELOMA; INTENSIVE THERAPY; SURVIVAL; BUSULFAN; CHEMORADIOTHERAPY; CYCLOPHOSPHAMIDE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP ANDERSON, KC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA50947, CA06516] NR 50 TC 102 Z9 102 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 OCT 15 PY 1993 VL 82 IS 8 BP 2568 EP 2576 PG 9 WC Hematology SC Hematology GA MC276 UT WOS:A1993MC27600039 PM 8400304 ER PT J AU PAIETTA, E WIERNIK, PH ANDERSEN, J BENNETT, J YUNIS, J AF PAIETTA, E WIERNIK, PH ANDERSEN, J BENNETT, J YUNIS, J TI ACUTE MYELOID-LEUKEMIA M4 WITH INV(16) (P13Q22) EXHIBITS A SPECIFIC IMMUNOPHENOTYPE WITH CD2 EXPRESSION SO BLOOD LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. UNIV ROCHESTER,DIV MED ONCOL,ROCHESTER,NY 14627. THOMAS JEFFERSON UNIV,DIV CANC BIOL,PHILADELPHIA,PA 19107. EASTERN COOPERAT ONCOL GRP,DENVER,CO. RP PAIETTA, E (reprint author), MONTEFIORE & ALBERT EINSTEIN CANC CTR,DEPT ONCOL,BRONX,NY, USA. NR 3 TC 29 Z9 30 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 OCT 15 PY 1993 VL 82 IS 8 BP 2595 EP 2595 PG 1 WC Hematology SC Hematology GA MC276 UT WOS:A1993MC27600042 PM 8104541 ER PT J AU ROTH, BJ YEAP, BY WILDING, G KASIMIS, B MCLEOD, D LOEHRER, PJ AF ROTH, BJ YEAP, BY WILDING, G KASIMIS, B MCLEOD, D LOEHRER, PJ TI TAXOL IN ADVANCED, HORMONE-REFRACTORY CARCINOMA OF THE PROSTATE - A PHASE-II TRIAL OF THE EASTERN-COOPERATIVE-ONCOLOGY-GROUP SO CANCER LA English DT Article DE MEDICAL ONCOLOGY; PROSTATE CANCER; HORMONE-REFRACTORY; TAXOL ID CANCER; ESTRAMUSTINE; VINBLASTINE AB Background. Recent clinical trials have documented activity for combinations of chemotherapeutic agents that target the microtubular apparatus in patients with hormone-refractory prostate cancer. Taxol has a novel antimicrotubular mechanism, acting by stabilizing polymerized tubulin. Methods. Twenty-three patients with hormone-refractory prostate cancer and bidimensionally measurable disease were treated with Taxol by 24-hour continuous infusion at 135-170 mg/M2 every 21 days for a maximum of 6 cycles. Results. Eighty-five courses of Taxol were administered to 23 patients. One patient (4.3%) experienced a partial response lasting 9 months, and four other patients with radiographically stable disease had minor reductions in the serum prostate-specific antigen (PSA) of 16-24%. Eleven patients (47.8%) had stable disease, and progressive disease developed in 9 patients (39.1%) during therapy. Median survival was 9 months. Leukopenia was the dose-limiting toxicity with 13% of patients having Grade 3 and 61% having Grade 4 toxicity, and granulocytopenic fever developed in 26%. Three patients experienced sudden cardiovascular events while participating in the study, including one patient with a nonfatal, non-Q-wave myocardial infarction that occurred during a taxol infusion, and two patients who had sudden deaths 9 days and 30 days after receiving their last taxol dose, respectively. Conclusions. In the subset of patients with hormone-refractory prostate cancer and bidimensionally measurable disease, Taxol at this dosage has only minor activity. C1 INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46204. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI 53706. NYU MED CTR,NEW YORK,NY 10016. VET ADM MED CTR,E ORANGE,NJ 07019. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. FU NCI NIH HHS [CA 49883, CA 21076, CA 23318] NR 13 TC 140 Z9 142 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 OCT 15 PY 1993 VL 72 IS 8 BP 2457 EP 2460 DI 10.1002/1097-0142(19931015)72:8<2457::AID-CNCR2820720825>3.0.CO;2-Z PG 4 WC Oncology SC Oncology GA MA713 UT WOS:A1993MA71300024 PM 8104680 ER PT J AU PARK, S TOMLINSON, G NISEN, P HABER, DA AF PARK, S TOMLINSON, G NISEN, P HABER, DA TI ALTERED TRANS-ACTIVATIONAL PROPERTIES OF A MUTATED WT1 GENE-PRODUCT IN A WAGR-ASSOCIATED WILMS-TUMOR SO CANCER RESEARCH LA English DT Note ID FACTOR-A-CHAIN; RETINOBLASTOMA GENE; HUMAN CHROMOSOME-11; POINT MUTATIONS; SUPPRESSOR WT1; DELETION; GROWTH; KIDNEY; IDENTIFICATION; REPRESSION AB WAGR syndrome is an acronym for a rare constellation of congenital abnormalities including predisposition to Wilms' tumor, Aniridia, Genitourinary malformations, and mental Retardation. These congenital defects at-e associated with a constitutional deletion affecting one copy of chromosome band 11p13, implicating the loss of one allele from a number of contiguous genes in this syndrome. Predisposition to Wilms' tumor and genitourinary abnormalities have been attributed to hemizygosity for the WT1 tumor suppressor gene, a transcriptional repressor that is normally expressed transiently during kidney development. Here we show that a Wilms' tumor arising in a child with WAGR syndrome contained a point, mutation within the remaining WT1 allele. This mutation resulted in a glycine to aspartic acid substitution within the putative trans-activation domain of WT1, converting the encoded protein from a transcriptional repressor to an activator of its target DNA sequence. Thus, a critical amino acid substitution can alter the functional properties of WT1 and provide the ''second hit'' required for Wilms tumorigenesis. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC GENET LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. UNIV TEXAS,SW MED CTR,DEPT PEDIAT,DALLAS,TX 75235. FU NCI NIH HHS [CA 58596] NR 36 TC 36 Z9 36 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1993 VL 53 IS 20 BP 4757 EP 4760 PG 4 WC Oncology SC Oncology GA MB993 UT WOS:A1993MB99300005 PM 8402654 ER PT J AU KRISTJANSEN, PEG BOUCHER, Y JAIN, RK AF KRISTJANSEN, PEG BOUCHER, Y JAIN, RK TI DEXAMETHASONE REDUCES THE INTERSTITIAL FLUID PRESSURE IN A HUMAN COLON ADENOCARCINOMA XENOGRAFT SO CANCER RESEARCH LA English DT Note ID HYPERTENSION; TUMORS; PERMEABILITY; TRANSPORT; STEROIDS AB The effect of dexamethasone on interstitial hypertension was evaluated in a human colonic adenocarcinoma. Two weeks after transplantation of the tumor line LS174T into SCID mice, recipients with tumors >8.5 mm in diameter received one daily injection i.p. on days 1-4, at five different doses in the range of 0.3-30 mg/kg. Controls received saline. The interstitial fluid pressure (IFP) was determined in all tumors pretherapeutically on days 1, 4, and 7. A total of 68 tumors were examined, and in an additional group of 22 mice, the effect of 4-day dexamethasone therapy on blood pressure was evaluated. In the 3-, 10-, and 30-mg/kg dose groups a significant reduction in IFP was found, comparing treated versus controls and individual measurements from day 1 versus day 4. No effects were observed on day 7. A marginal effect was observed after 1.0 mg/kg, whereas 0.3 mg/kg did not affect the IFP. The systemic blood pressure was slightly increased by the dexamethasone therapy, and no treatment related changes in tumor sizes were observed. Our findings indicate that the reversible decrease in tumor IFP by dexamethasone is an effect of a reduced microvascular permeability and vascular hydraulic conductivity in the tumors. RP KRISTJANSEN, PEG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-56591] NR 22 TC 64 Z9 67 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1993 VL 53 IS 20 BP 4764 EP 4766 PG 3 WC Oncology SC Oncology GA MB993 UT WOS:A1993MB99300007 PM 8402656 ER PT J AU MAYTIN, EV MURPHY, LA MERRILL, MA AF MAYTIN, EV MURPHY, LA MERRILL, MA TI HYPERTHERMIA INDUCES RESISTANCE TO ULTRAVIOLET LIGHT-B IN PRIMARY AND IMMORTALIZED EPIDERMAL-KERATINOCYTES SO CANCER RESEARCH LA English DT Article ID HEAT-SHOCK PROTEINS; CHINESE-HAMSTER FIBROBLASTS; INDUCED DNA DAMAGE; CELL-CYCLE; HUMAN-SKIN; VIOLET RADIATIONS; PYRIMIDINE DIMERS; ESCHERICHIA-COLI; UV IRRADIATION; ACTION SPECTRA AB Environmental exposure to UVB (290-320 nm) wavelengths of the solar spectrum causes major damage, including carcinogenesis, in the skin. Therefore, cellular responses that protect against UVB damage are of particular interest in cutaneous epithelial cells. In cultured keratinocytes, mild hyperthermia generates a classical stress response with acquired thermotolerance and elevated stress protein synthesis (E. V. Maytin, J. Biol. Chem., 267: 23189-23196, 1992). To test the ability of this stress response to protect against UVB damage, monolayers of primary murine keratinocytes or BALB/MK keratinocytes were heated at 42-degrees-C for 1 h and then exposed to UVB at 6 h (typical dose, 40 mJ/cm2). Survival was assessed by fluorescein diacetate/ethidium bromide vital dye uptake and video microscopy. With heat-conditioning prior to UVB, a significant increase in both the percentage viability (2- to 3-fold) and in the absolute number of living (fluorescein diacetate-positive) cells was measurable at 24-48 h. Steady-state incorporation into [H-3]DNA and S-35-protein, while suppressed immediately after UVB, showed greater recovery in heat-conditioned cultures compared to sham-conditioned cultures at 48 h. Increased metabolic activity was accompanied by increased proliferative potential since colonies of BALB/MK cells observed at 72 h were larger, more numerous, and more active in the uptake of 5-bromo-2'-deoxyuridine in heat-conditioned cultures. A time course for the development of UVB resistance showed maximal protection when heat and UVB were spaced approximately 6 h apart. Hyperthermic conditioning could induce UVB protection in nonproliferating cells, indicating that cell cycle arrest was not primarily responsible for the UVB-protective effect. In summary, hyperthermia induces a mechanism in epithelial cells which can ameliorate damage from UVB. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MAYTIN, EV (reprint author), MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,CUTANEOUS BIOL RES CTR,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 73 TC 38 Z9 39 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1993 VL 53 IS 20 BP 4952 EP 4959 PG 8 WC Oncology SC Oncology GA MB993 UT WOS:A1993MB99300039 PM 8402686 ER PT J AU ZAJCHOWSKI, DA SAGER, R WEBSTER, L AF ZAJCHOWSKI, DA SAGER, R WEBSTER, L TI ESTROGEN INHIBITS THE GROWTH OF ESTROGEN RECEPTOR-NEGATIVE, BUT NOT ESTROGEN RECEPTOR-POSITIVE, HUMAN MAMMARY EPITHELIAL-CELLS EXPRESSING A RECOMBINANT ESTROGEN-RECEPTOR SO CANCER RESEARCH LA English DT Article ID HUMAN-BREAST-CANCER; STEROID-HORMONE RECEPTORS; PROGESTERONE-RECEPTOR; MENSTRUAL-CYCLE; DNA-SYNTHESIS; ESTRADIOL; LINES; PROLIFERATION; ACTIVATION; CULTURE AB Estrogen is essential for the growth of the normal mammary gland and most estrogen receptor (ER)-positive mammary carcinomas. To better understand the differences between the estrogen response pathways in normal and tumor cells, we have stably transfected ER-negative immortal, nontumorigenic human mammary epithelial cells and ER-negative breast cancer cells with an ER-encoding expression vector. Unexpectedly, estrogen treatment (1.0 nM) inhibited the proliferation of ER-transfected non-tumorigenic and tumor-derived cells. The control transfectants and parental cells exhibited no response to estrogen concentrations as high as 1.0 muM. This inhibitory effect was attributed to a decreased growth rate and a perturbation of the cell cycle distribution by estrogen treatment of the ER transfectants. The inhibitory response was blocked by cotreatment with the antiestrogen ICI 164,384 as predicted for a pure antagonist of estrogen action. However, treatment with the antiestrogen hydroxytamoxifen caused growth inhibition, implying that hydroxytamoxifen acts as an agonist of estrogen action in ER-transfected cells. Since estrogen is a mitogenic and not a growth-inhibitory stimulus for ER-positive breast cancers and cell lines, we tested the effect of constitutive, high level expression of the ER in ER-positive tumor cells. Stabler transfection of ER-positive MCF-7 and T47D cells with the ER expression vector yielded cells with varying amounts of ER. At ER levels comparable to those found in the ER-negative transfected cells, the MCF-7 and T47D ER transfectants were not inhibited by estrogen. These data suggest that ER-positive breast cancer cells can tolerate higher constitutive levels of ER expression than ER-negative cells. The mechanism by which this is accomplished may be an essential step in the process which yields ER-positive tumors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC GENET,BOSTON,MA 02115. RP ZAJCHOWSKI, DA (reprint author), BERLEX BIOSCI,DEPT CELL BIOL & IMMUNOL,RICHMOND,CA 94804, USA. NR 47 TC 117 Z9 118 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1993 VL 53 IS 20 BP 5004 EP 5011 PG 8 WC Oncology SC Oncology GA MB993 UT WOS:A1993MB99300046 PM 8402691 ER PT J AU TAGHIAN, A BUDACH, W ZIETMAN, A FREEMAN, J GIOIOSO, D RUKA, W SUIT, HD AF TAGHIAN, A BUDACH, W ZIETMAN, A FREEMAN, J GIOIOSO, D RUKA, W SUIT, HD TI QUANTITATIVE COMPARISON BETWEEN THE TRANSPLANTABILITY OF HUMAN AND MURINE TUMORS INTO THE SUBCUTANEOUS TISSUE OF NCR/SED-NU/NU NUDE AND SEVERE COMBINED IMMUNODEFICIENT MICE SO CANCER RESEARCH LA English DT Article ID SCID MICE; GROWTH; IRRADIATION; MOUSE AB In previous reports, nude mice have demonstrated residual immunoreactivity against xenografts. Severe combined immunodeficient (SCID) mice lack functional T- and B-cells. These animals are expected to be better hosts in which to perform preclinical studies on human tumors. The purpose of this study is to quantitate the advantage of SCID mice over nude mice in terms of transplantability of human and murine tumors and the importance of residual immunity in SCID mice. The transplantation assays are described by an assay based on the number of tumor cells required to transplant tumor into 50% of recipients (TD50). Seven human tumors of different histology and four murine tumor cell lines were used. Serial 2-10-fold dilutions of cells were injected (0.1 ml) into the flanks of normal and whole-body irradiated WBI nude and SCID mice. The results showed that in 6 of 6 human tumor cell lines studied, TD50s for SCID mice were 2.4 to 200 times lower than that of nude mice (significant in 5 cell lines). In contrast, in 2 of 3 murine tumors, TD50s in WBI SCID mice were significantly higher than that found in nude mice. When SCID and nude mice received WBI, TD50s were lower than those of nonirradiated animals in 5 of 5 xenografts (significant in 2 cell lines for nude mice and in 5 cell lines for SCID mice). We concluded that WBI SCID mice are significantly better recipients of human tumor xenografts than nude mice. There is a factor of 10-1625 gain in TD50s in favor of the WBI SCID mice when compared to nonirradiated nude mice. WBI has, however, an important effect on SCID mice which may suggest a detectable residual immunoreactivity, perhaps due to natural killer cells. These data demonstrate that WBI SCID mice are better models for human tumor transplantation than nude mice and, although WBI at 6 Gy suppressed significantly the immune system of nude mice, a certain level of immunoreactivity against xenografts is still maintained. C1 BOSTON UNIV,MED CTR,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02118. RP TAGHIAN, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB RADIAT PHYS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA13311] NR 22 TC 31 Z9 31 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1993 VL 53 IS 20 BP 5012 EP 5017 PG 6 WC Oncology SC Oncology GA MB993 UT WOS:A1993MB99300047 PM 8402692 ER PT J AU TAGHIAN, A BUDACH, W ZIETMAN, A FREEMAN, J GIOIOSO, D SUIT, HD AF TAGHIAN, A BUDACH, W ZIETMAN, A FREEMAN, J GIOIOSO, D SUIT, HD TI QUANTITATIVE COMPARISON BETWEEN THE TRANSPLANTABILITY OF HUMAN AND MURINE TUMORS INTO THE BRAIN OF NCR/SED-NU/NU NUDE AND SEVERE COMBINED IMMUNODEFICIENT MICE SO CANCER RESEARCH LA English DT Article AB We have demonstrated (A. Taghian et al., Cancer Res., 53: 5012-5017, 1993) that the take rate of human xenografts in the s.c. tissue of severe combined immunodeficient (SCID) mice is significantly higher than that of nude mice. Earlier, this laboratory reported that the transplantability of tumor xenografts was significantly higher for intracranial (i.c.) injection than for s.c. injection in nude mice. The purpose of this study is to assess: (a) the relative i.c. transplantability of human and murine tumors in comparison with s.c. tissue in SCID mice; (b) the relative i.c. transplantability in SCID mice in comparison to nude mice; and (c) the influence of whole-body irradiation on i.c. transplantability of SCID and nude mice. The assay based on the number of cells required to transplant tumors into 50% of recipients (TD50) was used to describe the transplantability assays. Five human and four murine tumor cell lines were used. Concurrent TD50 assays were performed i.c. in whole-body irradiated and non-irradiated SCID and nude mice. Serial 2-10-fold dilutions of cells were injected in a 10-mul volume into the right parietal lobe 3 mm below the skin. The results showed that in all tumors studied the i.c. TD50s were significantly lower than the s.c. TD50s by a factor of 1.7-1580. The average enhancement ratio (s.c. TD50/i.c. TD50) in nude mice was twice that in SCID mice. No significant difference was found between the i.c. TD50s in SCID and in nude mice, contrary to the significant difference in s.c. TD50s between both strains of mice (A. Taghian et al., Cancer Res., 53: 5012-5017, 1993). Whole-body irradiation did not significantly affect the i.c. TD50 in nude mice; however, it did affect two of three xenografts in SCID mice. In conclusion, despite the significantly lower s.c. TD50s of human xenografts in SCID mice, i.c. TD50S were almost similar to those of NCr/Sed-nu/nu nude mice. This suggests the presence of different immunoreactivities between nude and SCID mice in s.c. transplantability; however, for i.c. transplantability, nude mice behaved equally as well as SCID mice. The significant enhancement ratio in SCID mice is further evidence that this strain of mice displays a residual systemic immunoreactivity, although the immunoreactivity is significantly lower than that of nude mice. C1 BOSTON UNIV,MED CTR,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02118. RP TAGHIAN, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB RADIAT BIOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA13311] NR 7 TC 18 Z9 18 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1993 VL 53 IS 20 BP 5018 EP 5021 PG 4 WC Oncology SC Oncology GA MB993 UT WOS:A1993MB99300048 PM 8402693 ER PT J AU LECHLEIDER, RJ SUGIMOTO, S BENNETT, AM KASHISHIAN, AS COOPER, JA SHOELSON, SE WALSH, CT NEEL, BG AF LECHLEIDER, RJ SUGIMOTO, S BENNETT, AM KASHISHIAN, AS COOPER, JA SHOELSON, SE WALSH, CT NEEL, BG TI ACTIVATION OF THE SH2-CONTAINING PHOSPHOTYROSINE PHOSPHATASE SH-PTP2 BY ITS BINDING-SITE, PHOSPHOTYROSINE-1009, ON THE HUMAN PLATELET-DERIVED GROWTH-FACTOR RECEPTOR-BETA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID PROTEIN-TYROSINE-PHOSPHATASE; PDGF RECEPTOR; SH3 DOMAINS; PHOSPHORYLATION; IDENTIFICATION; CORKSCREW; SUBUNIT; SIGNAL AB Much progress has been made in elucidating early events in signal transduction by growth factor receptors with intrinsic tyrosine kinase activity. Upon ligand addition, these receptors dimerize and activate, becoming phosphorylated at a number of tyrosyl residues. These phosphorylation sites serve as docking points for proteins containing src homology-2 (SH2) domains. However, little is known about how phosphotyrosine phosphatases (PTPs), participate in these events. Recently, we and others molecularly cloned a ubiquitously expressed SH2 domain-containing PTP, SH-PTP2 (Syp, PTP1D, PTP2C), and found that it interacts directly with several activated growth factor receptors via its SH2 domains. Using a peptide competition assay, we now demonstrate that the major binding site for SH-PTP2 on the platelet-derived growth factor receptor is phosphotyrosine 1009. Immunoprecipitation studies indicate that SH-PTP2 is the previously unidentified ''64-kDa'' protein known to bind at this site. Addition of a phosphotyrosyl peptide comprising the region around Tyr-1009 stimulates SH-PTP2 activity 5-10-fold, whereas other phosphotyrosyl peptides from the platelet-derived growth factor receptor have no stimulatory effect. Our data suggest that binding of SH-PTP2 to the activated receptor in vivo should result in stimulation of SH-PTP2 activity. C1 BETH ISRAEL HOSP,MOLEC MED UNIT,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DIV PULM MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. FU NCI NIH HHS [CA49152, CA54786]; NIGMS NIH HHS [GM20011] NR 34 TC 275 Z9 277 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 OCT 15 PY 1993 VL 268 IS 29 BP 21478 EP 21481 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MC809 UT WOS:A1993MC80900007 PM 7691811 ER PT J AU SCHILDBACH, JF NEAR, RI BRUCCOLERI, RE HABER, E JEFFREY, PD NG, SC NOVOTNY, J SHERIFF, S MARGOLIES, MN AF SCHILDBACH, JF NEAR, RI BRUCCOLERI, RE HABER, E JEFFREY, PD NG, SC NOVOTNY, J SHERIFF, S MARGOLIES, MN TI HEAVY-CHAIN POSITION-50 IS A DETERMINANT OF AFFINITY AND SPECIFICITY FOR THE ANTIDIGOXIN ANTIBODY-26-10 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SITE-DIRECTED MUTAGENESIS; SOMATIC MUTATION; BINDING; ENERGY; ANTIBODIES; PROTEINS; DIVERSITY; COMPLEXES AB Antibody produced by a variant of the murine anti-digoxin hybridoma 26-10 has reduced afrinity for digoxin but enhanced recognition of the digoxin 12-hydroxyl due to a Tyr to His substitution at heavy chain position 50 (Schildbach, J. F., Panka, D. J., Parks, D. R., Jager, G. C., Novotny, J., Herzenberg, L. A., Mudgett-Hunter, M., Bruccoleri, R. E., Haber, E., and Margolies, M. N. (1991) J. Biol. Chem. 266, 4640-4647). Consistent with these data, the 26-10 Fab-digoxin x-ray crystal structure (Jeffrey, P. D., Strong, R. K., Sieker, L. C., Chang, C. Y., Campbell, R. L., Petsko, G. A., Haber, E., Margolies, M. N., and Sheriff, S. (1993) Proc. Natl. Acad. Sci. U. S. A., in press) reveals that Tyr-50 contacts a region of digoxin that includes the hapten- 12 carbon. To determine the effects of other heavy chain position 50 substitutions, mutant antibodies were engineered, and their affinities for digoxin and digoxin analogues were measured. The affinity of the mutant antibodies for digoxin roughly correlates with the size of the position 50 side chain. Substitutions of Trp or Phe have no effect on affinity, whereas substitutions of Asn, His, Leu, Ala, Gly, and Asp confer progressively lower affinities. Although Trp and Phe mutants exhibit wild-type specificity, Asn and Asp mutants have improved affinity for digoxin relative to digitoxin (12-deshydroxydigoxin). Leu, Ala, and Gly mutants have improved affinity for 12-acetyldigoxin relative to digoxin as compared with 26-10. These results indicate that position 50 is a determinant of both antibody affinity and fine specificity for antibody 26-10 and that single-amino acid substitutions can alter antibody fine specificity. Models of the mutants were computationally constructed, and haptens were docked into the modeled binding sites. The results suggest that 12-acetyldigoxigenin occupies different orientations in the 26-10 and in the Ala mutant binding sites, resulting in altered binding. C1 MASSACHUSETTS GEN HOSP,DEPT MED,JACKSON 1402,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,GRAD SCH ARTS & SCI,PROGRAM IMMUNOL,CAMBRIDGE,MA 02138. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ 08543. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOL SCI,CARDIOVASC BIOL LAB,BOSTON,MA 02115. FU NHLBI NIH HHS [R01-HL47415, P01-HL19259] NR 50 TC 33 Z9 33 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 15 PY 1993 VL 268 IS 29 BP 21739 EP 21747 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MC809 UT WOS:A1993MC80900050 PM 7691815 ER PT J AU GOLENBOCK, DT LIU, YN MILLHAM, FH FREEMAN, MW ZOELLER, RA AF GOLENBOCK, DT LIU, YN MILLHAM, FH FREEMAN, MW ZOELLER, RA TI SURFACE EXPRESSION OF HUMAN CD14 IN CHINESE-HAMSTER OVARY FIBROBLASTS IMPARTS MACROPHAGE-LIKE RESPONSIVENESS TO BACTERIAL-ENDOTOXIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LPS BINDING-PROTEIN; LIPOPOLYSACCHARIDE LPS; SCAVENGER RECEPTORS; BEARING PARTICLES; HUMAN MONOCYTES; CELL-LINE; RECOGNITION; ACCUMULATION; NEUTROPHILS; LIPOPROTEIN AB Cardiovascular collapse associated with Gram-negative septicemia is believed to result from the stimulation of phagocytes by bacterial lipopolysaccharide (endotoxin, LPS). It remains unclear how endotoxin activates phagocytes, but recent evidence suggests the involvement of the glycosyl phosphatidylinositol-linked myelocyte antigen, CD14. We report that transfection of human CD14 into Chinese hamster ovary fibroblasts transfers macrophage-like responsiveness to otherwise LPS-unresponsive cells. These data demonstrate that LPS-induced responsiveness can be transferred to a heterologous non-responder cell type by expression of a single leukocyte-specific gene product. C1 BOSTON CITY HOSP,DEPT INTERNAL MED,DIV INFECT DIS,BOSTON,MA 02118. BOSTON CITY HOSP,DEPT SURG,CRIT CARE SECT,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT BIOPHYS,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,LIPID METAB UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [R01 HL45098]; NIAID NIH HHS [P01-AI33087]; NIGMS NIH HHS [R29GM47127] NR 36 TC 126 Z9 128 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 OCT 15 PY 1993 VL 268 IS 29 BP 22055 EP 22059 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MC809 UT WOS:A1993MC80900092 PM 7691822 ER PT J AU CHUNG, GH SCOTT, MG KIM, KH KEARNEY, J SIBER, GR AMBROSINO, DM NAHM, MH AF CHUNG, GH SCOTT, MG KIM, KH KEARNEY, J SIBER, GR AMBROSINO, DM NAHM, MH TI CLONAL CHARACTERIZATION OF THE HUMAN-IGG ANTIBODY REPERTOIRE TO HAEMOPHILUS-INFLUENZAE TYPE-B POLYSACCHARIDE .5. IN-VIVO EXPRESSION OF INDIVIDUAL ANTIBODY CLONES IS DEPENDENT ON IG C(H) HAPLOTYPES AND THE CATEGORIES OF ANTIGEN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CAPSULAR POLYSACCHARIDE; STREPTOCOCCUS-PNEUMONIAE; IMMUNOGLOBULIN ALLOTYPE; IMMUNOLOGICAL MEMORY; CONJUGATE VACCINE; GERM-LINE; PHOSPHORYLCHOLINE ANTIBODIES; 6-MONTH-OLD INFANTS; VARIABLE REGION; CHAIN ISOTYPES AB Antibodies (Ab) to the polysaccharide capsule of Haemophilus influenzae type b (Hib-PS) provide protection against Haemophilus influenzae type b disease in children, and Hib-PS vaccines with different immunologic properties are widely used clinically. The repertoire of human anti-Hib-PS Ab induced by these vaccines is relatively restricted and can be divided into two types by the structure of the light chain V region. Ab using A2-VkappaII gene product, which account for the majority of anti-Hib-PS Ab response in most patients, show little somatic mutations. In contrast, non-Ab using A2-VkappaII gene product use V(L) genes from the VkappaI, VkappaII, VkappaIII, VkappaIV, and V(lambda) subgroups, are variably expressed among patients, and contain somatic mutations. To further study the expression of these two types of anti-Hib-PS Ab, we have produced KB13, a mAb specific for V(kappa)II subgroup, and used mAb specific for various other V(L) subgroups to develop immunoassays specific for anti-Hib-PS Ab of each V(L) subgroup. When Ig allotypes were studied for the effect on the Ab repertoire, A2-V(kappa)II (A2) Ab were found to be expressed less in patients expressing fb or zag C(H) haplotypes (p < 0.05). When the T cell-independent Hib-PS carbohydrate vaccine was compared to two T cell-dependent Hib-PS protein conjugate vaccines for their effect on Ab repertoire, Ab using V(kappa)III V(L) were found to be more often elicited with the conjugate vaccines than with the Hib-PS carbohydrate vaccine (p < 0.01). Thus, individual members of the anti-Hib-PS Ab repertoire differ not only in their V region structure but also in the control of their expression. C1 WASHINGTON UNIV,SCH MED,DEPT PATHOL,BOX 8118,660 S EUCLID AVE,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. FU NIAID NIH HHS [AI-31473] NR 48 TC 20 Z9 20 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 OCT 15 PY 1993 VL 151 IS 8 BP 4352 EP 4361 PG 10 WC Immunology SC Immunology GA MB163 UT WOS:A1993MB16300043 PM 8409407 ER PT J AU MOLINA, IJ SANCHO, J TERHORST, C ROSEN, FS REMOLDODONNELL, E AF MOLINA, IJ SANCHO, J TERHORST, C ROSEN, FS REMOLDODONNELL, E TI T-CELLS OF PATIENTS WITH THE WISKOTT-ALDRICH SYNDROME HAVE A RESTRICTED DEFECT IN PROLIFERATIVE RESPONSES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LYMPHOCYTE SURFACE SIALOGLYCOPROTEIN; MONOCLONAL-ANTIBODIES; ANTIGEN; RECEPTOR; ABNORMALITIES; EXPRESSION; PLATELETS; CD3-ZETA; SIGNALS; BINDING AB The Wiskott-Aldrich syndrome (WAS) is a disease of profound thrombocytopenia and severe immune defects caused by an unidentified defective X chromosome gene. In this study, T lymphocyte function is examined using a panel of allospecific WAS patient T cell lines, previously found to express the abnormal disease gene and the cytoarchitectural defect characteristic of the disease. Although T cell lines from normal individuals proliferate vigorously in response to immobilized anti-CD3 mAb OKT3 and SPV-T3b, five of seven WAS patient T cell lines failed to proliferate and two lines showed significantly decreased proliferation when challenged with the immobilized anti-CD3 mAb. The deficient responsiveness of the WAS T cell lines to immobilized anti-CD3 mAb is a restricted defect, because the cells proliferate normally when challenged with allospecific Ag, PHA, or PMA plus ionomycin. Addition of anti-CD28 mAb did not correct the deficient proliferation of the WAS cells challenged with immobilized anti-CD3. Deficient response of the WAS T cell lines to immobilized anti-CD3 was detected also when earlier events of the proliferation process, IL-2 production and up-regulation of activation Ag CD69 and CD28, were measured. On the other hand, WAS cell lines did not differ from normal cell lines in binding of anti-CD3 mAb, mobilization of Ca2+ in response to soluble OKT3, and tyrosine phosphorylation and GTP binding of the CD3 zeta-chain in response to OKT3. Cumulatively, these findings demonstrate a striking restricted defect in the proliferative response of WAS T cells, which because it is found in cell lines free of secondary changes that occur in the patient circulation must be a reflection of the inherited defective disease gene product. C1 CHILDRENS HOSP MED CTR,CTR BLOOD RES,DIV IMMUNOL,800 HUNTINGTON AVE,BOSTON,MA 02115. BETH ISRAEL HOSP,DIV IMMUNOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RI Sancho, Jaime/O-3228-2013 OI Sancho, Jaime/0000-0003-3852-7951 FU NCRR NIH HHS [RR02172]; NIAID NIH HHS [AI31541]; NIGMS NIH HHS [GM37298] NR 34 TC 156 Z9 159 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 OCT 15 PY 1993 VL 151 IS 8 BP 4383 EP 4390 PG 8 WC Immunology SC Immunology GA MB163 UT WOS:A1993MB16300046 PM 8409409 ER PT J AU ROSOWSKY, A MOTA, CE WRIGHT, JE FREISHEIM, JH HEUSNER, JJ MCCORMACK, JJ QUEENER, SF AF ROSOWSKY, A MOTA, CE WRIGHT, JE FREISHEIM, JH HEUSNER, JJ MCCORMACK, JJ QUEENER, SF TI 2,4-DIAMINOTHIENO[2,3-D]PYRIMIDINE ANALOGS OF TRIMETREXATE AND PIRITREXIM AS POTENTIAL INHIBITORS OF PNEUMOCYSTIS-CARINII AND TOXOPLASMA-GONDII DIHYDROFOLATE-REDUCTASE SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; LIPID-SOLUBLE ANTIFOLATE; PNEUMONIA; THERAPY; PYRIMETHAMINE; RESISTANCE; EFFICACY; INVITRO; 566C80; HYDROXYNAPHTHOQUINONE AB A series of eight previously undescribed 2,4-diaminothieno[2,3-d]pyrimidine analogues of the potent dihydrofolate reductase (DHFR) inhibitors trimetrexate (TMQ) and piritrexim (PTX) were synthesized as potential drugs against Pneumocystis carinii and Toxoplasma gondii, which are major causes of severe opportunistic infections in AIDS patients. 2,4-Diamino-5-methyl-6-(aryl/aralkyl)thieno[2,3-d]pyrimidines with 3,4,5-trimethoxy or 2,5-dimethoxy substitution in the aryl/aralkyl moiety and 2,4-diamino-5-(aryl/aralkyl)thieno[2,3-d]pyrimidines with 2,5-dimethoxy substitution in the aryl/aralkyl moiety were obtained by reaction of the corresponding 2-amino-3-cyanothiophenes with chloroformamidine hydrochloride. The aryl group in the 5,6-disubstituted analogues was either attached directly to the hetero ring or was separated from it by one or two carbons, whereas the aryl group in the 5-monosubstituted analogues was separated from the hetero ring by two or three carbons. 2-Amino-3-cyano-5-methyl-6-(aryl/alkyl)thiophene intermediates for the preparation of the 5,6-disubstituted analogues were prepared from omega-aryl-2-alkylidene-malononitriles and sulfur in the presence of a secondary amine, and 2-amino-3-cyano-4-(aryl/aralkyl)thiophene intermediates for the preparation of the 5-monosubstituted analogues were obtained from omega-aryl-1-chloro-2-alkylidenemalononitriles and sodium hydrosulfide. Synthetic routes to the heretofore unknown ylidenemalononitriles, and the ketone precursors thereof, were developed. The final products were tested in vitro as inhibitors of DHFR from Pneumocystis carinii, Toxoplasma gondii, rat liver, beef liver, and Lactobacillus casei. A selected number of previously known 2,4-diaminothieno[2,3-d]pyrimidines lacking the 3,4,5-trimethoxyphenyl and 2,5-dimethoxyphenyl substitution pattern of TMQ and PTX, respectively, were also tested for comparison. None of the compounds was as potent as TMQ or PTX, and while some of them showed some selectivity in their binding to Pneumocystis cariniii and Toxoplasma gondii versus rat liver DHFR, this effect was not deemed large enough to warrant further preclinical evaluation. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MED COLL OHIO,DEPT BIOCHEM & MOLEC BIOL,TOLEDO,OH 43699. UNIV VERMONT,DEPT PHARMACOL,BURLINGTON,VT 05405. INDIANA UNIV,SCH MED,DEPT PHARMACOL & TOXICOL,INDIANAPOLIS,IN 46202. UNIV VERMONT,COLL MED,VERMONT REG CANC CTR,BURLINGTON,VT 05405. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [NCI RO1-CA41461]; NIAID NIH HHS [NIAID RO1-AI29904, NIAID NO1-AI87240] NR 37 TC 65 Z9 66 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD OCT 15 PY 1993 VL 36 IS 21 BP 3103 EP 3112 DI 10.1021/jm00073a009 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA MC619 UT WOS:A1993MC61900009 PM 8230096 ER PT J AU ANDO, K AJCHENBAUMCYMBALISTA, F GRIFFIN, JD AF ANDO, K AJCHENBAUMCYMBALISTA, F GRIFFIN, JD TI REGULATION OF G(1)/S TRANSITION BY CYCLIN-D2 AND CYCLIN-D3 IN HEMATOPOIETIC-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID SACCHAROMYCES-CEREVISIAE; G1-SPECIFIC CYCLINS; YEAST; GENE; KINASE; PHASE; ACTIVATION; EXPRESSION; APOPTOSIS; ONCOGENE AB Identification of the genes that control passage through the G1 phase of the cell cycle in mammalian cells is of particular interest because virtually all external events that regulate proliferation act primarily or exclusively during G1. Cyclins are likely to play a key role in controlling cell cycle progression, although their role during G1 in higher eukaryotic cells is unclear. In the hematopoietic cell line 32Dcl3, both cyclins D2 and D3 were expressed in proliferating cells, while cyclin D1 was undetectable. Expression of D2, and to a lesser extent D3, was interleukin 3 (IL-3) dependent and declined rapidly in the absence of this growth factor. To investigate the potential role of D cyclins in regulating cell growth, cell lines overexpressing either D2 or D3 were generated by transfection. Constitutive overexpression of either D2 or D3 did not affect cell viability, rate of cell proliferation, or dependence on IL-3 for growth. However, the distribution of cells through the cell cycle was dramatically altered, with both cyclins causing an increase in the fraction of cells in S phase, apparently related to a shortening of G1. Also, when deprived of IL-3, D3-overexpressing cells failed to arrest in G1, and apoptotic cell death in the absence of IL-3 was delayed. These results suggest a role for cyclins D2 and D3 in controlling passage of hematopoietic cells through G1 in the presence of growth factors and in effecting G1 arrest in the absence of growth factors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA36167]; NIDDK NIH HHS [DK43904] NR 32 TC 165 Z9 166 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 OCT 15 PY 1993 VL 90 IS 20 BP 9571 EP 9575 DI 10.1073/pnas.90.20.9571 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MC570 UT WOS:A1993MC57000071 PM 8415743 ER PT J AU NATHANSON, JA HUNNICUTT, EJ KANTHAM, L SCAVONE, C AF NATHANSON, JA HUNNICUTT, EJ KANTHAM, L SCAVONE, C TI COCAINE AS A NATURALLY-OCCURRING INSECTICIDE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MONOAMINES; OCTOPAMINE; PLANT DEFENSE; ANTIDEPRESSANTS; TRANSPORTERS ID SENSITIVE ADENYLATE-CYCLASE; DOPAMINE UPTAKE COMPLEX; GBR-12935 BINDING; SEROTONIN TRANSPORTER; OCTOPAMINE RECEPTORS; UPTAKE MECHANISM; NERVOUS-SYSTEM; CLONING; EXPRESSION; NOREPINEPHRINE AB Although cocaine has a fascinating and complex medicinal history in man, its natural function in plants is unknown. The present studies demonstrate that cocaine exerts insecticidal effects at concentrations which occur naturally in coca leaves. Unlike its known action on dopamine reuptake in mammals, cocaine's pesticidal effects are shown to result from a potentiation of insect octopaminergic neurotransmission. Amine-reuptake blockers of other structural classes also exert pesticidal activity with a rank order of potency distinct from that known to affect vertebrate amine transporters. These findings suggest that cocaine functions in plants as a natural insecticide and that octopamine transporters may be useful sites for targeting pesticides with selectivity toward invertebrates. RP NATHANSON, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROPHARMACOL LAB,CNY-6,BOSTON,MA 02114, USA. OI Scavone, Cristoforo/0000-0002-1206-0882 NR 31 TC 58 Z9 59 U1 2 U2 13 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 OCT 15 PY 1993 VL 90 IS 20 BP 9645 EP 9648 DI 10.1073/pnas.90.20.9645 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MC570 UT WOS:A1993MC57000086 PM 8415755 ER PT J AU HERBERT, V AF HERBERT, V TI HEALTH QUACKERY - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 BRONX VET AFFAIRS MED CTR,BRONX,NY 10468. RP HERBERT, V (reprint author), MT SINAI MED CTR,NEW YORK,NY 10029, USA. NR 3 TC 2 Z9 2 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 OCT 14 PY 1993 VL 329 IS 16 BP 1204 EP 1204 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MA667 UT WOS:A1993MA66700029 ER PT J AU JELLINEK, MS NURCOMBE, B AF JELLINEK, MS NURCOMBE, B TI 2 WRONGS DONT MAKE A RIGHT - MANAGED CARE, MENTAL-HEALTH, AND THE MARKETPLACE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. VANDERBILT UNIV,MED CTR,SCH MED,DIV CHILD & ADOLESCENT PSYCHIAT,NASHVILLE,TN 37232. RP JELLINEK, MS (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,15 PARKMAN ST,ACC 725,BOSTON,MA 02114, USA. NR 18 TC 65 Z9 65 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 OCT 13 PY 1993 VL 270 IS 14 BP 1737 EP 1739 DI 10.1001/jama.270.14.1737 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA MA294 UT WOS:A1993MA29400032 PM 8411506 ER PT J AU MANOME, Y DATTA, R TANEJA, N SHAFMAN, T BUMP, E HASS, R WEICHSELBAUM, R KUFE, D AF MANOME, Y DATTA, R TANEJA, N SHAFMAN, T BUMP, E HASS, R WEICHSELBAUM, R KUFE, D TI COINDUCTION OF C-JUN GENE-EXPRESSION AND INTERNUCLEOSOMAL DNA FRAGMENTATION BY IONIZING-RADIATION SO BIOCHEMISTRY LA English DT Article ID MYELOID-LEUKEMIA CELLS; TRANSCRIPTION FACTOR AP-1; FACTOR-KAPPA-B; PROTO-ONCOGENE; GROWTH-FACTORS; N-ACETYLCYSTEINE; BINDING PROTEIN; ACTIVATION; P53; PROTOONCOGENE AB Previous work has demonstrated that the cellular response to ionizing radiation includes transcriptional activation of the c-jun early response gene. The present studies demonstrate that this induction of c-jun expression is temporally related to the appearance of internucleosomal DNA fragmentation. These events were maximal at 6 h and transient after exposure to lethal doses (20 Gy) of ionizing radiation. We also demonstrate that N-acetyl-L-cysteine (NAC), an antioxidant, inhibits X-ray-induced c-jun expression and endonucleolytic DNA cleavage. These findings suggested that both events are mediated at least in part through the formation of reactive oxygen intermediates (ROIs). Since ROIs damage DNA and X-ray-induced DNA damage is associated with activation of poly(ADP-ribose) polymerase (ADPRP), we studied the effects of the ADPRP inhibitors 3-aminobenzamide (3-AB), nicotinamide, and theophylline. 3-AB blocked both X-ray-induced c-jun expression and internucleosomal DNA fragmentation. Similar findings were obtained with nicotinamide and theophylline. In contrast, 3-AB had little if any effect on induction of c-jun transcripts or DNA fragmentation induced by the alkylating agent mitomycin C. While c-jun expression is restricted to cells in G1 and G1/S phases, we have found that X-ray-induced c-jun transcripts are detectable throughout all phases of the cell cycle. The induction of internucleosomal DNA fragmentation by X-rays was also detectable throughout the cell cycle. Taken together, these results support the coinduction of c-jun transcription and internucleosomal DNA fragmentation by ionizing radiation. Similar studies were performed with H2O2 since this agent also results in the production of ROIs. While H2O2 induced c-jun expression by an NAC-sensitive mechanism, this event was not affected by 3-AB and was not associated with internucleosomal DNA fragmentation. These findings suggest that while activation of the c-jun gene and endonucleolytic DNA cleavage are coinduced by ionizing radiation, these events are differentially regulated by other ROI-mediated mechanisms. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. UNIV CHICAGO,PRITZKER SCH MED,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 FU NCI NIH HHS [CA55241] NR 51 TC 73 Z9 74 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 12 PY 1993 VL 32 IS 40 BP 10607 EP 10613 DI 10.1021/bi00091a010 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MB497 UT WOS:A1993MB49700010 PM 8399205 ER PT J AU NADOL, JB AF NADOL, JB TI HEARING-LOSS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID INNER-EAR; DOUBLE-BLIND; OTITIS-MEDIA; MANIFESTATIONS; MENINGITIS; THERAPY; PHARMACOKINETICS; OTOTOXICITY; GENTAMICIN; TOBRAMYCIN C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. RP NADOL, JB (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 95 TC 130 Z9 132 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 OCT 7 PY 1993 VL 329 IS 15 BP 1092 EP 1102 DI 10.1056/NEJM199310073291507 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA LZ640 UT WOS:A1993LZ64000007 PM 8371732 ER PT J AU WEBER, BL GARBER, JE AF WEBER, BL GARBER, JE TI FAMILY HISTORY AND BREAST-CANCER - PROBABILITIES AND POSSIBILITIES SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID RISK C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP WEBER, BL (reprint author), UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,ANN ARBOR,MI 48109, USA. NR 11 TC 9 Z9 9 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 OCT 6 PY 1993 VL 270 IS 13 BP 1602 EP 1603 DI 10.1001/jama.270.13.1602 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA LZ334 UT WOS:A1993LZ33400037 PM 8371474 ER PT J AU FREBOURG, T FRIEND, SH AF FREBOURG, T FRIEND, SH TI THE IMPORTANCE OF P53 GENE ALTERATIONS IN HUMAN CANCER - IS THERE MORE THAN CIRCUMSTANTIAL EVIDENCE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Note ID WILD-TYPE P53; TUMOR SUPPRESSOR GENE; TRANSCRIPTIONAL ACTIVATION; BINDING-SITE; MUTATIONS; PROTEIN; P53-PROTEIN; EXPRESSION; CARCINOMA; SPECTRUM C1 MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,BOSTON,MA. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP FREBOURG, T (reprint author), CHU ROUEN,UNITE GENET MOLEC,1 RUE GERMONT,F-76031 ROUEN,FRANCE. NR 64 TC 40 Z9 40 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 OCT 6 PY 1993 VL 85 IS 19 BP 1554 EP 1557 DI 10.1093/jnci/85.19.1554 PG 4 WC Oncology SC Oncology GA LZ632 UT WOS:A1993LZ63200010 PM 8411229 ER PT J AU KAMITANI, T CHANG, HM ROLLINS, C WANECK, GL YEH, ETH AF KAMITANI, T CHANG, HM ROLLINS, C WANECK, GL YEH, ETH TI CORRECTION OF THE CLASS-H DEFECT IN GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR BIOSYNTHESIS IN LTK- CELLS BY A HUMAN CDNA CLONE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID VARIANT SURFACE GLYCOPROTEINS; PHOSPHATIDYLINOSITOL MEMBRANE ANCHORS; PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; GLYCOSYL-PHOSPHATIDYLINOSITOL; MAMMALIAN-CELLS; STRUCTURAL CHARACTERIZATION; GLYCOLIPID PRECURSORS; RESISTANT GLYCOLIPIDS; MOLECULAR-CLONING; PROTEINS AB Previous attempts to express glycosylphosphatidylinositol-anchored proteins in Ltk- cells have not been successful because Ltk- cells cannot synthesize N-acetylglucosamine-phosphatidylinositol, the first intermediate in anchor biosynthesis. Using complementation cloning, we have identified a human cDNA that corrects the defect in anchor biosynthesis and allows the expression of glycosylphosphatidylinositol-anchored proteins in Ltk- cells. The nucleotide sequence predicts a novel cytosolic protein of 188 amino acids. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,6431 FANNIN,SUITE 4200,HOUSTON,TX 77030. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. UNIV TEXAS,HLTH SCI CTR,DEPT ANESTHESIA,HOUSTON,TX 77030. FU NHLBI NIH HHS [HL-45851]; NIAMS NIH HHS [AR-03564]; NIGMS NIH HHS [GM-46467] NR 39 TC 78 Z9 79 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 OCT 5 PY 1993 VL 268 IS 28 BP 20733 EP 20736 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MA288 UT WOS:A1993MA28800014 PM 8407896 ER PT J AU SLACK, BE NITSCH, RM LIVNEH, E KUNZ, GM BREU, J ELDAR, H WURTMAN, RJ AF SLACK, BE NITSCH, RM LIVNEH, E KUNZ, GM BREU, J ELDAR, H WURTMAN, RJ TI REGULATION BY PHORBOL ESTERS OF AMYLOID PRECURSOR PROTEIN RELEASE FROM SWISS 3T3 FIBROBLASTS OVEREXPRESSING PROTEIN KINASE-C-ALPHA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ALZHEIMERS-DISEASE; BETA-PROTEIN; PHOSPHORYLATION; CELLS; IDENTIFICATION; PEPTIDE; BIOGENESIS; EXPRESSION; ACTIVATION; SECRETION AB Release of large soluble NH2-terminal fragments of the amyloid precursor protein (APP) of Alzheimer's disease was measured in two Swiss 3T3 fibroblast cell lines (designated SF1.4 and SF3.2), overexpressing the alpha subtype of protein kinase C, and in two control cell lines (SC1 and SC2) (Eldar, H., Zisman, Y., Ullrich, A., and Livneh, E. (1990) J. Biol. Chem. 265, 13290-13296). Basal release of APP was significantly increased in SF1.4 cells, but not in SF3.2 cells, relative to controls. Phorbol 12-myristate 13-acetate, an activator of protein kinase C, elicited a concentration-dependent increase in APP release in all four cell lines. However, the estimated EC50 for this effect was lower in the two cell lines overexpressing protein kinase C-alpha (7 and 6 nM, in SF1.4 and SF3.2 cells, respectively) than in control SC1 and SC2 cells (56 and 22 nM, respectively). The absolute amount of APP released by maximal concentrations of phorbol ester was not altered by overexpression of protein kinase Calpha. The protein kinase C inhibitor H-7 (1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride) significantly reduced the response to phorbol esters in control (SC1) cells but not in cells (SF1.4) that overexpress protein kinase Calpha. Levels of cell-associated APP were slightly elevated, and rates of APP turnover were unchanged, in SF1.4 cells relative to controls. However, cell-associated APP levels were lower in SF3.2 cells than in controls. The results demonstrate that protein kinase Calpha regulates APP release in Swiss 3T3 fibroblasts, and perhaps in other tissues, including brain, and may be the isozyme that mediates receptor-evoked release of APP. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. WEIZMANN INST SCI,DEPT CHEM IMMUNOL,IL-76100 REHOVOT,ISRAEL. RP SLACK, BE (reprint author), MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139, USA. FU NIMH NIH HHS [MH-28783] NR 33 TC 97 Z9 97 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 OCT 5 PY 1993 VL 268 IS 28 BP 21097 EP 21101 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MA288 UT WOS:A1993MA28800070 PM 8407946 ER PT J AU LIGGINS, GC FRANCE, JT SCHNEIDER, RC KNOX, BS ZAPOL, WM AF LIGGINS, GC FRANCE, JT SCHNEIDER, RC KNOX, BS ZAPOL, WM TI CONCENTRATIONS, METABOLIC-CLEARANCE RATES, PRODUCTION-RATES AND PLASMA-BINDING OF CORTISOL IN ANTARCTIC PHOCID SEALS SO ACTA ENDOCRINOLOGICA LA English DT Article ID PRIMATE EVOLUTION; SQUIRREL-MONKEY; HARBOR SEAL; VITULINA AB We have reported previously that plasma of the Weddell seal, a member of the phocid family, contains a very high concentration of cortisol. The present study was undertaken to determine whether high cortisol levels were common to seals in the Antarctic environment, or to other phocidae, and to determine the mechanism of the hypercortisolaemia. High levels of cortisol (0.82-2.38 mumol/l) were found in 4 phocidae (Weddell, crabeater, leopard and Southern elephant seals), whereas levels in a member of the otariid family (Antarctic fur seal) were similar to human values. Metabolic clearance rates (MCR) and production rates (PR) of cortisol were determined in the field in Weddell (N = 1), crabeater (N = 3) and leopard (N = 3) seals following bolus injections of [H-3] cortisol. The MCR and PR did not differ between the three phocids, but whereas the MCR of 410-590 l/day was twice that of human values, the PR of 460-1180 mumol.m-2.d-1 was up to 40-fold greater. The binding capacity of corticosteroid-binding globulin (CBG) was equal to or greater than the plasma concentrations of cortisol, resulting in relatively low concentrations of free cortisol. We conclude that hypercortisolaemia is maintained in phocid seals mainly by a high production rate-the highest (corrected for surface area) reported in any species. The relatively low cortisol levels in otariid seals studied in the same environment suggest that the high PR in phocidae is unrelated to the harsh climatic conditions, but may be part of their adaptation for diving to extreme depths. The phocid seals and New World primates have similarly high levels of cortisol and a high PR but CBG in the primates has low binding capacity and affinity and cortisol is mainly free. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. UNIV AUCKLAND,REPROD MED RES CTR,AUCKLAND,NEW ZEALAND. NR 17 TC 10 Z9 11 U1 0 U2 7 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-5598 J9 ACTA ENDOCRINOL-COP JI Acta Endocrinol. PD OCT PY 1993 VL 129 IS 4 BP 356 EP 359 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ME956 UT WOS:A1993ME95600015 PM 8237255 ER PT J AU MATSUYAMA, SS JARVIK, LF AF MATSUYAMA, SS JARVIK, LF TI ABNORMAL FIBROBLAST MICROTUBULE RESPONSE IN FAMILIAL ALZHEIMER-DISEASE SO AGE LA English DT Article ID PAIRED HELICAL FILAMENTS; PROTEIN-TAU TAU; AMYLOID PRECURSOR; PHILOTHERMAL RESPONSE; TRANSPORT INVIVO; SKIN FIBROBLASTS; GENE-MUTATIONS; DEMENTIA; LINKAGE; BRAIN AB There is increasing evidence that cytoskeletal changes, in particular perturbation of the microtubule (MT) system, play a role in the pathogenesis of Alzheimer disease (AD). The reappearance of the cytoplasmic MT network following treatment with the MT disrupting agent colchicine was investigated in commercially available (Human Genetic Cell Repository, Camden, NJ) fibroblasts derived from 11 patients with familial AD and 11 controls. The AD cells revealed a significant delay in the reappearance of that network following release from treatment with colchicine. Further research with larger samples is needed to determine the sensitivity and specificity of this finding for AD as well as research into the underlying bases for the observed differences. C1 W LOS ANGELES VA MED CTR,PSYCHOGERIATR UNIT & LAB,BRENTWOOD DIV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. NR 47 TC 3 Z9 3 U1 1 U2 1 PU AMER AGING ASSOC PI CHESTER PA 2129 PROVIDENCE AVENUE, CHESTER, PA 19013 SN 0161-9152 J9 AGE JI Age PD OCT PY 1993 VL 16 IS 4 BP 152 EP 158 DI 10.1007/BF02434992 PG 7 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA NA507 UT WOS:A1993NA50700003 ER PT J AU JOHNSON, RP TROCHA, A HAMMOND, S SILICIANO, R BLATTNER, W WALKER, BD AF JOHNSON, RP TROCHA, A HAMMOND, S SILICIANO, R BLATTNER, W WALKER, BD TI EFFECTS OF SEQUENCE VARIATION ON RECOGNITION OF HIV-1 BY HUMAN CYTOTOXIC T-LYMPHOCYTES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 OCT PY 1993 VL 9 SU 1 BP S44 EP S44 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA ME188 UT WOS:A1993ME18800029 ER PT J AU KALAMS, S JOHNSON, RP TROCHA, A DYNAN, MJ KURNICK, JT WALKER, BD AF KALAMS, S JOHNSON, RP TROCHA, A DYNAN, MJ KURNICK, JT WALKER, BD TI LIMITED T-CELL RECEPTOR GENE USAGE IN HIV-1 ENVELOPE SPECIFIC CYTOTOXIC T-LYMPHOCYTES FROM AN INFECTED INDIVIDUAL SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02129. NR 0 TC 0 Z9 0 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 OCT PY 1993 VL 9 SU 1 BP S44 EP S44 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA ME188 UT WOS:A1993ME18800030 ER PT J AU LI, J LORD, C HASELTINE, W LETVIN, N SODROSKI, J AF LI, J LORD, C HASELTINE, W LETVIN, N SODROSKI, J TI INFECTION OF CYNOMOLGUS MONKEYS WITH A CHIMERIC HIV/SIV(MAC) VIRUS THAT EXPRESSES THE HIV-1 ENVELOPE GLYCOPROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. NR 0 TC 0 Z9 0 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 OCT PY 1993 VL 9 SU 1 BP S106 EP S106 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA ME188 UT WOS:A1993ME18800088 ER PT J AU RUPRECHT, RM FRATAZZI, C SHARMA, PL GREENE, MF WYAND, MS PENNINCK, D AF RUPRECHT, RM FRATAZZI, C SHARMA, PL GREENE, MF WYAND, MS PENNINCK, D TI A PRIMATE MODEL TO STUDY IMMUNOPROPHYLAXIS FOR PERINATAL LENTIVIRAL INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1993 VL 9 SU 1 BP S86 EP S86 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA ME188 UT WOS:A1993ME18800058 ER PT J AU COLES, NA HIBBERD, M RUSSELL, M LOVE, T ORY, D FIELD, TS DEC, GW EAGLE, KA AF COLES, NA HIBBERD, M RUSSELL, M LOVE, T ORY, D FIELD, TS DEC, GW EAGLE, KA TI POTENTIAL IMPACT OF PULMONARY-ARTERY CATHETER PLACEMENT ON SHORT-TERM MANAGEMENT DECISIONS IN THE MEDICAL INTENSIVE-CARE UNIT SO AMERICAN HEART JOURNAL LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; CRITICALLY ILL PATIENTS; HEART AB The purpose of this study was to examine the potential impact of pulmonary artery (PA) catheter placement on short-term management decisions in the medical intensive care unit (ICU). One hundred three patients were examined over an 18-month period. The predominant indications for PA-catheter placement included refractory congestive heart failure, airspace disease, uncertain cardiac filling pressures, or hypotension. In 58 (56%) of the 103 patients, management recommendations changed as a direct result of knowledge gained by PA catheter placement. These changes involved fluid therapy recommendations in 41 patients, vasopressor use in 17 patients, intravenous vasodilator use in 24 patients, and recommendations for the use of inotropic agents in 15 patients. Although 18 patients experienced early or late complications, major events were limited to a single pneumothorax requiring chest tube insertion and four episodes of bacteremia. No deaths were directly attributable to the catheter insertion. In critically ill patients in the medical intensive care unit, PA-catheter placement leads to changes in recommendations for management in a substantial portion of patients with little risk of life-threatening complications in those who receive such invasive monitoring. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,15 PARKMAN ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN MED UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 16 TC 7 Z9 9 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD OCT PY 1993 VL 126 IS 4 BP 815 EP 819 DI 10.1016/0002-8703(93)90693-4 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MA334 UT WOS:A1993MA33400002 PM 8213436 ER PT J AU MARCIAL, VA PAJAK, TF ROTMAN, M BRADY, LW AMATO, D AF MARCIAL, VA PAJAK, TF ROTMAN, M BRADY, LW AMATO, D TI COMPENSATED SPLIT-COURSE VERSUS CONTINUOUS RADIATION-THERAPY OF CARCINOMA OF THE TONSILLAR FOSSA - FINAL RESULTS OF A PROSPECTIVE RANDOMIZED CLINICAL-TRIAL OF THE RADIATION-THERAPY ONCOLOGY GROUP SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE TONSILLAR FOSSA; RADIOTHERAPY; SPLIT-COURSE RADIOTHERAPY; HEAD AND NECK SQUAMOUS CELL CARCINOMA AB The Radiation Therapy Oncology Group conducted a prospective comparison of a compensated split course radiotherapy technique (300 cGy x 10. 3 weeks rest. 300 cGy X 10), versus continuous radiotherapy (200-220 cGy up to 6000-6600 cGy), in 137 evaluable patients. The complete response (CR) was 57% in 63 patients, treated with the split-technique vs 61% in 74 patients submitted to continuous course radiotherapy. The completion of therapy as planned was better in the split-technique, but acute and late tissue reactions were the same. Locoregional control of tumor at 5 years was 25% for split and 28% for continuous therapy. At 7 years this was 25% and 24%, respectively. Absolute survival in the split-course patients tended to be lower than in the continuous group, but when the sample of patients was enlarged by the addition of cases from similar trials of nasopharynx and base of tongue lesions, the survival difference was eliminated. On the basis of the results of this study we conclude that the stated compensated split-course technique gives equal clinical results as conventional continuous therapy, with the advantage of requiring fewer radiation fractions, and less burden on the patient and therapy facilities. C1 RADIAT ONCOL CTR,SAN JUAN,PR. RADIAT THERAPY ONCOL GRP,STAT UNIT,PHILADELPHIA,PA. SUNY HLTH SCI CTR,DEPT RADIAT ONCOL,BROOKLYN,NY. HAHNEMANN UNIV,DEPT RADIAT ONCOL,PHILADELPHIA,PA 19102. SIDNEY FARBER CANC INST,CTR STAT,BOSTON,MA 02115. FU NCI NIH HHS [CA-12258, CA-32115] NR 12 TC 7 Z9 7 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 OCT PY 1993 VL 16 IS 5 BP 389 EP 396 DI 10.1097/00000421-199310000-00004 PG 8 WC Oncology SC Oncology GA MB181 UT WOS:A1993MB18100005 PM 8213620 ER PT J AU ZUKERBERG, LR MEDEIROS, LJL FERRY, JA HARRIS, NL AF ZUKERBERG, LR MEDEIROS, LJL FERRY, JA HARRIS, NL TI DIFFUSE LOW-GRADE B-CELL LYMPHOMAS - 4 CLINICALLY DISTINCT SUBTYPES DEFINED BY A COMBINATION OF MORPHOLOGIC AND IMMUNOPHENOTYPIC FEATURES SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE CENTROCYTIC LYMPHOMA; MANTLE CELL LYMPHOMA; IMMUNOCYTOMA; MALTTOMA; MONOCYTOID B-CELL LYMPHOMA ID SMALL-CLEAVED-CELL; INTERMEDIATE LYMPHOCYTIC LYMPHOMA; NON-HODGKINS LYMPHOMA; MANTLE ZONE LYMPHOMA; MALIGNANT-LYMPHOMA; MONOCLONAL-ANTIBODIES; CENTROCYTIC LYMPHOMA; ANTIGEN EXPRESSION; TISSUE MALT; DIFFERENTIATION AB The authors studied 56 cases of diffuse low-grade B-cell lymphoma using frozen tissue sections and a large panel of monoclonal antibodies that distinguish subsets of normal B cells. They compared the immunophenotypes with the histologic subtypes defined by the Rappaport classification, Working Formulation, and Kiel classification to correlate antigen expression with the morphologic subtypes defined in these classification schemes and to define the contribution of immunophenotype to clinically relevant subclassification. All categories in all classifications showed some heterogeneity of antigen expression; however, antigen expression correlated better with four major subgroups defined by the Kiel classification: (1) CD5+CD10-CD23+CD43+: chronic lymphocytic leukemia (CLL); (2) CD5+CD10-/+CD23-CD43+: centrocytic (mantle cell) lymphoma; (3) CD5-CD10+/-CD23-/+ CD43-: centroblastic/centrocytic (CB/CC) lymphoma; and (4) CD5-CD10-CD23-/+CD43-/+: immunocytoma, mucosa-associated lymphoid tissue (MALT)-type, and monocytoid B-cell lymphoma. These subgroups had distinctive clinical features. Patients with centrocytic lymphoma were predominantly male (5.5:1) and had a significantly worse probability of survival than those with either CLL or MALT-type lymphoma (P = 0.001). The group with CB/CC lymphoma had an equal male-female ratio and an intermediate prognosis. Most patients with MALT-type and nodal monocytoid B-cell lymphomas were female (2:1); the disease-free survival for patients with extranodal MALT-type lymphoma was significantly better than that for all patients with other lymphoma subtypes except CB/CC (P < 0.01). The group with non-MALT immunocytoma had a slight male predominance, a high frequency of monoclonal gammopathy, and an intermediate prognosis. In differential diagnosis, CD23 was useful in distinguishing B-cell CLL from centrocytic lymphoma (P < 0.0001); CD5 (P < 0.0001), CD6 (P < 0.005), and CD43 (P < 0.0001) distinguish centrocytic lymphoma from CB/CC lymphoma; and CD10 (P < 0.005), CD43 (P = 0.06), Leu-8 (P = 0.08), and Ig heavy chain (P = 0.01) may help distinguish CB/CC lymphoma from immunocytoma, monocytoid B-cell lymphoma, and MALT-type lymphoma. Differences in antigen expression and clinical features among these Kiel classification subgroups suggest that they represent distinct biologic entities. The Working Formulation categories do not delineate these diseases clearly. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LAB,WARREN 2,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 58 TC 120 Z9 120 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD OCT PY 1993 VL 100 IS 4 BP 373 EP 385 PG 13 WC Pathology SC Pathology GA MB215 UT WOS:A1993MB21500004 PM 8213632 ER PT J AU LEWANDROWSKI, KB WARSHAW, AL COMPTON, CC PINS, MR SOUTHERN, JF AF LEWANDROWSKI, KB WARSHAW, AL COMPTON, CC PINS, MR SOUTHERN, JF TI VARIABILITY IN CYST FLUID CARCINOEMBRYONIC ANTIGEN LEVEL, FLUID VISCOSITY, AMYLASE CONTENT, AND CYTOLOGIC FINDINGS AMONG MULTIPLE LOCULI OF A PANCREATIC MUCINOUS CYSTIC NEOPLASM SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Note DE FINE-NEEDLE ASPIRATION; PANCREATIC NEOPLASMS; BORDERLINE TUMORS ID CYSTADENOCARCINOMA; CYSTADENOMA; DIAGNOSIS; TUMORS AB The procedure of percutaneous aspiration and analysis of cyst contents has been advocated to provide a preoperative diagnosis of pancreatic cystic lesions (pseudocysts and cystic tumors), but it is not known whether variation in the contents of separate loculi of a multilocular neoplasm might misrepresent the identity of the tumor. The authors measured the cyst fluid carcinoembryonic antigen (CEA) level, fluid viscosity, and amylase content and performed cytologic analysis on aspirates from ten different loculi of a single mucinous cystic neoplasm (of the pancreas. The CEA levels were highly variable (median, 6,326 ng/mL; range, 962-64,670 ng/mL) but in all cases were diagnostic of a mucinous tumor. Fluid relative viscosity values were also variable (median, 2.4; range, 1.3-10+) but diagnostic in eight of nine aspirates. The amylase content in all of the loculi was low (< 91 U/1.), and values were consistent with a cystic tumor. Cytologic analysis showed diagnostic mucin-secreting epithelial cells in nine of ten loculi. Although cytologic examination was nondiagnostic in one loculus, there were no false-positive results for malignancy. The combination of all four tests would not have resulted in misclassification of any of the tumors. The authors conclude that the characteristics of the contents of different loculi of pancreatic cystic neoplasms may be variable, but the use of a combination of tests still ensures accurate diagnosis. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. RP LEWANDROWSKI, KB (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,CLIN CHEM,GRAY 5,BOSTON,MA 02114, USA. NR 11 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD OCT PY 1993 VL 100 IS 4 BP 425 EP 427 PG 3 WC Pathology SC Pathology GA MB215 UT WOS:A1993MB21500012 PM 7692722 ER PT J AU SOBER, AJ AF SOBER, AJ TI MELANOMA THICKNESS AND PROGNOSIS SO AMERICAN JOURNAL OF DERMATOPATHOLOGY LA English DT Article RP SOBER, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0193-1091 J9 AM J DERMATOPATH JI Am. J. Dermatopathol. PD OCT PY 1993 VL 15 IS 5 BP 477 EP 477 DI 10.1097/00000372-199310000-00011 PG 1 WC Dermatology SC Dermatology GA MB169 UT WOS:A1993MB16900011 PM 8238785 ER PT J AU SIMON, JA AF SIMON, JA TI SERUM CERULOPLASMIN LEVEL AND THE RISK OF MYOCARDIAL-INFARCTION AND STROKE SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter ID VITAMIN-C; DISEASE RP SIMON, JA (reprint author), SAN FRANCISCO VET AFFAIRS MED CTR,GEN INTERNAL MED SECT,SAN FRANCISCO,CA 94121, USA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD OCT 1 PY 1993 VL 138 IS 7 BP 550 EP 550 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MC311 UT WOS:A1993MC31100009 PM 8213759 ER PT J AU RABENECK, L CRANE, MM RISSER, JMH LACKE, CE WRAY, NP AF RABENECK, L CRANE, MM RISSER, JMH LACKE, CE WRAY, NP TI EFFECT OF HIV TRANSMISSION CATEGORY AND CD4 COUNT ON THE OCCURRENCE OF DIARRHEA IN HIV-INFECTED PATIENTS SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; HOMOSEXUAL MEN; INTESTINAL INFECTIONS; RECTAL MUCOSA; SYNDROME AIDS; MANIFESTATIONS; PREDICTORS; COHORT; VIRUS AB This study was designed to assess the relative contributions of HIV transmission category and immunodeficiency to the risk of HIV-related diarrhea. We reviewed the medical records of 169 HIV-infected non-AIDS patients seen between 1986 and 1990 at the Houston VA Special Medicine Clinic. The prevalence of diarrhea at any given clinic visit ranged from 3% to 7%. Diarrhea was three times more common in homosexual/bisexual men [odds ratio = 3.0 (1.01-9.53)], and this pattern persisted when stratified by CD4 count. Previous studies have focused mainly on the detection of enteric organisms in patients with HIV-related diarrhea. Studies of the temporal relationships between sexual practices, enteric pathogens, diarrhea, and immunodeficiency are needed to clarify the pathogenesis of HIV-related diarrhea. C1 UNIV TEXAS,SCH PUBL HLTH,EPIDEMIOL DISCIPLINE,HOUSTON,TX 77025. RP RABENECK, L (reprint author), VET ADM MED CTR 111D,BAYLOR COLL MED,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 16 TC 14 Z9 14 U1 0 U2 1 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 OCT PY 1993 VL 88 IS 10 BP 1720 EP 1723 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MB687 UT WOS:A1993MB68700012 PM 8105679 ER PT J AU ROSS, DS AF ROSS, DS TI BONE-DENSITY IS NOT REDUCED DURING THE SHORT-TERM ADMINISTRATION OF LEVOTHYROXINE TO POSTMENOPAUSAL WOMEN WITH SUBCLINICAL HYPOTHYROIDISM - A RANDOMIZED, PROSPECTIVE-STUDY SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID L-THYROXINE THERAPY; MINERAL DENSITY; PREMENOPAUSAL WOMEN; HORMONE REPLACEMENT; THYROID-HORMONE; DOUBLE-BLIND; HYPERTHYROIDISM AB PURPOSE: Controversy exists as to whether patients with subclinical hypothyroidism benefit from treatment. Two randomized trials reported that hypothyroid symptoms improved following thyroid hormone replacement therapy. However, during the initial treatment of overt hypothyroidism with levothyroxine, three studies have demonstrated short-term (6 to 12 months) 5% to 13% reductions in bone density. The current study measures bone density during the initial treatment of subclinical hypothyroidism. PATIENTS: Seventeen postmenopausal women with subclinical hypothyroidism (elevated serum thyrotropin [TSH] and normal serum free thyroxine concentrations) and no prior history of thyroid disease were randomly assigned to levothyroxine treatment or no treatment and followed prospectively. Patients in the treatment group had similar initial serum TSH concentrations (9.8 +/- 3.3 versus 8.4 +/- 2.7 muU/mL) but were slightly older (68 +/- 7 years versus 60 +/- 5 years [p < 0.02]). The average dose of levothyroxine needed to normalize serum TSH concentration was 0.072 +/- 0.027 mg. RESULTS: Bone density determinations were not significantly different between the two groups at baseline. After 14 +/- 1 months, single-photon absorptiometry of the wrist decreased by 1.8% +/- 3.2% in the untreated patients and 0.5% +/- 4.1% in the levothyroxine-treated patients (p = NS). Dual-energy X-ray absorptiometry of the lumbar spine decreased by 0.7% +/- 2.9% in the untreated patients and rose 0.1% +/- 4.75% in the levothyroxine-treated patients (p = NS). CONCLUSIONS: Unlike the early treatment of overt hypothyroidism, there is no short-term reduction of bone density with levothyroxine treatment of subclinical hypothyroidism in postmenopausal women. These data suggest that potentially symptomatic women with subclinical hypothyroidism should be given a trial of levothyroxine therapy without concern about adverse effects on skeletal integrity. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP ROSS, DS (reprint author), MASSACHUSETTS GEN HOSP, DEPT MED, THYROID UNIT, BOSTON, MA 02114 USA. FU NCRR NIH HHS [RR-01066] NR 19 TC 31 Z9 31 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9343 EI 1555-7162 J9 AM J MED JI Am. J. Med. PD OCT PY 1993 VL 95 IS 4 BP 385 EP 388 DI 10.1016/0002-9343(93)90307-B PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA MB684 UT WOS:A1993MB68400008 PM 8213870 ER PT J AU CASTILLO, L CHAPMAN, TE YU, YM AJAMI, A BURKE, JF YOUNG, VR AF CASTILLO, L CHAPMAN, TE YU, YM AJAMI, A BURKE, JF YOUNG, VR TI DIETARY ARGININE UPTAKE BY THE SPLANCHNIC REGION IN ADULT HUMANS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE LEUCINE; SPLANCHNIC UPTAKE; 1ST PASS ID AMINO-ACIDS; GAS-CHROMATOGRAPHY; LEUCINE METABOLISM; NITROGEN-METABOLISM; BIOLOGICAL-FLUIDS; MASS-SPECTROMETRY; KINETICS; DERIVATIVES; INGESTION; L-<1-C-13,N-15>LEUCINE AB To determine the uptake of dietary arginine and leucine by the splanchnic region, two experiments were carried out, each involving four healthy young adult men who received a diet supplying 1 g1 protein . kg-1 . day-1 for 7 and 10 days before conducting a primed constant tracer infusion protocol. In study 1, subjects received for 8 h (3-h fast; 5-h fed state, achieved by a constant intragastric infusion of the diet formula) L-[5,5-H-2(2); guanidino-N-15(2)]arginine ([M4]Arg), L-[guanidino-C-13]arginine ([C-13]Arg), and L-[5,5,5-H-2(3)]leucine ([H-2(3)]Leu) simultaneously by an intragastric infusion on day 7 and a repeat of this protocol on day 10 except with tracer administration given by vein. Plasma arginine fluxes were essentially the same for the two arginine tracers but differed significantly with route of administration. In study 2 the subjects received on day 7 a constant intravenous infusion of [C-13]Arg and [H-2(3)]Leu and a simultaneous intragastric infusion of [M4]Arg and [1-C-13]eucine. On day 10 the routes of administration of these tracer pairs were reversed. During the fed state in study 1, splanchnic uptake of dietary arginine was 31 +/- 10 and 34 +/- 8%, based on the [C-13]Arg and [M4]Arg tracers, respectively, and it was significantly higher (P < 0.01) than for leucine, which was 10 +/- 6%. In study 2, splanchnic uptake of dietary arginine, estimated from a series of tracer-protocol combinations for the fed state, was approximately 38% compared with a lower (P < 0.01) value of approximately 15% for leucine. C1 MIT, CLIN RES CTR, HUMAN NUTR LAB, RM E18-613, CAMBRIDGE, MA 02139 USA. SHRINERS BURNS INST, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. TRACER TECHNOL, SOMERVILLE, MA 02145 USA. FU NCRR NIH HHS [RR-88]; NIDDK NIH HHS [DK-15856]; NIGMS NIH HHS [GM-02700] NR 43 TC 88 Z9 89 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD OCT PY 1993 VL 265 IS 4 BP E532 EP E539 PN 1 PG 8 WC Physiology SC Physiology GA ME480 UT WOS:A1993ME48000038 PM 8238326 ER PT J AU ANDERSON, S JUNG, FF INGELFINGER, JR AF ANDERSON, S JUNG, FF INGELFINGER, JR TI RENAL RENIN-ANGIOTENSIN SYSTEM IN DIABETES - FUNCTIONAL, IMMUNOHISTOCHEMICAL, AND MOLECULAR BIOLOGICAL CORRELATIONS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HYPERTENSION; CHRONIC RENAL FAILURE; ANGIOTENSIN-CONVERTING ENZYME; ANGIOTENSIN-II RECEPTOR ANTAGONIST ID CONVERTING ENZYME; MESSENGER-RNA; GLOMERULAR INJURY; SODIUM-REGULATION; RATS; EXPRESSION; MELLITUS; TISSUE; HYPERTENSION; THROMBOXANE AB Recent evidence indicates a role for the renin-angiotensin system (RAS) in the pathogenesis of glomerular injury in diabetes. To further explore the RAS in diabetes, studies were conducted in nondiabetic control rats and in moderately hyperglycemic diabetic (DM) rats. In DM rats, both acute and chronic therapy with the specific angiotensin II (ANG II) receptor antagonist losartan did not affect glomerular hyperfiltration or hyperperfusion but selectively normalized the glomerular capillary hydraulic pressure and ultrafiltration coefficient. To determine the basis of intrarenal hemodynamic responsiveness to RAS inhibition, we conducted biochemical, molecular biological, and immunohistochemical studies to assess endogenous RAS activity. Values for plasma renin concentration and serum angiotensin-converting enzyme (ACE) activity in DM rats were normal. In contrast, intrarenal renin protein content, and renin and angiotensinogen mRNAs, were increased in DM rats, suggesting disproportionate activation of the intrarenal RAS. Total renal ACE activity was significantly reduced in DM rats, but immunohistochemical studies indicated redistribution of ACE in the diabetic kidney. Proximal tubule ACE activity was reduced, but ACE immunostaining intensity was enhanced in glomeruli and renal vasculature. Together, these observations indicate increased RAS activity in those sites (glomeruli and vasculature) most likely to regulate hemodynamic function, potentially explaining the prominent responses to pharmacological blockade of ANG II formation and/or action. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV RENAL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIV PEDIAT NEPHROL,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-40210]; NIADDK NIH HHS [AM-30410] NR 39 TC 225 Z9 230 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 OCT PY 1993 VL 265 IS 4 BP F477 EP F486 PN 2 PG 10 WC Physiology SC Physiology GA ME481 UT WOS:A1993ME48100099 PM 8238377 ER PT J AU TARI, A YAMAMOTO, G SUMII, K SUMII, M TAKEHARA, Y HARUMA, K KAJIYAMA, G WU, V SACHS, G WALSH, JH AF TARI, A YAMAMOTO, G SUMII, K SUMII, M TAKEHARA, Y HARUMA, K KAJIYAMA, G WU, V SACHS, G WALSH, JH TI ROLE OF HISTAMINE(2) RECEPTOR IN INCREASED EXPRESSION OF RAT GASTRIC H+-K+-ATPASE ALPHA-SUBUNIT INDUCED BY OMEPRAZOLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GASTRIC ADENOSINE-TRIPHOSPHATASE; ACID SECRETION; GASTRIN; FAMOTIDINE ID PARIETAL-CELLS; MESSENGER-RNA; BETA-SUBUNIT; MEMBRANES; CLONING; STOMACH; MUCOSA; GENE AB Omeprazole is a specific inhibitor in vivo of the functioning gastric acid pump, the H+-K+-adenosinetriphosphatase (ATPase), in the secretory canaliculus of the parietal cell. It has been shown previously that omeprazole in rats led to an increase in the mRNA for the alpha-subunit of the H+-K+-ATPase. Omeprazole causes a marked increase in circulating gastrin in this species, which in turn stimulates release of histamine from the enterochromaffin-like cell. The possible role of this pathway was investigated by the in vivo administration of famotidine, a potent H-2 receptor antagonist. A single intraperitoneal dose of famotidine, 200 mg/kg, produced a transient hypergastrinemia peaking at 3 h and normalizing at 12 h, inhibition of secretion that lasted for 12 h, but no change in the level of the alpha-subunit mRNA or of beta-actin mRNA. In contrast, a single dose of omeprazole, 100 mg/kg, inhibited acid secretion and produced hypergastrinemia, peaking at 12 h, both effects lasting for the 24-h observation period. Omeprazole elevated the alpha-subunit mRNA transiently by more than threefold at 3 h, with normal levels being restored at 24 h. The administration of famotidine 1 h after omeprazole did not change the effects of omeprazole on acid secretion but elevated the gastrin levels further. There was now no elevation of the alpha-subunit mRNA for the first 6 h, but a small increase at 12 h and a further increase to approximately 2.5-fold at 24 h. Hence the acute effect of omeprazole on alpha-subunit mRNA transcription appears to require activation of the H-2 receptor on the parietal cell, probably resulting from the histamine release induced by hypergastrinemia. C1 W LOS ANGELES VET AFFAIRS MED CTR,BLDG 115,RM 115,LOS ANGELES,CA 90073. HIROSHIMA UNIV,SCH MED,DEPT INTERNAL MED 1,HIROSHIMA 734,JAPAN. UNIV CALIF LOS ANGELES,CTR ULCER RES & EDUC,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PHYSIOL,LOS ANGELES,CA 90024. FU NIDDK NIH HHS [DK-41301, DK-17294] NR 28 TC 22 Z9 22 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 OCT PY 1993 VL 265 IS 4 BP G752 EP G758 PN 1 PG 7 WC Physiology SC Physiology GA ME480 UT WOS:A1993ME48000075 PM 8238359 ER PT J AU MULLIGAN, LJ ESCOBEDO, D FREEMAN, GL AF MULLIGAN, LJ ESCOBEDO, D FREEMAN, GL TI MECHANICAL DETERMINANTS OF CORONARY BLOOD-FLOW DURING DYNAMIC ALTERATIONS IN MYOCARDIAL-CONTRACTILITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PULSUS ALTERNANS; ELASTANCE; MYOCARDIAL BLOOD FLOW ID CLOSED-CHEST DOGS; ANESTHETIZED GOAT; VARYING ELASTANCE; END-EJECTION; HEART-RATE; PRESSURE; IMPEDIMENT; VENTRICLE AB Recently it has been proposed that the decrease in coronary blood flow (CBF) resulting from cardiac contraction referred to as systolic flow impediment (SFI) is dependent on the level of left ventricular elastance (E(es)) The average rate of LV relaxation (R(avg)) has been shown to be major determinant of diastolic flow development (DFD). We tested these hypotheses using the unique hemodynamic condition of pulsus alternans (PA) where end-systolic LV pressure and instantaneous E(es) vary on beat-to-beat basis. In six mongrel dogs instrumented with LV and aortic manometers, ultrasonic dimension crystals, and Doppler coronary flow probes we measured phasic CBF and E(es) during PA and control conditions. Maximal pressure development over time (dP/dt(max)) and SFI were significantly different between weak (WB) and strong beats (SB) as were R(avg) and DFD. Minimum CBF (Q(min)) was not different between SB and WB; however, Q(min) and peak E(es) occurred nearly simultaneously in the WB. Q(min) occurred much earlier than peak E(es) in the strong and control beats. Plots of instantaneous LV elastance and CBF showed that for control beats and for the strong beats of PA CBF was similar during systole and diastole, suggesting elastance is a unique determinant of CBF. This was quantified as CBF at the time in either systole or diastole when elastance was half-maximal for that beat (E50). During the WB of PA, however, CBF at E50 was significantly higher during systole than during diastole. We conclude that while SFI and DFD are highly dependent on the dP/dt and R(avg), E(es) is not a unique determinant of CBF under all conditions. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED & CARDIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 19 TC 6 Z9 6 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 OCT PY 1993 VL 265 IS 4 BP H1112 EP H1118 PN 2 PG 7 WC Physiology SC Physiology GA ME481 UT WOS:A1993ME48100011 ER PT J AU PRABHU, SD FREEMAN, GL AF PRABHU, SD FREEMAN, GL TI LEFT-VENTRICULAR ENERGETICS IN CLOSED-CHEST DOGS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE OXYGEN CONSUMPTION; MYOCARDIAL MECHANICS; CONTRACTILITY ID PRESSURE-VOLUME AREA; MYOCARDIAL OXYGEN-CONSUMPTION; CONSCIOUS DOGS; HEART-RATE; CONTRACTILITY; TACHYCARDIA; MUSCLE; PERFORMANCE; DYSFUNCTION; AFTERLOAD AB Studies of ventricular energetics using the relation between myocardial O2 consumption (MVo2) and pressure-volume area (PVA) have been performed extensively in the isolated heart, but not in the intact animal. We characterized the MVo2-PVA relation and its response to heart rate (HR) in eight closed-chest dogs instrumented with high-fidelity micromanometers, piezoelectric crystals, coronary flow probes, and coronary sinus oximetric catheters. The effect of dobutamine was studied in five dogs. MVo2 is linearly related to PVA with lower MVo2 required for the generation of smaller PVAs. Baseline contractile efficiency (EFF) was 25.6 +/- 2.8%. High pacing rates reduced EFF (25.7 +/- 3.2% at a HR of 107 +/- 3 beats/min vs. 16.3 +/- 2.4% at a HR of 194 +/- 5 beats/min, P < 0.0167) and load-independent MVo2 per beat (0.562 +/- 0.119 vs. 0.377 +/- 0.074 J.beat-1.100 g LV-1, P < 0.0167) while increasing end-systolic elastance (E(es)) (9.4 +/- 1.3 vs. 18.6 +/- 3.1 mmHg/ml, P < 0.0167). Dobutamine administration increased load-independent MVo2 per beat (0.392 +/- 0.108 vs. 0.607 +/- 0.083 J.beat-1.100 g LV-1, P < 0.05) and contractility (E(es) 10.1 +/- 1.5 vs. 32.0 +/- 7.6 mmHg/ml, P < 0.05) without changing EFF (28.8 +/- 3.8 vs. 30.3 +/- 3.8%, P = NS). Thus the intact animal displays loss of EFF at high heart rates but maintains EFF during dobutamine stimulation. Both interventions increased load-independent MVo2 per minute, indicating increased O2 requirements for excitation-contraction coupling. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Prabhu, Sumanth/D-5223-2009 NR 45 TC 7 Z9 8 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD OCT PY 1993 VL 265 IS 4 BP H1048 EP H1055 PN 2 PG 8 WC Physiology SC Physiology GA ME481 UT WOS:A1993ME48100003 ER PT J AU OTTO, MW POLLACK, MH SACHS, GS REITER, SR MELTZERBRODY, S ROSENBAUM, JF AF OTTO, MW POLLACK, MH SACHS, GS REITER, SR MELTZERBRODY, S ROSENBAUM, JF TI DISCONTINUATION OF BENZODIAZEPINE TREATMENT - EFFICACY OF COGNITIVE-BEHAVIORAL THERAPY FOR PATIENTS WITH PANIC DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID FOLLOW-UP; CARBAMAZEPINE TREATMENT; WITHDRAWAL; ALPRAZOLAM; DEPENDENCE; AGORAPHOBIA; ANXIETY AB Objective: The primary disadvantage of high-potency benzodiazepine treatment or panic disorder is the difficulty of discontinuing the treatment. During treatment discontinuation, new symptoms may emerge and anxiety may return, preventing many patients from successfully discontinuing their treatment. In this controlled, randomized trial the authors investigated the efficacy of a cognitive-behavioral program for patients with panic disorder who were attempting to discontinue treatment with high-potency benzodiazepines. Method: Outpatients treated for panic disorder with alprazolam or clonazepam for a minimum of 6 months and expressing a desire to stop taking the medication (N=33) were randomly assigned to one of two taper conditions: a slow taper condition alone or a slow taper condition in conjunction with 10 weeks of group cognitive-behavioral therapy. Results: The rate of successful discontinuation of benzodiazepine treatment was significantly higher for the patients receiving the cognitive-behavioral program (13 of 17; 76%) than for the patients receiving the slow taper program alone (four of 16; 25%). There was no difference in the likelihood of discontinuation success between the patients treated with alprazolam and those who received clonazepam. At the 3-month follow-up evaluation, 77% of the patients in the cognitive-behavioral program who successfully discontinued benzodiazepine treatment remained benzodiazepine free. Conclusions: These findings support the efficacy of cognitive-behavioral interventions in aiding benzodiazepine discontinuation for patients with panic disorder. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC-815,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [NIMH MH-19600] NR 37 TC 160 Z9 161 U1 0 U2 7 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 OCT PY 1993 VL 150 IS 10 BP 1485 EP 1490 PG 6 WC Psychiatry SC Psychiatry GA MA342 UT WOS:A1993MA34200007 PM 8379551 ER PT J AU KOPANS, DB FEIG, SA AF KOPANS, DB FEIG, SA TI THE CANADIAN NATIONAL BREAST SCREENING STUDY - A CRITICAL-REVIEW SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material ID CANCER-DETECTION; WOMEN AB Public health planners around the world had been awaiting the preliminary results of the randomized, controlled trial of breast cancer screening performed by the Canadian National Breast Screening Study (CNBSS) during the 1980s. It had been hoped that this large study would answer, with statistical validity, many of the questions concerning breast cancer screening that had not been answered satisfactorily by previous studies. Among the major unresolved issues is the desire to establish ''absolute'' proof that mammographic screening can benefit women who are between 40 and 49 years old. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. THOMAS JEFFERSON UNIV HOSP,DEPT RADIOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 21 TC 107 Z9 108 U1 1 U2 2 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 OCT PY 1993 VL 161 IS 4 BP 755 EP 760 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG651 UT WOS:A1993MG65100012 PM 8372752 ER PT J AU BENNETT, GL CHEW, FS AF BENNETT, GL CHEW, FS TI SEROUS CYSTADENOMA OF THE PANCREAS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note ID MICROCYSTIC ADENOMA; SPECTRUM C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 4 TC 3 Z9 3 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 OCT PY 1993 VL 161 IS 4 BP 786 EP 786 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MG651 UT WOS:A1993MG65100018 PM 8372758 ER PT J AU YOUNG, RH GILKS, CB SCULLY, RE AF YOUNG, RH GILKS, CB SCULLY, RE TI PSEUDOMYXOMA PERITONEI SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter ID MUCINOUS TUMORS; OVARY C1 UNIV HOSP BRITISH COLUMBIA,VANCOUVER,BC,CANADA. RP YOUNG, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114, USA. NR 5 TC 13 Z9 15 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD OCT PY 1993 VL 17 IS 10 BP 1068 EP 1070 PG 3 WC Pathology; Surgery SC Pathology; Surgery GA LZ182 UT WOS:A1993LZ18200017 PM 8372947 ER PT J AU HU, H BECKETT, L KELSEY, K CHRISTIANI, D AF HU, H BECKETT, L KELSEY, K CHRISTIANI, D TI THE LEFT-SIDED PREDOMINANCE OF ASBESTOS-RELATED PLEURAL DISEASE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID LOCATION; FIBROSIS AB In a series of 406 subjects with a diagnosis of asbestos-related pleural disease (ARPD), the left-right symmetry of radiographically diagnosed ARPD was assessed using the International Labour Organization (ILO) system for classifying radiographic abnormalities and three different statistical models for testing the degree of symmetry. The extent of chest disease was found to be greater on the left than on the right for a number of parameters of pleural disease, including the width and extent of localized pleural thickening, the extent of enface pleural thickening, and the extent of diaphragmatic and chest wall calcification. Current cigarette smoking significantly enhanced the observed asymmetry, with the most pronounced effect being in diaphragmatic calcification. Using a composite scale for each subject's pleural disease, the left side had 1.6 times more localized disease than did the right (p < 0.001). Asymmetry in one parameter was associated with asymmetry in another for a number of pairs. The most significant of these associations was between enface pleural thickening and chest wall calcification (Kendall's tau B = 0.42). The pathophysiologic mechanisms that explain these findings remain elusive and need further investigation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH SCI,OCCUPAT HLTH PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,RADIOL LAB,BOSTON,MA 02115. MASSACHUSETTS RESP HOSP,CTR OCCUPAT & ENVIRONM MED,BRAINTREE,MA. RUSH PRESBYTERIAN ST LUKES MED CTR,CTR RES HLTH & AGING,CHICAGO,IL 60612. RP HU, H (reprint author), BRIGHAM & WOMENS HOSP,CHANNING LAB,180 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIEHS NIH HHS [2 P30 ES-00002] NR 17 TC 14 Z9 16 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD OCT PY 1993 VL 148 IS 4 BP 981 EP 984 PG 4 WC Respiratory System SC Respiratory System GA MC073 UT WOS:A1993MC07300025 PM 8214954 ER PT J AU FRATACCI, MD KIMBALL, WR WAIN, JC KACMAREK, RM POLANER, DM ZAPOL, WM AF FRATACCI, MD KIMBALL, WR WAIN, JC KACMAREK, RM POLANER, DM ZAPOL, WM TI DIAPHRAGMATIC SHORTENING AFTER THORACIC-SURGERY IN HUMANS - EFFECTS OF MECHANICAL VENTILATION AND THORACIC EPIDURAL-ANESTHESIA SO ANESTHESIOLOGY LA English DT Article DE ANESTHETIC TECHNIQUE, EPIDURAL; INSTRUMENT TECHNIQUES, ELECTROMYOGRAPHY; SONOMICROMETRY; LUNG, VENTILATION, MECHANICAL VENTILATION; SPONTANEOUS VENTILATION; MUSCLE, DIAPHRAGM, COSTAL DIAPHRAGMATIC CONTRACTION; POSTOPERATIVE FUNCTION; SURGERY, THORACIC PULMONARY RESECTION ID UPPER ABDOMINAL-SURGERY; RESPIRATORY INDUCTIVE PLETHYSMOGRAPH; CANINE DIAPHRAGM; BODY POSITION; RIB CAGE; LENGTH; CALIBRATION; DOGS; RECOVERY; MODEL AB Background: Diaphragmatic function is believed to be inhibited after thoracic surgery and may be improved by thoracic epidural anesthesia. Methods: Diaphragmatic function after a thoracotomy was monitored by implanting one pair of sonomicrometry crystals and two electromyogram (EMG) electrodes on the costal diaphragm of six patients undergoing an elective pulmonary resection. Crystals and EMG electrodes remained in place for 12-24 h. Results: During mechanical ventilation, costal diaphragmatic length (as a percent of rest length; %L(FRC)) decreased passively as tidal volume (V(T)) increased (%L(FRC) = 2.81 +/- 1.12 X 10(-2) V(T) (ml), r = 0.99). During spontaneous ventilation, the costal shortening (2.1 +/- 2.3 %L(FRC)) was less than during mechanical ventilation (7.9 +/- 3.0 %L(FRC), P < 0.05) at the same V(T). Comparing spontaneous ventilation before and 30 min after thoracic epidural anesthesia, there were increases of V(T) (390 +/- 78 to 555 +/- 75 ml), vital capacity (1.37 +/- 0.16 to 1.68 +/- 0.21 l), and esophageal ( 8.5 +/- 1.5 to 10.6 +/- 1.7 cmH2O), gastric (-0.7 +/- 0.8 to +0.8 +/- 0.8 cmH2O), and transdiaphragmatic (7.7 +/- 1.5 to 11.5 +/- 1.9 cmH2O) pressures, but diaphragmatic EMG and shortening fraction remained constant. In three of six patients, epidural anesthesia produced paradoxical segment lengthening upon inspiration. Conclusions: Thoracotomy and pulmonary resection produce a marked reduction of active diaphragmatic shortening, which is not reversed by thoracic epidural anesthesia despite improvement of other indices of respiratory function. C1 MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT ANAESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HARVARD MED SCH,ANAESTHESIA LABS,BOSTON,MA 02114. OI Polaner, David/0000-0001-8716-6289 FU NHLBI NIH HHS [HL 42397] NR 37 TC 41 Z9 45 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD OCT PY 1993 VL 79 IS 4 BP 654 EP 665 DI 10.1097/00000542-199310000-00005 PG 12 WC Anesthesiology SC Anesthesiology GA MA814 UT WOS:A1993MA81400004 PM 8214744 ER PT J AU POLANER, DM KIMBALL, WR FRATACCI, MD WAIN, JC ZAPOL, WM AF POLANER, DM KIMBALL, WR FRATACCI, MD WAIN, JC ZAPOL, WM TI THORACIC EPIDURAL-ANESTHESIA INCREASES DIAPHRAGMATIC SHORTENING AFTER THORACOTOMY IN THE AWAKE LAMB SO ANESTHESIOLOGY LA English DT Article DE ANESTHETIC TECHNIQUES, EPIDURAL; DIAPHRAGM, INHIBITION; LUNG, POSTOPERATIVE RESPIRATORY FUNCTION; MEASUREMENT TECHNIQUES, SONOMICROMETRY; SURGERY, THORACIC ID UPPER ABDOMINAL-SURGERY; EXTRADURAL BLOCK; RIB CAGE; LUNG; MORPHINE; DOGS AB Background. Prolonged inhibition of diaphragmatic function occurs after thoracic and upper abdominal surgery. It was hypothesized that thoracic epidural anesthesia on the day after a thoracotomy could block inhibitory neural pathways and increase the shortening of costal and crural diaphragmatic segments. Methods. Pairs of sonomicrometer crystals were implanted into the costal and crural regions of the diaphragm through a right lateral thoracotomy in 14 30-kg, 4-5-month-old lambs. One day after surgery, a thoracic epidural catheter was placed at the T8-T9 level. Regional diaphragmatic shortening normalized to end-expiratory length (%L(FRC)), was measured by sonomicrometry in these awake lambs. Changes in gastric (DELTAP(gas)), esophageal (DELTAP(es)), and transdiaphragmatic (DELTAP(dl)) pressures were measured with transnasal balloon catheters. End-tidal carbon dioxide (FET(CO2)), costal and crural electromyogram (E(dl)), and tidal volume (V(T)) were measured. Inductance plethysmography was used in four lambs to assess relative contributions of the rib cage and abdomen to V(T). Control values were obtained during quiet breathing and while rebreathing at up to 10% FET(CO2). To block thoracic dermatomes, 1% or 2% lidocaine was injected through the epidural catheter. Measurements were repeated after each lidocaine injection. Results: There was no change of resting length with 1% lidocaine; costal resting length increased by 22% with 2% lidocaine. After 2% lidocaine, costal %L(FRC) increased from control both during quiet breathing (8.7 +/- 0.7 to 18.1 +/- 1, xBAR +/- SEM%) and at FET(CO2) 10% (22.1 +/- 2 to 33.7 +/- 3%). V(T) during quiet breathing was unchanged after 1% lidocaine but increased from 235 +/- 16 to 283 +/- 28 ml after 2% lidocaine. At 10% FET(CO2) DELTAP(dl) was unchanged after 1% lidocaine and decreased from 36.5 +/- 4.3 to 26.3 +/- 4.9 cmH2O after 2% lidocaine. Regional DELTAE(dl) was unchanged with both 1% and 2% lidocaine at rest and during carbon dioxide rebreathing. Plethysmography in three lambs showed a reduction in rib cage contribution to tidal volume with 2% lidocaine during quiet breathing. Conclusions: Improved postoperative tidal volume and diaphragmatic shortening after thoracic epidural blockade may be due to changes of chest wall conformation and resting length and a shift of the workload of breathing from the rib cage to the diaphragm caused by intercostal muscle paralysis. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MADIGAN ARMY MED CTR,DEPT SURG,TACOMA,WA 98431. OI Polaner, David/0000-0001-8716-6289 FU NHLBI NIH HHS [HL 42397] NR 21 TC 19 Z9 20 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD OCT PY 1993 VL 79 IS 4 BP 808 EP 816 PG 9 WC Anesthesiology SC Anesthesiology GA MA814 UT WOS:A1993MA81400023 PM 8214761 ER PT J AU DANIELS, GH AF DANIELS, GH TI MANAGEMENT OF THYROID-NODULES SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP DANIELS, GH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 1 Z9 1 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 OCT 1 PY 1993 VL 119 IS 7 BP 634 EP 634 PN 1 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MA291 UT WOS:A1993MA29100019 PM 8363179 ER PT J AU MECOCCI, P MACGARVEY, U KAUFMAN, AE KOONTZ, D SHOFFNER, JM WALLACE, DC BEAL, MF AF MECOCCI, P MACGARVEY, U KAUFMAN, AE KOONTZ, D SHOFFNER, JM WALLACE, DC BEAL, MF TI OXIDATIVE DAMAGE TO MITOCHONDRIAL-DNA SHOWS MARKED AGE-DEPENDENT INCREASES IN HUMAN BRAIN SO ANNALS OF NEUROLOGY LA English DT Article ID RESPIRATORY-CHAIN FUNCTION; CEREBRAL BLOOD-FLOW; DEGENERATIVE DISEASES; OXYGEN-CONSUMPTION; SKELETAL-MUSCLE; MONKEY BRAIN; MUTATION; 8-HYDROXY-2'-DEOXYGUANOSINE; 8-HYDROXYDEOXYGUANOSINE; 8-HYDROXYGUANINE AB A major theory of aging is that oxidative damage may accumulate in DNA and contribute to physiological changes associated with aging. We examined age-related accumulation of oxidative damage to both nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) in human brain tissue. We measured the oxidized nucleoside, 8-hydroxy-2'-deoxyguanosine (OH8dG), in DNA isolated from 3 regions of cerebral cortex and cerebellum from 10 normal humans aged 42 to 97 years. The amount of OH8dG, expressed as a ratio of the amount of deoxyguanosine (dG) or as fmol/mug of DNA, increased progressively with normal aging in both nDNA and mtDNA; however, the rate of increase with age was much greater in mtDNA. There was a significant 10-fold increase in the amount of OH8dG in mtDNA as compared with nDNA in the entire group of samples, and a 15-fold significant increase in patients older than 70 years. These results show for the first time that there is a progressive age-related accumulation in oxidative damage to DNA in human brain, and that the mtDNA is preferentially affected. It is possible that such damage may contribute to age-dependent increases in incidence of neurodegenerative diseases. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROL SERV,NEUROCHEM LAB,WARREN 408,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. EMORY UNIV,DEPT NEUROL,ATLANTA,GA 30322. EMORY UNIV,DEPT GENET & MOLEC MED,ATLANTA,GA 30322. FU NIA NIH HHS [IP50AG05134]; NINDS NIH HHS [NS21328]; PHS HHS [16367] NR 50 TC 508 Z9 529 U1 4 U2 19 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 1993 VL 34 IS 4 BP 609 EP 616 DI 10.1002/ana.410340416 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MA624 UT WOS:A1993MA62400015 PM 8215249 ER PT J AU FALCONE, PM BROCKHURST, RJ AF FALCONE, PM BROCKHURST, RJ TI DELAYED-ONSET OF BILATERAL ACUTE RETINAL NECROSIS SYNDROME - A 34-YEAR INTERVAL SO ANNALS OF OPHTHALMOLOGY LA English DT Article AB The case is described of a male patient who had a history of acute retinal necrosis (ARN) OS at age 13 years. The eye subsequently had an inoperable retinal detachment with residual light perception visual acuity. After a 34-year disease-free interval, ARN developed OD that responded to medical treatment. This case represents the longest reported interval of ARN quiescence with eventual bilateral involvement and illustrates the importance of long-term patient follow-up. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 7 TC 19 Z9 22 U1 0 U2 1 PU AMER SOC CONTEMPORARY OPHTHALMOLOGY PI SKOKIE PA 4711 GOLF RD, SUITE 408, SKOKIE, IL 60076-1242 SN 0003-4886 J9 ANN OPHTHALMOL JI Ann. Ophthalmol. PD OCT PY 1993 VL 25 IS 10 BP 373 EP 374 PG 2 WC Ophthalmology SC Ophthalmology GA MM910 UT WOS:A1993MM91000003 PM 8304688 ER PT J AU FALCONE, PM PAOLINI, L LOU, PL AF FALCONE, PM PAOLINI, L LOU, PL TI HYDROXYCHLOROQUINE TOXICITY DESPITE NORMAL DOSE THERAPY SO ANNALS OF OPHTHALMOLOGY LA English DT Article ID CHLOROQUINE RETINOPATHY; RHEUMATOID-ARTHRITIS AB The risk of retinopathy associated with the use of hydroxychloroquine is said to be nullified if the dosage recommendations are followed strictly. In this case report, we describe an elderly patient with rheumatoid arthritis who had bilateral maculopathy, presumably secondary to hydroxychloroquine therapy, despite a dosing regimen within therapeutic guidelines. We believe special attention should be given to elderly patients who are being treated with hydroxychloroquine because their retinal pigment epithelium may be more susceptible to the toxic effects of this drug. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. W READING OPHTHALM ASSOCIATES,W READING,PA. ST LUKES ROOSEVELT HOSP,DEPT OPHTHALMOL,NEW YORK,NY. NR 22 TC 29 Z9 30 U1 0 U2 1 PU AMER SOC CONTEMPORARY OPHTHALMOLOGY PI SKOKIE PA 4711 GOLF RD, SUITE 408, SKOKIE, IL 60076-1242 SN 0003-4886 J9 ANN OPHTHALMOL JI Ann. Ophthalmol. PD OCT PY 1993 VL 25 IS 10 BP 385 EP 388 PG 4 WC Ophthalmology SC Ophthalmology GA MM910 UT WOS:A1993MM91000006 PM 8304691 ER PT J AU JENNINGS, TS HARDIN, TC AF JENNINGS, TS HARDIN, TC TI TREATMENT OF ASPERGILLOSIS WITH ITRACONAZOLE SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; INVASIVE ASPERGILLOSIS; PULMONARY ASPERGILLOSIS; THERAPY; ANTIFUNGAL; MYCOSES AB OBJECTIVE: To review the role of itraconazole as oral therapy for the major infections caused by Aspergillus spp.: allergic bronchopulmonary aspergillosis, aspergilloma, and invasive aspergillosis. DATA SOURCES: A MEDLINE search of articles published in the English language between 1986 and 1993 was used to identify relevant citations, including review articles. In addition, a search of die published abstracts of the past two Interscience Conferences on Antimicrobial Agents and Chemotherapy (ICAAC) was performed. STUDY SELECTION: Clinical trials that evaluated itraconazole therapy in either allergic bronchopulmonary aspergillosis, aspergilloma, or invasive aspergillosis were critically reviewed. Trials were evaluated based upon entry criteria for die diagnosis of each type of aspergillosis, risk factors for the development of aspergillosis (neutropenia, transplant recipient, hematologic malignancy), prior antifungal chemotherapy, and dose and duration of itraconazole therapy. DATA SYNTHESIS: Overall, the clinical trials of itraconazole therapy for aspergillosis are limited and of variable quality. In the treatment of allergic bronchopulmonary aspergillosis, itraconazole has been reported to prompt a reduction in corticosteroid dosage in selected patients. There have been no controlled trials of itraconazole as treatment for aspergilloma, but data from several open-label trials suggest that this agent may be of clinical benefit in aspergilloma, primarily as an alternative to surgery. The use of itraconazole for invasive aspergillosis has been evaluated in several trials, most often in patients who were intolerant to amphotericin B treatment. Response to oral itraconazole has generally been promising. CONCLUSIONS: Although itraconazole offers promise for oral therapy against infections caused by Aspergillus spp., it should not presently be regarded as primary therapy for any of these diseases. Amphotericin B, in doses ranging from 1 to 1.5 mg/kg to a total dose of 1.5-4.0 g, should remain the treatment of choice in both aspergilloma and invasive aspergillosis. Itraconazole use should be restricted to patients who experience severe toxicity with amphotericin B therapy. Corticosteroids continue to be first-line therapy for allergic bronchopulmonary aspergillosis, with the use of itraconazole reserved for those patients who would benefit from a reduction in corticosteroid dose. C1 UNIV TEXAS, COLL PHARM, AUSTIN, TX 78712 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT PHARMACOL, SAN ANTONIO, TX 78284 USA. RP JENNINGS, TS (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR, PHARM SERV, 7400 MERTON MINTER BLVD, SAN ANTONIO, TX 78284 USA. NR 25 TC 32 Z9 32 U1 1 U2 2 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD OCT PY 1993 VL 27 IS 10 BP 1206 EP 1211 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MC459 UT WOS:A1993MC45900013 PM 8251691 ER PT J AU FISCHMAN, AJ LIVNI, E BABICH, J ALPERT, NM LIU, YY THOM, E CLEELAND, R PROSSER, BL CORREIA, JA STRAUSS, HW RUBIN, RH AF FISCHMAN, AJ LIVNI, E BABICH, J ALPERT, NM LIU, YY THOM, E CLEELAND, R PROSSER, BL CORREIA, JA STRAUSS, HW RUBIN, RH TI PHARMACOKINETICS OF [F-18] FLEROXACIN IN HEALTHY-HUMAN SUBJECTS STUDIED BY USING POSITRON EMISSION TOMOGRAPHY SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID LIQUID-CHROMATOGRAPHIC DETERMINATION; FLEROXACIN RO 23-6240; INVITRO ACTIVITY; CLINICAL PHARMACOKINETICS; CHLAMYDIA-TRACHOMATIS; PERFORMANCE; EFFICACY; TISSUE; PENETRATION; VOLUNTEERS AB Positron emission tomography (PET) with [F-18]fleroxacin was used to study the pharmacokinetics of fleroxacin, a new broad-spectrum fluoroquinolone, in 12 healthy volunteers (9 men and 3 women). The subjects were infused with a standard therapeutic dose of fleroxacin (400 mg) supplemented with approximately 20 mCi of [F-18]fleroxacin. Serial PET images were made and blood samples were collected for 8 h, starting at the initiation of the infusion. The subjects were then treated with unlabeled drug for 3 days (400 mg/day). On the fifth day, infusion of radiolabeled drug, PET imaging, and blood collection were repeated. In most organs, there was rapid accumulation of radiolabeled drug, with stable levels achieved within 1 h after completion of the infusion. Especially high peak concentrations (in micrograms per gram) were achieved in the kidney (>34), liver (>25), lung >20), myocardium (>19), and spleen (>18). Peak concentrations of drug more than two times the MIC for 90% of Enterobacteriaceae strains tested (>10-fold for most organisms) were achieved in all tissues except the brain and remained above this level for more than 6 to 8 h. The plateau concentrations in tissues (2 to 8 h, in micrograms per gram +/- standard error of the mean) of drug were as follows: brain, 0.83 +/- 0.032; myocardium, 4.53 +/- 0.24; lung, 5.80 +/- 0.48; liver, 7.31 +/- 0.33; spleen, 6.00 +/- 0.47; bowel, 3.53 +/- 0.74; kidney, 8.85 +/- 0.64; bone, 2.87 +/- 0.29; muscle, 4.60 +/- 0.33; prostate, 4.65 +/- 0.48; uterus, 3.87 +/- 0.39; breast, 2.68 +/- 0.11; and blood, 2.35 +/- 0.09. Concentrations of fleroxacin in tissue were similar in males and females, before and after pretreatment with unlabeled drug. C1 MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114, USA. NR 54 TC 35 Z9 35 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 OCT PY 1993 VL 37 IS 10 BP 2144 EP 2152 PG 9 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA MA179 UT WOS:A1993MA17900017 PM 8257137 ER PT J AU VOLPE, NJ LESSELL, S AF VOLPE, NJ LESSELL, S TI REMITTING 6TH NERVE PALSY IN SKULL BASE TUMORS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID ABERRANT OCULOMOTOR REGENERATION; PARALYSIS; PROGNOSIS; CHILDREN; PARESIS; ADULTS; SIGN; IV; VI AB Objective: Spontaneous recovery of a sixth nerve palsy is thought to rule out a neoplastic origin. We reviewed cases of sixth nerve palsy that improved without treatment but that ultimately proved to be caused by a tumor at the base of the skull. Design: Case series. Setting: Hospital-based, neuro-ophthalmology referral practice. Patients: Seven patients with an age range from 7 to 61 years had sixth nerve palsy secondary to a slow-growing neoplasm at the skull base. Main Outcome Measures: Return of lateral rectus function and resolution of diplopia without intervention. Results: Seven patients with sixth nerve palsy caused by skull base tumors experienced spontaneous improvement of their deficit. Recovery time ranged from 1 week to 18 months. No patient was diabetic or had evidence of vascular disease. In one patient, the palsy improved once prior to becoming a fixed deficit, and spontaneous improvement occurred on two to five occasions in the other patients. Conclusion: Spontaneous recovery of a sixth nerve palsy can occur in the presence of an extramedullary compression by a tumor at the base of the brain. Possible mechanisms for recovery include remyelination, axonal regeneration, relief of transient compression (eg, resorption of hemorrhage), restoration of impaired blood flow, slippage of a nerve previously stretched over the tumor, or immune responses to the tumor. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,NEUROOPHTHALMOL UNIT,BOSTON,MA 02115. NR 24 TC 31 Z9 31 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD OCT PY 1993 VL 111 IS 10 BP 1391 EP 1395 PG 5 WC Ophthalmology SC Ophthalmology GA MB502 UT WOS:A1993MB50200033 PM 8216020 ER PT J AU TANAKA, M MORENO, EC MARGOLIS, HC AF TANAKA, M MORENO, EC MARGOLIS, HC TI EFFECT OF FLUORIDE INCORPORATION INTO HUMAN DENTAL ENAMEL ON ITS DEMINERALIZATION IN-VITRO SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE ENAMEL; FLUORIDE; DEMINERALIZATION; CARIES ID TOOTH DEMINERALIZATION; CARIES EXPERIENCE; DISSOLUTION; HYDROXYAPATITE; BEHAVIOR AB Coronal surfaces of extracted human teeth were ground to a depth of about 1 mm and then cut in half labiolingually. One half was used as a control; the other half was exposed, for 3 days, to a fluoride-enriching buffer (0.1 mol/l lactic acid, 19.7 mmol/l CaCl2, 10.8 mmol/l KH2PO4, 3 mmol/l NaN3; Ph adjusted to 4.68 with KOH) having fluoride concentrations from 0.0002 to 2.2 parts/10(6). This exposure resulted in an uptake of fluoride by the enamel to a depth of 2 mum without any apparent demineralization. The fluoride uptake was proportional to the F concentration of the enriching solution, reaching concentrations of about 8000 parts/10(6) within the first micrometre of enamel exposed to the highest F concentration; the controls had uniform F concentrations not exceeding 50 parts/10(6) along the 2.5 mum of enamel depth sampled. Thin sections (140-160 mum) were cut perpendicularly to the lingual surface, coated with protective resin except for a window about 1 mm long on the ground lingual surface, and exposed to a demineralizing buffer. The mineral losses of the sections were followed over 5 days by microradiography and image analysis. Fluoride enrichment resulted in reduced demineralization and the reduction was inversely related to the enamel fluoride content. The controls displayed a uniform erosion of the surface enamel whereas all the treatments below 1.5 parts/10(6) in the enriching solutions developed typical subsurface 'lesions'. The mineral content of the surface layer increased with increasing time of exposure to the demineralizing buffer. In enamel having 5000-6000 part/10(6) F within the first 1-2 mum from the surface, no detectable loss of enamel mineral was observed after the 5-day exposure to the demineralizing buffer. Incorporation of fluoride into enamel is explained by a process of dissolution and reprecipitation yielding a mineral that is more resistant to acid demineralization. C1 FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115. FU NIDCR NIH HHS [DE-07009, DE-07493, DE-03187] NR 27 TC 14 Z9 15 U1 1 U2 2 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 OCT PY 1993 VL 38 IS 10 BP 863 EP 869 DI 10.1016/0003-9969(93)90095-4 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MD997 UT WOS:A1993MD99700005 PM 8279991 ER PT J AU SCHULTE, L ROBERTS, MS ZIMMERMAN, C KETLER, J SIMON, LS AF SCHULTE, L ROBERTS, MS ZIMMERMAN, C KETLER, J SIMON, LS TI A QUANTITATIVE ASSESSMENT OF LIMITED JOINT MOBILITY IN PATIENTS WITH DIABETES - GONIOMETRIC ANALYSIS OF UPPER EXTREMITY PASSIVE RANGE OF MOTION SO ARTHRITIS AND RHEUMATISM LA English DT Article ID DUPUYTRENS CONTRACTURE; HAND ABNORMALITIES; NATURAL-HISTORY; MELLITUS; CHILDHOOD; COMPLICATIONS; RETINOPATHY; SHOULDER; COLLAGEN; ASSOCIATION AB Objective. The syndrome of limited joint mobility is a common but not widely recognized musculoskeletal complication of diabetes. The purpose of this study was to further characterize this syndrome using quantitative goniometric measures. Methods. Cross-sectional analysis of a sample population was performed to establish the prevalence, location, and severity of limited joint mobility and to determine its relationship to extraarticular manifestations and complications of diabetes. Passive range of motion of both upper extremities was measured by goniometry in 70 adult patients with insulin-dependent diabetes mellitus and 70 nondiabetic controls who were group-matched for age, sex, and general activity level. Joint mobility was assessed by both individual joint motions and a composite scoring technique. Results. Analysis of individual joints and composite scores revealed significant differences between dominant and nondominant extremities in both the control and the diabetic groups. Diabetic patients were generally less flexible than nondiabetic subjects throughout the arm, especially in shoulder and finger joints. In the full study population, multivariate analysis revealed that advanced age, male sex, and the presence of diabetes were associated with decreased passive range of motion for a majority of joints (P < 0.05). In the diabetes group, passive range of motion was significantly correlated (P < 0.05) with age, sex, duration of diabetes, and to a variable extent, glucose control, but was not correlated with the presence of clinically significant neuropathy, retinopathy, nephropathy, or peripheral vascular disease, with activity level, or with hand dominance. Stepwise regression analysis failed to identify single key joint. motion(s) to serve as possible screening tests in predicting generalized limited joint mobility of the upper extremity. Finally, the effect of limb usage on range of motion in flexion may differ in diabetic and nondiabetic subjects. Conclusion. Limited joint mobility is a generalized phenomenon occurring throughout the upper extremities of many diabetic patients. It is significantly related to age, sex, and to a variable extent duration of diabetes and glucose control. It is not related to the standard complications of diabetes as defined in this study. C1 NEW ENGLAND DEACONESS HOSP,DIV RHEUMATOL,110 FRANCIS ST,SUITE 5A,BOSTON,MA 02215. NEW ENGLAND DEACONESS HOSP,DEPT REHABIL SERV,BOSTON,MA 02215. NEW ENGLAND DEACONESS HOSP,DIV GEN INTERNAL MED,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT REHABIL SERV,MED SERV,ARTHRIT UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT REHABIL SERV,BOSTON,MA 02115. BOSTON UNIV,DEPT HLTH SCI,BOSTON,MA 02215. NR 41 TC 28 Z9 30 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD OCT PY 1993 VL 36 IS 10 BP 1429 EP 1443 DI 10.1002/art.1780361016 PG 15 WC Rheumatology SC Rheumatology GA MC066 UT WOS:A1993MC06600015 PM 8216403 ER PT J AU ZARINS, B AF ZARINS, B TI ARTHROSCOPIC REPAIR OF A TYPE-IV SLAP LESION - THE RED-ON-WHITE LESION AS A COMPONENT OF ANTERIOR INSTABILITY - REVIEW SO ARTHROSCOPY LA English DT Editorial Material RP ZARINS, B (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,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 0749-8063 J9 ARTHROSCOPY JI Arthroscopy PD OCT PY 1993 VL 9 IS 5 BP 493 EP 493 DI 10.1016/S0749-8063(05)80393-7 PG 1 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MD090 UT WOS:A1993MD09000003 ER PT J AU TAKAHASHI, LK RUBIN, WW AF TAKAHASHI, LK RUBIN, WW TI CORTICOSTEROID INDUCTION OF THREAT-INDUCED BEHAVIORAL-INHIBITION IN PREWEANLING RATS SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID 2-WEEK-OLD RATS; MINERALOCORTICOID RECEPTORS; ULTRASONIC VOCALIZATION; SEXUAL-DIFFERENTIATION; EARLY ADRENALECTOMY; RATTUS-NORVEGICUS; BRAIN GROWTH; GLUCOCORTICOIDS; RESPONSES; ONTOGENY AB Termination of ongoing behavior and assumption of defensive postures when threatened are adaptive characteristics of vertebrates. Altricial rat pups develop these characteristics by 14 days of age. At this time, pups inhibit their ultrasonic vocalizations and freeze when threatened. This emergence of behavioral inhibition is impaired when rats are adrenalectomized (ADX) at 10 days of age. That is, 14-day-old ADX pups exhibit deficits in freezing and continue to emit ultrasounds when confronted by an adult male rat. Studies also showed that removal of adrenal hormones does not potentiate vocalizations or render pups incapable of reducing their ultrasounds. More important, 3.0 mg/kg of corticosterone (CORT), but not lower doses, administered daily to ADX pups restored freezing, with lesser effects on ultrasound inhibition. Disrupting the developmental action of endogenous CORT appears to impair the ontogenetic expression of behavioral inhibition. C1 DUKE UNIV,DEPT NEUROBIOL,DURHAM,NC 27706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [MH-43986] NR 54 TC 51 Z9 51 U1 0 U2 1 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 OCT PY 1993 VL 107 IS 5 BP 860 EP 866 DI 10.1037//0735-7044.107.5.860 PG 7 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA MG763 UT WOS:A1993MG76300013 PM 8280395 ER PT J AU VOGT, JA CHAPMAN, TE WAGNER, DA YOUNG, VR BURKE, JF AF VOGT, JA CHAPMAN, TE WAGNER, DA YOUNG, VR BURKE, JF TI DETERMINATION OF THE ISOTOPE ENRICHMENT OF ONE OR A MIXTURE OF 2 STABLE LABELED TRACERS OF THE SAME COMPOUND USING THE COMPLETE ISOTOPOMER DISTRIBUTION OF AN ION FRAGMENT, THEORY AND APPLICATION TO IN-VIVO HUMAN TRACER STUDIES SO BIOLOGICAL MASS SPECTROMETRY LA English DT Article ID SUBSTRATE TURNOVER RATE; MASS-SPECTROMETRY; GAS-CHROMATOGRAPHY; YOUNG MEN; KINETICS; LEUCINE AB Calculations of flux rates for stable isotope tracer studies are based upon enrichment values of an infused tracer. We propose the determination of enrichment values by gas chromatography/mass spectrometry, which is based on tracer mole fraction and mass spectrometer signals, normalized over the total signal of an ion fragment isotopomer distribution. The method accounts for overlap of the signals of one or two tracers and the tracee, high tracer mole fraction and incomplete labelling of the (infused) tracer. For the single and multiple tracer case a linear relationship between tracer mole fraction (from zero to one) and all normalized mass spectrometer signals is derived. This linearity over the entire range is demonstrated with a single (1-C-13)glucose tracer and for mixtures of (1-C-13)- and (3,3-H-2(2))tyrosine tracers. The linearity allows determination of the tracer mole fraction for two tracers, using multiple linear regression. The corresponding calibration can rely on measurements of the pure tracer and tracee compound, without weighing or check for chemical purity. This is compared with a calibration based on tracer/tracee mixtures. Estimates for the tracer mole fraction are slightly better if based on a calibration, using standard mixtures. In all cases the tracer mole fraction can be determined with high precision (coefficient of variation smaller than 5%) and high accuracy. For tyrosine it is demonstrated that the measurement of seven channels rather than three, for the main isotopomers, does not reduce the precision in the prediction of the tracer mole fraction. Equations are also derived to use the tracer mole fraction to estimate the endogenous production of the tracee under study conditions, assuming a steady state of the host metabolism. C1 SHRINERS BURNS INST,BOSTON,MA 02114. MIT,HUMAN NUTR LAB,CAMBRIDGE,MA 02139. RP VOGT, JA (reprint author), MASSACHUSETTS GEN HOSP,TRAUMA SERV,1 FRUIT ST,BOSTON,MA 02114, USA. NR 26 TC 39 Z9 39 U1 1 U2 3 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 1052-9306 J9 BIOL MASS SPECTROM JI Biol. Mass Spectrom. PD OCT PY 1993 VL 22 IS 10 BP 600 EP 612 DI 10.1002/bms.1200221008 PG 13 WC Biophysics; Spectroscopy SC Biophysics; Spectroscopy GA LY774 UT WOS:A1993LY77400007 PM 8218425 ER PT J AU CAPLAN, D AF CAPLAN, D TI LANGUAGE - STRUCTURE, PROCESSING AND DISORDERS - REPLY SO BIOLOGICAL PSYCHOLOGY LA English DT Note ID MODEL RP CAPLAN, D (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0301-0511 J9 BIOL PSYCHOL JI Biol. Psychol. PD OCT PY 1993 VL 37 IS 1 BP 87 EP 88 DI 10.1016/0301-0511(93)90073-H PG 2 WC Psychology, Biological; Behavioral Sciences; Psychology; Psychology, Experimental SC Psychology; Behavioral Sciences GA ML666 UT WOS:A1993ML66600051 ER PT J AU DALTON, LA MILLER, KW AF DALTON, LA MILLER, KW TI TRANS-UNSATURATED LIPID DYNAMICS - MODULATION OF DIELAIDOYLPHOSPHATIDYLCHOLINE ACYL-CHAIN MOTION BY ETHANOL SO BIOPHYSICAL JOURNAL LA English DT Article ID ELECTRON-PARAMAGNETIC RESONANCE; NUCLEAR MAGNETIC-RESONANCE; INTERDIGITATED GEL PHASE; SATURATION-TRANSFER; SPIN-RESONANCE; PHOSPHOLIPID-MEMBRANES; ROTATIONAL DIFFUSION; MOLECULAR-MOTION; BILAYERS; TEMPERATURE AB Acyl chain dynamics of the trans-unsaturated lipid, dielaidoylphosphatidylcholine (DEPC), were studied by conventional and saturation transfer electron paramagnetic resonance spectroscopy of aqueous dispersions of DEPC spin labeled with lecithins having doxyl groups at positions 5, 10, and 14 on the sn-2 chain. The gel to liquid crystalline transition is concerted with simultaneous increases in rotational motion about the long axis of the acyl chain (libration) and in gauche-trans conformational interconversions (wobble). Relative to saturated lecithins at similar reduced temperatures the double bond (a) slowed libration by an order of magnitude in both phases, while wobble motions were several times slower, and (b) produced a pronounced stiffness of the acyl chain near the double bond. Ethanol (0-1.6 M), in addition to its well-known colligative effect on the phase transition, was found to decrease the bilayer order in a concentration-dependent manner. This effect was smaller in the gel than in the liquid crystalline phase, most pronounced next to the double bond, and weakest deep in the bilayer. Ethanol affected slow motions little in the gel phase but wobble and libration correlation times were markedly decreased in the liquid crystalline phase. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,WHITE BLDG,ROOM 430,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIAAA NIH HHS [R01 AA07040] NR 44 TC 8 Z9 8 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD OCT PY 1993 VL 65 IS 4 BP 1620 EP 1631 PG 12 WC Biophysics SC Biophysics GA MC124 UT WOS:A1993MC12400031 PM 8274650 ER PT J AU SOIFFER, RJ GONIN, R MURRAY, C ROBERTSON, MJ COCHRAN, K CHARTIER, S CAMERON, C DALEY, J LEVINE, H NADLER, LM RITZ, J AF SOIFFER, RJ GONIN, R MURRAY, C ROBERTSON, MJ COCHRAN, K CHARTIER, S CAMERON, C DALEY, J LEVINE, H NADLER, LM RITZ, J TI PREDICTION OF GRAFT-VERSUS-HOST DISEASE BY PHENOTYPIC ANALYSIS OF EARLY IMMUNE RECONSTITUTION AFTER CD6-DEPLETED ALLOGENEIC BONE-MARROW TRANSPLANTATION SO BLOOD LA English DT Article ID LYMPHOCYTES-T; SELECTIVE DEPLETION; RISK-FACTORS; RECIPIENTS; PREVENTION; LEUKEMIA; CORRELATE; ANTIGEN; CELLS; SKIN C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI29530] NR 41 TC 30 Z9 30 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 OCT 1 PY 1993 VL 82 IS 7 BP 2216 EP 2223 PG 8 WC Hematology SC Hematology GA MA663 UT WOS:A1993MA66300040 PM 7691252 ER PT J AU DUKECOHAN, JS MORIMOTO, C SCHLOSSMAN, SF AF DUKECOHAN, JS MORIMOTO, C SCHLOSSMAN, SF TI TARGETING OF AN ACTIVATED T-CELL SUBSET USING A BISPECIFIC ANTIBODY-TOXIN CONJUGATE DIRECTED AGAINST CD4 AND CD26 SO BLOOD LA English DT Article ID MONOCLONAL-ANTIBODIES; ORGAN-TRANSPLANTATION; MOLECULE; CYCLOSPORINE; CYTOTOXICITY; MAINTENANCE; EXPRESSION; DIAGNOSIS; DISEASE; BINDING C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP DUKECOHAN, JS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Duke-Cohan, Jonathan/A-5812-2010 OI Duke-Cohan, Jonathan/0000-0002-9478-9609 FU NIAID NIH HHS [AI-23360-08, AI-29530] NR 34 TC 13 Z9 13 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 1 PY 1993 VL 82 IS 7 BP 2224 EP 2234 PG 11 WC Hematology SC Hematology GA MA663 UT WOS:A1993MA66300041 PM 8104537 ER PT J AU STOREY, E BEAL, MF AF STOREY, E BEAL, MF TI NEUROCHEMICAL SUBSTRATES OF RIGIDITY AND CHOREA IN HUNTINGTONS-DISEASE SO BRAIN LA English DT Article ID STRIATAL PROJECTION NEURONS; DOPAMINE RECEPTOR SUBTYPES; P-LIKE IMMUNOREACTIVITY; BASAL GANGLIA; SUBSTANCE-P; HUMAN-BRAIN; SUBTHALAMIC NUCLEUS; FUNCTIONAL-ANATOMY; NEURAL MECHANISMS; ENKEPHALIN AB Huntington's disease is a progressive degenerative neurological disorder which produces a characteristic movement disorder termed chorea. Although chorea is associated with dysfunction of the basal ganglia, the underlying mechanisms by which dyskinesias such as chorea are produced, are poorly understood. Recent studies in primates have led to experimental models of chorea with postulated involvement of specific neural pathways. In the present study we attempted to determine the validity of the experimental models by measuring concentrations of gamma-aminobutyric acid (GABA), glutamate, substance P and met-enkephalin in the basal ganglia of Huntington's disease patients who manifested either chorea or rigidity/bradykinesia within 6 months of death. We also characterized changes in the Huntington's disease patients according to pathological grade, since this may be a confounding factor. We analysed post-mortem brain tissue from 12 controls, and 11 grade 3 and 12 grade 4 Huntington's disease patients. The grade 3 and 4 cases consisted of eight adult-onset choreic, nine adult-onset rigid and six juvenile-onset rigid patients. We also analysed the putamen and globus pallidus from 11 grade 2 adult onset choreic Huntington's disease patients. A model of chorea based on experimental studies in primates proposes that a loss of striatal GABAergic inhibitory projections to the globus pallidus externa leads to increased activity of the inhibitory globus pallidus externa GABAergic neurons which project to the subthalamic nucleus. It is believed that the loss of GABAergic inputs to the globus pallidus externa precedes a loss of GABAergic input to the globus pallidus interna, which occurs later in the disease and is associated with the development of rigidity and bradykinesia. In the choreic Huntington's disease patients whom we studied, there was a greater loss of GABA in the globus pallidus externa than in the globus pallidus interna, and the globus pallidus interna:globus pallidus externa GABA ratio was significantly increased compared with rigid patients. There were also increases in GABA in the subthalamic nucleus in the choreic patients, although this did not reach significance. A differential loss of met-enkephalin in the globus pallidus externa compared with substance P loss in the globus pallidus interna was not observed in either the choreic patients with advanced disease or the grade II patients. There was a significant increase in GABA concentrations in the ventroanterior nucleus of the thalamus in the choreic patients compared with rigid/bradykinetic patients. These results are in accord with major tenets of proposed models of dyskinesia in experimental animals; however, the finding of increased GABA in the thalamus requires modification of current theories. C1 MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Storey, Elsdon/A-9889-2013 FU DS NIH HHS [NINDS 16367]; NIMH NIH HHS [MH31862] NR 39 TC 76 Z9 78 U1 0 U2 1 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 OCT PY 1993 VL 116 BP 1201 EP 1222 DI 10.1093/brain/116.5.1201 PN 5 PG 22 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MH349 UT WOS:A1993MH34900013 PM 7693298 ER PT J AU SWIERGIEL, AH TAKAHASHI, LK KALIN, NH AF SWIERGIEL, AH TAKAHASHI, LK KALIN, NH TI ATTENUATION OF STRESS-INDUCED BEHAVIOR BY ANTAGONISM OF CORTICOTROPIN-RELEASING FACTOR RECEPTORS IN THE CENTRAL AMYGDALA IN THE RAT SO BRAIN RESEARCH LA English DT Article DE AMYGDALA; CORTICOTROPIN-RELEASING FACTOR; STRESS; DEFENSIVE BEHAVIOR; FREEZING ID LOCUS-CERULEUS; IMMUNOREACTIVE NEURONS; EXPLORATORY-BEHAVIOR; CENTRAL NUCLEUS; BRAIN; CRF; HYPOTHALAMUS; ORGANIZATION; PROJECTIONS; INJECTIONS AB Research suggests that endogenous corticotropin-releasing factor (CRF) in the amygdala plays a role in the expression of stress-induced behavior. This study examined in rats whether antagonism of CRF receptors in the central amygdala (CA) region using alpha-helical CRF9-41, a CRF antagonist, was effective in attenuating the occurrence of stress-induced freezing. Bilateral infusions of 50, 100, or 200 ng of the CRF antagonist were made in the CA region using 33-gauge cannula immediately prior to testing. Freezing was measured in two test conditions. In one condition, the effects of the CRF antagonist on freezing was assessed immediately after exposure to electric foot shock. In the other condition, freezing was examined in shock-experienced rats that were re-exposed to the shock environment. Results suggested that 50 and 100 ng of the CRF antagonist were effective in reducing the duration of freezing in the immediate post-shock period. In addition, the 100 ng dose produced a significant reduction in freezing duration after rats were re-exposed to the shock environment. Collectively, data suggest that antagonizing the action of endogenous CRF in the CA region contributes to a general alleviation of stress-induced freezing. C1 UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NIMH NIH HHS [NIMH MH-40855] NR 34 TC 173 Z9 175 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 OCT 1 PY 1993 VL 623 IS 2 BP 229 EP 234 DI 10.1016/0006-8993(93)91432-R PG 6 WC Neurosciences SC Neurosciences & Neurology GA LY947 UT WOS:A1993LY94700008 PM 8221104 ER PT J AU FONG, DS RAIZMAN, MB AF FONG, DS RAIZMAN, MB TI SPONTANEOUS HYPHEMA ASSOCIATED WITH ANTERIOR UVEITIS SO BRITISH JOURNAL OF OPHTHALMOLOGY LA English DT Article AB Few reports have described hyphaema in association with anterior uveitis. Five cases of anterior chamber haemorrhage are reported in patients with five different anterior uveitic entities: Reiter's syndrome, juvenile chronic arthritis, ankylosing spondylitis, idiopathic anterior uveitis, and herpes simplex. Hyphaema has been reported in association with idiopathic non-granulomatous anterior uveitis, but not with the other four entities. In three cases, iris rubeosis was present. In two cases the patients were taking non-steroidal anti-inflammatory agents. The hyphaemas occurred at times of heightened inflammation and resolved spontaneously without complication in all but one case, a boy with idiopathic uveitis who required surgery to remove the blood. The clinical outcome of these cases provides evidence that conservative medical management is usually sufficient. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FONG, DS (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 10 TC 12 Z9 12 U1 0 U2 1 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-1161 J9 BRIT J OPHTHALMOL JI Br. J. Ophthalmol. PD OCT PY 1993 VL 77 IS 10 BP 635 EP 638 DI 10.1136/bjo.77.10.635 PG 4 WC Ophthalmology SC Ophthalmology GA MA928 UT WOS:A1993MA92800006 PM 8218031 ER PT J AU SAVAGE, AP PICARD, M HOPKINS, CC MALT, RA AF SAVAGE, AP PICARD, M HOPKINS, CC MALT, RA TI COMPLICATIONS AND SURVIVAL OF MULTILUMEN CENTRAL VENOUS CATHETERS USED FOR TOTAL PARENTERAL-NUTRITION SO BRITISH JOURNAL OF SURGERY LA English DT Article ID PULMONARY-ARTERY CATHETERS; 200 CONSECUTIVE PATIENTS; TRIPLE-LUMEN; CARE; INFECTION; SUPPORT; SEPSIS; TEAM AB In a prospective study of 879 triple-lumen catheters, 219 pulmonary artery catheters, 31 double-lumen and six single-lumen catheters used for the administration of total parenteral nutrition over a 1-year period, the overall complication rate was 12.5 per cent (14.7 complications per 1000 catheter-days) and the catheter-related sepsis rate 4.4 per cent (5-2 per 1000 catheter-days). The probability of development of catheter-related sepsis did not increase with the duration of catheterization. There were no differences in the rate of complications associated with 427 catheters changed by replacement at a new site compared with 159 lines changed over a guidewire. These data support the use of multilumen central venous catheters for the administration of total parenteral nutrition. They suggest that a routine weekly change of line is unnecessary; catheters should be changed only on the development of a complication. When it is required, a catheter should be changed by replacement over a guidewire. C1 MASSACHUSETTS GEN HOSP,SURG SERV,NUTR SUPPORT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,INFECT CONTROL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. OI Picard, Michael/0000-0002-9264-3243 NR 23 TC 20 Z9 21 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1323 J9 BRIT J SURG JI Br. J. Surg. PD OCT PY 1993 VL 80 IS 10 BP 1287 EP 1290 DI 10.1002/bjs.1800801021 PG 4 WC Surgery SC Surgery GA MA921 UT WOS:A1993MA92100018 PM 8242300 ER PT J AU MIAKE, Y SHIMODA, S FUKAE, M AOBA, T AF MIAKE, Y SHIMODA, S FUKAE, M AOBA, T TI EPITAXIAL OVERGROWTH OF APATITE CRYSTALS ON THE THIN-RIBBON PRECURSOR AT EARLY STAGES OF PORCINE ENAMEL MINERALIZATION SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE ENAMEL; AMELOGENESIS; CRYSTAL GROWTH; CALCIUM PHOSPHATES; BIOMINERALIZATION ID RESOLUTION ELECTRON-MICROSCOPY; OCTACALCIUM PHOSPHATE; CALCIUM-PHOSPHATE; MODEL SYSTEM; AMELOGENESIS; MORPHOLOGY; GROWTH; HYDROXYAPATITE; TRANSPORT; PHASES AB The aim of the present work was to investigate changes in cross-sectional morphologies of enamel crystallites as a function of location in secretory porcine enamel. Enamel tissues were obtained from 5- to 6-month-old slaughtered piglets. For examination by electron microscopy, a portion of the secretory enamel was embedded in resin and ultrathin sections were prepared with a diamond knife. In parallel studies, compositional and structural changes of enamel mineral were assessed by chemical analysis and Fourier transform infrared (FTIR) spectroscopy. For this purpose, two consecutive layers of the outer secretory enamel, each approximately 30 mum thick, were separated from the labial side of permanent incisors. Using high-resolution electron microscopy, early events of enamel crystal growth were characterized as the epitaxial growth of small apatite units on the lateral surfaces of the initially precipitated thin ribbon. These apatite units had regular triangle or trapezoid cross-sections. After fusions of those isolated trapezoids on both lateral sides of the platy template, the resulting enamel crystallites had the well-documented flattened-hexagonal shapes in cross-sections. The initially precipitated thin plate was buried inside the overgrown apatite lamella and then retained as a central dark line. Similar morphological evidence for the epitaxial nucleation and overgrowth of carbon-atoapatite on the platy template was obtained in vitro. Chemical and FTIR analyses of the enamel layer samples showed that the characteristics of the youngest enamel mineral were distinct from those of enamel crystals found in older secretory enamel. The overall results support the concept that initial enamel mineralization comprises two events: the initial precipitation of thin ribbons and the subsequent epitaxial growth of apatite crystals on the two-dimensional octacalcium phosphate-like precursor. C1 FORSYTH DENT CTR,BOSTON,MA 02115. TOKYO DENT COLL,CHIBA,JAPAN. TSURUMI UNIV,SCH DENT,YOKOHAMA 230,JAPAN. FU NIDCR NIH HHS [DE07623, DE08670] NR 32 TC 72 Z9 78 U1 1 U2 8 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD OCT PY 1993 VL 53 IS 4 BP 249 EP 256 DI 10.1007/BF01320910 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LX472 UT WOS:A1993LX47200007 PM 8275353 ER PT J AU TEICHER, BA HOLDEN, SA MENON, K HOPKINS, RE GAWRYL, MS AF TEICHER, BA HOLDEN, SA MENON, K HOPKINS, RE GAWRYL, MS TI EFFECT OF HEMOGLOBIN SOLUTION ON THE RESPONSE OF INTRACRANIAL AND SUBCUTANEOUS 9L TUMORS TO ANTITUMOR ALKYLATING-AGENTS SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE HEMOGLOBIN SOLUTION; ALKYLATING AGENTS; INTRACRANIAL TUMORS ID BRAIN-TUMORS; RADIATION-THERAPY; BOVINE HEMOGLOBIN; FSAIIC FIBROSARCOMA; FLUOSOL-DA; CHEMOTHERAPY; CHILDREN; 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA; MEDULLOBLASTOMA; OXYGENATION AB The 9L gliosarcoma growing subcutaneously in the hind leg of the Fisher 344 rat contains major areas of severe (<5 mmHg) hypoxia, making up about 49% of the tumor. Intravenous administration of an ultrapurified polymerized bovine hemoglobin solution (8 ml/kg) along with normal air breathing reduces the percentage of severe hypoxia to about 24% and increases oxygenation throughout the tumor. Coadministration of the hemoglobin solution increased the tumor growth delay of subcutaneously implanted 9L tumors treated with carmustine (BCNU), cyclophosphamide, or ifosfamide but did not significantly change the tumor growth delay produced by cisplatin (CDDP). Coadministration of the hemoglobin solution with each of the four antitumor alkylating agents resulted in a near doubling of the percentage of increase in life span in animals bearing intracranial tumors treated with the combination as compared with animals treated with the drugs alone. Increases in serum blood urea nitrogen (BUN) and creatinine levels in treated animals returned to normal by 11 days posttreatment. Major changes in liver enzymes occurred with the combination of cyclophosphamide and the hemoglobin solution at 4 days posttreatment; however, these values returned to the levels in the untreated control animals within 1 week thereafter. These results indicate that further exploration of the use of hemoglobin solutions in cancer therapy is warranted. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. BIOPURE CORP,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 [NCI PO1-CA38493] NR 38 TC 20 Z9 20 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 OCT PY 1993 VL 33 IS 1 BP 57 EP 62 DI 10.1007/BF00686024 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA MC707 UT WOS:A1993MC70700010 PM 8269590 ER PT J AU MASHAL, RD LESTER, SC SKLAR, J AF MASHAL, RD LESTER, SC SKLAR, J TI CLONAL ANALYSIS BY STUDY OF X-CHROMOSOME INACTIVATION IN FORMALIN-FIXED PARAFFIN-EMBEDDED TISSUE SO CANCER RESEARCH LA English DT Article ID POLYMERASE CHAIN-REACTION; HUMAN ANDROGEN-RECEPTOR; HUMAN-TUMORS; DNA; POLYMORPHISMS; AMPLIFICATION; SPECIMENS; ORIGIN; GENE; SIZE AB Analysis of clonality by X chromosome inactivation has proven to be a powerful strategy in the study of neoplastic and preneoplastic disorders (P. J. Fialkow, Biochim. Biophys. Acta, 458: 283-321, 1976; B. Vogelstein et al., Cancer Res., 47: 4806-4813, 1987). Recently, the gene for the androgen receptor has been shown to be a highly polymorphic locus in which methylation of DNA correlates with inactivation of one or the other X homologue (R. C. Allen et al., Am. J. Hum. Genet., 51: 1229-1239, 1992). Unlike other loci used for analysis of X inactivation, the methylation sites within the androgen receptor gene lie close to the region of DNA containing the polymorphism. Consequently, it should be possible to use methylation-sensitive restriction enzymes and polymerase chain reaction to study differential methylation among alleles of this gene in formalin-fixed and paraffin-embedded archival tissue specimens. To investigate this question, we performed clonal analysis on a variety of randomly selected, formalin-fixed, paraffin-embedded tumor tissues from 15 women. Thirteen of the women were found to be heterozygous for polymorphisms at the androgen receptor locus. Among these women, 11 tumors were clearly clonal in assays of methylation of the androgen receptor gene. Interpretation of results for the remaining two cases was complicated because of a skewed pattern of X chromosome inactivation found in normal control tissues. We conclude that analysis of methylation in the androgen receptor gene should allow study of clonality in most formalin-fixed, paraffin-embedded tissue specimens from women, including small preneoplastic lesions or rare conditions for which sufficient material is not available for analysis by other techniques. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,DIV MOLEC ONCOL,75 FRANCIS ST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,DIV SURG PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA-01556, CA-58203] NR 22 TC 87 Z9 88 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 1 PY 1993 VL 53 IS 19 BP 4676 EP 4679 PG 4 WC Oncology SC Oncology GA LZ637 UT WOS:A1993LZ63700042 PM 8402645 ER PT J AU WANG, CY STILES, CD AF WANG, CY STILES, CD TI REGULATION OF PLATELET-DERIVED GROWTH FACTOR-A MESSENGER-RNA TRANSLATION IN DIFFERENTIATING F9-TERATOCARCINOMA CELLS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID TERATOCARCINOMA STEM-CELLS; SIMIAN SARCOMA-VIRUS; RETINOIC ACID; FACTOR RECEPTORS; PDGF-A; GENE; EXPRESSION; INDUCTION; SIS; EMBRYOGENESIS AB We have monitored production of platelet-derived growth factor (PDGF) in F9 teratocarcinoma cells. We show that undifferentiated F9 cells express PDGF A mRNA and produce biologically active PDGF AA homodimers. When differentiation is induced by treatment with retinoic acid and cyclic AMP, the production of PDGF AA protein is terminated. Contrary to expectation, inhibition of PDGF synthesis is exerted at a posttranscriptional level. Both undifferentiated and differentiated (1 day) F9 cell cultures contain comparable amounts of PDGF A mRNA. However, this mRNA becomes dissociated from polysomes during F9 cell differentiation. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. NR 37 TC 11 Z9 11 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD OCT PY 1993 VL 4 IS 10 BP 871 EP 877 PG 7 WC Cell Biology SC Cell Biology GA MA997 UT WOS:A1993MA99700009 PM 8274456 ER PT J AU ANDERSEN, JK FRIM, DM ISACSON, O BREAKEFIELD, XO AF ANDERSEN, JK FRIM, DM ISACSON, O BREAKEFIELD, XO TI HERPESVIRUS-MEDIATED GENE DELIVERY INTO THE RAT-BRAIN - SPECIFICITY AND EFFICIENCY OF THE NEURON-SPECIFIC ENOLASE PROMOTER SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE HERPESVIRUS VECTOR; GENE TRANSFER; NEURON-SPECIFIC ENOLASE (NSE) PROMOTER; LACZ; STEREOTAXIC DELIVERY; RAT CNS ID GENETICALLY MODIFIED CELLS; SIMPLEX VIRUS NEUROVIRULENCE; BETA-GALACTOSIDASE; THYMIDINE KINASE; EXPRESSION; LATENT; GANGLIA; IMPLANTATION; INFECTION; VECTORS AB 1. Herpesvirus infection with genetically engineered vectors is a way to deliver foreign gene products to various cell populations in culture and in vivo. Selective neuronal gene expression can be achieved using the neuron-specific enolase (NSE) promoter regulating expression of a transgene placed in and delivered by a herpesvirus vector. 2. We sought to determine the anatomical specificity and efficiency of herpesvirus-mediated gene transfer into the rat brain following placement of virus particles carrying a transgene (lacZ) under control of the NSE promoter. The virus utilized was thymidine kinase (TK) deficient and therefore replication deficient in the brain. 3. Infusion of 10(6) plaque-forming units of virus into the striatum caused a limited number of striatal neurons to express the lacZ transgene mRNA and protein product 7 days postinfection. In addition, small numbers of neurons expressing the transgene mRNA and protein were found ipsilateral to the viral injection in the frontal cortex, substantia nigra pars compacta, and thalamus. Neurons at these anatomic loci project directly to the striatal injection site. No other cells within the brains of injected animals expressed the lacZ gene. 4. While this herpesvirus NSE vector was capable of introducing novel functional genetic information into postmitotic neurons within defined neuroanatomic constraints, the numbers of neurons expressing detectable levels of beta-galactosidase was minimal. The calculated efficiency of delivery and transgene expression at 7 days postinfection was 1 transgenic neuron per 10(4) virus particles infused. 5. We conclude that NSE probably is not an optimal promoter for use in gene delivery to CNS neurons in herpesvirus vectors and that the efficacy of gene delivery using other neuron-specific promoters placed at various sites in the herpes viral genome needs to be explored. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROGENET UNIT,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA. MCLEAN HOSP,NEUROREGENERAT LAB,BELMONT,MA. FU NINDS NIH HHS [NS30064, NS24279, NS29178] NR 47 TC 33 Z9 33 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD OCT PY 1993 VL 13 IS 5 BP 503 EP 515 DI 10.1007/BF00711459 PG 13 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA MM970 UT WOS:A1993MM97000003 PM 8111822 ER PT J AU WILLIAMS, AJ AF WILLIAMS, AJ TI THE NOSE AND OBSTRUCTIVE SLEEP-APNEA SO CHEST LA English DT Editorial Material ID NASAL RESISTANCE; FLOW C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. RP WILLIAMS, AJ (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VA MED CTR, CTR SLEEP DISORDERS, LOS ANGELES, CA USA. NR 11 TC 3 Z9 3 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1993 VL 104 IS 4 BP 993 EP 993 PG 1 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MC283 UT WOS:A1993MC28300004 PM 8404236 ER PT J AU KINANE, BT MANSELL, AL ZWERDLING, RG LAPEY, A SHANNON, DC AF KINANE, BT MANSELL, AL ZWERDLING, RG LAPEY, A SHANNON, DC TI FOLLICULAR BRONCHITIS IN THE PEDIATRIC POPULATION SO CHEST LA English DT Article AB Five patients in a pediatric population were identified with idiopathic follicular bronchitis (IFB) by open lung biopsy and their case records were reviewed. All were tachypneic and had a chronic cough by 6 weeks of age. The physical examination was characterized by diffuse fine crackles in four patients and by coarse rhonchi in one. The chest radiographs in all demonstrated a diffuse interstitial pattern. None had a collagen vascular or an autoimmune disease demonstrable. Response to corticosteroid therapy was minimal. Associated or coincidental esophageal reflux was treated surgically in two. No viral or bacterial agents were isolated in the sputum or the biopsy specimens. Patients have been followed up for 2 to 15 years; the conditions of all patients improved at about 2 to 4 years of age. The older patients have residual mild obstructive lung disease. To our knowledge, this is the first reported series of IFB in the pediatric population. C1 UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA 01605. RHODE ISL HOSP,DEPT PEDIAT,PROVIDENCE,RI 02902. RP KINANE, BT (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,PEDIAT PULM UNIT,BOSTON,MA 02114, USA. NR 7 TC 32 Z9 33 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 OCT PY 1993 VL 104 IS 4 BP 1183 EP 1186 DI 10.1378/chest.104.4.1183 PG 4 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MC283 UT WOS:A1993MC28300042 PM 8404188 ER PT J AU PAUL, SD LITALIEN, GJ HENDEL, RC LEPPO, JA EAGLE, KA AF PAUL, SD LITALIEN, GJ HENDEL, RC LEPPO, JA EAGLE, KA TI LONG-TERM PROGNOSIS AFTER GERIATRIC VASCULAR-SURGERY - DOES PREOPERATIVE CLINICAL-EVALUATION AND DIPYRIDAMOLE-THALLIUM TESTING MAKE A DIFFERENCE SO CIRCULATION LA English DT Meeting Abstract C1 UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA 01605. 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 11 EP 11 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200096 ER PT J AU SCHWAMMENTHAL, E CHEN, CG SAGIE, A DEPRADA, JV GUERRERO, JL WEYMAN, AE LEVINE, RA AF SCHWAMMENTHAL, E CHEN, CG SAGIE, A DEPRADA, JV GUERRERO, JL WEYMAN, AE LEVINE, RA TI AN OBJECTIVE METHOD TO DERIVE THE OPTIMAL ALIAS VELOCITY FOR FLOW-RATE CALCULATION FROM ANALYSIS OF THE PROXIMAL FLOW-FIELD SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 26 EP 26 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200168 ER PT J AU OSSWALD, S TROUTON, TG ONUNAIN, SS ROELKE, M SOSASUAREZ, GE MCGOVERN, BA GARAN, H RUSKIN, JN BROOKS, R AF OSSWALD, S TROUTON, TG ONUNAIN, SS ROELKE, M SOSASUAREZ, GE MCGOVERN, BA GARAN, H RUSKIN, JN BROOKS, R TI ELECTROCARDIOGRAPHIC PSEUDO-INFARCT PATTERN AFTER IMPLANTATION OF INTERNAL CARDIOVERTER-DEFIBRILLATOR SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 54 EP 54 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200318 ER PT J AU OSSWALD, S TROUTON, TG HOLDEN, HB ONUNAIN, SS GARAN, H RUSKIN, JN AF OSSWALD, S TROUTON, TG HOLDEN, HB ONUNAIN, SS GARAN, H RUSKIN, JN TI MYOCARDIAL ELECTRICAL INJURY - DEPRESSION OF OXIDATIVE-METABOLISM AFTER INTERNAL COUNTERSHOCK DURING SINUS RHYTHM IN A CANINE MODEL SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 61 EP 61 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200358 ER PT J AU JIANG, L DEPRADA, JV HE, J PADIAL, LR FALLON, JT KING, ME LEVINE, RA AF JIANG, L DEPRADA, JV HE, J PADIAL, LR FALLON, JT KING, ME LEVINE, RA TI QUANTITATIVE ASSESSMENT OF STENOTIC AORTIC-VALVE AREA USING INTRAVASCULAR ECHOCARDIOGRAPHY - IN-VITRO VALIDATION SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 103 EP 103 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200584 ER PT J AU TICHO, BS STAINIER, DYR FISHMAN, MC BREITBART, RE AF TICHO, BS STAINIER, DYR FISHMAN, MC BREITBART, RE TI MEF2 FACTORS FROM ZEBRAFISH EMBRYOS AND THEIR ROLE IN EARLY CARDIAC DEVELOPMENT SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 129 EP 129 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200724 ER PT J AU FILIPPOV, G BLOCH, KD AF FILIPPOV, G BLOCH, KD TI SOLUBLE GUANYLATE-CYCLASE GENE-EXPRESSION IS DECREASED IN CULTURED RAT AORTIC SMOOTH-MUSCLE CELLS EXPOSED TO CYTOKINES SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 141 EP 141 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200790 ER PT J AU PICARD, MH HOCHMAN, JS HAHN, R VUILLE, C PALMERI, S SONNENBLICK, EH LEJEMTEL, T AF PICARD, MH HOCHMAN, JS HAHN, R VUILLE, C PALMERI, S SONNENBLICK, EH LEJEMTEL, T TI TIMING AND MAGNITUDE OF VENTRICULAR DILATION FOLLOWING THROMBOLYTIC THERAPY IN ACUTE ANTERIOR MYOCARDIAL-INFARCTION SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CAPTAIN STUDY,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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 158 EP 158 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200879 ER PT J AU DEPRADA, JV PADIAL, LR CHEN, MH LENG, JA JUN, H KING, ME WEYMAN, AE CHEN, CG AF DEPRADA, JV PADIAL, LR CHEN, MH LENG, JA JUN, H KING, ME WEYMAN, AE CHEN, CG TI ASSESSMENT OF RIGHT-VENTRICULAR VOLUME USING A NEW 10MHZ INTRACARDIAC ULTRASOUND CATHETER - AN IN-VITRO VALIDATION-STUDY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 160 EP 160 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200892 ER PT J AU LENG, JA DEPRADA, JV GUERRERO, JL HANDSCHUMACHER, MD PICARD, MH FALLON, JT WEYMAN, AE LEVINE, RA AF LENG, JA DEPRADA, JV GUERRERO, JL HANDSCHUMACHER, MD PICARD, MH FALLON, JT WEYMAN, AE LEVINE, RA TI QUANTITATIVE 3-DIMENSIONAL RECONSTRUCTION OF ANEURYSMAL LEFT-VENTRICLES - IN-VITRO AND IN-VIVO VALIDATION SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 160 EP 160 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200891 ER PT J AU CHEN, CG GUERRERO, L DEPRADA, JV SCHWAMMENTHAL, E PADIAL, LR LENG, JA HELGE, S SVIZZERO, T WEYMAN, AE AF CHEN, CG GUERRERO, L DEPRADA, JV SCHWAMMENTHAL, E PADIAL, LR LENG, JA HELGE, S SVIZZERO, T WEYMAN, AE TI INTRACARDIAC ULTRASOUND MEASUREMENT OF VOLUMES AND FUNCTION IN NORMAL AND INFARCTED ANEURYSMAL LEFT-VENTRICLES - IN-VIVO VALIDATION SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 161 EP 161 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200898 ER PT J AU CHEN, MH PADIAL, L LENG, JA WEYMAN, A CHEN, CG AF CHEN, MH PADIAL, L LENG, JA WEYMAN, A CHEN, CG TI FEASIBILITY AND ACCURACY OF QUANTIFYING LEFT-VENTRICULAR MASS WITH USE OF A 10-MHZ INTRACARDIAC ULTRASOUND CATHETER SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 161 EP 161 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200893 ER PT J AU LENG, JA MORRISSEY, R HANDSCHUMACHER, MD HE, J PICARD, MH WEYMAN, AE LEVINE, RA AF LENG, JA MORRISSEY, R HANDSCHUMACHER, MD HE, J PICARD, MH WEYMAN, AE LEVINE, RA TI CAN ACOUSTIC QUANTIFICATION BE APPLIED TO 3-DIMENSIONAL ECHOCARDIOGRAPHIC RECONSTRUCTION SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 161 EP 161 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200897 ER PT J AU CHEN, CG GUERRERO, JL PADIAL, LR DEPRADA, JV SIMON, H SVIZZERO, T LEVINE, RA AF CHEN, CG GUERRERO, JL PADIAL, LR DEPRADA, JV SIMON, H SVIZZERO, T LEVINE, RA TI CONTRAST INTRACARDIAC ULTRASOUND QUANTIFICATION OF CORONARY PERFUSION TERRITORY USING A 10-MHZ ULTRASOUND CATHETER SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 163 EP 163 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200909 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 CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 4 Z9 4 U1 0 U2 4 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 190 EP 190 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201053 ER PT J AU SMITH, AJC GOLD, HK WERNER, W HOLT, R FITZPATRICK, K BOVILL, EG FUSTER, V JANG, IK AF SMITH, AJC GOLD, HK WERNER, W HOLT, R FITZPATRICK, K BOVILL, EG FUSTER, V JANG, IK TI TRANSIENT HYPERCOAGULABLE STATE AFTER ABRUPT DISCONTINUATION OF HEPARIN IN PATIENTS UNDERGOING PERCUTANEOUS CORONARY ANGIOPLASTY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. NR 0 TC 2 Z9 2 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 OCT PY 1993 VL 88 IS 4 BP 209 EP 209 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201155 ER PT J AU CARTER, ME GULICK, T MOORE, DD KELLY, DP AF CARTER, ME GULICK, T MOORE, DD KELLY, DP TI MODULATION OF TRANSCRIPTION BY COMPETITIVE INTERACTION OF NUCLEAR RECEPTORS ON A PLEIOTROPIC ELEMENT IN THE MEDIUM-CHAIN ACYL-COA DEHYDROGENASE (MCAD) GENE SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. WASHINGTON UNIV,ST LOUIS,MO 63130. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 234 EP 234 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201290 ER PT J AU GULICK, T CRESCI, S CARTER, ME CAIRA, T MOORE, DD KELLY, DP AF GULICK, T CRESCI, S CARTER, ME CAIRA, T MOORE, DD KELLY, DP TI FATTY-ACIDS REGULATE MITOCHONDRIAL FATTY-ACID BETA-OXIDATION GENE-EXPRESSION THROUGH NUCLEAR RECEPTOR TRANSCRIPTION FACTORS SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. WASHINGTON UNIV,ST LOUIS,MO 63130. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 234 EP 234 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201291 ER PT J AU NARULA, J PETROV, A DITLOW, C CHEN, F KHAW, BA AF NARULA, J PETROV, A DITLOW, C CHEN, F KHAW, BA TI LOCALIZATION OF EXPERIMENTAL ATHEROSCLEROTIC LESIONS WITH NEGATIVELY-CHARGED POLYMER-MODIFIED CHIMERIC ANTIBODY SPECIFIC FOR PROLIFERATING NEOINTIMAL SMOOTH-MUSCLE CELLS SO CIRCULATION LA English DT Meeting Abstract C1 NORTHEASTERN UNIV,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SCOTGEN,MENLO PK,CA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 250 EP 250 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201381 ER PT J AU ROLLER, M PERRY, C SUTTON, JM GRAMBOW, D KANDALWAL, M PALACIOS, I ROSENSCHEIN, U AF ROLLER, M PERRY, C SUTTON, JM GRAMBOW, D KANDALWAL, M PALACIOS, I ROSENSCHEIN, U TI UROKINASE THERAPY IN THE CATHETERIZATION LABORATORY IS ASSOCIATED WITH HIGH-RATE OF BLEEDING SO CIRCULATION LA English DT Meeting Abstract C1 CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MICHIGAN,ANN ARBOR,MI 48109. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 252 EP 252 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201392 ER PT J AU SHAH, PK FALK, E BADIMON, JJ LEVY, G ORTIZ, AF FALLON, J FUSTER, V AF SHAH, PK FALK, E BADIMON, JJ LEVY, G ORTIZ, AF FALLON, J FUSTER, V TI HUMAN MONOCYTE-DERIVED MACROPHAGES EXPRESS COLLAGENASE AND INDUCE COLLAGEN BREAKDOWN IN ATHEROSCLEROTIC FIBROUS CAPS - IMPLICATIONS FOR PLAQUE RUPTURE SO CIRCULATION LA English DT Meeting Abstract C1 CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 10 Z9 10 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 OCT PY 1993 VL 88 IS 4 BP 254 EP 254 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201401 ER PT J AU GARABEDIAN, HD GOLD, HK HAGSTROM, JN COLLEN, D BOVILL, EG AF GARABEDIAN, HD GOLD, HK HAGSTROM, JN COLLEN, D BOVILL, EG TI ACCELERATED THROMBIN GENERATION ACCOMPANYING SPECIFIC THROMBIN INHIBITION IN UNSTABLE ANGINA PATIENTS SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV VERMONT,COLL MED,BURLINGTON,VT. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 264 EP 264 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201459 ER PT J AU CANNON, MB VINE, AJ ALLYN, JW TORCHIANA, DF KANTOR, HL TITUS, JS PELTON, M TEPLICK, RS GEFFIN, GA DAGGETT, WM AF CANNON, MB VINE, AJ ALLYN, JW TORCHIANA, DF KANTOR, HL TITUS, JS PELTON, M TEPLICK, RS GEFFIN, GA DAGGETT, WM TI WARM AND COLD BLOOD CARDIOPLEGIA - A COMPARISON OF MYOCARDIAL-FUNCTION AND METABOLISM UTILIZING 31-PHOSPHORUS MAGNETIC-RESONANCE SPECTROSCOPY SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 289 EP 289 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201582 ER PT J AU RIHAL, CS MICKEL, M EAGLE, KA GERSH, BJ AF RIHAL, CS MICKEL, M EAGLE, KA GERSH, BJ TI SURGERY FOR PATIENTS IN THE CORONARY-ARTERY SURGERY STUDY REGISTRY WITH COMBINED CORONARY AND PERIPHERAL VASCULAR-DISEASE SO CIRCULATION LA English DT Meeting Abstract C1 UNIV WASHINGTON,SEATTLE,WA 98195. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 297 EP 297 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201627 ER PT J AU FERNANDEZORTIZ, A MEYER, BJ MAILHAC, A CHESEBRO, JH BADIMON, L HASSINGER, N OWEN, WG FUSTER, V BADIMON, JJ AF FERNANDEZORTIZ, A MEYER, BJ MAILHAC, A CHESEBRO, JH BADIMON, L HASSINGER, N OWEN, WG FUSTER, V BADIMON, JJ TI INTRAVASCULAR LOCAL-DELIVERY - AN IONTOPHORETIC APPROACH SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI BADIMON, LINA/O-4711-2014 OI BADIMON, LINA/0000-0002-9162-2459 NR 0 TC 2 Z9 2 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 OCT PY 1993 VL 88 IS 4 BP 309 EP 309 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201693 ER PT J AU MORENO, PR JANG, IK BLOCK, PC PALACIOS, IF AF MORENO, PR JANG, IK BLOCK, PC PALACIOS, IF TI LONG-TERM FOLLOW-UP OF PERCUTANEOUS AORTIC BALLOON VALVULOPLASTY IN THE ELDERLY - THE MASSACHUSETTS-GENERAL-HOSPITAL EXPERIENCE SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 340 EP 340 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201859 ER PT J AU PALACIOS, IF BLOCK, PC HARRELL, L FISHER, G WEYMAN, AE AF PALACIOS, IF BLOCK, PC HARRELL, L FISHER, G WEYMAN, AE TI LONG-TERM FOLLOW-UP OF PATIENTS UNDERGOING PERCUTANEOUS MITRAL BALLOON VALVOTOMY - THE MASSACHUSETTS-GENERAL-HOSPITAL EXPERIENCE SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 340 EP 340 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201862 ER PT J AU SAGIE, A SCHWAMMENTHAL, E HARRELL, L WEYMAN, AE PALACIOS, IF AF SAGIE, A SCHWAMMENTHAL, E HARRELL, L WEYMAN, AE PALACIOS, IF TI SIGNIFICANT TRICUSPID REGURGITATION IS A MARKER FOR ADVERSE OUTCOME IN PATIENTS UNDERGOING MITRAL BALLOON VALVOTOMY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 340 EP 340 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201861 ER PT J AU CHEN, MH SEMIGRAN, MJ HARRELL, L PALACIOS, IF AF CHEN, MH SEMIGRAN, MJ HARRELL, L PALACIOS, IF TI RELATIONSHIP OF PULMONARY-ARTERY RESISTANCE TO SHORT-TERM SUCCESS AND LONG-TERM SURVIVAL AFTER PERCUTANEOUS MITRAL VALVULOPLASTY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 341 EP 341 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201863 ER PT J AU SEMIGRAN, MJ CHEN, MH HARRELL, L PALACIOS, IF AF SEMIGRAN, MJ CHEN, MH HARRELL, L PALACIOS, IF TI EFFECTIVE BALLOON DILATING AREA PREDICTS THE DEVELOPMENT OF MITRAL REGURGITATION AND NEED FOR SURGERY IN PATIENTS UNDERGOING PERCUTANEOUS MITRAL VALVULOPLASTY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 351 EP 351 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68201920 ER PT J AU CANNISTRA, LB DAVIDOFF, R PICARD, MH OMALLEY, CJ DEMPSEY, AL RYAN, TJ BALADY, GJ AF CANNISTRA, LB DAVIDOFF, R PICARD, MH OMALLEY, CJ DEMPSEY, AL RYAN, TJ BALADY, GJ TI DOES EXERCISE TRAINING AFFECT LEFT-VENTRICULAR REMODELING AFTER MYOCARDIAL-INFARCTION SO CIRCULATION LA English DT Meeting Abstract C1 BOSTON UNIV,MED CTR,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 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 OCT PY 1993 VL 88 IS 4 BP 406 EP 406 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202216 ER PT J AU LEWANDOWSKI, ED WHITE, LT AF LEWANDOWSKI, ED WHITE, LT TI DIFFERENCES IN CARBON FLUX FROM LACTATE VERSUS PYRUVATE DURING STIMULATED OXIDATION BY INTACT HEARTS SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 427 EP 427 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202332 ER PT J AU BADIMON, JJ WENG, D CHESEBRO, JH FUSTER, V BADIMON, L AF BADIMON, JJ WENG, D CHESEBRO, JH FUSTER, V BADIMON, L TI COMBINED SPECIFIC THROMBIN AND CYCLOOXYGENASE INHIBITION REDUCES ARTERIAL PLATELET DEPOSITION MORE EFFECTIVELY THAN EITHER ALONE AT HIGH-SHEAR RATE SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RI BADIMON, LINA/O-4711-2014 OI BADIMON, LINA/0000-0002-9162-2459 NR 0 TC 0 Z9 0 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 OCT PY 1993 VL 88 IS 4 BP 458 EP 458 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202499 ER PT J AU LI, HM FREEMAN, M LIBBY, P AF LI, HM FREEMAN, M LIBBY, P TI REGULATION OF SMOOTH-MUSCLE CELL SCAVENGER RECEPTOR EXPRESSION IN-VIVO BY ATHEROGENIC DIETS AND IN-VITRO BY CYTOKINES SO CIRCULATION LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 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 OCT PY 1993 VL 88 IS 4 BP 464 EP 464 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202532 ER PT J AU KAWAI, N FILIPPOV, G RABKINA, DJ SUEN, HC JANSSENS, SP BLOCH, DB BLOCH, KD AF KAWAI, N FILIPPOV, G RABKINA, DJ SUEN, HC JANSSENS, SP BLOCH, DB BLOCH, KD TI CONSTITUTIVE ENDOTHELIAL NITRIC-OXIDE SYNTHASE GENE-EXPRESSION IN RAT LUNG IS DEVELOPMENTALLY-REGULATED SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 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 OCT PY 1993 VL 88 IS 4 BP 477 EP 477 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202600 ER PT J AU PAUL, SD EAGLE, KA OGARA, PT AF PAUL, SD EAGLE, KA OGARA, PT TI WEEKLY RHYTHM OF ACUTE MYOCARDIAL-INFARCTION - ARE PHYSICIANS MORE AGGRESSIVE WITH THROMBOLYSIS AFTER THE WEEKEND SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 509 EP 509 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202774 ER PT J AU TOUSSAINT, JF SOUTHERN, JF FALK, E FUSTER, V KANTOR, HL AF TOUSSAINT, JF SOUTHERN, JF FALK, E FUSTER, V KANTOR, HL TI ATHEROSCLEROTIC PLAQUE COMPONENTS IMAGED BY NUCLEAR-MAGNETIC-RESONANCE SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 2 Z9 2 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 OCT PY 1993 VL 88 IS 4 BP 520 EP 520 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202832 ER PT J AU HAJJAR, RJ GWATHMEY, JK AF HAJJAR, RJ GWATHMEY, JK TI DIFFERENTIAL-EFFECTS OF P(I) AND PH ON CA2+-ACTIVATION IN NONFAILING AND FAILING HUMAN HEARTS SO CIRCULATION LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 542 EP 542 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68202955 ER PT J AU CARROLL, DL AF CARROLL, DL TI RECOVERY IN THE ELDERLY AFTER CORONARY-ARTERY BYPASS-SURGERY SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 578 EP 578 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68203142 ER PT J AU MENDES, LA PICARD, MH DEC, GW PALACIOS, IF RYAN, TJ DAVIDOFF, R AF MENDES, LA PICARD, MH DEC, GW PALACIOS, IF RYAN, TJ DAVIDOFF, R TI LEFT-VENTRICULAR SPHERICITY IN ACTIVE MYOCARDITIS SO CIRCULATION LA English DT Meeting Abstract C1 BOSTON UNIV,MED CTR,BOSTON,MA 02215. 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 599 EP 599 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68203253 ER PT J AU SIU, SC RIVERA, JM GUERRERO, JL HANDSCHUMACHER, MD LETHOR, JP WEYMAN, AE LEVINE, RA PICARD, MH AF SIU, SC RIVERA, JM GUERRERO, JL HANDSCHUMACHER, MD LETHOR, JP WEYMAN, AE LEVINE, RA PICARD, MH TI 3-DIMENSIONAL ECHOCARDIOGRAPHY - IN-VIVO VALIDATION FOR LEFT-VENTRICULAR VOLUME AND FUNCTION SO CIRCULATION LA English DT Article DE ECHOCARDIOGRAPHY; LEFT VENTRICLE; ULTRASOUND ID CARDIAC-OUTPUT; MITRAL-VALVE; RECONSTRUCTION; THERMODILUTION; REGURGITATION; PERFORMANCE; OVERLOAD; FLOW AB Background. Current two-dimensional quantitative echocardiographic methods of volume assessment require image acquisition from standardized scanning planes. Left ventricular volume and ejection fraction are then calculated by assuming ventricular symmetry and geometry. These assumptions may not be valid in distorted ventricles. Three-dimensional echocardiography can quantify left ventricular volume without the limitations imposed by the assumptions of two-dimensional methods. We have developed a three-dimensional system that automatically integrates two-dimensional echocardiographic images and their positions in real time and calculates left ventricular volume directly from traced endocardial contours without geometric assumptions. Methods and Results. To study the accuracy of this method in quantifying left ventricular volume and performance in vivo, a canine model was developed in which instantaneous left ventricular volume can be measured directly with an intracavitary balloon connected to an external column. Ten dogs were studied at 84 different cavity volumes (4 to 85 cm3) and in conditions of altered left ventricular shape produced by either coronary occlusion or right ventricular volume overload. To demonstrate clinical feasibility, 19 adult human subjects were then studied by this method for quantification of stroke volume. Left ventricular volume, stroke volume, and ejection fraction calculated by three-dimensional echocardiography correlated well with directly measured values (r=.98, .96, .96 for volume, stroke volume, and ejection fraction, respectively) and agreed closely with them (mean difference, -0.78 cm3, -0.60 cm3, -0.32%). In humans, there was a good correlation (r=.94, SEE=4.29 cm3) and agreement (mean difference, -0.98+/-4.2 cm3) between three-dimensional echocardiography and Doppler-derived stroke volumes. Conclusions. Three-dimensional echocardiography allows accurate assessment of left ventricular volume and systolic function. C1 MASSACHUSETTS GEN HOSP, CARDIAC UNIT, CARDIAC ULTRASOUND LAB, FRUIT ST, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RI rivera, miguel/D-5026-2014; Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 FU NHLBI NIH HHS [HL-38176] NR 35 TC 125 Z9 130 U1 0 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 1715 EP 1723 PN 1 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA678 UT WOS:A1993MA67800034 PM 8403317 ER PT J AU TANAKA, H SUKHOVA, GK SWANSON, SJ CLINTON, SK GANZ, P CYBULSKY, MI LIBBY, P AF TANAKA, H SUKHOVA, GK SWANSON, SJ CLINTON, SK GANZ, P CYBULSKY, MI LIBBY, P TI SUSTAINED ACTIVATION OF VASCULAR CELLS AND LEUKOCYTES IN THE RABBIT AORTA AFTER BALLOON INJURY SO CIRCULATION LA English DT Article DE ENDOTHELIAL CELLS; SMOOTH MUSCLE CELLS; VASCULAR CELL ADHESION MOLECULE-1; INTERCELLULAR ADHESION MOLECULE-1; ANGIOPLASTY ID SMOOTH-MUSCLE CELLS; LUMINAL CORONARY ANGIOPLASTY; FIBROBLAST GROWTH-FACTOR; HUMAN-ENDOTHELIAL CELLS; GENE-EXPRESSION; IMMUNE INTERFERON; CAROTID-ARTERY; MESSENGER-RNA; TIME COURSE; PROLIFERATION AB Background. To improve understanding of the cellular basis of the arterial response to injury, we tested whether balloon withdrawal can induce certain inflammatory functions of vascular cells and leukocytes and whether such ''activation'' persists even after the acute phase of injury. Methods and Results. We examined the expression of several inducible cell surface molecules in the rabbit aorta at 2, 5, 10, and 30 days after balloon injury. Longitudinal sections encompassing parts of the uninjured, border, and injured zones were examined for expression of vascular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), class II major histocompatibility (MHC) antigens, and markers for smooth muscle cells (SMCs), macrophages, endothelial cells, and T-lymphocytes. Endothelial cell healing involved true endothelial regeneration as well as migration, as shown by nuclear incorporation of bromodeoxyuridine. Luminal endothelial cells at the leading edge of repopulation at each time point expressed VCAM-1. As healing progressed, VCAM-1 expression decreased in the regenerated endothelial cells. The neointimal endothelium also expressed high levels of ICAM-1 that persisted longer than the elevation of VCAM-1. SMCs in the neointima also showed increased levels of ICAM-1. Some neointimal endothelial cells, SMCs, and macrophages also expressed high levels of class II MHC antigens during 30 days after injury. Conclusions. Local inflammatory activation of endothelial cells, SMCs, and leukocytes occurs in a predictable sequence and persists up to 30 days after balloon injury to the rabbit aorta. Our findings suggest that ongoing local signals persisting after the original balloon injury may contribute to later phases of intimal thickening. C1 BRIGHAM & WOMENS HOSP,VASC MED & ATHEROSCLEROSIS UNIT,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,VASC RES DIV,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NHLBI NIH HHS [P0-1-HL-48743] NR 46 TC 209 Z9 210 U1 0 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP 1788 EP 1803 PN 1 PG 16 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA678 UT WOS:A1993MA67800043 PM 7691431 ER PT J AU FUSTER, V AF FUSTER, V TI MECHANISMS LEADING TO MYOCARDIAL-INFARCTION - INSIGHTS FROM STUDIES OF VASCULAR BIOLOGY SO CIRCULATION LA English DT Meeting Abstract RP FUSTER, V (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIOVASC UNIT,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 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 OCT PY 1993 VL 88 IS 4 BP A EP B PN 2 PG 0 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200001 ER PT J AU SCHWAMMENTHAL, E CHEN, CG SAGIE, A DEPRADA, JV GUERRERO, JL WEYMAN, AE LEVINE, RA AF SCHWAMMENTHAL, E CHEN, CG SAGIE, A DEPRADA, JV GUERRERO, JL WEYMAN, AE LEVINE, RA TI AN OBJECTIVE METHOD TO DERIVE THE OPTIMAL ALIAS VELOCITY FOR FLOW-RATE CALCULATION FROM ANALYSIS OF THE PROXIMAL FLOW-FIELD SO CIRCULATION 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 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1993 VL 88 IS 4 BP N EP N PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MA682 UT WOS:A1993MA68200037 ER PT J AU REINECKER, HC STEFFEN, M WITTHOEFT, T PFLUEGER, I SCHREIBER, S MACDERMOTT, RP RAEDLER, A AF REINECKER, HC STEFFEN, M WITTHOEFT, T PFLUEGER, I SCHREIBER, S MACDERMOTT, RP RAEDLER, A TI ENHANCED SECRETION OF TUMOR-NECROSIS-FACTOR-ALPHA, IL-6, AND IL-1-BETA BY ISOLATED LAMINA PROPRIA MONONUCLEAR-CELLS FROM PATIENTS WITH ULCERATIVE-COLITIS AND CROHNS-DISEASE SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE TUMOR NECROSIS FACTOR; IL-6; IL-1; ULCERATIVE COLITIS; CROHNS DISEASE; LAMINA PROPRIA MONONUCLEAR CELLS ID INFLAMMATORY BOWEL-DISEASE; COLONY-STIMULATING FACTOR; ADHESION MOLECULE-1; INTERLEUKIN-6 PRODUCTION; RECEPTOR EXPRESSION; ANTIBODY SECRETION; ENDOTHELIAL-CELLS; MESSENGER-RNA; T-CELLS; LYMPHOCYTES AB The perpetuation of inflammation in ulcerative colitis and Crohn's disease may be regulated in part by an increased secretion of proinflammatory cytokines due to either an appropriate response to initial stimulating agents, and/or due to an impaired down-regulation of cytokine secretion. The aim of this study was to determine the secretion patterns of the proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), IL-6 and IL-1beta, from isolated lamina propria mononuclear cells (LPMNC) isolated from colonic biopsies from patients with untreated ulcerative colitis or Crohn's disease. LPMNC isolated from involved inflammatory bowel disease (IBD) mucosa spontaneously produced increased amounts of TNF-alpha, IL-6, and IL-1beta. The TNF-alpha secretion from IBD LPMNC could be further enhanced by pokeweed mitogen stimulation. The secretion patterns of TNF-alpha and IL-1beta by LPMNC from patients with either ulcerative colitis or Crohn's disease demonstrated a close correlation with the degree of tissue involvement and mucosal inflammation. LPMNC from non-involved ulcerative colitis mucosa secreted markedly increased levels of IL-6 compared with non-involved Crohn's disease mucosa or control mucosa. The heightened IL-6 secretion from LPMNC from non-involved ulcerative colitis mucosa without visible or microscopic signs of inflammation indicates that the pathophysiologic mechanisms involved in the initiation of inflammation may differ between ulcerative colitis and Crohn's disease. The determination of proinflammatory cytokine secretion by isolated LPMNC from colonoscopic biopsies may be a sensitive method for monitoring the severity of mucosal inflammation in IBD patients. C1 UNIV PENN,MED CTR,DEPT MED,DIV GASTROENTEROL,PHILADELPHIA,PA 19104. UNIV HAMBURG,UNIV HOSP EPPENDORF,DEPT MED,W-2000 HAMBURG 13,GERMANY. LAHEY CLIN MED CTR,GASTROENTEROL SECT,BURLINGTON,MA. RP REINECKER, HC (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,JACKSON BLDG R719,FRUIT ST,BOSTON,MA 02114, USA. RI Schreiber, Stefan/B-6748-2008 OI Schreiber, Stefan/0000-0003-2254-7771 FU NIDDK NIH HHS [DK-21474] NR 55 TC 613 Z9 620 U1 1 U2 17 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD OCT PY 1993 VL 94 IS 1 BP 174 EP 181 PG 8 WC Immunology SC Immunology GA LZ385 UT WOS:A1993LZ38500031 PM 8403503 ER PT J AU LAUDE, D GOLDMAN, M ESCOURROU, P ELGHOZI, JL AF LAUDE, D GOLDMAN, M ESCOURROU, P ELGHOZI, JL TI EFFECT OF BREATHING PATTERN ON BLOOD-PRESSURE AND HEART-RATE OSCILLATIONS IN HUMANS SO CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY LA English DT Article DE BLOOD PRESSURE; FINGER BLOOD PRESSURE; HEART RATE; PARADOXICAL PULSE; RESPIRATION; RESPIRATORY SINUS ARRHYTHMIA; SYSTOLIC BLOOD PRESSURE; TIDAL VOLUME; VARIABILITY ID RESPIRATORY SINUS ARRHYTHMIA; RATE-VARIABILITY; SPECTRAL-ANALYSIS; ORTHOSTATIC LOAD; FLUCTUATIONS AB 1. The relationships of respiratory sinus arrhythmia (RSA) and respiratory changes in systolic blood pressure (SBP) to tidal volume (V(T)) and breathing frequency (BF), were quantified during voluntary control of V(T) and BF in healthy subjects. 2. Respiration was measured non-invasively with a respiratory inductive plethysmograph, which was calibrated prior to each study while breathing through a pneumotachygraph. Finger arterial blood pressure was measured non-invasively by the Finapres. 3. Heart rate (HR) increased during inspiration, with a nearly fixed time delay for most V(T) and BF approximating 0.9 s. The magnitude of RSA increased with increases in V(T) and with decreases in BF. SBP decreased during inspiration, with a time delay which increased as BF decreased, resulting in a phase delay approximating 160-degrees. The magnitude of the inspiratory fall in SBP increased with increases in V(T). Increased amplitudes of RSA and SBP variation occurred at the lowest BF, consistent with the possibility of interactions between respiratory-related influences and those due to slow waves' of vasomotor tone. 4. The present results are consistent with the conclusion that respiratory effects on SBP are caused by a mechanism other that simply changes in HR. C1 W LOS ANGELES VA MED CTR,PULM SECT,LOS ANGELES,CA. HOP ANTOINE BECLERE,SERV EXPLORAT FONCT,CLAMART,FRANCE. RP LAUDE, D (reprint author), FAC MED NECKER ENFANTS MALAD,PHARMACOL LAB,CNRS,URA 1482,156 RUE VAUGIRARD,F-75015 PARIS,FRANCE. NR 30 TC 49 Z9 50 U1 2 U2 6 PU BLACKWELL SCIENCE PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON VICTORIA 3053, AUSTRALIA SN 0305-1870 J9 CLIN EXP PHARMACOL P JI Clin. Exp. Pharmacol. Physiol. PD OCT PY 1993 VL 20 IS 10 BP 619 EP 626 DI 10.1111/j.1440-1681.1993.tb01643.x PG 8 WC Pharmacology & Pharmacy; Physiology SC Pharmacology & Pharmacy; Physiology GA MD396 UT WOS:A1993MD39600002 PM 8261656 ER PT J AU PARKER, SW AF PARKER, SW TI VESTIBULAR EVALUATION - ELECTRONYSTAGMOGRAPHY, ROTATIONAL TESTING, AND POSTUROGRAPHY SO CLINICAL ELECTROENCEPHALOGRAPHY LA English DT Article DE DYNAMIC POSTUROGRAPHY; ELECTRONYSTAGMOGRAM; ROTATIONAL TESTING; SINUSOIDAL VERTICAL AXIS ROTATION; VISUAL VESTIBULAR INTERACTION ROTATION TESTING ID DYNAMIC POSTUROGRAPHY RP PARKER, SW (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,15 PARKMAN ST,SUITE 835,BOSTON,MA 02114, USA. NR 17 TC 23 Z9 23 U1 0 U2 1 PU CLINICAL EEG PI ELM GROVE PA 850 ELM GROVE RD,SUITE 11, ELM GROVE, WI 53122 SN 0009-9155 J9 CLIN ELECTROENCEPHAL JI Clin. Electroencephalogr. PD OCT PY 1993 VL 24 IS 4 BP 151 EP 159 PG 9 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA MD814 UT WOS:A1993MD81400001 PM 8261636 ER PT J AU WILZ, SW KURNICK, JT PANDOLFI, F RUBIN, RH WARREN, HS GOLDSTEIN, R KERSTEN, CM MCCLUSKEY, RT AF WILZ, SW KURNICK, JT PANDOLFI, F RUBIN, RH WARREN, HS GOLDSTEIN, R KERSTEN, CM MCCLUSKEY, RT TI T-LYMPHOCYTE RESPONSES TO ANTIGENS OF GRAM-NEGATIVE BACTERIA IN PYELONEPHRITIS SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID ESCHERICHIA-COLI; PROTEIN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,149 13TH ST,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02129. BOSTON UNIV,SCH MED,DEPT MOLEC GENET & EPIDEMIOL,BOSTON,MA 02215. FU NHLBI NIH HHS [HL-43793]; NIAID NIH HHS [AI-28943]; NIAMS NIH HHS [AR-39993] NR 19 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD OCT PY 1993 VL 69 IS 1 BP 36 EP 42 DI 10.1006/clin.1993.1147 PG 7 WC Immunology; Pathology SC Immunology; Pathology GA MA656 UT WOS:A1993MA65600006 PM 8403542 ER PT J AU SINGER, DE AF SINGER, DE TI PROBLEMS WITH STOPPING RULES IN TRIALS OF RISKY THERAPIES - THE CASE OF WARFARIN TO PREVENT STROKE IN ATRIAL-FIBRILLATION SO CLINICAL RESEARCH LA English DT Editorial Material ID CLINICAL-TRIALS; ANTICOAGULATION RP SINGER, DE (reprint author), MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BULFINCH 1,BOSTON,MA 02114, USA. NR 20 TC 3 Z9 3 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD OCT PY 1993 VL 41 IS 3 BP 482 EP 486 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LY017 UT WOS:A1993LY01700002 PM 8403778 ER PT J AU KLEINMAN, JG BROWN, D BONVENTRE, JV BESHENSKY, AM WORCESTER, EM AF KLEINMAN, JG BROWN, D BONVENTRE, JV BESHENSKY, AM WORCESTER, EM TI DISTRIBUTION OF OSTEOPONTIN IN RAT-KIDNEY - UP-REGULATION IN ISCHEMIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VAMC,MILWAUKEE,WI. MED COLL WISCONSIN,MILWAUKEE,WI 53226. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 1 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 OCT PY 1993 VL 41 IS 3 BP A686 EP A686 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LY017 UT WOS:A1993LY01700507 ER PT J AU MOBINI, N AHMED, AR AF MOBINI, N AHMED, AR TI IMMUNOGENETICS OF DRUG-INDUCED BULLOUS DISEASES SO CLINICS IN DERMATOLOGY LA English DT Review C1 HARVARD SCH DENT MED,CTR BLOOD RES,DEPT ORAL MED & PATHOL,BOSTON,MA. NR 0 TC 12 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0738-081X J9 CLIN DERMATOL JI Clin. Dermatol. PD OCT-DEC PY 1993 VL 11 IS 4 BP 449 EP 460 DI 10.1016/0738-081X(93)90151-2 PG 12 WC Dermatology SC Dermatology GA MQ178 UT WOS:A1993MQ17800005 PM 8124633 ER PT J AU FLICK, MR WEBSTER, RO HOEFFEL, JM JULIEN, M MILLIGAN, SA KENT, B LESSER, M AF FLICK, MR WEBSTER, RO HOEFFEL, JM JULIEN, M MILLIGAN, SA KENT, B LESSER, M TI EFFECT OF PHENYTOIN ON ACUTE LUNG INJURIES IN UNANESTHETIZED SHEEP SO CRITICAL CARE MEDICINE LA English DT Article DE ADULT RESPIRATORY DISTRESS SYNDROME; ENDOTOXIN; PHENYTOIN; EMBOLISM, AIR; OLEIC ACID; SEPTICEMIA; NEUTROPHILS; LUNGS; LYMPH; ESCHERICHIA-COLI ID RESPIRATORY-DISTRESS SYNDROME; MICRO-VASCULAR PERMEABILITY; MEDIASTINAL LYMPH-NODE; SEPTIC SHOCK; AIR EMBOLI; ANESTHETIZED SHEEP; N-ACETYLCYSTEINE; PULMONARY-EDEMA; DOUBLE-BLIND; ENDOTOXIN AB Objective. To determine if the intravenous administration of phenytoin attenuates or prevents acute experimental lung injury. Design: Placebo-controlled, longitudinal animal investigative study. Setting. University research laboratory. Subjects: Sixteen yearling female lambs weighing 30 +/- 3 kg. Intervention: After administration of anesthesia, the animals were endotracheally intubated and mechanically ventilated. Using sterile techniques, four thoracotomies were performed. Through the left fourth intercostal space, cannulas for pressure measurements were inserted directly into the main pulmonary artery and left atrium. An ultrasound flow cuff for determination of cardiac output was placed around the main pulmonary artery. Through the left tenth intercostal space, the diaphragmatic and mediastinal parietal pleura were widely cauterized. Through the right tenth intercostal space, the caudal mediastinal lymph node was identified and divided at the caudal margin of the right pulmonary ligament, and a 1- to 2-cm portion of the node distal to the ligament was resected. The diaphragmatic and mediastinal parietal pleura were widely cauterized. Through the right sixth intercostal space, the efferent duct (or ducts) was identified, ligated at the site of entry into the thoracic duct, and cannulated. The lymph cannula was brought to the outside of the thorax through a separate stab wound. Measurements and Main Results: Unanesthetized sheep were studied 7 to 10 days after surgery. Hemodynamic, lung fluid balance, and arterial blood variables were measured in uninjured sheep and in sheep injured by intravenous infusions of Escherichia coli endotoxin (1 mug/kg iv over 30 mins), air bubbles (0.056 to 0.074 mL/kg/min over 4 hrs), or oleic acid (0.06 mL/kg over 1 hr). The sheep were studied when untreated and after pretreatment with phenytoin. We found that the expected increase in protein-rich lung lymph flow with injuries, resulting from increased microvascular permeability in the lungs, was attenuated by phenytoin when the lungs were injured by endotoxin or air bubbles. In contrast, phenytoin had no effect on oleic acid-induced lung injury or on uninjured lungs. Conclusions. Phenytoin attenuates acute lung injuries in sheep that are thought to be caused by stimulation of host inflammatory responses (e.g., endotoxin and air bubbles), but has no effect on direct injuries to the lungs (e.g., oleic acid). A plausible mechanism for this finding is phenytoin inhibition of polymorphonuclear leukocyte function. C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,MED CTR,ROSALIND RUSSELL ARTHRITIS RES LAB,SAN FRANCISCO,CA 94110. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94143. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT SURG,NEW YORK,NY 10029. BRONX VET ADM MED CTR,NEW YORK,NY. RP FLICK, MR (reprint author), UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,MED CTR,MED SERV,SAN FRANCISCO,CA 94110, USA. FU NHLBI NIH HHS [HL-26913, HL-19155] NR 45 TC 2 Z9 2 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD OCT PY 1993 VL 21 IS 10 BP 1563 EP 1571 DI 10.1097/00003246-199310000-00027 PG 9 WC Critical Care Medicine SC General & Internal Medicine GA MB228 UT WOS:A1993MB22800027 PM 8403968 ER PT J AU BURAKOFF, SJ LAFFERTY, KJ AF BURAKOFF, SJ LAFFERTY, KJ TI ANTIGEN, CO-STIMULATORS AND CYTOKINES - REGULATORS OF ALLOGENEIC INTERACTIONS - EDITORIAL OVERVIEW SO CURRENT OPINION IN IMMUNOLOGY LA English DT Editorial Material C1 UNIV COLORADO,HLTH SCI CTR,BARBARA DAVIS CTR CHILDHOOD DIABET,1200 E 9TH AVE,DENVER,CO 80262. RP BURAKOFF, SJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 6 TC 1 Z9 1 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD OCT PY 1993 VL 5 IS 5 BP 745 EP 746 DI 10.1016/0952-7915(93)90131-B PG 2 WC Immunology SC Immunology GA MB868 UT WOS:A1993MB86800011 PM 8240737 ER PT J AU BIERER, BE HOLLANDER, G FRUMAN, D BURAKOFF, SJ AF BIERER, BE HOLLANDER, G FRUMAN, D BURAKOFF, SJ TI CYCLOSPORINE-A AND FK506 - MOLECULAR MECHANISMS OF IMMUNOSUPPRESSION AND PROBES FOR TRANSPLANTATION BIOLOGY SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID VERSUS-HOST DISEASE; T-CELL ACTIVATION; BONE-MARROW TRANSPLANTATION; CALCINEURIN PHOSPHATASE-ACTIVITY; CYTOSOLIC BINDING-PROTEIN; PEPTIDYL-PROLYL ISOMERASE; CIS-TRANS ISOMERASE; CLONAL DELETION; LYMPHOCYTE-T; POSITIVE SELECTION AB The microbial products cyclosporin A (CsA), FK506 and rapamycin are potent immunosuppressive agents. The introduction of CsA in the early 1970's, significantly improved the outcome of organ and bone marrow allograft transplantation and advanced therapeutic options in autoimmune diseases. FK506 appears to have a higher therapeutic index than CsA, and has been used with encouraging results in clinical transplantation trials. FK506 and CsA, although structurally unrelated, appear to target similar signal transduction pathways in hematopoietic cells by inhibiting the action of calcineurin, a serine/threonine phosphatase. A structural analog of FK506, rapamycin, inhibits cellular function by a different molecular mechanism. These agents have advanced our understanding of signal transmission pathways in lymphocyte activation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BIERER, BE (reprint author), BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,DIV PEDIAT ONCOL,DANA 1710A,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 39542]; NIAID NIH HHS [AI32514] NR 105 TC 144 Z9 144 U1 0 U2 8 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD OCT PY 1993 VL 5 IS 5 BP 763 EP 773 DI 10.1016/0952-7915(93)90135-F PG 11 WC Immunology SC Immunology GA MB868 UT WOS:A1993MB86800015 PM 7694595 ER PT J AU FERRARA, JLM AF FERRARA, JLM TI CYTOKINE DYSREGULATION AS A MECHANISM OF GRAFT-VERSUS-HOST DISEASE SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID BONE-MARROW TRANSPLANTATION; NECROSIS-FACTOR-ALPHA; NITRIC-OXIDE; IFN-GAMMA; RECEPTOR ANTAGONIST; SERUM LEVELS; INVIVO; LIPOPOLYSACCHARIDE; INTERLEUKIN-1; ANTIBODIES AB Craft versus host disease (GVHD) remains the major complication of allogeneic bone marrow transplantation. T cells in the donor bone marrow recognize and react against host alloantigens and thereby initiate GVHD, but the precise mechanisms by which host tissues are damaged remain unclear. Recently, several convergent lines of evidence have suggested that inflammatory cytokines act as mediators of acute GVHD. Most of the clinical manifestations of GVHD may in fact be due to the dysregulated production of cytokines by T cells and other inflammatory cells. The complex interactions among cytokines and their cellular targets suggest that individual cytokines may play an important and distinctive role in the pathophysiology of GVHD. Perturbation of the cytokine network may function as a final common pathway of target organ damage, and the rapid onset of severe, acute GVHD can be considered a 'cytokine storm.' RP FERRARA, JLM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,ROOM DANA 1640A,44 BINNEY ST,BOSTON,MA 02115, USA. NR 36 TC 139 Z9 141 U1 1 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD OCT PY 1993 VL 5 IS 5 BP 794 EP 799 DI 10.1016/0952-7915(93)90139-J PG 6 WC Immunology SC Immunology GA MB868 UT WOS:A1993MB86800019 PM 8240742 ER PT J AU RUBIN, PAD AF RUBIN, PAD TI ENUCLEATION, EVISCERATION, AND EXENTERATION SO CURRENT OPINION IN OPHTHALMOLOGY LA English DT Article AB This review outlines many of the recent advancements in the understanding and management of the anophthalmic patient. A population-based study demonstrated that the annual incidence of enucleations for all causes was about 3 to 5 per 100,000. Application of expandable orbital implants appears to be promising in the management of microphthalmia or anophthalmia in infants to maximize orbital growth. Some reports on the use of hydroxyapatite enucleation implants are encouraging, with no major complications observed in one large series. Yet other reports of hydroxyapatite implant exposures, at a very concerning frequency, are also beginning to emerge. Few of the exposures heal spontaneously; however, infections or extrusions are very rare, and they are attributable to the porous composition of the implant. Conjunctival flaps alone are suboptimal in the management of exposures. Adjunctive autologous fascial grafts seem preferable to heterologous sclera in the management of these exposures. Magnetic resonance imaging of the hydroxyapatite implant appears to be superior to bone scan in the noninvasive assessment of vascularization of these implants. Further advancements are necessary to achieve a more optimal enucleation implant. RP RUBIN, PAD (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE PLAST & ORBIT SERV,50 STANIFORD ST,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1040-8738 J9 CURR OPIN OPHTHALMOL PD OCT PY 1993 VL 4 IS 5 BP 39 EP 48 DI 10.1097/00055735-199310000-00009 PG 10 WC Ophthalmology SC Ophthalmology GA MJ176 UT WOS:A1993MJ17600009 PM 10146486 ER PT J AU BILYK, JR AF BILYK, JR TI ORBITAL AND OPTIC-NERVE TRAUMA SO CURRENT OPINION IN OPHTHALMOLOGY LA English DT Article AB The evaluation and management of orbital trauma continues to evolve. The application of plating systems for rigid fixation of complex orbital fractures has allowed the surgeon to reapproximate the normal bony anatomy to a greater degree than was previously available with wiring. Porous implants, including hydroxyapatite and porous polyethylene, have also been used in periorbital reconstruction with success. Improved resolution and new imaging modalities have not only allowed the clinician a better view of the traumatized orbit, but have also aided in developing an understanding of the complexities of the orbital apex and optic canal region. Other issues of trauma are also well represented in this year's literature. The clinician is reminded once again that, although certain patterns of trauma are recognized, all patients without exception must be carefully evaluated for occult ocular, periorbital, neurological, or systemic injuries. The sequelae and complications of orbital trauma are also important to remember, and should be reviewed with the patient and the patient's family during the initial evaluation. Excellent reviews of orbital implant and ocular motility complications are included in this year's literature. RP BILYK, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,CTR EYE PLAST & ORBIT,50 STANIFORD ST,3RD FLOOR,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1040-8738 J9 CURR OPIN OPHTHALMOL PD OCT PY 1993 VL 4 IS 5 BP 49 EP 55 DI 10.1097/00055735-199310000-00010 PG 7 WC Ophthalmology SC Ophthalmology GA MJ176 UT WOS:A1993MJ17600010 ER PT J AU BLEICH, D POLAK, M EISENBARTH, GS JACKSON, RA AF BLEICH, D POLAK, M EISENBARTH, GS JACKSON, RA TI DECREASED RISK OF TYPE-I DIABETES IN OFFSPRING OF MOTHERS WHO ACQUIRE DIABETES DURING ADRENARCHY SO DIABETES LA English DT Article ID IMMUNE-SYSTEM; SEX STEROIDS; IDDM; DETERMINANTS; CHILDREN; MELLITUS; DISEASE; AGE AB Fathers with type I diabetes transmit diabetes to their offspring 2-3 times more frequently than mothers with type I diabetes. This phenomenon has provoked both genetic and nongenetic hypotheses, but the mechanism remains obscure. We find that mothers who develop diabetes before age 8 transmit diabetes at the same rate as diabetic fathers, and that the sex difference in diabetes transmission is explained by a decreased transmission rate in mothers who acquired diabetes after age 8. We constructed a data base containing 2156 nondiabetic and diabetic offspring of parents with type I diabetes. Families were selected from our main data base, which contains demographic information and diabetes autoantibody test results on >8000 first-degree relatives of patients with type I diabetes and diabetic probands. Identification of offspring was made through diabetic parents who had participated in our autoantibody screening program at the Joslin Diabetes Center between 1983 and 1990. Questionnaires were sent to all other family members to determine the number of diabetic and nondiabetic offspring in each family. The 20-yr life-table risk of diabetes in offspring of diabetic fathers and mothers is 8.9 +/- 1.0 and 3.4 +/- 0.6%, respectively. For mothers acquiring diabetes before or after age 8, the risk of diabetes in offspring is 13.9 +/- 4.4 and 2.4 +/- 0.6% at 20 yr of age, respectively. Furthermore, we find that duration of diabetes in mothers before pregnancy has no effect on the risk of diabetes in their offspring. The increased transmission rate of diabetes in diabetic fathers is explained by a decreased transmission rate of diabetes in mothers who acquire diabetes after age 8. Because women acquiring diabetes after age 8 transmit less diabetes to their offspring, we propose that adrenarchy may have an apparent protective effect on diabetes transmission. We speculate that mothers who acquire diabetes after age 8 are more susceptible to this disorder (similar to susceptibility to other organ-specific autoimmune diseases) and may possess and transmit fewer genetic susceptibility determinants to their offspring. C1 JOSLIN DIABET CTR,DIV IMMUNOL & IMMUNOGENET,BOSTON,MA. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-36836, DK-32083] NR 16 TC 30 Z9 30 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD OCT PY 1993 VL 42 IS 10 BP 1433 EP 1439 DI 10.2337/diabetes.42.10.1433 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LY402 UT WOS:A1993LY40200007 PM 8375582 ER PT J AU PUGH, JA MEDINA, R RAMIREZ, M AF PUGH, JA MEDINA, R RAMIREZ, M TI COMPARISON OF THE COURSE TO END-STAGE RENAL-DISEASE OF TYPE-1 (INSULIN-DEPENDENT) AND TYPE-2 (NON-INSULIN-DEPENDENT) DIABETIC NEPHROPATHY SO DIABETOLOGIA LA English DT Article; Proceedings Paper CT SYMP ON DIABETIC RENAL DISEASE IN TYPE-2 DIABETIC PATIENT : A MAJOR WORLDWIDE HEALTH PROBLEM CY SEP 07, 1992 CL PRAGUE, CZECHOSLOVAKIA SP HOECHST AKTIENGESELL DE END-STAGE RENAL DISEASE; TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS; TYPE-1 (INSULIN-DEPENDENT) DIABETES ID MELLITUS; ONSET; PRESSURE; FAILURE; KIDNEY AB Is the course leading to diabetic end-stage renal disease similar for Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus? We identified all diabetic end-stage renal disease patients starting renal replacement therapy from 1989 to 1991 in two urban counties in Texas. Three ethnic/racial groups were enrolled: Mexican Americans, non-Hispanic Whites, African Americans. Patients were interviewed and their medical records, both inpatient and out-patient, were abstracted for relevant diagnostic and therapeutic information. We attempted to obtain records as far back as the onset of diabetes or hypertension and from all physicians who had cared for the patient. An historical algorithm was used to determine diabetic type. Of the patients enrolled, 91 were Type 1 and 438 were Type 2 diabetic patients. Type 1 diabetic patients had higher mean glucose levels in the first 10 years of diabetes (16.3 vs 11.4 mmol/l) but lower systolic blood pressures (148 vs 157 mm Hg). The duration of diabetes prior to end-stage renal disease was longer for Type 1 than Type 2 patients (22 vs 17 years). Type 1 diabetic patients were more likely to have other microvascular complications (retinopathy, neuropathy, gastroparesis), less likely to have coronary disease (myocardial infarction and congestive heart failure), and had similar rates of stroke and vascular surgery procedures (carotid endarterectomy, coronary artery bypass surgery, aorto-femoral bypass). Type 1 and Type 2 diabetic patients were just as likely to have a first degree relative with hypertension (60.5 vs 65.5 %). The late manifestations of end-stage renal disease were similar between the two groups (kidney size, proteinuria, slope of the inverse of creatinine, laboratory data prior to end-stage renal disease, reasons for starting dialysis). The course to end-stage renal disease may be different for Type 1 and Type 2 diabetes, with hyperglycaemia playing a more dominant role in Type 1 and hypertension playing a more dominant role for Type 2. The Type 1/Type 2 differences in patterns of other diabetic complications add weight to this hypothesis. However, the late course of the renal disease and the end result on the kidney is very similar. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. MEXICAN AMER MED TREATMENT EFFECTIVENESS CTR,SAN ANTONIO,TX. RP PUGH, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,AMBULATORY CARE 11C6,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. OI Pugh, Jacqueline/0000-0003-4933-141X FU AHRQ HHS [1-U01-HS07397-01]; NIDDK NIH HHS [DK38392] NR 19 TC 46 Z9 46 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD OCT PY 1993 VL 36 IS 10 BP 1094 EP 1098 DI 10.1007/BF02374504 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LZ223 UT WOS:A1993LZ22300039 PM 8243860 ER PT J AU FURUTA, GT BROSS, DA DOODY, D KLEINMAN, RE AF FURUTA, GT BROSS, DA DOODY, D KLEINMAN, RE TI INTUSSUSCEPTION AND LEIOMYOSARCOMA OF THE GASTROINTESTINAL-TRACT IN A PEDIATRIC-PATIENT - CASE-REPORT AND REVIEW OF THE LITERATURE SO DIGESTIVE DISEASES AND SCIENCES LA English DT Note DE LEIOMYOSARCOMA; INTUSSUSCEPTION; PEDIATRIC PATIENT ID SOFT-TISSUE SARCOMAS; SMOOTH-MUSCLE TUMORS; INTESTINAL LEIOMYOSARCOMA; GASTRIC LEIOMYOSARCOMA; PROGNOSTIC FACTORS; CHILDHOOD; COLON; DUODENUM; TRIAD C1 MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIV PEDIAT SURG,BOSTON,MA 02114. NR 46 TC 9 Z9 9 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD OCT PY 1993 VL 38 IS 10 BP 1933 EP 1937 DI 10.1007/BF01296122 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MB727 UT WOS:A1993MB72700026 PM 8404418 ER PT J AU KOLTUN, WA SMITH, RJ LOEHNER, D DURDEY, P COLLER, JA MURRAY, JJ ROBERTS, PL VEIDENHEIMER, MC SCHOETZ, DJ AF KOLTUN, WA SMITH, RJ LOEHNER, D DURDEY, P COLLER, JA MURRAY, JJ ROBERTS, PL VEIDENHEIMER, MC SCHOETZ, DJ TI ALTERATION IN INTESTINAL PERMEABILITY AFTER ILEAL POUCH-ANAL ANASTOMOSIS SO DISEASES OF THE COLON & RECTUM LA English DT Article ID CROHNS-DISEASE; ENZYMATIC METHOD; CELIAC-DISEASE; LACTULOSE; SUGARS AB The physiologic changes that occur when the small bowel is used as a reservoir, as in the ileal pouch-anal anastomosis, are poorly understood. Alterations in bowel permeability, which may lead to bacterial translocation that could result in illness or dysfunction of the pouch, may be one such consequence of the pouch procedure. METHODS: Whole-bowel permeability was evaluated in patients with and without the pouch through the use of an orally consumed nonmetabolizable sugar clearance technique. Patients in whom the ileal pouch-anal anastomosis was performed for ulcerative colitis (17 patients) and patients with familial polyposis (7 patients) were compared with normal healthy volunteers (10 patients) and patients with ulcerative colitis with and without curative colectomy and ileostomy (6 and 5 patients, respectively). RESULTS: Measured by this technique, no differences were noted in bowel permeability between the volunteers and patients with ulcerative colitis, even after colectomy and ileostomy (1.7 +/- 0.4 in normal healthy volunteers, 1.8 +/- 0.5 in patients with ulcerative colitis without stoma, and 1.4 +/- 0.2 in patients with ulcerative colitis with ileostomy). The group of patients with an ileal reservoir, however, had a significantly increased index of measured bowel permeability (3.5 +/- 0.5 in patients with ulcerative colitis and 5.1 +/- 0.7 in patients with familial polyposis; P < 0.05 by analysis of variance compared with normal healthy volunteers and patients with ulcerative colitis with or without ileostomy). CONCLUSION: The exact site, cause, and consequence of this possible alteration of bowel permeability are unclear but appear to be related to the presence of the pouch and are not caused by the underlying pathologic diagnosis. C1 LAHEY CLIN MED CTR,DEPT COLON & RECTAL SURG,41 MALL RD,BURLINGTON,MA 01805. JOSLIN DIABETES CTR,BOSTON,MA. NR 14 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0012-3706 J9 DIS COLON RECTUM JI Dis. Colon Rectum PD OCT PY 1993 VL 36 IS 10 BP 922 EP 926 DI 10.1007/BF02050626 PG 5 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA MB730 UT WOS:A1993MB73000005 PM 8404382 ER PT J AU NOBLE, EP BLUM, K KHALSA, ME RITCHIE, T MONTGOMERY, A WOOD, RC FITCH, RJ OZKARAGOZ, T SHERIDAN, PJ ANGLIN, MD PAREDES, A TREIMAN, LJ SPARKES, RS AF NOBLE, EP BLUM, K KHALSA, ME RITCHIE, T MONTGOMERY, A WOOD, RC FITCH, RJ OZKARAGOZ, T SHERIDAN, PJ ANGLIN, MD PAREDES, A TREIMAN, LJ SPARKES, RS TI ALLELIC ASSOCIATION OF THE D(2) DOPAMINE-RECEPTOR GENE WITH COCAINE DEPENDENCE SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE D(2) DOPAMINE RECEPTOR GENE; COCAINE DEPENDENCE; TAQ1-A AND TAQ1-B ALLELES; FAMILY HISTORY OF ALCOHOLISM; DEVIANT BEHAVIORS ID DRUG-ABUSE; D2-DOPAMINE RECEPTOR; ALCOHOLISM; FAMILY; MECHANISMS; ADDICTION; DISORDER; LOCUS AB The objective of the present study was to examine allelic prevalence of the D2 dopamine receptor (DRD2) gene in male cocaine-dependent (CD) Caucasian (non-Hispanic) subjects and to determine the relationship of DRD2 alleles to family history and selected behavioral measures. The prevalence of the A1 allele in CD subjects (n = 53) was 50.9%. It was significantly higher than either the 16.0% prevalence (P < 10(-4)) in non-substance abusing controls (n = 100) or the 30.9% prevalence (P < 10(-2)) in population controls (n = 265) wherein substance abusers were not excluded. Similarly, a significantly higher prevalence (p < 10(-2)) of the B1 allele was found in CD subjects (n = 52) compared with non-substance abusing controls (n = 53); 38.5% vs. 13.2%. Logistic regression analysis of CD subjects identified potent routes of cocaine use and the interaction of early deviant behaviors and parental alcoholism as significant risk factors associated with the A1 allele. The cumulative number of these three risk factors in CD subjects was positively and significantly (P < 10(-3)) related to A1 allelic prevalence. The data showing a strong association of the minor alleles (A1 and B1) of the DRD2 with cocaine dependence suggest that a gene, located on the q22-q23 region of chromosome 11, confers susceptibility to this drug disorder. C1 UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, ALCOHOL RES CTR, INST NEUROPSYCHIAT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, DRUG ABUSE RES CTR, LOS ANGELES, CA USA. UTHSC, DEPT CELLULAR & STRUCT BIOL, SAN ANTONIO, TX USA. UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA USA. UNIV TEXAS, HLTH SCI CTR,DEPT PHARMACOL,DIV ADDICT DIS, PHARMACOGENET LAB, SAN ANTONIO, TX 78284 USA. UTHSC, DEPT COMP RESOURCES, SAN ANTONIO, TX USA. RP NOBLE, EP (reprint author), UNIV CALIF LOS ANGELES, DEPT PSYCHIAT & BEHAV SCI, LOS ANGELES, CA 90024 USA. FU NIDA NIH HHS [NIDA DA06250, NIDA DA00146, NIDA DA04268] NR 66 TC 181 Z9 182 U1 0 U2 3 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0376-8716 EI 1879-0046 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD OCT PY 1993 VL 33 IS 3 BP 271 EP 285 DI 10.1016/0376-8716(93)90113-5 PG 15 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA MD306 UT WOS:A1993MD30600006 PM 8261891 ER PT J AU ELLIOTT, ME GOODFRIEND, TL JEFCOATE, CR AF ELLIOTT, ME GOODFRIEND, TL JEFCOATE, CR TI BOVINE ADRENAL GLOMERULOSA AND FASCICULATA CELLS EXHIBIT 28.5-KILODALTON PROTEINS SENSITIVE TO ANGIOTENSIN, OTHER AGONISTS, AND ATRIAL-NATRIURETIC-PEPTIDE SO ENDOCRINOLOGY LA English DT Article ID STIMULATED ALDOSTERONE SYNTHESIS; LEYDIG TUMOR-CELLS; CORPUS-LUTEUM; RAPID ACCUMULATION; CORTEX CELLS; STEROIDOGENESIS; PHOSPHOPROTEIN; BIOSYNTHESIS; SECRETION; CAMP AB Protein synthesis by bovine adrenal glomerulosa and fasciculata cells in response to various modulators of steroid synthesis was examined using [S-35]methionine labeling and two-dimensional gel electrophoresis. Both cell types responded to steroidogenic stimuli with rapid changes in a family of 28- to 30-kilodalton (kDa) proteins similar to those described in rat fasciculata by Epstein and Orme-Johnson. In glomerulosa, angiotensin-II (AII), potassium, and (Bu)2cAMP stimulated the appearance of two 28.5-kDa proteins (no. 3 and 4) with pI values of 6.44 and 6.33 and decreased labeling of two other 28.5-kDa proteins (no. 1 and 2) with pI values of 6.9 and 6.59. The rank order of potency on aldosterone synthesis and that on proteins 1-4 were the same: (Bu)2cAMP > AII > potassium. Atrial natriuretic peptide blocked the effects of AII on all four proteins and on aldosterone synthesis. Adrenal secretagogues also affected labeling of four slightly larger (30 kDa) proteins (no. 5-8). Corresponding proteins in each quartet are separated by the same difference in isoelectric points. These eight proteins may represent a core protein systematically modified in a number of ways. Aldosterone synthesis in glomerulosa, like glucocorticoid synthesis in fasciculata, requires ongoing protein synthesis. The 28- to 30-kDa proteins increased by steroidogenic stimuli in both cells and decreased by atrial natriuretic peptide in glomerulosa may be the proteins whose synthesis is crucial to acute control of steroidogenesis. Our results indicate that these proteins are made in response to calcium- or calcium/phosphoinositide-dependent mechanisms as well as by cAMP. C1 UNIV WISCONSIN, SCH MED, DEPT MED, MADISON, WI 53705 USA. UNIV WISCONSIN, SCH MED, DEPT PHARMACOL, MADISON, WI 53705 USA. RP ELLIOTT, ME (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR, HYPERTENS RES LAB, ROOM C4114, 2500 OVERLOOK TERRACE, MADISON, WI 53705 USA. FU NIDDK NIH HHS [DK-18585] NR 32 TC 50 Z9 50 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD OCT PY 1993 VL 133 IS 4 BP 1669 EP 1677 DI 10.1210/en.133.4.1669 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MA411 UT WOS:A1993MA41100025 PM 8404608 ER PT J AU ELLIOT, SJ STRIKER, LJ HATTORI, M YANG, CW HE, CJ PETEN, EP STRIKER, GE AF ELLIOT, SJ STRIKER, LJ HATTORI, M YANG, CW HE, CJ PETEN, EP STRIKER, GE TI MESANGIAL CELLS FROM DIABETIC NOD MICE CONSTITUTIVELY SECRETE INCREASED AMOUNTS OF INSULIN-LIKE GROWTH FACTOR-I SO ENDOCRINOLOGY LA English DT Article ID SOMATOMEDIN-C; IGF-I; BINDING; KIDNEY; RECEPTORS; MOUSE; RAT; NEPHROPATHY; FIBROBLASTS; MECHANISM AB Experimental evidence has suggested that insulin-like growth factor-I (IGF-I) may contribute to diabetic complications. Previously, we and others have shown that normal glomerular mesangial cells have receptors for, synthesize, and exhibit a mitogenic response to IGF-I. We investigated the IGF-I response in cells derived from a genetic model of diabetes, the nonobese diabetic (NOD) mouse. Mesangial cell lines were derived from diabetic (D-NOD) and nondiabetic adult mice. D-NOD cells released more IGF-I into the supernatant and had a decreased binding of IGF-I to surface receptors. Analysis according to Scatchard revealed a decreased number of receptor sites on D-NOD cells, although the structure of the IGF-I receptor visualized by crosslinking was identical for both cell types. Preincubation of D-NOD cells with an antibody to IGF-I resulted in an increase in the number of receptor sites. This suggested that autocrine IGF-I was responsible for the decrease in D-NOD receptor number and that diabetes had resulted in a stable phenotypic change. C1 NIDDKD, METAB DIS BRANCH,RENAL CELL BIOL SECT,BLDG 10, ROOM 3N110,9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. JOSLIN DIABET CTR, BOSTON, MA 02215 USA. FU NIDDK NIH HHS [P30 RO1DK-43613, DK-36836] NR 27 TC 44 Z9 45 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD OCT PY 1993 VL 133 IS 4 BP 1783 EP 1788 DI 10.1210/en.133.4.1783 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MA411 UT WOS:A1993MA41100040 PM 7691581 ER PT J AU BAUERDANTOIN, AC HOLLENBERG, AN JAMESON, JL AF BAUERDANTOIN, AC HOLLENBERG, AN JAMESON, JL TI DYNAMIC REGULATION OF GONADOTROPIN-RELEASING-HORMONE RECEPTOR MESSENGER-RNA LEVELS IN THE ANTERIOR-PITUITARY GLAND DURING THE RAT ESTROUS-CYCLE SO ENDOCRINOLOGY LA English DT Note ID ESTRADIOL AB The number of gonadotropin-releasing hormone (GnRH) receptors on pituitary gonadotropes varies substantially during the rat estrous cycle and may modulate pituitary responsiveness to GnRH. The present studies were undertaken to determine to what extent these changes in GnRH receptor number reflect a change in GnRH receptor mRNA expression in the anterior pituitary gland. Using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), pituitary GnRH receptor mRNA levels were measured at various timepoints throughout the rat estrous cycle. There was a three-fold increase in GnRH receptor mRNA levels on the afternoon of proestrus (PRO) when compared to levels observed on the morning of metestrus (MET). This rise preceded the onset of the LH surge by Sh (1200h). GnRH receptor mRNA levels remained elevated through 2100h PRO, after which they dropped dramatically, and by 2400h PRO were not significantly different from levels observed at 0900h MET. A two-fold increase in GnRH receptor mRNA expression was also observed during the early stages of the estrous cycle (0900h to 1800h MET), and this increase was sustained until 1800h on diestrus, at which time mRNA levels decreased to levels observed at 0900h MET. These results demonstrate that pituitary GnRH receptor mRNAs are dynamically regulated during the rat estrous cycle, with receptor mRNA expression being greatest on the afternoon of PRO, the time of the estrous cycle at which gonadotropes are most sensitive to GnRH stimulation. RP BAUERDANTOIN, AC (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, DEPT MED, THYROID UNIT, BOSTON, MA 02114 USA. FU NICHD NIH HHS [HD28138, HD29164] NR 13 TC 98 Z9 98 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD OCT PY 1993 VL 133 IS 4 BP 1911 EP 1914 DI 10.1210/en.133.4.1911 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MA411 UT WOS:A1993MA41100058 PM 8404635 ER PT J AU KELSEY, KT CAGGANA, M MAUCH, PM COLEMAN, CN CLARK, JR LIBER, HL AF KELSEY, KT CAGGANA, M MAUCH, PM COLEMAN, CN CLARK, JR LIBER, HL TI MUTAGENESIS AFTER CANCER-THERAPY SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID HUMAN LYMPHOCYTES-T; PERIPHERAL-BLOOD LYMPHOCYTES; RESISTANT MUTANT FREQUENCY; HUMAN RETINOBLASTOMA GENE; OXIDE-EXPOSED PRIMATES; INVIVO HPRT MUTATIONS; HODGKINS-DISEASE; 6-THIOGUANINE-RESISTANT LYMPHOCYTES; CLONING ASSAY; BREAST-CANCER AB A subset of Hodgkin's disease (HD) and breast cancer Patients have been reported to have elevated hprt mutant frequencies in peripheral blood lymphocytes after cessation of therapy. A subset of these patients are also known to develop second therapy-related malignancies. Therefore, it is clearly important to determine if these elevations in mutant frequency represent true, persistently elevated mutation frequencies. As a follow-up to our study of patients previously treated for HD, we recruited for a prospective study six previously treated HD patients and five patients who had been treated for squamous cell carcinoma of the head and neck. These individuals were studied several times over a 6-7 months. The results confirmed that a subset of patients have persistently high mutant frequencies when compared to 71 previously studied controls. The study was designed to determine if the elevated mutant frequencies of treated patients represented independent mutations or resulted from the in vivo expansion of single mutant cells. We used the polymerase chain reaction to examine DNA single strand conformation polymorphisms at the T-cell receptor-gamma locus of individual mutant clones. This analysis showed that 20.1% of the mutants from Hodgkin's disease patients and 17.5% of the mutants from squamous cell carcinoma patients were siblings. The sibling mutants generally did not persist over time. However, one patient had one mutant clone that persisted, but slowly decreased in prevalence over a 7 month sampling period. The data demonstrate that treatments for cancer result in persistently elevated mutation frequencies at the hprt locus in some, but not all, patients. In addition, our results confirm previous studies indicating that it is not always appropriate to assume equality between mutant and mutation frequencies when studying individuals exposed to significant doses of known mutagens or carcinogens. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP KELSEY, KT (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,RADIOBIOL LAB,665 HUNTINGTON AVE,BOSTON,MA 02115, USA. RI Kelsey, Karl/I-1252-2014 FU NCI NIH HHS [CA-09078]; NIEHS NIH HHS [ES-00002] NR 49 TC 7 Z9 7 U1 0 U2 0 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 1993 VL 101 SU 3 BP 177 EP 184 DI 10.2307/3431722 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA MN668 UT WOS:A1993MN66800033 PM 8143613 ER PT J AU DUBEY, DP MIRZA, NM ZAHARIAN, BI YUNIS, EJ AF DUBEY, DP MIRZA, NM ZAHARIAN, BI YUNIS, EJ TI ROLE OF A GENETIC REGION ON CHROMOSOME-4 IN THE REGULATION OF NATURAL-KILLER-CELL ACTIVITY IN MICE SO EUROPEAN JOURNAL OF IMMUNOGENETICS LA English DT Article ID HYBRID RESISTANCE; CYTO-TOXICITY; INTERFERON; MOUSE; IDENTIFICATION; ASSOCIATION; LOCATION; LINKAGE; ANTIGEN; LY-49 AB Natural killer cell (NK) activity is regulated by both the H-2 and non-H-2 genes. Using bilineal congenic HW26C and HW13 mice which differ from the background strain C57BL/6By (B6) in a region of chromosome 4, we investigated the role played by a gene/genes in a segment of chromosome 4 of BALB/cBy on NK cell activity. Percoll separated low density spleen cells from young HW26C and HW13 mice showed a 3.5 fold higher NK activity than the B6. We also observed that the increase in NK activity of HW26C was not due to an increase in the number of NK cells. Using five other bilineal congenics containing different regions of chromosome 4 of BALB/cBy, we observed that the putative gene(s) regulating NK activity may be located between b and IFN-alpha/beta genes of chromosome 4. The level of NK activity of (B6xHW26C)F1 ranked between the HW26C and B6 suggesting that the gene product described is inherited in an incompletely dominant fashion. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP DUBEY, DP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA06516-29]; NIA NIH HHS [AG02329]; NIAID NIH HHS [AI26817] NR 37 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0960-7420 J9 EUR J IMMUNOGENET JI Eur. J. Immunogenet. PD OCT PY 1993 VL 20 IS 5 BP 381 EP 389 DI 10.1111/j.1744-313X.1993.tb00157.x PG 9 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA LZ761 UT WOS:A1993LZ76100007 PM 9098406 ER PT J AU IGLESIAS, A NICHOGIANNOPOULOU, A WILLIAMS, GS FLASWINKEL, H KOHLER, G AF IGLESIAS, A NICHOGIANNOPOULOU, A WILLIAMS, GS FLASWINKEL, H KOHLER, G TI EARLY B-CELL DEVELOPMENT REQUIRES MU-SIGNALING SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE PRE-B CELL RECEPTOR; TRANSGENIC MICE; MUTANT IMMUNOGLOBULIN ID PRE-B; LIGHT-CHAIN; GENE REARRANGEMENT; ANTIGEN RECEPTOR; SURFACE EXPRESSION; TRANSGENIC MICE; LYMPHOCYTES-B; HEAVY-CHAINS; KAPPA-GENES; IGM AB In vitro studies with Abelson murine leukemia virus (AMuLV)-transformed murine pre-B cell lines demonstrated that wild-type mu but not mutant mu chains lacking the first constant domain (muDELTA1) can efficiently induce Ig light (L) chain gene rearrangement. Using antibodies against the cytoplasmic tail of the immunoglobulin co-receptor beta (Igbeta) chain we find mu, but not muDELTA1 chains associated with Igbeta. Since a heterodimer of surface-labeled proteins was co-precipitated with mu we conclude that only wild-type mu is associated with the Igalpha/Igbeta co-receptor on the surface of pre-B cell lines. Mutant muDELTA1 chains achieve their surface expression by utilizing a glycophospholipid anchor. In vivo analysis of transgenic mcie expressing either mu or muDELTA1 transgenes revealed the expected ''normal'' B cell development in the case of wild-type mu transgenic lymphocytes, but a block in differentiation of muDELTA1 transgenic lymphocytes. The maturation block occurs at the developmental transition of pre-B lymphocytes from the CD43/S7+, CD45R/B220low stage to the CD43/S7-, B220low/high stage in which the majority of L chain gene rearrangements occur. These results, together with the observed inability of the muDELTA1 chains to signal activation of L chain gene joining and to associate Igalpha/Igbeta in pre-B cell lines suggest that signals mediated by the protein complex composed of mu/Igalpha/Igbeta are crucial during differentiation of pre-B lymphocytes. C1 MPI PSYCHIAT,D-82152 MARTINSRIED,GERMANY. CNRS,F-67085 STRASBOURG,FRANCE. HARVARD UNIV,CTR BLOOD RES,CAMBRIDGE,MA 02138. NR 38 TC 24 Z9 24 U1 1 U2 2 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD OCT PY 1993 VL 23 IS 10 BP 2622 EP 2630 DI 10.1002/eji.1830231036 PG 9 WC Immunology SC Immunology GA MD626 UT WOS:A1993MD62600035 PM 8405063 ER PT J AU EZZELL, RM TONER, M HENDRICKS, K DUNN, JCY TOMPKINS, RG YARMUSH, ML AF EZZELL, RM TONER, M HENDRICKS, K DUNN, JCY TOMPKINS, RG YARMUSH, ML TI EFFECT OF COLLAGEN GEL CONFIGURATION ON THE CYTOSKELETON IN CULTURED RAT HEPATOCYTES SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID SANDWICH CONFIGURATION; EXTRACELLULAR-MATRIX; SUBSTRATE ADHESION; LIVER; CELL; FIBRONECTIN; TRANSCRIPTION; ATTACHMENT; RECEPTORS; LAMININ C1 SHRINERS BURN INST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. RUTGERS UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. RP YARMUSH, ML (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BIGELOW 1302,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 43371, DK 43351, DK 41709] NR 37 TC 73 Z9 73 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD OCT PY 1993 VL 208 IS 2 BP 442 EP 452 DI 10.1006/excr.1993.1266 PG 11 WC Oncology; Cell Biology SC Oncology; Cell Biology GA MA098 UT WOS:A1993MA09800013 PM 8375473 ER PT J AU MATULONIS, U SALGIA, R OKUDA, K DRUKER, B GRIFFIN, JD AF MATULONIS, U SALGIA, R OKUDA, K DRUKER, B GRIFFIN, JD TI INTERLEUKIN-3 AND P210 BCR/ABL ACTIVATE BOTH UNIQUE AND OVERLAPPING PATHWAYS OF SIGNAL-TRANSDUCTION IN A FACTOR-DEPENDENT MYELOID CELL-LINE SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE IL-3; P210 BCR/ABL; MYELOID CELLS; SIGNAL TRANSDUCTION ID CHRONIC MYELOGENOUS LEUKEMIA; COLONY-STIMULATING FACTOR; TYROSINE KINASE-ACTIVITY; C-ABL; PHILADELPHIA-CHROMOSOME; ABELSON VIRUS; MURINE IL-3; MAP KINASE; V-ABL; PROTEIN AB Chronic myelogenous leukemia (Civil) is characterized by a specific chromosomal translocation occurring between the long arms of chromosomes 9 and 22 resulting in a fusion product, p210 BCR/ABL, which has elevated tyrosine kinase activity. Expression of p210 BCR/ABL in murine interleukin-3 (IL-3)-dependent cell lines typically converts these cell lines to factor-independence by a non-autocrine mechanism. The IL-3 receptor is believed to function in part by activating a receptor-associated tyrosine kinase, leading to the hypothesis that p210 BCR/ABL may induce factor-independence of myeloid cells by constitutively phosphorylating some common signal-transducing proteins that normally would be phosphorylated on tyrosine residues in response to IL-3. p210 BCR/ABL subclones were constructed from an IL-3-dependent murine myeloid cell line, 32Dc13, by transfection of a plasmid containing a full-length p210 BCR/ABL cDNA. Following transfection, the cells became completely factor-independent within 3 weeks. We examined the effects of p210 BCR/ABL and IL-3 on the pattern of tyrosine phosphorylation of cellular proteins in 32Dc13 cells using one- and two-dimensional antiphosphotyrosine immunoblotting. WEHI-3B conditioned media (WEHI-CM) was used as a source of n-3. The introduction of p210 BCR/ABL results in constitutively increased levels of tyrosine phosphorylation of more than 20 new proteins, while WEHI-CM induced transient tyrosine phosphorylation of 6 to 10 new proteins. Using two-dimensional immunoblots to examine phosphoproteins, four categories could be identified: (1) proteins that are inducibly tyrosine phosphorylated in response to WEHI-CM in 32Dc13 cells only, (2) proteins inducibly tyrosine phosphorylated by WEHI-CM only in p210 BCR/ABL(+) cells, (3) proteins that are inducibly tyrosine phosphorylated in response to WEHI-CM in both 32Dc13 cells and p210 BCR/ABL(+) cells, and (4) proteins inducibly tyrosine phosphorylated in response to WEHI-CM and constitutively phosphorylated in the presence of p210 BCR/ABL. We have identified one of the proteins in category 4 as p42 mitogen-activated protein (MAP) kinase (ERK2). Overall, however, we found that the signal transduction pathways of IL-3 and BCR/ABL are strikingly different, suggesting that most of the immediate substrates of the IL-3 receptor-activated tyrosine kinase and p210 BCR/ABL kinase are different. Convergence of signaling pathways at p42 MAP kinase is of interest since activation of this kinase has been linked to mitogenesis in many systems. Identification of the overlapping proteins of both IL-3 signal transduction in 32Dc13 cells and p210 BCR/ABL(+) cells may help explain the growth-promoting effects of this oncogene. C1 DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02215. DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. NR 33 TC 91 Z9 91 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD OCT PY 1993 VL 21 IS 11 BP 1460 EP 1466 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA MW617 UT WOS:A1993MW61700014 PM 8405226 ER PT J AU ENOCHS, WS SCHAFFER, B BHIDE, PG NOSSIFF, N PAPISOV, M BOGDANOV, A BRADY, TJ WEISSLEDER, R AF ENOCHS, WS SCHAFFER, B BHIDE, PG NOSSIFF, N PAPISOV, M BOGDANOV, A BRADY, TJ WEISSLEDER, R TI MR-IMAGING OF SLOW AXONAL-TRANSPORT IN-VIVO SO EXPERIMENTAL NEUROLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP ENOCHS, WS (reprint author), MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,MRPP,BOSTON,MA 02114, USA. FU NCI NIH HHS [1ROI CA 54886-01] NR 10 TC 24 Z9 24 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD OCT PY 1993 VL 123 IS 2 BP 235 EP 242 DI 10.1006/exnr.1993.1156 PG 8 WC Neurosciences SC Neurosciences & Neurology GA MC851 UT WOS:A1993MC85100008 PM 8405287 ER PT J AU SANDERSON, IR OUELLETTE, AJ CARTER, EA HARMATZ, PR AF SANDERSON, IR OUELLETTE, AJ CARTER, EA HARMATZ, PR TI ONTOGENY OF LA-MESSENGER RNA IN THE MOUSE SMALL-INTESTINAL EPITHELIUM IS MODULATED BY AGE OF WEANING AND DIET SO GASTROENTEROLOGY LA English DT Article ID IA-ANTIGEN; INVARIANT CHAIN; ELEMENTAL DIET; CROHNS-DISEASE; SMALL BOWEL; HLA-DR; EXPRESSION; CELLS; RAT; GUT C1 MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,MUCOSAL IMMUNOL LAB,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA. CHILDRENS HOSP OAKLAND,RES CTR,OAKLAND,CA. FU NICHD NIH HHS [HD12437]; NIDDK NIH HHS [DK34854, DK33506] NR 36 TC 26 Z9 26 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD OCT PY 1993 VL 105 IS 4 BP 974 EP 980 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LZ246 UT WOS:A1993LZ24600003 PM 8405883 ER PT J AU HELIN, K WU, CL FATTAEY, AR LEES, JA DYNLACHT, BD NGWU, C HARLOW, E AF HELIN, K WU, CL FATTAEY, AR LEES, JA DYNLACHT, BD NGWU, C HARLOW, E TI HETERODIMERIZATION OF THE TRANSCRIPTION FACTORS E2F-1 AND DP-1 LEADS TO COOPERATIVE TRANSACTIVATION SO GENES & DEVELOPMENT LA English DT Article DE E2F/DP-1; RETINOBLASTOMA PROTEIN; HETERODIMERIZATION; TRANSACTIVATION ID RETINOBLASTOMA GENE-PRODUCT; REGION 1A PROTEINS; HUMAN MYC PROMOTER; DNA-BINDING; CELL-CYCLE; C-MYC; ADENOVIRUS-E1A PREVENTS; EXPRESSION; FOS; POLYPEPTIDES AB The E2F transcription factor has been implicated in the regulation of genes whose products are involved in cell proliferation. Two proteins have recently been identified with E2F-like properties. One of these proteins, E2F-1, has been shown to mediate E2F-dependent trans-activation and to bind the hypophosphorylated form of the retinoblastoma protein (pRB). The other protein, murine DP-1, was purified from an E2F DNA-affinity column, and it was subsequently shown to bind the consensus E2F DNA-binding site. To study a possible interaction between E2F-1 and DP-1, we have now isolated a cDNA for the human homolog of DP-1. Human DP-1 and E2F-1 associate both in vivo and in vitro, and this interaction leads to enhanced binding to E2F DNA-binding sites. The association of E2F-1 and DP-1 leads to cooperative activation of an E2F-responsive promoter. Finally, we demonstrate that E2F-1 and DP-1 association is required for stable interaction with pRB in vivo and that trans-activation by E2F-1/DP-1 heterodimers is inhibited by pRB. We suggest that ''E2F'' is the activity that is formed when an E2F-1-related protein and a DP-1-related protein dimerize. RP HELIN, K (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129, USA. NR 66 TC 419 Z9 426 U1 0 U2 4 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD OCT PY 1993 VL 7 IS 10 BP 1850 EP 1861 DI 10.1101/gad.7.10.1850 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA MB745 UT WOS:A1993MB74500002 PM 8405995 ER PT J AU MROZ, EA NISSIM, KR LECHENE, C AF MROZ, EA NISSIM, KR LECHENE, C TI ELECTRON-PROBE ANALYSIS OF ISOLATED GOLDFISH HAIR-CELLS - IMPLICATIONS FOR PREPARING HEALTHY CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; ION COMPOSITION; ELECTRON-PROBE ANALYSIS; CULTURE MEDIA; CELL ISOLATION ID GUINEA-PIG COCHLEA; INNER-EAR; CONCANAVALIN-A; IONIC BASIS; TRANSPORT; CALCIUM; TRANSDUCTION; TRANSMISSION; CURRENTS; MODEL AB Electron-probe analysis provides an objective criterion for the physiological status of cells: whether they show the high potassium and low sodium that are expected of healthy animal cells. Preparing isolated goldfish hair cells that were healthy by this criterion required several precautions, including: limited exposure to enzymes and to simple salt solutions, a rest period between enzyme treatment and mechanical disruption of the tissue, and presence of bovine albumin in the medium both during the rest period and during mechanical dispersion and plating. Cells prepared with these precautions from the saccule and lagena and kept in an enriched medium had the following elemental composition (mole percentages with respect to phosphorus): K, 103; Na, 18; Cl, 23; S, 13; Mg, 8; Ca, 1.5. These mole percentages were close to these elements' total millimolar concentrations in the cells. If the precautions were not taken, cells with intact surface membranes (as assessed by exclusion and retention of dyes) could be obtained, but the cells had elevated cell sodium and low cell potassium. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NCRR NIH HHS [RR 02604]; NIDCD NIH HHS [R01 DC000033, DC00033]; NINDS NIH HHS [NS13126] NR 53 TC 10 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1993 VL 70 IS 1 BP 9 EP 21 DI 10.1016/0378-5955(93)90048-6 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000002 PM 7506249 ER PT J AU MROZ, EA NISSIM, KR LECHENE, C AF MROZ, EA NISSIM, KR LECHENE, C TI RAPID RESTING ION FLUXES IN GOLDFISH HAIR-CELLS ARE BALANCED BY (NA+,K+)-ATPASE SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; CELL VOLUME; ION TRANSPORT; SODIUM-POTASSIUM ATPASE; ELECTRON-PROBE ANALYSIS; MENIERES DISEASE ID INNER-EAR; PUMP ACTIVITY; TRANSDUCTION; COCHLEA; K+; NA+,K+-ATPASE; POTENTIALS; SACCULUS; OUABAIN; MODEL AB Inhibition of sodium/potassium pumping by isolated goldfish hair cells led to a rapid gain of sodium and loss of potassium. Half-times for turnover were about 10 min, among the fastest of any cell type examined by electron-probe analysis. Pumping was inhibited by removal of extracellular potassium or by treatment with 1 mM ouabain, as expected of a classical (Na+,K+)-ATPase. The initial rate of entry of sodium after inhibition, about 4 mM/min, provided an estimate of resting sodium-entry and sodium-pumping rates. After return to control medium, cells loaded with sodium by removal of extracellular potassium could recover their normal high-potassium/low-sodium status. The initial rate of recovery (an estimate of the cells' maximum sodium-pumping rate) was sufficient to lower cell sodium by 10 mM/min. This functional estimate of hair-cell (Na+,K+)-ATPase activity was of the same order of magnitude as the biochemical activity of (Na+,K+)-ATPase previously reported for sensory epithelia of other species. The balance between sodium entry and sodium pumping determines hair-cell ionic composition, and thus the resting potential and the driving forces for sodium-coupled transport processes. Imbalance due to excess sodium entry or loss of pump capacity could have significant consequences for hair-cell function and integrity. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NCRR NIH HHS [RR 02604]; NIDCD NIH HHS [R01 DC000033, DC00033]; NINDS NIH HHS [NS13126] NR 44 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1993 VL 70 IS 1 BP 22 EP 30 DI 10.1016/0378-5955(93)90049-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000003 PM 8276730 ER PT J AU AMBROSINO, DM MOLRINE, DC AF AMBROSINO, DM MOLRINE, DC TI CRITICAL-APPRAISAL OF IMMUNIZATION STRATEGIES FOR PREVENTION OF INFECTION IN THE COMPROMISED HOST SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID BONE-MARROW TRANSPLANTATION; INFLUENZAE TYPE-B; CHRONIC LYMPHOCYTIC-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; IMPAIRED ANTIBODY-RESPONSE; GRAM-NEGATIVE BACTEREMIA; LIVE ATTENUATED MEASLES; NON-HODGKINS LYMPHOMA; LONG-TERM SURVIVORS; SICKLE-CELL-ANEMIA RP AMBROSINO, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. NR 103 TC 29 Z9 30 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD OCT PY 1993 VL 7 IS 5 BP 1027 EP 1050 PG 24 WC Oncology; Hematology SC Oncology; Hematology GA LZ421 UT WOS:A1993LZ42100006 PM 8226564 ER PT J AU DELCASTILLO, CF WARSHAW, L AF DELCASTILLO, CF WARSHAW, L TI PERITONEAL METASTASES IN PANCREATIC-CARCINOMA SO HEPATO-GASTROENTEROLOGY LA English DT Article DE PANCREATIC CANCER; METASTASES; PERITONEUM ID CANCER; BIOPSY; LAPAROSCOPY; DIAGNOSIS; CYTOLOGY; AUTOPSY AB Peritoneal metastases are present in about 50 % of patients with pancreatic cancer at the time of death, and are the second most common site of involvement, following the liver. The small size of peritoneal metastases precludes their identification by CT scan, and thus they have to be identified by direct visualization, either at laparotomy or through laparoscopy. Adding laparoscopy to the staging protocol permits pre-operative identification of patients who will not benefit from surgery. Malignant cells are also found within the peritoneal cavity in 20 to 30 % of patients with pancreatic cancer who otherwise have no peritoneal or liver metastases. Their presence, documented by peritoneal washings during laparoscopy or at the time of surgery, seems to be associated with an adverse prognosis. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DELCASTILLO, CF (reprint author), MASSACHUSETTS GEN HOSP,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 18 TC 27 Z9 27 U1 0 U2 3 PU H G E UPDATE MEDICAL PUBL LTD. PI ATHENS PA PO BOX 17160, ATHENS GR-10024, GREECE SN 0172-6390 J9 HEPATO-GASTROENTEROL JI Hepato-Gastroenterol. PD OCT PY 1993 VL 40 IS 5 BP 430 EP 432 PG 3 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA MC533 UT WOS:A1993MC53300005 PM 8270231 ER PT J AU MORADPOUR, D WANDS, JR MELEGARI, M AF MORADPOUR, D WANDS, JR MELEGARI, M TI CHASING THE ESCAPE MUTANT SO HEPATOLOGY LA English DT Note ID HEPATITIS-B VIRUS; LIVER-DISEASE; INFECTION; MUTATION; ANTIGEN; HBSAG RP MORADPOUR, D (reprint author), MASSACHUSETTS GEN HOSP CANC CTR,MOLEC HEPATOL LAB,BOSTON,MA 02129, USA. NR 18 TC 1 Z9 1 U1 0 U2 2 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 OCT PY 1993 VL 18 IS 4 BP 1011 EP 1014 DI 10.1002/hep.1840180438 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MA114 UT WOS:A1993MA11400037 PM 7691705 ER PT J AU HARUTA, I WANDS, JR DELAMONTE, SM AF HARUTA, I WANDS, JR DELAMONTE, SM TI IMPAIRED INSULIN-MEDIATED UP-REGULATION OF GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE-EXPRESSION IN HEPATOCELLULAR-CARCINOMA CELLS INDUCED BY ACUTE ETHANOL INTOXICATION SO HEPATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,MOLEC HEPATOL LAB,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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1993 VL 18 IS 4 BP A268 EP A268 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LY995 UT WOS:A1993LY99500846 ER PT J AU HASEGAWA, K HUANG, JK LIANG, TJ AF HASEGAWA, K HUANG, JK LIANG, TJ TI ENHANCED VIRAL REPLICATION OF A HEPATITIS-B VIRUS MUTANT ASSOCIATED WITH AN EPIDEMIC OF FULMINANT-HEPATITIS SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1993 VL 18 IS 4 BP A145 EP A145 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LY995 UT WOS:A1993LY99500355 ER PT J AU KOZIEL, MJ DUDLEY, D CHOO, QL HOUGHTON, M RALSTON, R WALKER, BD AF KOZIEL, MJ DUDLEY, D CHOO, QL HOUGHTON, M RALSTON, R WALKER, BD TI RECOGNITION OF HCV PROTEINS BY INTRAHEPATIC CYTOTOXIC T-LYMPHOCYTES IN PERSONS WITH CHRONIC HEPATITIS SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHIRON CORP,EMERYVILLE,CA. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1993 VL 18 IS 4 BP A111 EP A111 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LY995 UT WOS:A1993LY99500219 ER PT J AU LINDSAY, KL DAVIS, GL SCHIFF, E BODENHEIMER, H BALART, L DIENSTAG, J PERRILLO, R TAMBURRO, C SILVA, M GOFF, C EVERSON, G SANGHVI, B ALBRECHT, J AF LINDSAY, KL DAVIS, GL SCHIFF, E BODENHEIMER, H BALART, L DIENSTAG, J PERRILLO, R TAMBURRO, C SILVA, M GOFF, C EVERSON, G SANGHVI, B ALBRECHT, J TI LONG-TERM RESPONSE TO HIGHER DOSES OF INTERFERON (IFN) ALFA-2B TREATMENT OF PATIENTS WITH CHRONIC HEPATITIS-C - A RANDOMIZED MULTICENTER TRIAL SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV SO CALIF,LOS ANGELES,CA 90089. UNIV FLORIDA,GAINESVILLE,FL 32611. UNIV MIAMI,MIAMI,FL 33152. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. SO BAPTIST HOSP,NEW ORLEANS,LA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. WASHINGTON UNIV,ST LOUIS,MO 63130. UNIV LOUISVILLE,LOUISVILLE,KY 40292. UNIV COLORADO,DENVER,CO 80202. SCHERING PLOUGH CORP,KENILWORTH,NJ. NR 0 TC 19 Z9 19 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1993 VL 18 IS 4 BP A106 EP A106 DI 10.1016/0270-9139(93)91952-O PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LY995 UT WOS:A1993LY99500199 ER PT J AU MAIA, M WANDS, JR AF MAIA, M WANDS, JR TI IMMUNO-PCR ASSAY FOR THE DETECTION OF LOW-LEVEL HEPATITIS-B SURFACE-ANTIGEN (HBSAG) SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1993 VL 18 IS 4 BP A241 EP A241 DI 10.1016/0270-9139(93)92489-M PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LY995 UT WOS:A1993LY99500735 ER PT J AU NANJI, AA ZHAO, S SADRZADEH, SMH WAXMAN, DJ AF NANJI, AA ZHAO, S SADRZADEH, SMH WAXMAN, DJ TI EVALUATION OF IN-VIVO CYTOKINE GENE-EXPRESSION IN CHRONIC ETHANOL-FED RATS SO HEPATOLOGY LA English DT Meeting Abstract C1 NEW ENGLAND DEACONESS HOSP,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1993 VL 18 IS 4 BP A272 EP A272 DI 10.1016/0270-9139(93)92613-5 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LY995 UT WOS:A1993LY99500859 ER PT J AU WANDS, JR HARUTA, I BROWN, NV CARLSON, RI RHOADS, DB DELAMONTE, SM AF WANDS, JR HARUTA, I BROWN, NV CARLSON, RI RHOADS, DB DELAMONTE, SM TI ETHANOL-INDUCED GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE DOWN-REGULATED GENE-EXPRESSION AND MUTED RESPONSE TO HORMONAL-STIMULATION IN PRIMARY RAT HEPATOCYTE CULTURES SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,TUMOR BIOL LAB,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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1993 VL 18 IS 4 BP A278 EP A278 DI 10.1016/0270-9139(93)92635-D PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LY995 UT WOS:A1993LY99500882 ER PT J AU SONG, BZ DONOFF, RB TSUJI, T TODD, R GALLAGHER, GT WONG, DTW AF SONG, BZ DONOFF, RB TSUJI, T TODD, R GALLAGHER, GT WONG, DTW TI IDENTIFICATION OF RABBIT EOSINOPHILS AND HETEROPHILS IN CUTANEOUS HEALING WOUNDS SO HISTOCHEMICAL JOURNAL LA English DT Article ID GROWTH FACTOR-ALPHA; PEROXIDASE AB The study of wound healing has traditionally used the rabbit as an experimental model. We have recently localized the production of the multifunctional cytokine, TGF-alpha, to eosinophils in rabbit skin wounds. It was evident that during the process of TGF-alpha localization, the distinction between the two granulocytic cell types, eosinophils and heterophils, was impossible by conventional histochemical techniques. This paper describes a rapid method to distinguish these two granulocytes by virtue of their endogenous peroxidases and differential resistance to blockade by inhibitors. In sections that have been blocked by hydrogen peroxide, the peroxidase substrate 3,3'-diaminobenzidine, together with nickel chloride (DAB-Ni), preferentially stained the cytoplasm of rabbit eosinophils while sparing those of heterophils. This selective DAB staining of rabbit eosinophil peroxidase in H2O2-blocked rabbit wounds was verified at the ultrastructural level by electron microscopy. We applied this technique to quantify eosinophil and heterophil infiltration into the 21-day rabbit cutaneous healing wound model. Heterophils were found infiltrated into all three layers of the wound (dot > granulation > base), but eventually all disappeared by day 21. As with the heterophils, eosinophils which had infiltrated into the clot and base of the wound had disappeared by day 21. Unlike the heterophils, eosinophils in the granulation layer of the wound continued to increase up to day 21. The continually increased and sustained presence of the eosinophils together with their demonstrated production of TGF-alpha, in the granulation layer of the healing wound suggests that these cells play an important role in the organizational aspects of healing wounds. C1 MASSACHUSETTS GEN HOSP,DEPT ORAL PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORAL & MAXILLOFACIAL SURG,BOSTON,MA 02114. HARVARD UNIV,SCH DENT MED,BOSTON,MA 02115. FU NIDCR NIH HHS [DE00318, DE-08680, DE-10335] NR 27 TC 9 Z9 9 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0018-2214 J9 HISTOCHEM J JI Histochem.J. PD OCT PY 1993 VL 25 IS 10 BP 762 EP 771 PG 10 WC Cell Biology SC Cell Biology GA MC731 UT WOS:A1993MC73100007 PM 7506704 ER PT J AU GUIGO, R SMITH, TF AF GUIGO, R SMITH, TF TI INFERRING CORRELATION BETWEEN DATABASE QUERIES - ANALYSIS OF PROTEIN-SEQUENCE PATTERNS SO IEEE TRANSACTIONS ON PATTERN ANALYSIS AND MACHINE INTELLIGENCE LA English DT Article DE DATABASE MINING; FUNCTIONAL AND STOCHASTIC DEPENDENCES; INDUCTIVE MACHINE LEARNING; KNOWLEDGE ACQUISITION; MOLECULAR BIOLOGY DATABASES; PATTERN ANALYSIS; PROBABILISTIC INFERENCE; PROTEIN SEQUENCES; SET SIMILARITIES ID MOTIFS AB Given a subset P of a database, we address the problem of finding the query phi in a given database attribute having the closest extension to P. In the particular case that we outline, P is the set of protein sequences in a protein sequence database matching a given protein sequence pattern, whereas phi is a query in the annotation of the database. Ideally, phi is the description of a biological function. If the extension of phi is very similar to P, we may infer association between the pattern and the biological function described by the query. We have developed an algorithm that efficiently searches the query space when negation is not considered. Since the query language is a first-order language, the query space may be mapped into a set algebra in which a measure of stochastic dependence-an assymptotic approximation of the correlation coefficient-is used as a measure of set similarity. The algorithm uses the algebraic properties of such a measure to reduce the time required to search the query space. A prototype implementation of the algorithm has been tested in different collections of protein sequence patterns. Results obtained show that appropriate descriptions for known biologically meaningful protein sequence patterns are found efficiently. We finally describe an application of the algorithm in which the database is automatically and exhaustively searched for potentially relevant protein sequence patterns, and we report a few interesting discoveries obtained in a test case. C1 HARVARD UNIV,DANA FARBER CANC INST,CAMBRIDGE,MA 02138. HARVARD UNIV,DEPT BIOSTAT,CAMBRIDGE,MA 02138. RI sebastianovitsch, stepan/G-8507-2013; Guigo, Roderic/D-1303-2010 OI Guigo, Roderic/0000-0002-5738-4477 NR 25 TC 5 Z9 5 U1 0 U2 1 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 SN 0162-8828 J9 IEEE T PATTERN ANAL JI IEEE Trans. Pattern Anal. Mach. Intell. PD OCT PY 1993 VL 15 IS 10 BP 1030 EP 1041 DI 10.1109/34.254060 PG 12 WC Computer Science, Artificial Intelligence; Engineering, Electrical & Electronic SC Computer Science; Engineering GA MD775 UT WOS:A1993MD77500005 ER PT J AU SUGITA, K DASGUPTA, JD NOJIMA, Y AGEMATSU, K SCHLOSSMAN, SF MORIMOTO, C AF SUGITA, K DASGUPTA, JD NOJIMA, Y AGEMATSU, K SCHLOSSMAN, SF MORIMOTO, C TI PROTEIN-KINASE A-MEDIATED PHOSPHORYLATION OF THE T-CELL SURFACE-ANTIGEN CD27 SO IMMUNOLOGY LA English DT Article ID GROWTH-FACTOR RECEPTOR; LYMPHOCYTES-T; DIFFERENTIATION ANTIGEN; ACTIVATION ANTIGEN; EXPRESSION; FAMILY; CAMP; MEMBRANE; PATHWAY; MEMBER AB CD27 is a T-cell surface antigen expressed on the majority of peripheral T cells and belongs to a newly defined receptor family including the low-affinity nerve growth factor receptor, tumour necrosis factor (TNF) receptors, the B-cell activation antigen CD40, and the Fas antigen. Although the function of CD27 has not been defined, several experimental observations support the notion that this molecule plays an important role in the process of T-cell activation. In this paper, we have demonstrated that a rapid hyperphosphorylation of CD27 is induced by a cyclic AMP-inducing agent, forskolin, and a membrane-permeable cAMP analogue, 8-bromo-cAMP, as well as phorbol 12-myristate 13-acetate (PMA). In addition, increased phosphorylation of CD27 in T-cell activation either via CD2 or CD3 pathways was strongly suppressed by a cyclic nucleotide-dependent kinase inhibitor, H-8, but only slightly by a protein kinase C inhibitor, staurosporine. These results suggest that protein kinase A might be a key kinase responsible for CD27 phosphorylation in the process of T-cell activation. CD27 is the first T-cell surface antigen demonstrated to be phosphorylated by the cyclic AMP-protein kinase A-mediated pathway. 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 NIAID NIH HHS [AI-29530, AI-12069]; NIAMS NIH HHS [AR-33713] NR 33 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD OCT PY 1993 VL 80 IS 2 BP 217 EP 221 PG 5 WC Immunology SC Immunology GA LZ829 UT WOS:A1993LZ82900009 PM 8262550 ER PT J AU MATULONIS, U ROSENFELD, CS SHADDUCK, RK AF MATULONIS, U ROSENFELD, CS SHADDUCK, RK TI PREVENTION OF LEGIONELLA INFECTIONS IN A BONE-MARROW TRANSPLANT UNIT - MULTIFACETED APPROACH TO DECONTAMINATION OF A WATER-SYSTEM SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID NOSOCOMIAL LEGIONNAIRES-DISEASE; DRINKING-WATER; PNEUMOPHILA; PNEUMONIA; CANCER; ERADICATION; RECIPIENTS; MICDADEI; CHLORINE; EFFICACY AB OBJECTIVE: To evaluate measures intended to reduce Legionella infections in patients undergoing bone marrow transplantation (BMT). DESIGN: Ongoing clinical and microbiological surveillance for Legionella colonization or infection was undertaken. All neutropenic patients with pulmonary infiltrates and fever unresponsive to broad-spectrum antibiotics were tested for Legionella organisms. SETTING: A 505-bed medical-surgical hospital with a designated BMT unit. PATIENTS: Two hundred twenty-five patients underwent BMT, 201 were treated on a new BMT unit. The incidence of Legionella infections was compared to that seen in an estimated 150 neutropenic patients treated on other units. INTERVENTION. A combined approach to decontamination of a hospital water supply was assessed. This included heating, particulate filtration, ultraviolet sterilization, and monthly pulse hyperchlorination of water supplied to the BMT unit. The incidence of Legionella infections was assessed on the BMT unit and compared with the frequency elsewhere in the hospital. RESULTS: There were only three cases of Legionella pneumonia among 201 patients undergoing transplantation on a new BMT unit. In contrast, 33 cases of Legionella infections were detected from approximately 1 50 patients treated on general medical floors. CONCLUSION. A multifaceted approach to decontamination of a hospital water system led to a marked reduction in Legionella infections. C1 W PENN HOSP,W PENN CANC INST,4800 FRIENDSHIP AVE,SUITE 2303,PITTSBURGH,PA 15224. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 29 TC 28 Z9 28 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD OCT PY 1993 VL 14 IS 10 BP 571 EP 575 PG 5 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA MB282 UT WOS:A1993MB28200009 PM 8228148 ER PT J AU HARUTA, I WANDS, JR DELAMONTE, SM AF HARUTA, I WANDS, JR DELAMONTE, SM TI IMPAIRED INSULIN-MEDIATED UP-REGULATION OF GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE-EXPRESSION BY ETHANOL EXPOSURE IN-VITRO SO INTERNATIONAL HEPATOLOGY COMMUNICATIONS LA English DT Article DE GAPDH; ETHANOL INTOXICATION; LIVER REGENERATION; HEPATOCELLULAR CARCINOMA ID PHOSPHOENOLPYRUVATE CARBOXYKINASE GENE; LIVER-REGENERATION; 6-PHOSPHOFRUCTO-2-KINASE FRUCTOSE-2,6-BISPHOSPHATASE; MULTIHORMONAL REGULATION; RAT-LIVER; IDENTIFICATION; TRANSCRIPTION; INHIBITION AB Ethanol exposure causes hepatocellular injury, hepatic insufficiency, and impaired hepatocellular regenerative capacity. In the present study, we examined insulin-responsive cell growth, DNA synthesis, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene expression in FOCUS hepatocellular carcinoma cells treated with 0 mM, 40 mM or 100 mM ethanol since, the GAPDH gene contains 5' insulin responsive regulatory sequences, and insulin is required for liver regeneration. Exposure of FOCUS hepatocellular carcinoma cells to ethanol resulted in an immediate reduction in GAPDH mRNA levels, and it abolished the sharp increase in GAPDH protein content observed at 24 and 48 h in control cultures. Diminished responsiveness of GAPDH gene expression to insulin stimulation could represent an important mechanism by which ethanol intoxication impairs liver regeneration. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,MGH E,149 13TH ST,BOSTON,MA 02129. NR 22 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0928-4346 J9 INT HEPATOL COMMUN JI Int. Hepatol. Commun. PD OCT 1 PY 1993 VL 1 IS 5 BP 260 EP 266 DI 10.1016/0928-4346(93)90073-O PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MP230 UT WOS:A1993MP23000004 ER PT J AU ALONSO, A RUTAN, JS AF ALONSO, A RUTAN, JS TI CHARACTER CHANGE IN-GROUP THERAPY SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article AB The treatment of character pathology in group therapy becomes ever more relevant in the current climate of health care delivery with the mounting awareness of the importance of the long-term treatment needed for such problems. This article reviews the psychodynamic meanings of character pathology and addresses the specific ways that psychodynamic group therapy is suited to its treatment. Clinical examples are offered to illustrate how the resolution of character difficulties occurs in group therapy. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR GRP PSYCHOTHERAPY,BOSTON,MA 02114. RP ALONSO, A (reprint author), MASSACHUSETTS GEN HOSP,ACC8 GEN PSYCHIAT PRACTICE,15 PARKHAM ST,BOSTON,MA 02114, USA. NR 15 TC 10 Z9 10 U1 0 U2 2 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0020-7284 J9 INT J GROUP PSYCHOTH JI Int. J. Group Psychother. PD OCT PY 1993 VL 43 IS 4 BP 439 EP 451 PG 13 WC Psychology, Clinical SC Psychology GA MB313 UT WOS:A1993MB31300003 PM 8244596 ER PT J AU ETOH, Y DEWHIRST, FE PASTER, BJ YAMAMOTO, A GOTO, N AF ETOH, Y DEWHIRST, FE PASTER, BJ YAMAMOTO, A GOTO, N TI CAMPYLOBACTER-SHOWAE SP-NOV, ISOLATED FROM THE HUMAN ORAL CAVITY SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID BACTEROIDES-GRACILIS; WOLINELLA-RECTA; EIKENELLA-CORRODENS; VIBRIO-SUCCINOGENES; PERIODONTAL-DISEASE; GEN-NOV; CONCISUS; IDENTIFICATION; HYBRIDIZATION; BACTERIA AB Nine Campylobacter-like strains were isolated from human gingival crevices and characterized. These strains were gram-negative, straight rods that were motile by means of multiple unipolar flagella. They were asaccharolytic and preferred an anaerobic atmosphere rather than a microaerophilic atmosphere for growth, and their growth was stimulated by formate and fumarate. These strains were biochemically similar to Campylobacter curvus and Campylobacter rectus, but were clearly distinguishable from these organisms by the number of flagella (two to five flagella at one end of the cell), by being catalase positive, by their whole-cell protein profiles, by their Western blot (immunoblot) patterns, and on the basis of DNA-DNA homology data. They could also be differentiated from the other species of the genus Campylobacter. The nine Campylobacter-like strains were compared with two strains (FDC 286 and VPI 10279) representing a previously described but unnamed Wolinella sp. The nine isolates and strains FDC 286 and VPI 10279 were found to be members of a single species. The 16S rRNA sequences of two strains of the newly identified species were compared with the rRNA sequences of 21 reference Campylobacter, Wolinella, and Helicobacter species in order to generate a phylogenetic tree. We propose the name Campylobacter showae for the newly identified strains; strain SU A4 (= ATCC 51146) is the type strain of this new species. C1 FORSYTH DENT CTR,BOSTON,MA 02115. RP ETOH, Y (reprint author), SHOWA UNIV,SCH DENT,DEPT ORAL MICROBIOL,1-5-8 HATANODAI,SHINAGAWA KU,TOKYO 142,JAPAN. FU NIDCR NIH HHS [DE-04881, DE-08303] NR 27 TC 47 Z9 48 U1 0 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD OCT PY 1993 VL 43 IS 4 BP 631 EP 639 PG 9 WC Microbiology SC Microbiology GA MC210 UT WOS:A1993MC21000001 PM 7694633 ER PT J AU LEVIN, LA ALBERT, DM JOHNSON, D AF LEVIN, LA ALBERT, DM JOHNSON, D TI MAST-CELLS IN HUMAN OPTIC-NERVE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE MAST CELL; OPTIC NERVE; MENINGS; CHLOROACETATE ESTERASE; OPTIC NEURITIS ID EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; DE-GRANULATION; SYSTEM; RATS; HISTAMINE; NUMBERS; BRAIN AB Purpose. Mast cells are classically found in ocular tissues within the conjunctiva, choroid, and iris. The aim of this study was to examine their distribution in the optic nerve and its meninges. Methods. Sixty-six human optic nerves were studied from normal subjects at autopsy, fetuses aborted for chromosomal abnormalities, and from enucleation specimens of patients with a variety of inflammatory, traumatic, neoplastic, and vascular disorders. Mast cells were identified using a stain for the enzyme chloracetate esterase, and confirmed using toluidine blue, revealing metachromatic cytoplasmic granules. Results. Mast cells were found scattered in the meninges of almost all optic nerves examined, frequently in perivascular locations, with densities up to 2325 mast cells/mm3 (mean 269.7 +/- 64.1 cells/mm3 in normal nerves). Mast cells were found in the optic nerve parenchyma in nerves from four eyes that had severe abnormality, often associated with neovascularization. Normal nerves, as well as nerves from fetuses aborted for congenital defects, had significantly fewer meningeal mast cells than those from eyes with inflammatory or vascular diseases. Degranulation of mast cells was observed more often in eyes with recent severe trauma. Conclusions. Based on their work and the work of others suggesting an association between mast cells and nervous system autoimmune disorders, the authors hypothesize a role for optic nerve mast cells in certain ocular inflammatory conditions. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. UNIV WISCONSIN,MADISON,WI 53706. BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 19 TC 11 Z9 12 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 OCT PY 1993 VL 34 IS 11 BP 3147 EP 3153 PG 7 WC Ophthalmology SC Ophthalmology GA MB601 UT WOS:A1993MB60100013 PM 8407223 ER PT J AU JUPITER, JB PALUMBO, MA NUNLEY, JA AULICINO, PL HERZENBERG, JE AF JUPITER, JB PALUMBO, MA NUNLEY, JA AULICINO, PL HERZENBERG, JE TI SECONDARY RECONSTRUCTION AFTER VASCULARIZED FIBULAR TRANSFER SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID AUTOGENOUS BONE-GRAFTS; TRANSPLANTATION; ANASTOMOSES; RESECTION; STRENGTH; DEFECTS; TUMORS; RADIUS; TIBIA AB We evaluated the results of skeletal reconstruction performed through a mature, vascularized fibular graft in five patients. The average time-interval between the original transplant and the secondary reconstruction was sixty-eight months. The indication for the initial graft had been the loss of bone secondary to trauma in one patient, a skeletal defect due to ablation of a tumor in two patients, and osseous loss due to resection of a congenital pseudarthrosis in two patients. The indication for the second reconstruction was non-union of a fracture as a result of a new traumatic injury in two patients and complex angular deformity in three patients; one of the patients in the latter group had an associated leg-length discrepancy. In all five patients, the second reconstruction was successful, and the vascularized fibular graft responded to the procedure in a manner similar to normal cortical bone. C1 DUKE UNIV,MED CTR,DURHAM,NC 27710. EASTERN VIRGINIA GRAD SCH MED,NORFOLK,VA. UNIV MARYLAND,COLL PK,MD 20742. RP JUPITER, JB (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED TRAUMA SERV,AMBULATORY CARE BLDG,ROOM 529A,BOSTON,MA 02114, USA. NR 47 TC 15 Z9 15 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 OCT PY 1993 VL 75A IS 10 BP 1442 EP 1450 PG 9 WC Orthopedics; Surgery SC Orthopedics; Surgery GA ME011 UT WOS:A1993ME01100004 PM 8408132 ER PT J AU SAMSON, IR SPRINGFIELD, DS SUIT, HD MANKIN, HJ AF SAMSON, IR SPRINGFIELD, DS SUIT, HD MANKIN, HJ TI OPERATIVE TREATMENT OF SACROCOCCYGEAL CHORDOMA - A REVIEW OF 21 CASES SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID TUMORS AB Between 1972 and 1992, twenty-one patients had a primary operation for the treatment of a sacrococcygeal chordoma; seventeen had had a diagnostic biopsy elsewhere. The average age at the time of the operation was fifty-five years (range, six to seventy-eight years); fourteen patients were male and seven were female. In all patients, a posterior approach was used, even for resections at the cephalic levels of the sacrum. In addition, sixteen of the twenty-one patients were treated with adjuvant radiation therapy. Four patients died; three died of metastatic chordoma. Of the remaining seventeen patients, fifteen were apparently free of disease and had not had a local recurrence at the time of the latest follow-up examination. The average duration of follow-up for these fifteen patients was four and one-half years. Of the nine patients who were followed for at least five years, seven were disease-free at the latest follow-up evaluation. Of the seven patients in whom both second sacral roots were the most caudad nerve-roots spared, four had normal bladder control and rive had normal bowel control. Of the four patients in whom the most caudad nerve-roots spared were the first sacral or more cephalic roots, all had impaired bladder control, one had impaired bowel control, and three had a colostomy. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED ONCOL UNIT,GRAY 6,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 14 TC 115 Z9 127 U1 1 U2 1 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 OCT PY 1993 VL 75A IS 10 BP 1476 EP 1484 PG 9 WC Orthopedics; Surgery SC Orthopedics; Surgery GA ME011 UT WOS:A1993ME01100008 PM 8408136 ER PT J AU REDDY, SV SCARCEZ, T WINDLE, JJ LEACH, RJ HUNDLEY, JE CHIRGWIN, JM CHOU, JY ROODMAN, GD AF REDDY, SV SCARCEZ, T WINDLE, JJ LEACH, RJ HUNDLEY, JE CHIRGWIN, JM CHOU, JY ROODMAN, GD TI CLONING AND CHARACTERIZATION OF THE 5'-FLANKING REGION OF THE MOUSE TARTRATE-RESISTANT ACID-PHOSPHATASE GENE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID MULTINUCLEATED CELLS; OSTEOCLAST PHENOTYPE; BONE-RESORPTION; SEQUENCE; PROMOTER; TYPE-5; TRANSCRIPTION; UTEROFERRIN; EXPRESSION; PROTEIN AB Little information is available on the molecular mechanisms controlling osteoclastic bone resorption. We used tartrate-resistant acid phosphatase (TRAP) to begin to investigate the regulation of bone resorption at the molecular level. TRAP is expressed at high levels in osteoclasts and may play an important role in the bone resorptive process. Therefore, we isolated the murine TRAP gene from a mouse spleen genomic library and characterized its promoter. A restriction map was generated for the 17 kb TRAP insert. A 2 kb SmaI fragment, containing the 5'-flanking region, was subcloned and the nucleotide sequence determined. Sequence analysis of the SmaI fragment revealed the presence of numerous candidate transcription factor binding sequences, including those for AP1 and H-APF-1. The H-APF-1 site matches the consensus sequence for the IL-6-regulated transcription factor. An intron was identified at -1 to -393 bp relative to the ATG. The presence of an intron was confirmed by PCR analysis of RNA isolated from murine osteoclasts. Primer extension analysis indicated the presence of a transcription initiation site at -552 bp from the ATG. The region from -1846 to 2 bp relative to the ATG initiation codon drove the transient expression of a luciferase reporter gene when transfected into HRE H9 rabbit endometrial cells. PMA treatment of HRE H9 cells enhanced luciferase transcription approximately threefold. These data suggest that the TRAP promoter is complex and contains multiple regulatory elements. The availability of the TRAP promoter may also permit production of transgenic mice, which can be used to develop previously unavailable osteoclast cell lines. C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT HEMATOL,SAN ANTONIO,TX 78284. CANC THERAPY & RES CTR S TEXAS,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT,SAN ANTONIO,TX 78284. NICHHD,BETHESDA,MD 20892. OI Windle, Jolene/0000-0001-6690-385X FU NIADDK NIH HHS [AM 35188]; NIAMS NIH HHS [AR 41336, AR 39539] NR 30 TC 28 Z9 29 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD OCT PY 1993 VL 8 IS 10 BP 1263 EP 1270 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LY890 UT WOS:A1993LY89000014 PM 8256664 ER PT J AU MASUMOTO, A HEMLER, ME AF MASUMOTO, A HEMLER, ME TI MUTATION OF PUTATIVE DIVALENT-CATION SITES IN THE ALPHA(4) SUBUNIT OF THE INTEGRIN VLA-4 - DISTINCT EFFECTS ON ADHESION TO CS1/FIBRONECTIN, VCAM-1, AND INVASIN SO JOURNAL OF CELL BIOLOGY LA English DT Article ID III CONNECTING SEGMENT; ACTIVATED T-CELLS; BINDING-SITE; ALPHA-4-BETA-1 INTEGRIN; MONOCLONAL-ANTIBODIES; REGULATED EXPRESSION; FIBRONECTIN MOLECULES; LYMPHOCYTE ADHERENCE; RECOGNITION SEQUENCE; PLATELET INTEGRIN AB To investigate the functional significance of putative integrin divalent cation binding sites, several mutated alpha4 subunit cDNAs were constructed. Mutants contained the conservative substitution of Glu for Asp or Asn at the third position in each of three putative divalent cation sites. Transfection of wild-type or mutated alpha4 into K562 cells yielded comparable expression levels and immunoprecipitation profiles. However, for all three alpha4 mutants, adhesion to CS1/fibronectin was greatly diminished in either the presence or absence of the stimulatory anti-beta1 mAb TS2/16. Constitutive adhesion to vascular cell adhesion molecule (VCAM) 1 was also diminished but, unlike CS1 adhesion, was restored upon TS2/16 stimulation. In contrast, adhesion to the bacterial protein invasin was minimally affected by any of the three mutations. For each of the mutants, the order of preference for divalent cations was unchanged compared to wild-type alpha4 on CS1/fibronectin (Mn2+ > Mg2+ > Ca2+), on VCAM-1 (Mn2+ > Mg2+ = Ca2+) and on invasin (Mg2+ = Ca2+). However for the three mutants, the efficiency of divalent cation utilization was decreased. On VCAM-1, 68-108 muM Mn2+ was required to support half-maximal adhesion for the mutants compared with 14-18 muM for wild-type alpha4 .These results indicate (a) that three different ligands for VLA-4 show widely differing sensitivities to mutations within putative divalent cation sites, and (b) each of the three putative divalent cation sites in alpha4 have comparable functional importance with respect to both divalent cation usage and cell adhesion. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MASUMOTO, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM46526, GM38903] NR 82 TC 96 Z9 96 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT PY 1993 VL 123 IS 1 BP 245 EP 253 DI 10.1083/jcb.123.1.245 PG 9 WC Cell Biology SC Cell Biology GA LZ631 UT WOS:A1993LZ63100023 PM 7691827 ER PT J AU BIEDERMAN, J FARAONE, SV DOYLE, A LEHMAN, BK KRAUS, I PERRIN, J TSUANG, MT AF BIEDERMAN, J FARAONE, SV DOYLE, A LEHMAN, BK KRAUS, I PERRIN, J TSUANG, MT TI CONVERGENCE OF THE CHILD-BEHAVIOR CHECKLIST WITH STRUCTURED INTERVIEW-BASED PSYCHIATRIC DIAGNOSES OF ADHD CHILDREN WITH AND WITHOUT COMORBIDITY SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE CHILD BEHAVIOR CHECKLIST; ADHD; COMORBIDITY; CHILDREN ID DEFICIT HYPERACTIVITY DISORDER; PROBANDS; PREVALENCE; RELATIVES; FAMILY AB We evaluated the convergence of CBCL scales with the diagnosis of ADHD and comorbid disorders in 133 ADHD and 118 normal control boys, aged 6-17 years old. We evaluated the strength of association between each CBCL scale and structured-interview derived diagnoses with Total Predictive Value (TPV) and the odds-ratio (OR). Excellent convergence was found between the CBCL Attention Problems scale with the diagnosis of ADHD, between the Delinquent Behavior scale and the diagnosis of CD, and between the Anxiety/Depression scale and the diagnoses of Anxiety Disorders. These findings indicate that the CBCL could serve as a rapid and useful screening instrument to identify comorbid and non-comorbid cases of ADHD. C1 HARVARD COMMUNITY HLTH PLAN,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. VET ADM MED CTR,BROCKTON,MA 02401. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,FRUIT ST,BOSTON,MA 02114, USA. OI Faraone, Stephen/0000-0002-9217-3982 NR 17 TC 183 Z9 184 U1 3 U2 6 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD OCT PY 1993 VL 34 IS 7 BP 1241 EP 1251 DI 10.1111/j.1469-7610.1993.tb01785.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA MA488 UT WOS:A1993MA48800012 PM 8245144 ER PT J AU NAGAYA, T EBERHARDT, NL JAMESON, JL AF NAGAYA, T EBERHARDT, NL JAMESON, JL TI THYROID-HORMONE RESISTANCE SYNDROME - CORRELATION OF DOMINANT-NEGATIVE ACTIVITY AND LOCATION OF MUTATIONS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID RECEPTOR-BETA-GENE; LIGAND-BINDING DOMAIN; C-ERBA PROTOONCOGENES; RETINOID X-RECEPTOR; RAT GROWTH-HORMONE; GENERALIZED RESISTANCE; 3,5,3'-TRIIODOTHYRONINE T3; TRANSCRIPTIONAL REGULATION; AUXILIARY PROTEIN; MAMMALIAN-CELLS AB Generalized resistance to thyroid hormone (GRTH) is caused by multiple distinct mutations that cluster in two regions of the hormone-binding domain of the thyroid hormone beta-receptor. The mutant receptors are functionally inactive, but nevertheless inhibit normal receptor activity in a dominant negative manner. Four different GRTH mutants were studied in the transient expression assays to further examine their functional properties. The transcriptional activity of the mutant receptors correlated with their T3 binding affinities. Two distal region mutants with partial T3 binding were transcriptionally active at high T3 concentrations, but exhibited potent dominant negative activity at low T3 concentrations. Two proximal region mutants that did not bind to T3 were 5- to 10-fold less effective inhibitors of normal receptor function, indicating that dominant negative inhibition is not correlated with T3 binding activity. Each of the proximal and distal region mutants retain the ability to form heterodimers with accessory proteins and to bind to DNA effectively. Because the non-T3 binding thyroid hormone receptor isoform alpha2 also exists in most tissues, its effects on mutant receptor function were also examined. The inhibitory activity of each of the GRTH mutants was potentiated by alpha2 but only in the context of a positively regulated reporter gene. Thus, alpha2 may selectively alter the degree of dominant negative activity that occurs for different target genes. We conclude that the locations of GRTH mutations may influence dominant negative activity by altering transactivating or other functions of the receptor, providing a potential basis for the phenotypic variability in different kindreds with GRTH. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, THYROID UNIT, BOSTON, MA 02114 USA. MAYO CLIN & MAYO FDN, DEPT MED & BIOCHEM, ROCHESTER, MN 55905 USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD-28138]; NIDDK NIH HHS [DK-42144] NR 52 TC 45 Z9 45 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 OCT PY 1993 VL 77 IS 4 BP 982 EP 990 DI 10.1210/jc.77.4.982 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MC303 UT WOS:A1993MC30300018 PM 8408475 ER PT J AU BERKMAN, LF SEEMAN, TE ALBERT, M BLAZER, D KAHN, R MOHS, R FINCH, C SCHNEIDER, E COTMAN, C MCCLEARN, G NESSELROADE, J FEATHERMAN, D GARMEZY, N MCKHANN, G BRIM, G PRAGER, D ROWE, J AF BERKMAN, LF SEEMAN, TE ALBERT, M BLAZER, D KAHN, R MOHS, R FINCH, C SCHNEIDER, E COTMAN, C MCCLEARN, G NESSELROADE, J FEATHERMAN, D GARMEZY, N MCKHANN, G BRIM, G PRAGER, D ROWE, J TI HIGH, USUAL AND IMPAIRED FUNCTIONING IN COMMUNITY-DWELLING OLDER MEN AND WOMEN - FINDINGS FROM THE MACARTHUR FOUNDATION RESEARCH NETWORK ON SUCCESSFUL AGING SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE SUCCESSFUL AGING; PHYSICAL FUNCTIONING; COGNITIVE FUNCTIONING ID ALZHEIMERS-DISEASE; STATE EXAMINATION; ELDERLY PATIENTS; INDEX; RISK; CHROMATOGRAPHY; QUESTIONNAIRE; ASSOCIATION; POPULATION; MORTALITY AB The objective of this study is to determine the range of complex physical and cognitive abilities of older men and women functioning at high, medium and impaired ranges and to determine the psychosocial and physiological conditions that discriminate those in the high functioning group from those functioning at middle or impaired ranges. The subjects for this study were drawn from men and women aged 70-79 from 3 Established Populations for the Epidemiologic Study of the Elderly (EPESE) programs in East Boston MA, New Haven CT, and Durham County NC screened on the basis of criteria of physical and cognitive function. In 1988, 4030 men and women were screened as part of their annual EPESE interview. 1192 men and women met criteria for ''high functioning''. Age and sex-matched subjects were selected to represent the medium (n = 80) and low (n = 82) functioning groups. Physical and cognitive functioning was assessed from performance-based examinations and self-reported abilities. Physical function measures focused on balance, gait, and upper body strength. Cognitive exams assessed memory, language, abstraction, and praxis. Significant differences for every performance-based examination of physical and cognitive function were observed across functioning groups. Low functioning subjects were almost 3 times as likely to have an income of less-than-or-equal-to $5000 compared to the high functioning group. They were less likely to have completed high school. High functioning subjects smoked cigarettes less and exercised more than others. They had higher levels of DHEA-S and peak expiratory flow rate. High functioning elders were more likely to engage in volunteer activities and score higher on scales of self-efficacy, mastery and report fewer psychiatric symptoms. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. DUKE UNIV,MED CTR,DEPT PSYCHIAT,DURHAM,NC 27710. UNIV MICHIGAN,SURVEY RES CTR,ANN ARBOR,MI 48109. VET ADM MED CTR,MT SINAI SCH MED,BRONX,NY 10468. UNIV SO CALIF,ANDRUS GERONTOL CTR,LOS ANGELES,CA 90089. UNIV CALIF IRVINE,DEPT PSYCHOBIOL,IRVINE,CA 92717. PENN STATE UNIV,PROGRAM BIOBEHAV SCI,UNIV PK,PA 16802. UNIV VIRGINIA,DEPT PSYCHOL,CHARLOTTESVILLE,VA 22903. SOCIAL SCI RES COUNCIL,NEW YORK,NY. UNIV MINNESOTA,DEPT PSYCHOL,MINNEAPOLIS,MN 55455. JOHNS HOPKINS UNIV,INST MIND BRAIN,BALTIMORE,MD 21218. MACARTHUR FDN RES NETWORK SUCCESSFUL MIDLIFE DEV,VERO BEACH,FL. JOHN D & LATHERINE T MACARTHUR FDN,CHICAGO,IL. MT SINAI MED CTR,NEW YORK,NY 10029. RP BERKMAN, LF (reprint author), YALE UNIV,DEPT EPIDEMIOL & PUBL HLTH,NEW HAVEN,CT 06510, USA. NR 47 TC 352 Z9 361 U1 1 U2 21 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD OCT PY 1993 VL 46 IS 10 BP 1129 EP 1140 DI 10.1016/0895-4356(93)90112-E PG 12 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA MC571 UT WOS:A1993MC57100010 PM 8410098 ER PT J AU FOLLI, F SAAD, MJA BACKER, JM KAHN, CR AF FOLLI, F SAAD, MJA BACKER, JM KAHN, CR TI REGULATION OF PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY IN LIVER AND MUSCLE OF ANIMAL-MODELS OF INSULIN-RESISTANT AND INSULIN-DEFICIENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INSULIN RECEPTOR KINASE; INSULIN RESISTANCE; INSULIN RECEPTOR SUBSTRATE; PHOSPHATIDYLINOSITOL 3-KINASE; DIABETES ID RECEPTOR TYROSINE KINASE; SKELETAL-MUSCLE; GLUCOSE-TRANSPORT; SIGNAL TRANSDUCTION; INTACT RAT; OB-OB; SUBSTRATE; BINDING; OBESE; AUTOPHOSPHORYLATION AB Insulin stimulates tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1 ), which in turn binds to and activates phosphatidylinositol 3-kinase (PI 3-kinase). In the present study, we have examined these processes in animal models of insulin-resistant and insulin-deficient diabetes mellitus. After in vivo insulin stimulation, there was a 60-80%, decrease in IRS-1 phosphorylation in liver and muscle of the ob / ob mouse. There was no insulin stimulation of PI 3-kinase (85 kD subunit) association with IRS-1, and IRS-1-associated PI 3-kinase activity was reduced 90%. Insulin-stimulated total PI 3-kinase activity was also absent in both tissues of the ob/ob mouse. By contrast, in the streptozotocin diabetic rat, IRS-1 phosphorylation increased 50% in muscle, IRS-1-associated Pt 3-kinase activity was increased two- to threefold in liver and muscle, and there was a 50% increase in the p85 associated with IRS-1 after insulin stimulation in muscle. In conclusion, (a) IRS-1-associated PI 3-kinase activity is differentially regulated in hyperinsulinemic and hypoinsulinemic diabetic states; (b) PI 3-kinase activation closely correlates with IRS-1 phosphorylation; and (c) reduced PI 3-kinase activity may play a role in the pathophysiology of insulin resistant diabetic states, such as that seen in the ob/ob mouse. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,DIV RES,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. OI folli, franco/0000-0001-9824-5222 FU NIDDK NIH HHS [DK 33201, DK 36836] NR 51 TC 211 Z9 212 U1 0 U2 3 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 OCT PY 1993 VL 92 IS 4 BP 1787 EP 1794 DI 10.1172/JCI116768 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MB166 UT WOS:A1993MB16600028 PM 7691886 ER PT J AU WETZLER, M TALPAZ, M VANETTEN, RA HIRSHGINSBERG, C BERAN, M KURZROCK, R AF WETZLER, M TALPAZ, M VANETTEN, RA HIRSHGINSBERG, C BERAN, M KURZROCK, R TI SUBCELLULAR-LOCALIZATION OF BCR, ABL, AND BCR-ABL PROTEINS IN NORMAL AND LEUKEMIC-CELLS AND CORRELATION OF EXPRESSION WITH MYELOID DIFFERENTIATION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CHRONIC MYELOGENOUS LEUKEMIA; HEMATOPOIESIS; BCR-ABL FUSION PROTEINS; C-ABL PROTOONCOGENE PROTEINS; IMMUNOHISTOCHEMISTRY ID CHRONIC MYELOGENOUS LEUKEMIA; CHROMOSOME-POSITIVE LEUKEMIAS; ACUTE LYMPHOBLASTIC-LEUKEMIA; TYROSINE KINASE-ACTIVITY; C-MYC EXPRESSION; PHILADELPHIA-CHROMOSOME; V-ABL; GENE-PRODUCT; ESCHERICHIA-COLI; MESSENGER-RNA AB We used specific antisera and immunohistochemical methods to investigate the subcellular localization and expression of Bcr, Abl, and Bcr-Abl proteins in leukemic cell lines and in fresh human leukemic and normal samples at various stages of myeloid differentiation. Earlier studies of the subcellular localization of transfected murine type IV c-Abl protein in fibroblasts have shown that this molecule resides largely in the nucleus, whereas transforming deletion variants are localized exclusively in the cytoplasm. Here, we demonstrate that the murine type IV c-Abl protein is also found in the nucleus when overexpressed in a mouse hematopoietic cell line. However, in both normal and leukemic human hematopoietic cells, c-Abl is discerned predominantly in the cytoplasm, with nuclear staining present, albeit at a lower level. In contrast, normal endogenous Bcr protein, as well as the aberrant p210BCR-ABL and p190BCR-ABL proteins consistently localize to the cytoplasm in both cell lines and fresh cells. The results with p210BCR-ABL were confirmed in a unique Ph1-positive chronic myelogenous leukemia (CML) cell line, KBM5, which lacks the normal chromosome 9 and hence the normal c-Abl product. Because the p210BCR-ABL protein appears cytoplasmic in both chronic phase and blast crisis CML cells, as does the p190BCR-ABL in Ph1-positive acute leukemia, a change in subcellular location of Bcr-Abl proteins between cytoplasm and nucleus cannot explain the different spectrum of leukemias associated with p210 and p190, nor the transition from the chronic to the acute leukemia phenotype seen in CML. Further analysis of fresh CML and normal hematopoietic bone marrow cells reveals that p210BCR-ABL , as well as the normal Bcr and Abl proteins, are expressed primarily in the early stages of myeloid maturation, and that levels of expression are reduced significantly as the cells mature to polymorphonuclear leukocytes. Similarly, a decrease in Bcr and Abl levels occurs in HL-60 cells induced by DMSO to undergo granulocytic differentiation. The action of p210BCR-ABL and its normal counterparts may, therefore, take place during the earlier stages of myeloid development. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT HEMATOL,HOUSTON,TX 77030. UNIV TEXAS,M D ANDERSON CANC CTR,DEPT LAB MED,HOUSTON,TX 77030. CTR BLOOD RES,BOSTON,MA 02115. RP WETZLER, M (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,DEPT CLIN INVEST,BIOL STUDIES SECT,HOUSTON,TX 77030, USA. NR 66 TC 156 Z9 161 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 OCT PY 1993 VL 92 IS 4 BP 1925 EP 1939 DI 10.1172/JCI116786 PG 15 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MB166 UT WOS:A1993MB16600046 PM 8408645 ER PT J AU SAAD, MJA FOLLI, F KAHN, JA KAHN, CR AF SAAD, MJA FOLLI, F KAHN, JA KAHN, CR TI MODULATION OF INSULIN-RECEPTOR, INSULIN-RECEPTOR SUBSTRATE-1, AND PHOSPHATIDYLINOSITOL 3-KINASE IN LIVER AND MUSCLE OF DEXAMETHASONE-TREATED RATS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INSULIN RESISTANCE; ANIMAL MODELS; TYROSINE KINASE; INSULIN RECEPTOR SUBSTRATE; PHOSPHATIDYLINOSITOL 3-KINASE ID TYROSINE KINASE; GLUCOSE-OXIDATION; SKELETAL-MUSCLE; ANIMAL-MODELS; INTACT RAT; BINDING; PHOSPHORYLATION; PROTEIN; HEPATOCYTES; RESISTANCE AB Insulin rapidly stimulates tyrosine kinase activity of its receptor resulting in phosphorylation of its cytosolic substrate, insulin receptor substrate-1 (IRS-1 ), which in turn associates with phosphatidylinositol 3-kinase (PI 3-kinase), thus activating the enzyme. Glucocorticoid treatment is known to produce insulin resistance, but the exact molecular mechanism is unknown. In the present study we have examined the levels and phosphorylation state of the insulin receptor and IRS-1, as well as the association / activation between IRS-1 and PI 3-kinase in the liver and muscle of rats treated with dexamethasone. After dexamethasone treatment (1 mg/kg per d for 5 d), there was no change in insulin receptor concentration in liver of rats as determined by immunoblotting with antibody to the COOH-terminus of the receptor. However, insulin stimulation of receptor autophosphorylation determined by immunoblotting with antiphosphotyrosine antibody was reduced by 46.7+/-9.1%. IRS-1 and PI 3-kinase protein levels increased in liver of dexamethasone-treated animals by 73 and 25%, respectively (P < 0.05). By contrast, IRS-1 phosphorylation was decreased by 31.3+/-10.9% (P < 0.05), and insulin stimulated PI 3-kinase activity in anti-IRS-1 immunoprecipitates was decreased by 79.5+/-11.2% (P < 0.02). In muscle, the changes were less dramatic, and often in opposite direction of those observed in liver. Thus, there was no significant change in insulin receptor level or phosphorylation after dexamethasone treatment. IRS-1 and PI 3-kinase levels were decreased to 38.6 and 65.6%, respectively (P < 0.01 and P < 0.05). IRS-1 phosphorylation showed no significant change in muscle, but insulin-stimulated IRS-1 associated PI 3-kinase was decreased by 41%. Thus, dexamethasone has differential effects on the proteins involved in the early steps in insulin action in liver and muscle. In both tissues, dexamethasone treatment results in a reduction in insulin-stimulated IRS-1-associated PI 3-kinase, which may play a role in the pathogenesis of insulin resistance at the cellular level in these animals. C1 BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. OI folli, franco/0000-0001-9824-5222 FU NIDDK NIH HHS [DK-33201, DK-36836] NR 41 TC 248 Z9 251 U1 0 U2 0 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 OCT PY 1993 VL 92 IS 4 BP 2065 EP 2072 DI 10.1172/JCI116803 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MB166 UT WOS:A1993MB16600063 PM 7691892 ER PT J AU HAMMER, S CRUMPACKER, C DAQUILA, R JACKSON, B LATHEY, J LIVNAT, D REICHELDERFER, P AF HAMMER, S CRUMPACKER, C DAQUILA, R JACKSON, B LATHEY, J LIVNAT, D REICHELDERFER, P TI USE OF VIROLOGICAL ASSAYS FOR DETECTION OF HUMAN-IMMUNODEFICIENCY-VIRUS IN CLINICAL-TRIALS - RECOMMENDATIONS OF THE AIDS CLINICAL-TRIALS GROUP VIROLOGY COMMITTEE SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Review ID POLYMERASE CHAIN-REACTION; HIV-INFECTED INDIVIDUALS; PLACEBO-CONTROLLED TRIAL; BLOOD MONONUCLEAR-CELLS; P24 ANTIGEN; PERIPHERAL-BLOOD; IMMUNE-COMPLEXES; EARLY DIAGNOSIS; HOMOSEXUAL MEN; ZIDOVUDINE AZT C1 NIAID,DIV AIDS,BETHESDA,MD 20892. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BETH ISRAEL HOSP,CAMBRIDGE,MA. MASSACHUSETTS GEN HOSP,CAMBRIDGE,MA. CASE WESTERN RESERVE UNIV,DEPT CLIN PATHOL,CLEVELAND,OH 44106. UNIV CALIF SAN DIEGO,DEPT INFECT DIS,SAN DIEGO,CA 92103. FU NIAID NIH HHS [NIAID UOI-AI25879, NIAID UOI-AI27659, NIAID UOI-AI27670] NR 64 TC 62 Z9 62 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD OCT PY 1993 VL 31 IS 10 BP 2557 EP 2564 PG 8 WC Microbiology SC Microbiology GA LY059 UT WOS:A1993LY05900001 PM 8253949 ER PT J AU MATTIA, AR WALDRON, MA SIERRA, LS AF MATTIA, AR WALDRON, MA SIERRA, LS TI USE OF THE QUANTITATIVE BUFFY COAT SYSTEM FOR DETECTION OF PARASITEMIA IN PATIENTS WITH BABESIOSIS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID TRANSFUSION-TRANSMITTED BABESIOSIS; RAPID DIAGNOSIS; INFECTION; MICROTI; BLOOD; MALARIA; DISEASE; ANTIBODY AB Quantitative Buffy Coat analysis and blood smears were performed on a total of 47 blood samples. The technique showed 100% correlation with the blood smears in 9 samples containing babesia and 10 samples containing malaria, with some differential features distinguishing the two infections. Quantitative Buffy Coat analysis provides a simple and rapid method for the detection of parasitemia in cases of babesiosis. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MATTIA, AR (reprint author), MASSACHUSETTS GEN HOSP,CLIN MICROBIOL LAB,PARASITOL SECT,BOSTON,MA 02114, USA. NR 27 TC 10 Z9 11 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD OCT PY 1993 VL 31 IS 10 BP 2816 EP 2818 PG 3 WC Microbiology SC Microbiology GA LY059 UT WOS:A1993LY05900054 PM 8253995 ER PT J AU MAZZULLI, T RUBIN, RH FERRARO, MJ DAQUILA, RT DOVEIKIS, SA SMITH, BR THE, TH HIRSCH, MS AF MAZZULLI, T RUBIN, RH FERRARO, MJ DAQUILA, RT DOVEIKIS, SA SMITH, BR THE, TH HIRSCH, MS TI CYTOMEGALOVIRUS ANTIGENEMIA - CLINICAL CORRELATIONS IN TRANSPLANT RECIPIENTS AND IN PERSONS WITH AIDS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID BLOOD LEUKOCYTES; ALLOGRAFT RECIPIENTS; MONOCLONAL-ANTIBODY; CMV ANTIGENEMIA; VIRUS; VIREMIA; INFECTION; DIAGNOSIS; SPECIMENS; CULTURES AB We evaluated a rapid immunoperoxidase technique for the detection of cytomegalovirus (CMV) antigenemia in peripheral blood neutrophils of 56 transplant recipients (117 specimens) and 36 persons with AIDS (59 specimens). Antigenemia was 92% sensitive and 98% specific for the detection of clinical CMV infection in transplant recipients and 100% sensitive and 86% specific in persons with AIDS. Overall, CMV antigenemia was a more rapid and sensitive method for the detection of clinical CMV infection than either shell vial culture or conventional tube culture of blood. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV MICROBIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV HOSP GRONINGEN,DEPT CLIN IMMUNOL,GRONINGEN,NETHERLANDS. FU NCI NIH HHS [CA54741, CA35020] NR 23 TC 68 Z9 68 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD OCT PY 1993 VL 31 IS 10 BP 2824 EP 2827 PG 4 WC Microbiology SC Microbiology GA LY059 UT WOS:A1993LY05900056 PM 8253997 ER PT J AU FREEDMAN, AS NADLER, LM AF FREEDMAN, AS NADLER, LM TI WHICH PATIENTS WITH RELAPSED NON-HODGKINS-LYMPHOMA BENEFIT FROM HIGH-DOSE THERAPY AND HEMATOPOIETIC STEM-CELL TRANSPLANTATION SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID BONE-MARROW TRANSPLANTATION; CHEMOTHERAPY; DISEASE; GRADE RP FREEDMAN, AS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 17 TC 27 Z9 27 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD OCT PY 1993 VL 11 IS 10 BP 1841 EP 1843 PG 3 WC Oncology SC Oncology GA MC299 UT WOS:A1993MC29900001 PM 8105033 ER PT J AU GILCHRIST, KW GRAY, R FOWBLE, B TORMEY, DC TAYLOR, SG AF GILCHRIST, KW GRAY, R FOWBLE, B TORMEY, DC TAYLOR, SG TI TUMOR NECROSIS IS A PROGNOSTIC PREDICTOR FOR EARLY RECURRENCE AND DEATH IN LYMPH-NODE POSITIVE BREAST-CANCER - A 10-YEAR FOLLOW-UP-STUDY OF 728 EASTERN-COOPERATIVE-ONCOLOGY-GROUP PATIENTS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID REGRESSION-MODELS; ESTROGEN-RECEPTOR; ADJUVANT THERAPY; STAGE-I; SURVIVAL; CARCINOMA; PROJECT; GRADE C1 UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI 53706. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HOSP UNIV PENN,PHILADELPHIA,PA 19104. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. FU NCI NIH HHS [CA 21076, CA 23318, CA21115] NR 53 TC 65 Z9 66 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD OCT PY 1993 VL 11 IS 10 BP 1929 EP 1935 PG 7 WC Oncology SC Oncology GA MC299 UT WOS:A1993MC29900015 PM 8410120 ER PT J AU KLASSEN, D GOODFRIEND, TL SCHUNA, AA YOUNG, DY PETERSON, CA AF KLASSEN, D GOODFRIEND, TL SCHUNA, AA YOUNG, DY PETERSON, CA TI ASSESSMENT OF BLOOD-PRESSURE DURING TREATMENT WITH NAPROXEN OR IBUPROFEN IN HYPERTENSIVE PATIENTS TREATED WITH HYDROCHLOROTHIAZIDE SO JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Article ID ANTI-INFLAMMATORY DRUGS; INDOMETHACIN; DIURETICS; PROSTAGLANDINS; PROPRANOLOL; CAPTOPRIL; SULINDAC; ASPIRIN; AGENTS AB This study determined the effect of nonsteroidal anti-inflammatory drug (NSAID) administration on blood pressure in hypertensive patients taking hydrochlorothiazide (HCTZ). Ninety-seven patients with mild essential hypertension and a musculoskeletal indication for NSAID use were studied in a three-phase, multi-center, double-blind, randomized, parallel study based in 15 academic and community clinics. Patients served as their own controls. Patients with stable hypertension, not taking antihypertensive or NSAID medications, were treated with HCTZ 50 mg/day. After 4 to 5 weeks of treatment and documented stable blood pressure, naproxen 375 mg twice a day or ibuprofen 800 mg three times a day was added. Blood pressure was measured at 2 and 4 weeks of NSAID therapy. The average diastolic blood pressure was 97.5 +/- 2.4 mm Hg and the average of the mean arterial pressure (MAP) was 116.8 +/- 6.04 before treatment with HCTZ. Hydrochlorothiazide treatment decreased diastolic blood pressure to 83.1 +/- 5.6 mm Hg, and MAP to 101. 1 +/- 6.5 mm Hg. With naproxen or ibuprofen treatments, mean diastolic blood pressure increased less than 3 mm Hg. At 2 weeks, ibuprofen increased diastolic blood pressure by 2.6 mm Hg (P = .004) and naproxen increased diastolic blood pressure 0.7 mm Hg (P = .40). Both ibuprofen and naproxen significantly increased diastolic pressure at 4 weeks (2.1 mm Hg, P = .042; and 1.8 mm Hg, P = .043, respectively). There was no correlation between the pre-NSAID blood pressure and the magnitude of change after 2 or 4 weeks of treatment. Changes in MAP reflected a pattern similar to diastolic pressure. Ibuprofen increased MAP 3.6 mm Hg (P < .001) and 2.7 mm Hg (P = .019) at 2 and 4 weeks, respectively. Naproxen increased MAP 1.1 mmHg(P = .29)and 1.5 mmHg(P = .16)at2 and 4 weeks, respectively. Patient weight increased 1.0 kg (P <.001) and 0.9 kg (P <.001) with ibuprofen and 0.3 kg (P = .24) and .5 (P = .12) with naproxen at 2 and 4 weeks, respectively. Comparing naproxen and ibuprofen treatments, there were no significant differences in blood pressure or body weight changes. In patients with mild essential hypertension controlled with a thiazide diuretic, the concurrent use of either naproxen or ibuprofen resulted in small but statistically significant increases in blood pressure. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. SYNTEX LABS INC,DIV MED AFFAIRS,DEPT CLIN INVEST,PALO ALTO,CA. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. SYNTEX LABS INC,DIV MED AFFAIRS,DEPT BIOSTAT,PALO ALTO,CA. RP KLASSEN, D (reprint author), UNIV MARYLAND,SCH MED,DEPT MED,DIV NEPHROL,22 S GREENE ST,BALTIMORE,MD 21201, USA. NR 29 TC 15 Z9 15 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0091-2700 J9 J CLIN PHARMACOL JI J. Clin. Pharmacol. PD OCT PY 1993 VL 33 IS 10 BP 971 EP 978 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MA786 UT WOS:A1993MA78600014 PM 8227469 ER PT J AU SELLERS, EM CIRAULO, DA DUPONT, RL GRIFFITHS, RR KOSTEN, TR ROMACH, MK WOODY, GE SHADER, RI SHEAR GREENBLATT, DJ BALLENGER, JC SCHATZBERG BARBEE, JG AF SELLERS, EM CIRAULO, DA DUPONT, RL GRIFFITHS, RR KOSTEN, TR ROMACH, MK WOODY, GE SHADER, RI SHEAR GREENBLATT, DJ BALLENGER, JC SCHATZBERG BARBEE, JG TI ALPRAZOLAM AND BENZODIAZEPINE DEPENDENCE SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on Issues in the Clinical Use of Alprazolam CY MAR 13, 1993 CL WASHINGTON, DC ID DISCRIMINATIVE STIMULUS PROPERTIES; ABUSE LIABILITY; PANIC DISORDER; ALCOHOL WITHDRAWAL; DRUG-USE; ANXIETY DISORDERS; MULTICENTER TRIAL; RELATIVE ABUSE; SELF-INJECTION; DIAZEPAM AB The incidence of nonmedical use of alprazolam is very low relative to its widespread legitimate medical use; in fact, given the millions of patients who have received this medication, the incidence is remarkably small. In particular, among patients with anxiety disorders, dependence does not appear to be a clinically important problem. Alprazolam abuse and dependence represent only a small fraction of the large and serious nonmedical use problem in the United States, and when they occur, are among individuals who abuse other drugs. For example, a serious problem of alprazolam abuse may exist among patients in methadone maintenance treatment. A similar problem exists with diazepam. Alcohol abusers and alcohol-dependent individuals are another group among whom concern about benzodiazepine and alprazolam abuse exists. However, more and better information about the extent and nature of this use is needed. Many patients with alcohol or drug abuse also have anxiety disorders for whom effective pharmacotherapy may be needed. In the interim, caution but not prohibition to use should prevail in prescribing alprazolam to such patients. To the extent that nonmedical alprazolam use exists, evidence suggests that the vast majority of such use is the consequence of the inappropriate prescribing of the medication by a small number of physicians. One way to reduce the inappropriate use of benzodiazepines in methadone programs is to drug test the methadone-maintenance patients and to link positive urine tests to contingency-management strategies. The available data provide some support to the idea that alprazolam and diazepam have more abuse liability than other benzodiazepines. C1 UNIV TORONTO,DEPT PHARMACOL,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT MED,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT PSYCHIAT,TORONTO M5S 1A1,ONTARIO,CANADA. TUFTS UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02111. DEPT VET AFFAIRS OUTPATIENT CLIN,BOSTON,MA. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20057. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06510. UNIV PENN,PHILADELPHIA VET AFFAIRS MED CTR,SUBST ABUSE TREATMENT & RES CTR,PHILADELPHIA,PA 19104. MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC 29425. LOUISIANA STATE UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,NEW ORLEANS,LA 70112. RP SELLERS, EM (reprint author), ADDICT RES FDN,33 RUSSELL ST,TORONTO M5S 2S1,ONTARIO,CANADA. OI Shader, Richard/0000-0002-1888-7565 NR 93 TC 46 Z9 47 U1 2 U2 3 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1993 VL 54 SU S BP 64 EP 77 PG 14 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA MQ072 UT WOS:A1993MQ07200006 PM 8262891 ER PT J AU BOWDEN, CL SCHATZBERG, AF ROSENBAUM, A CONTRERAS, SA SAMSON, JA DESSAIN, E SAYLER, M AF BOWDEN, CL SCHATZBERG, AF ROSENBAUM, A CONTRERAS, SA SAMSON, JA DESSAIN, E SAYLER, M TI FLUOXETINE AND DESIPRAMINE IN MAJOR DEPRESSIVE DISORDER SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID CLINICAL-TRIAL; OUTPATIENTS; AMITRIPTYLINE; CLOMIPRAMINE; IMIPRAMINE AB The efficacy and safety of fluoxetine and desipramine were compared in a 6-week double-blind, parallel group study of patients with major depression. Twenty-five were studied while hospitalized for treatment, and 33 were studied as outpatients. Improvement on the Hamilton Rating Scale for Depression was significant for both treatments from week 1 through the end of the study and did not differ between the two treatments at any week. Overall, 64% of fluoxetine-treated patients and 68% of desipramine-treated patients had at least a 50% reduction in Hamilton Depression score. We assessed whether improvement relatively early in treatment was predictive of categorical response at 6 weeks. Among fluoxetine-treated patients, but not desipramine-treated patients, the week 3 change in the Hamilton Depression mood item was significantly predictive of the response at 6 weeks. Patients treated with fluoxetine had significantly fewer side effects than those treated with desipramine. Desipramine, but not fluoxetine, caused a persistent increase in heart rate. The results suggest that early signs of response to fluoxetine are not dependent on achieving steady-state levels of the drug. C1 MASSACHUSETTS MENTAL HLTH CTR,NEUROPSYCHOPHARMACOL LAB,BOSTON,MA 02115. STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. HARPER GRACE HOSP,DETROIT,MI 48201. TEXAS TECH UNIV,HLTH SCI CTR,LUBBOCK,TX 79430. MCLEAN HOSP,AFFECT DIS PROGRAM,BELMONT,MA 02178. RP BOWDEN, CL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 17 TC 67 Z9 67 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD OCT PY 1993 VL 13 IS 5 BP 305 EP 310 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LZ737 UT WOS:A1993LZ73700002 PM 8227488 ER PT J AU FRYE, MA WIRSHING, WC AMES, D AF FRYE, MA WIRSHING, WC AMES, D TI CLOZAPINE AS A DIAGNOSTIC-TOOL FOR A PSYCHOTIC PARKINSONIAN PATIENT SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter RP FRYE, MA (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA 90073 USA. NR 10 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD OCT PY 1993 VL 13 IS 5 BP 359 EP 360 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LZ737 UT WOS:A1993LZ73700010 PM 7901246 ER PT J AU PERRIN, JM AF PERRIN, JM TI BUILDING THE HEALING PARTNERSHIP - PARENTS, PROFESSIONALS, AND CHILDREN WITH CHRONIC ILLNESSES AND DISABILITIES - LEFF,PT, WALIZER,EH SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review RP PERRIN, JM (reprint author), MASSACHUSETTS GEN HOSP,AMBULATORY CARE PROGRAMS,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD OCT PY 1993 VL 14 IS 5 BP 352 EP 352 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA MB379 UT WOS:A1993MB37900014 ER PT J AU DRETLER, SP AF DRETLER, SP TI UROLITHIASIS - ELECTROHYDRAULIC AND LASER LITHOTRIPSY - REVIEW SO JOURNAL OF ENDOUROLOGY LA English DT Article ID PULSED DYE-LASER; CALCULI C1 HARVARD UNIV,SCH MED,DEPT SURG UROL,BOSTON,MA 02115. RP DRETLER, SP (reprint author), MASSACHUSETTS GEN HOSP,LITHOTRIPTER UNIT,14 FRUIT ST,BOSTON,MA 02114, USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0892-7790 J9 J ENDOUROL JI J. Endourol. PD OCT PY 1993 VL 7 IS 5 BP 387 EP 388 DI 10.1089/end.1993.7.387 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA ME701 UT WOS:A1993ME70100009 PM 8298619 ER PT J AU GOLDFELD, AE MCCAFFREY, PG STROMINGER, JL RAO, A AF GOLDFELD, AE MCCAFFREY, PG STROMINGER, JL RAO, A TI IDENTIFICATION OF A NOVEL CYCLOSPORINE-SENSITIVE ELEMENT IN THE HUMAN TUMOR-NECROSIS-FACTOR-ALPHA GENE PROMOTER SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID NF-KAPPA-B; HUMAN-IMMUNODEFICIENCY-VIRUS; LYMPHOCYTE-SPECIFIC FACTORS; CELL ACTIVATION GENES; BETA-INTERFERON GENE; T-CELL; FACTOR CACHECTIN; NUCLEAR FACTOR; INTERLEUKIN-2 PROMOTER; ENHANCER ELEMENTS AB Tumor necrosis factor alpha (TNF-alpha), a cytokine with pleiotropic biological effects, is produced by a variety of cell types in response to induction by diverse stimuli. In this paper, TNF-alpha mRNA is shown to be highly induced in a murine T cell clone by stimulation with T cell receptor (TCR) ligands or by calcium ionophores alone. Induction is rapid, does not require de novo protein synthesis, and is completely blocked by the immunosuppressant cyclosporin A (CsA). We have identified a human TNF-alpha promoter element, kappa3, which plays a key role in the calcium-mediated inducibility and CsA sensitivity of the gene. In electrophoretic mobility shift assays, an oligonucleotide containing kappa3 forms two DNA protein complexes with proteins that are present in extracts from unstimulated T cells. These complexes appear in nuclear extracts only after T cell stimulation. Induction of the inducible nuclear complexes is rapid, independent of protein synthesis, and blocked by CsA, and thus, exactly parallels the induction of TNF-alpha mRNA by TCR ligands or by calcium ionophore. Our studies indicate that the kappa3 binding factor resembles the preexisting component of nuclear factor of activated T cells. Thus, the TNF-alpha gene is an immediate early gene in activated T cells and provides a new model system in which to study CsA-sensitive gene induction in activated T cells. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP GOLDFELD, AE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-42471, CA-58735]; NIAID NIH HHS [AI-00683] NR 71 TC 196 Z9 198 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 OCT 1 PY 1993 VL 178 IS 4 BP 1365 EP 1379 DI 10.1084/jem.178.4.1365 PG 15 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LY323 UT WOS:A1993LY32300021 PM 8376940 ER PT J AU MATSUMOTO, AK MARTIN, DR CARTER, RH KLICKSTEIN, LB AHEARN, JM FEARON, DT AF MATSUMOTO, AK MARTIN, DR CARTER, RH KLICKSTEIN, LB AHEARN, JM FEARON, DT TI FUNCTIONAL DISSECTION OF THE CD21/CD19/TAPA-1/LEU-13 COMPLEX OF B-LYMPHOCYTES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID EPSTEIN-BARR-VIRUS; KINASE-DEPENDENT PATHWAY; MONOCLONAL-ANTIBODY; RECEPTOR TYPE-2; CELL-SURFACE; ANTIGEN RECEPTORS; ANTIPROLIFERATIVE ANTIBODY; TYROSINE PHOSPHORYLATION; INTERLEUKIN-2 RECEPTOR; ENDOTHELIAL-CELLS AB The CD21/CD19/TAPA-1 complex of B lymphocytes amplifies signal transduction through membrane immunoglobulin (mIg), recruits phosphatidylinositol 3-kinase (PI3-kinase), and induces homotypic cellular aggregation. The complex is unique among known membrane protein complexes of the immune system because its components represent different protein families, and can be expressed individually. By constructing chimeric molecules replacing the extracellular, transmembrane, and cytoplasmic regions of CD19 and CD21 with those of HLA-A2 and CD4, we have determined that CD19 and TAPA-1 interact through their extracellular domains, CD19 and CD21 through their extracellular and transmembrane domains, and, in a separate complex, CD21 and CD35 through their extracellular domains. A chimeric form of CD19 that does not interact with CD21 or TAPA-1 was expressed in Daudi B lymphoblastoid cells and was shown to replicate two functions of wild-type CD19 contained within the complex: synergistic interaction with mIgM to increase intracellular free calcium and tyrosine phosphorylation and association with the p85 subunit of PI3-kinase after ligation of mIgM. The chimeric CD19 lacked the capacity of the wild-type CD19 to induce homotypic cellular aggregation, a function of the complex that can be ascribed to the TAPA-1 component. The CD21/CD19/TAPA-1 complex brings together independently functioning subunits to enable the B cell to respond to low concentrations of antigen. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DIV MOLEC & CLIN RHEUMATOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. FU NIAID NIH HHS [5 RO1 AI22833, 5 RO1 AI28191] NR 48 TC 176 Z9 178 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 OCT 1 PY 1993 VL 178 IS 4 BP 1407 EP 1417 DI 10.1084/jem.178.4.1407 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LY323 UT WOS:A1993LY32300025 PM 7690834 ER PT J AU STOECKLE, JD RONAN, L EHRLICH, C ROBERTS, D AF STOECKLE, JD RONAN, L EHRLICH, C ROBERTS, D TI THE USES OF SHADOWING THE DOCTOR - AND PATIENT - ON SEEING AND HEARING THEIR WORK OF CARE SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,PRIMARY CARE PROGRAM,BOSTON,MA 02114, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD OCT PY 1993 VL 8 IS 10 BP 561 EP 563 DI 10.1007/BF02599640 PG 3 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA MC438 UT WOS:A1993MC43800007 PM 8271089 ER PT J AU STANLEY, J LINTON, D BURNENS, AP DEWHIRST, FE OWEN, RJ PORTER, A ON, SLW COSTAS, M AF STANLEY, J LINTON, D BURNENS, AP DEWHIRST, FE OWEN, RJ PORTER, A ON, SLW COSTAS, M TI HELICOBACTER-CANIS SP-NOV, A NEW SPECIES FROM DOGS - AN INTEGRATED STUDY OF PHENOTYPE AND GENOTYPE SO JOURNAL OF GENERAL MICROBIOLOGY LA English DT Article ID CAMPYLOBACTER-LIKE ORGANISMS; HOMOSEXUAL MEN; GEN-NOV; CINAEDI; DNA; IDENTIFICATION; FENNELLIAE; BACTERIUM; PYLORI; BACTEREMIA AB A group of Campylobacter-like organisms (CLOs) were isolated from the faeces of diarrhoeic or healthy dogs, constituting 4% of all CLOs from this source. Since they formed a unique DNA homology group within the genus Helicobacter, and exhibited distinctive phenotypic properties, they were collectively termed the HC group. A polyphasic taxonomic analysis was made of this group. The phenotype of four dog isolates and a single human isolate was unique and could be distinguished bacteriologically from other helicobacters. Electron microscopic ultrastructure revealed defining characteristics of Helicobacter. The 16S rRNA gene of the nominated type strain NCTC 12739T was sequenced, and its analysis delineated the group as a new species of Helicobacter. This conclusion was supported by relative DNA homology and whole-cell protein electrophoretic patterns. We therefore propose the name Helicobacter canis sp. nov. for this group. The species most closely related to H. canis sp. nov. were H. cinaedi, 'Flexispira rappini' and H. fennelliae. A species-specific recombinant DNA probe was cloned from NCTC 12739T for use in routine laboratory identification and epidemiological studies. The faecal source, bile tolerance and lack of urease activity of H. canis sp. nov. suggest that this new Helicobacter species colonizes the lower bowel rather than the stomach. C1 UNIV BERN,INST VET BACTERIOL,SWISS NATIONAL REFERENCE LAB FOODBORNE DIS,CH-3012 BERN,SWITZERLAND. FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02115. RP STANLEY, J (reprint author), CENT PUBL HLTH LAB,NATL COLLECT TYPE CULTURES,61 COLINDALE AVE,LONDON NW9 5HT,ENGLAND. NR 44 TC 135 Z9 136 U1 0 U2 0 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1287 J9 J GEN MICROBIOL JI J. Gen. Microbiol. PD OCT PY 1993 VL 139 BP 2495 EP 2504 PN 10 PG 10 WC Microbiology SC Microbiology GA MC996 UT WOS:A1993MC99600024 PM 8254320 ER PT J AU GRABBE, S GALLO, RL LINDGREN, A GRANSTEIN, RD AF GRABBE, S GALLO, RL LINDGREN, A GRANSTEIN, RD TI DEFICIENT ANTIGEN PRESENTATION BY LANGERHANS CELLS FROM ATHYMIC (NU/NU) MICE - RESTORATION WITH THYMIC TRANSPLANTATION OR ADMINISTRATION OF CYTOKINES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; NECROSIS-FACTOR-ALPHA; GRANULOCYTE-MACROPHAGE; DENDRITIC CELLS; GM-CSF; PRESENTING CELLS; GROWTH-FACTOR; FACTOR-BETA; DIFFERENTIATION; LYMPHOCYTES AB Epidermal Langerhans cells (LC) are a unique subtype of I-A+ dendritic cells able to present Ag for CD4-dependent immune responses. To investigate whether cutaneous Ag presentation is regulated by thymic elements or soluble factors produced by thymus-derived cells, we compared LC function in athymic nude mice and euthymic normal controls. Examination of the ability of LC to present alloantigens to T cell-enriched responder populations, and insulin to an insulin-specific T cell hybridoma, demonstrated that this function is deficient in LC from inbred and outbred strains of congenitally athymic (nu/nu) mice compared with euthymic litter mates. Adoptive transfer of thymic tissue from euthymic to athymic mice reconstituted the ability of LC derived from athymic mice to present alloantigens. To investigate whether an altered local cytokine microenvironment was responsible for the diminished LC function in athymic mice, various cytokines were administered in vivo and in vitro before determination of alloantigen presentation by epidermal cells from athymic and euthymic mice. Continuous intraperitoneal infusion of granulocyte-macrophage colony stimulating factor (GM-CSF) or TNF-alpha, but not IL-1alpha or IL-2, restored alloantigen presenting ability in athymic LC. In vitro preincubation of LC in GM-CSF or TNF-alpha but not in other cytokines tested also reconstituted alloantigen presentation by LC from athymic mice in most, but not all, of the experiments performed. Furthermore, analysis of cytokine production by epidermal cells in athymic and euthymic mice revealed that epidermal cells from athymic mice produce less GM-CSF and more TNF-alpha, but normal amounts of various other cytokines. However, reconstitution of athymic mice with thymic tissue did not result in normalization of GM-CSF or TNF-alpha production by epidermal cells. These data suggest that LC Ag presenting ability is regulated by thymic factors and that adequate function of cutaneous APC in situ may require the continuous presence of sufficient amounts of cytokines including GM-CSF and TNF-alpha. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, CUTANEOUS BIOL RES CTR, BOSTON, MA 02114 USA. RI Gallo, Richard/A-8931-2009 FU NEI NIH HHS [EY07782]; NIAMS NIH HHS [AR40667] NR 34 TC 31 Z9 31 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 1 PY 1993 VL 151 IS 7 BP 3430 EP 3439 PG 10 WC Immunology SC Immunology GA LZ636 UT WOS:A1993LZ63600003 PM 8376784 ER PT J AU LINDSTEN, T LEE, KP HARRIS, ES PETRYNIAK, B CRAIGHEAD, N REYNOLDS, PJ LOMBARD, DB FREEMAN, GJ NADLER, LM GRAY, GS THOMPSON, CB JUNE, CH AF LINDSTEN, T LEE, KP HARRIS, ES PETRYNIAK, B CRAIGHEAD, N REYNOLDS, PJ LOMBARD, DB FREEMAN, GJ NADLER, LM GRAY, GS THOMPSON, CB JUNE, CH TI CHARACTERIZATION OF CTLA-4 STRUCTURE AND EXPRESSION ON HUMAN T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ACTIVATION ANTIGEN B7; IG-SUPERFAMILY GENES; HUMAN LYMPHOCYTES-T; CD28 MESSENGER-RNA; COSTIMULATORY SIGNAL; PROLIFERATIVE RESPONSES; GENOMIC ORGANIZATION; CHROMOSOMAL LOCATION; INTERLEUKIN-2; SURFACE AB CTLA-4 is an adhesion receptor expressed on activated T cells. The amino acid sequence of CTLA-4 is related to CD28, and although the function of CTLA-4 remains unknown, it shares several features with CD28, including a common counter-receptor, B7, that is present on Ag-presenting cells. In a recent study we found that CD28 and CTLA-4 were coexpressed at the mRNA level on activated T cells but that only CD28 was expressed on resting T cells. Here we show that within the T cell population, CTLA-4 expression is restricted to the subset of T cells that also express cell surface CD28. CTLA-4 mRNA expression can be induced on quiescent T cells via phorbol ester-mediated activation of protein kinase C but not with calcium ionophore treatment alone. Phorbol ester-induced expression of CTLA-4 mRNA could be enhanced with calcium ionophore treatment, and treatment of cells in this manner resulted in a reciprocal decrease in expression of CD28 mRNA. Ligation of CD28 with monoclonal antibody also resulted in the specific and rapid induction of CTLA-4 mRNA. To study the expression of CTLA-4 at the protein level, a rabbit antiserum against a recombinant protein derived from CTLA-4 cDNA was generated. When activated T cells were labeled with [S-35]methionine, the rabbit antiserum precipitated a 41- to 43-kDa protein from whole cell lysates. Similar results were found when detergent-soluble lysates from I-125 surface-labeled resting and activated T cells were analyzed by SDS-PAGE. Surprisingly, under the conditions tested, CTLA-4 migrated primarily as a monomer at the cell surface, and could not be shown to exist as a disulfide-bonded homodimer or as a heterodimer consisting of CTLA-4 and CD28. These results suggest that B7 can bind to T cells via distinct receptor complexes consisting of either CD28 or CTLA-4, and that these complexes may potentially mediate distinct biologic functions. Further, the present results suggest that noncovalent interactions might mediate association of CTLA-4 and/or CD28 at the cell surface. C1 UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT MICROBIOL IMMUNOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. REPLIGEN CORP,CAMBRIDGE,MA 02139. USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20889. FU NCI NIH HHS [CA 54521] NR 51 TC 222 Z9 232 U1 0 U2 5 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 1 PY 1993 VL 151 IS 7 BP 3489 EP 3499 PG 11 WC Immunology SC Immunology GA LZ636 UT WOS:A1993LZ63600009 PM 8397258 ER PT J AU SUBRAMANIAN, R VOLOVSEK, A HO, YS AF SUBRAMANIAN, R VOLOVSEK, A HO, YS TI LACK OF CHANGE IN MNSOD DURING ISCHEMIA-REPERFUSION OF ISOLATED RAT-HEART SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE ISCHEMIA; REPERFUSION; SUPEROXIDE DISMUTASE; MYOCARDIUM; RAT; CARDIAC OUTPUT; LACTATE; LACTIC DEHYDROGENASE ID MITOCHONDRIAL SUPEROXIDE-DISMUTASE; FREE-RADICAL GENERATION; MYOCARDIAL ISCHEMIA; INJURY; OXYGEN; PROTEINS; NITRONE; DAMAGE C1 UNIV WISCONSIN, DEPT PATHOL, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, LAB SERV, MADISON, WI USA. DUKE UNIV, MED CTR, DEPT PULM MED, DURHAM, NC 27710 USA. FU NHLBI NIH HHS [HL-39585] NR 30 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD OCT PY 1993 VL 25 IS 10 BP 1179 EP 1186 DI 10.1006/jmcc.1993.1131 PG 8 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA ME936 UT WOS:A1993ME93600006 PM 8263952 ER PT J AU GOFF, DC SIMMS, CA AF GOFF, DC SIMMS, CA TI HAS MULTIPLE PERSONALITY-DISORDER REMAINED CONSISTENT OVER TIME - A COMPARISON OF PAST AND RECENT CASES SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID DIAGNOSIS AB The purpose of this study was to determine whether recent descriptions of multiple personality disorder are consistent with descriptions from the past. Clinical presentations and childhood histories obtained from early case reports of multiple personality disorder published between 1800 and 1965 (N = 52) were compared with recent case reports published in the 1980s (N = 54). Recent and past cases did not differ in age at diagnosis, length of treatment, duration of follow-up, presence of child and opposite gender personalities, and exposure to hypnosis. Recent cases differed significantly from past cases in mean number of personalities (12 vs. 3), age of onset (11 vs. 20 years), proportion of males (24% vs. 44%), and in prevalence of childhood abuse histories (81% vs. 29%). The authors discuss clinical and cultural factors that may have contributed to the change over time in the number of reported cases, complexity of personality structure, and description of etiological childhood trauma. Although a core set of symptoms has consistently been associated with this disorder over time, other important aspects have not been stable. C1 MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. HARVARD UNIV,DEPT PSYCHOL,CAMBRIDGE,MA 02138. RI toro, edgardo/F-2748-2014 NR 39 TC 10 Z9 10 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD OCT PY 1993 VL 181 IS 10 BP 595 EP 600 DI 10.1097/00005053-199310000-00003 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MD299 UT WOS:A1993MD29900003 PM 8409958 ER PT J AU GOFF, DC AF GOFF, DC TI IS ANYTHING CONSISTENT OVER TIME - REPLY SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD OCT PY 1993 VL 181 IS 10 BP 604 EP 605 DI 10.1097/00005053-199310000-00005 PG 2 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MD299 UT WOS:A1993MD29900005 ER PT J AU BEAL, MF BROUILLET, E JENKINS, BG FERRANTE, RJ KOWALL, NW MILLER, JM STOREY, E SRIVASTAVA, R ROSEN, BR HYMAN, BT AF BEAL, MF BROUILLET, E JENKINS, BG FERRANTE, RJ KOWALL, NW MILLER, JM STOREY, E SRIVASTAVA, R ROSEN, BR HYMAN, BT TI NEUROCHEMICAL AND HISTOLOGIC CHARACTERIZATION OF STRIATAL EXCITOTOXIC LESIONS PRODUCED BY THE MITOCHONDRIAL TOXIN 3-NITROPROPIONIC ACID SO JOURNAL OF NEUROSCIENCE LA English DT Article DE MITOCHONDRIA; EXCITOTOXICITY; HUNTINGTONS DISEASE; STRIATUM; MAGNETIC RESONANCE SPECTROSCOPY ID CYANIDE-INDUCED PARKINSONISM; D-ASPARTATE RECEPTOR; HUNTINGTONS-DISEASE; SUCCINATE-DEHYDROGENASE; ENERGY-METABOLISM; BRAIN-LESIONS; IMPAIRMENT; INHIBITION; GLUTAMATE; IMMUNOREACTIVITY AB An impairment of energy metabolism may underlie slow excitotoxic neuronal death in neurodegenerative diseases. We therefore examined the effects of intrastriatal, subacute systemic, or chronic systemic administration of the mitochondrial toxin 3-nitropropionic acid (3-NP) in rats. Following intrastriatal injection 3-NP produced dose-dependent striatal lesions. Neurochemical and histologic evaluation showed that markers of both spiny projection neurons (GABA, substance P, calbindin) and aspiny interneurons (somatostatin, neuropeptide Y, NADPH-diaphorase) were equally affected. Subacute systemic administration of 3-NP produced age-dependent bilateral striatal lesions with a similar neurochemical profile. However, in contrast to the intrastriatal injections, striatal dopaminergic afferent projections were spared. Both freeze-clamp measurements and chemical shift magnetic resonance spectroscopy showed that 3-NP impairs energy metabolism in the striatum in vivo. Microdialysis showed no increase in extracellular glutamate concentrations after systemic administration of 3-NP. The lesions produced by intrastriatal injection or systemic administration of 3-NP were blocked by prior decortication. However, the NMDA antagonist MK-801 did not block the effects of intrastriatal 3-NP, consistent with a non-NMDA excitotoxic mechanism. In contrast to subacute systemic administration of 3-NP, chronic (1 month) administration produced lesions confined to the striatum in which there was relative sparing of NADPH-diaphorase interneurons, consistent with an NMDA excitotoxic process. Chronic administration showed growth-related proliferative changes in dendrites of spiny neurons similar to changes in Huntington's disease (HD). These results are consistent with in vitro studies showing that mild metabolic compromise can selectively activate NMDA receptors while more severe compromise activates both NMDA and non-NMDA receptors. Chronic administration of 3-NP over 1 month produces selective striatal lesions that replicate many of the characteristic histologic and neurochemical features of HD. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,WARREN 408,BOSTON,MA 02114, USA. RI Kowall, Neil/G-6364-2012; Storey, Elsdon/A-9889-2013; Brouillet, Emmanuel/B-4784-2014 OI Kowall, Neil/0000-0002-6624-0213; Brouillet, Emmanuel/0000-0001-6322-7403 FU DS NIH HHS [NINDS 16367]; NINDS NIH HHS [NINDS NS 10828] NR 46 TC 741 Z9 749 U1 3 U2 11 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD OCT PY 1993 VL 13 IS 10 BP 4181 EP 4192 PG 12 WC Neurosciences SC Neurosciences & Neurology GA MB164 UT WOS:A1993MB16400006 PM 7692009 ER PT J AU HALLIDAY, AL OGILVY, CS CROWELL, RM AF HALLIDAY, AL OGILVY, CS CROWELL, RM TI INTRACRANIAL VERTEBRAL ARTERIOVENOUS-FISTULA SO JOURNAL OF NEUROSURGERY LA English DT Note DE ARTERIOVENOUS FISTULA; VERTEBRAL ARTERY; SUBARACHNOID HEMORRHAGE; ARTERIOVENOUS MALFORMATION ID BALLOON OCCLUSION; ARTERY AB True intracranial arteriovenous fistulas are rare. The authors report a case of a direct fistula between the intracranial portion of the vertebral artery and the lateral medullary venous system. The patient initially presented with a subarachnoid hemorrhage. An open surgical approach with clip obliteration of the lesion was used. The anatomy of this lesion and its surgical management are described. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114. NR 16 TC 13 Z9 13 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 OCT PY 1993 VL 79 IS 4 BP 589 EP 591 DI 10.3171/jns.1993.79.4.0589 PG 3 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA LZ628 UT WOS:A1993LZ62800017 PM 8410229 ER PT J AU FRIM, DM ISACSON, O AF FRIM, DM ISACSON, O TI NEURONAL PROTECTION AGAINST EXCITOTOXICITY - RESPONSE SO JOURNAL OF NEUROSURGERY LA English DT Letter ID NERVE GROWTH-FACTOR; NEOSTRIATUM; STRIATUM C1 MCLEAN HOSP,BELMONT,MA 02178. RP FRIM, DM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 8 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 OCT PY 1993 VL 79 IS 4 BP 640 EP 641 PG 2 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA LZ628 UT WOS:A1993LZ62800035 ER PT J AU SCHIFFRIN, EJ CARTER, EA WALKER, WA FRIEBERG, E BENJAMIN, J ISRAEL, EJ AF SCHIFFRIN, EJ CARTER, EA WALKER, WA FRIEBERG, E BENJAMIN, J ISRAEL, EJ TI INFLUENCE OF PRENATAL CORTICOSTEROIDS ON BACTERIAL-COLONIZATION IN THE NEWBORN RAT SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION LA English DT Article DE BACTERIAL COLONIZATION; CORTICOSTEROIDS; NEWBORN MICROFLORA ID GASTROINTESTINAL MUCOSAL BARRIER; MATURATION; CORTISONE; THYROXINE; SURFACE; TRACT; MICE; AGE AB The interactions between bacteria and the host's intestinal barrier appear to be important regulators of bacterial colonization. In this study we investigated the effect of prenatal corticosteroids, known to accelerate the intestinal maturation of newborn rats, on bacterial colonization in the rat pup. Pregnant rats were treated with either cortisone acetate or normal saline on days 18-21 of gestation and were allowed to deliver spontaneously. The pups, after normal delivery, were sacrificed at different times during the first 10 days of life. The entire small intestine was removed, and each lumen was flushed to exclude nonadherent, transient organisms and homogenized. Tenfold dilutions were plated on horse-blood agar (total bacteria) and MacConkey's medium (gram-negatives). Quantitation and bacterial typification was determined after 24 h of incubation at 37-degrees-C. Total bacteria and gram-negatives found in association with the mucosa were significantly lower in pups prenatally treated with steroids. These changes were not related to any changes in motility or intraluminal digestion. This suggests that the developmental condition of the host's intestinal barrier may be an important regulator of the bacterial microenvironment of the newborn small intestinal mucosa. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. SHRINERS HOSP CRIPPLED CHILDREN,BOSTON,MA. FU NICHD NIH HHS [HD00938-02, HD12437] NR 24 TC 21 Z9 21 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-2116 J9 J PEDIATR GASTR NUTR JI J. Pediatr. Gastroenterol. Nutr. PD OCT PY 1993 VL 17 IS 3 BP 271 EP 275 PG 5 WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics GA MD148 UT WOS:A1993MD14800007 PM 8271126 ER PT J AU REYNOLDS, EM RYAN, DP DOODY, DP AF REYNOLDS, EM RYAN, DP DOODY, DP TI MORTALITY AND RESPIRATORY-FAILURE IN A PEDIATRIC BURN POPULATION SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article; Proceedings Paper CT 1992 ANNUAL MEETING OF THE SECTION-ON-SURGERY OF THE AMERICAN-ACADEMY-OF-PEDIATRICS CY OCT 09-11, 1992 CL SAN FRANCISCO, CA SP AMER ACAD PEDIAT, SECT SURG DE RESPIRATORY DISTRESS SYNDROME; ADULT; BURNS; PEDIATRIC ID PROMPT ESCHAR EXCISION; ACUTE THERMAL-INJURY; DISTRESS SYNDROME; MECHANICAL VENTILATION; MANAGEMENT; PRESSURE C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT SURG,55 FRUIT ST,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 22 TC 8 Z9 8 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0022-3468 J9 J PEDIATR SURG JI J. Pediatr. Surg. PD OCT PY 1993 VL 28 IS 10 BP 1326 EP 1331 DI 10.1016/S0022-3468(05)80322-7 PG 6 WC Pediatrics; Surgery SC Pediatrics; Surgery GA MD716 UT WOS:A1993MD71600021 PM 8263696 ER PT J AU POLYKOFF, GI DRETLER, SP AF POLYKOFF, GI DRETLER, SP TI AMMONIUM URATE CALCULI - REVIEW OF 26 CASES SO JOURNAL OF STONE DISEASE LA English DT Article AB A retrospective review of 2,217 consecutive urinary calculi treated at the Massachusetts General Hospital, Boston, MA revealed that 26 (1.2%) were composed wholly or partly of ammonium urate. Two populations of ammonium urate calculi were identified: Type A or ''septic'' stones (15/26) occurred in patients with chronic urinary tract infection, and the ammonium urate was combined with struvite/apatite. Five of 15 were radiolucent and 6/15 also had proven laxative abuse, dietary or bowel disorders. Type B or ''aseptic'' stones (11/26) occurred in patients with ''sterile'' urine; 4/11 were pure ammonium urate, 5/11 were combined with calcium oxalate and 2/11 were associated with uric acid or apatite with no evidence of struvite: 9/11 had a proven history of either laxative abuse, dietary or bowel disorders; 2/11 were radiolucent. ''Aseptic'' or ''septic'' ammonium urate calculi may be associated with laxative abuse or other gastrointestinal disorders. All patients with ammonium urate calculi should be questioned regarding laxative overuse and if denied, undergo a spot urine test for Phenolphthalein. Excessive urinary uric acid may occur in some patients with ''septic'' ammonium urate stones. These patients may benefit from treatment with Allopurinol. C1 MASSACHUSETTS GEN HOSP,DEPT UROL,LITHOTRIPTOR UNIT,WACC 4,SUITE 486,15 PARKMAN ST,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 1059-9509 J9 J STONE DIS PD OCT PY 1993 VL 5 IS 4 BP 208 EP 212 PG 5 WC Gastroenterology & Hepatology; Urology & Nephrology SC Gastroenterology & Hepatology; Urology & Nephrology GA MA966 UT WOS:A1993MA96600002 ER PT J AU FEWKES, JL SALASCHE, SJ AF FEWKES, JL SALASCHE, SJ TI SURGICAL PEARL - A USER-FRIENDLY DRESSING SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article C1 ARIZONA HLTH SCI CTR,DERMATOL SECT,TUCSON,AZ 85724. RP FEWKES, JL (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD OCT PY 1993 VL 29 IS 4 BP 633 EP 635 PG 3 WC Dermatology SC Dermatology GA MA281 UT WOS:A1993MA28100016 PM 8408799 ER PT J AU RODRIGUEZ, A BOULLON, F PEREZBALINO, N PAVIOTTI, C LIPRANDI, MIS PALACIOS, IF MELE, E PEIREGNE, E DIAZ, R LUGONES, M SANTAERA, OA RISAU, G FERNANDEZ, M SZEJNFELD, M AHUALLI, P VITALE, G PALACIOS, IF BLASKSLEY, E NEWELL, JB PUJADAS, G PAOLASSO, E BAUDINO, C MADOERY, R AF RODRIGUEZ, A BOULLON, F PEREZBALINO, N PAVIOTTI, C LIPRANDI, MIS PALACIOS, IF MELE, E PEIREGNE, E DIAZ, R LUGONES, M SANTAERA, OA RISAU, G FERNANDEZ, M SZEJNFELD, M AHUALLI, P VITALE, G PALACIOS, IF BLASKSLEY, E NEWELL, JB PUJADAS, G PAOLASSO, E BAUDINO, C MADOERY, R TI ARGENTINE RANDOMIZED TRIAL OF PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY VERSUS CORONARY-ARTERY BYPASS-SURGERY IN MULTIVESSEL DISEASE (ERACI) - IN-HOSPITAL RESULTS AND 1-YEAR FOLLOW-UP SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID UNSTABLE ANGINA; COMPLETE REVASCULARIZATION; MYOCARDIAL REVASCULARIZATION; SURVIVAL; DETERMINANTS; EXPERIENCE AB Objectives. This study was designed to compare freedom from combined cardiac events (death, angina, myocardial infarction) at 1-, 3- and 5-year follow-up in patients with multivessel disease randomized to either percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery. Background. Percutaneous transluminal coronary angioplasty has been an effective approach in patients with coronary artery disease, but its role in patients with multivessel coronary artery disease is still controversial. Methods. One-hundred twenty-seven patients with multivessel disease and lesions suitable for either form of therapy were randomized to either coronary artery bypass grafting (n = 64) or coronary angioplasty (n = 63). In this study we report the immediate results and freedom from combined cardiac events at 1-year follow-up. Results. Demographic, clinical and angiographic characteristics were similar in both groups. There were no differences in in-hospital deaths, frequency of periprocedure myocardial infarction or need for emergency revascularization procedures between the two groups. At 1-year follow-up, there were no differences in mortality or in the incidence of myocardial infarction between the groups. However, patients treated with coronary artery bypass grafting were more frequently free of angina, reinterventions and combined cardiac events than were patients treated with coronary angioplasty (83.5% vs. 63.7%, p < 0.005). In-hospital cost and cumulative cost at 1-year follow-up were greater for the coronary artery bypass grafting than for the coronary angioplasty group. Conclusions. No significant differences were found in major in-hospital complications between patients treated with coronary artery bypass grafting or coronary angioplasty. Although at 1-year follow-up there were no differences in survival and freedom from myocardial infarction, patients in the coronary artery bypass grafting group were more frequently free from angina, reinterventions and combined events than were patients in the coronary angioplasty group. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. ANCHORENA HOSP,CARDIAC UNIT,BUENOS AIRES,ARGENTINA. NR 30 TC 233 Z9 238 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD OCT PY 1993 VL 22 IS 4 BP 1060 EP 1067 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ362 UT WOS:A1993MQ36200014 PM 8409041 ER PT J AU COLUCCI, WS SONNENBLICK, EH ADAMS, KF BERK, M BROZENA, SC GRABICKI, JM KUBO, SA LEJEMTEL, T LITTLER, WA SHABETAI, R SHANNON, J STARLING, MR WASSERMAN, AG BERGSTEN, L BOGART, D BROOKS, N CABANISS, D ALPERT, MA CHAITMAN, B COWLEY, AJ DEBONO, DP DEQUATTRO, V MICHAEL, AD FENSTER, PE FREEDMAN, RE GOODMAN, MA GORWITT, JI HOGLUND, C JENNINGS, K JEWITT, DE KIRBY, BJ KONECKE, LL LINDENFIELD, J MOBLEY, RA MUIR, AL PIETILA, K QUIGG, R ROBSON, RH STEPHENS, JD TIMMIS, AD TORP, A TOUCHON, RC WEISSBERG, PL WESTCOTT, RJ ATWOOD, JE BROZENA, S CARVER, JR CHESEBRO, JH RODEHEFFER, RJ CURTIS, GP DEWOOD, M FARNHAM, J FROELICHER, V GREEN, RJ ITELD, BJ MCBRIDE, JW MOHIUDDIN, SM NADEMANEE, K YELLEN, LG SILVER, M STEVENSON, LW WRIGHT, RF AF COLUCCI, WS SONNENBLICK, EH ADAMS, KF BERK, M BROZENA, SC GRABICKI, JM KUBO, SA LEJEMTEL, T LITTLER, WA SHABETAI, R SHANNON, J STARLING, MR WASSERMAN, AG BERGSTEN, L BOGART, D BROOKS, N CABANISS, D ALPERT, MA CHAITMAN, B COWLEY, AJ DEBONO, DP DEQUATTRO, V MICHAEL, AD FENSTER, PE FREEDMAN, RE GOODMAN, MA GORWITT, JI HOGLUND, C JENNINGS, K JEWITT, DE KIRBY, BJ KONECKE, LL LINDENFIELD, J MOBLEY, RA MUIR, AL PIETILA, K QUIGG, R ROBSON, RH STEPHENS, JD TIMMIS, AD TORP, A TOUCHON, RC WEISSBERG, PL WESTCOTT, RJ ATWOOD, JE BROZENA, S CARVER, JR CHESEBRO, JH RODEHEFFER, RJ CURTIS, GP DEWOOD, M FARNHAM, J FROELICHER, V GREEN, RJ ITELD, BJ MCBRIDE, JW MOHIUDDIN, SM NADEMANEE, K YELLEN, LG SILVER, M STEVENSON, LW WRIGHT, RF TI EFFICACY OF PHOSPHODIESTERASE INHIBITION WITH MILRINONE IN COMBINATION WITH CONVERTING-ENZYME INHIBITORS IN PATIENTS WITH HEART-FAILURE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID EXERCISE TOLERANCE; ORAL MILRINONE; BIPYRIDINE; DISEASE; AGENT AB We describe the results of two placebo controlled trials (MIL-1077 and MIL-1078) designed to evaluate the clinical efficacy of oral milrinone administered together with converting enzyme inhibitors to patients with congestive heart failure. Although these trials were terminated prematurely, they provide the only controlled data regarding the effect of oral milrinone on exercise capacity in patients receiving converting enzyme inhibitors. Of the 254 patients randomized, 140 completed one of the trials or reached an end point and are the basis of this report. In both trials, there was a clear trend for an increase in exercise capacity in the milrinone-treated patients (+26 +/- 8% vs. +5 +/- 7% in MIL-1077 and +11 +/- 5% vs. +2 +/- 4% in MIL-1078). Symptoms of congestive heart failure were decreased in one trial but not the other. Quality of life, as assessed by a questionnaire, was not effected in either trial. There was an increased incidence of adverse events in milrinone treated patients. Adverse events related primarily to hypotension and vasodilation led to discontinuation of drug in 18 milrinone-treated patients vs. 1 placebo-treated patient. Milrinone had little or no proarrhythmic effect and cardiovascular deaths were distributed equally between the milrinone and placebo groups. These data suggest that when used in combination with a converting enzyme inhibitor, oral milrinone improves exercise capacity but is associated with a high incidence of adverse events that appear to be related to excessive vasodilation. C1 UNIV KENTUCKY, LEXINGTON, KY USA. PENN VALLEY MED GRP, KANSAS CITY, MO USA. WYTHENSHAWE HOSP, MANCHESTER M23 9LT, LANCS, ENGLAND. UNIV SO ALABAMA, MOBILE, AL USA. ST LOUIS UNIV, MED CTR, ST LOUIS, MO USA. UNIV NOTTINGHAM HOSP, QUEENS MED CTR, NOTTINGHAM, NOTTS, ENGLAND. GROBY RD HOSP, LEICESTER, LEICS, ENGLAND. USC, SCH MED, LOS ANGELES, CA USA. CENT CARDIOL MED CLIN, BAKERSFIELD, CA USA. UNIV ARIZONA HOSP, TUCSON, AZ USA. FREEDMAN CLIN, ALEXANDRIA, LA USA. CARDIOVASC MED ASSOCIATES, MINEOLA, NY USA. ESCONDIDO CARDIOL ASSOCIATES, ESCONDIDO, CA USA. ABERDEEN ROYAL INFIRM, ABERDEEN, SCOTLAND. KINGS COLL HOSP, LONDON, ENGLAND. ROYAL DEVON & EXETER HOSP, EXETER EX2 5DW, DEVON, ENGLAND. UNIV COLORADO, CTR HLTH & SCI, DENVER, CO USA. UNIV BIRMINGHAM, QUEEN ELIZABETH HOSP, BIRMINGHAM B15 2TH, W MIDLANDS, ENGLAND. ROYAL INFIRM, EDINBURGH, SCOTLAND. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, RICHMOND, VA 23298 USA. CUMBERLAND INFIRM, CARLISLE, CUMBRIA, ENGLAND. VET ADM MED CTR, ANN ARBOR, MI USA. OLDCHURCH HOSP, ROMFORD, ESSEX, ENGLAND. NEWHAM DIST GEN HOSP, LONDON, ENGLAND. MARSHALL UNIV, SCH MED, HUNTINGTON, WV USA. GEORGE WASHINGTON UNIV, MED CTR, WASHINGTON, DC 20037 USA. ADDENBROOKES HOSP, CAMBRIDGE, ENGLAND. SEATTLE HEART CLIN, SEATTLE, WA USA. UNIV N CAROLINA, CHAPEL HILL, NC USA. VET ADM MED CTR, PALO ALTO, CA USA. TEMPLE UNIV HOSP & MED SCH, PHILADELPHIA, PA USA. MAYO CLIN & MAYO FDN, ROCHESTER, MN 55905 USA. BRIGHAM & WOMENS HOSP, BOSTON, MA USA. SCRIPPS CLIN, MED GRP, LA JOLLA, CA USA. DEACONESS MED CTR, BOSTON, MA USA. JACKSON CLIN, MADISON, WI USA. UNIV FLORIDA, GAINESVILLE, FL USA. UNIV MINNESOTA, CTR HLTH, MINNEAPOLIS, MN 55455 USA. ALBERT EINSTEIN COLL MED, BRONX, NY USA. ST PAUL RAMSEY MED CTR, ST PAUL, MN USA. CREIGHTON CARDIAC CTR, OMAHA, NE USA. DENVER GEN HOSP, DENVER, CO USA. VET AFFAIRS MED CTR, SAN DIEGO, CA USA. MICHAEL REESE HOSP, CHICAGO, IL USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. WESTSIDE CARDIOL CONSULTANTS, SANTA MONICA, CA USA. CARDIOL ASSOCIATES MED GRP E SAN DIEGO, SAN DIEGO, CA USA. RP COLUCCI, WS (reprint author), BRIGHAM & WOMENS HOSP, DIV CARDIOVASC, 75 FRANCIS ST, BOSTON, MA 02115 USA. NR 13 TC 21 Z9 21 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD OCT PY 1993 VL 22 IS 4 SU A BP A113 EP A118 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MR869 UT WOS:A1993MR86900020 PM 8376682 ER PT J AU DELAHANTY, LM ANDERSON, EJ AF DELAHANTY, LM ANDERSON, EJ TI CARBOHYDRATE COUNTING ALTERNATIVE IN GLUCOSE CONTROL - REPLY SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Letter RP DELAHANTY, LM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 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 OCT PY 1993 VL 93 IS 10 BP 1104 EP 1104 DI 10.1016/0002-8223(93)92748-M PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MC632 UT WOS:A1993MC63200005 ER PT J AU KIRN, DH LYNCH, TJ MENTZER, SJ LEE, TH STRAUSS, GM ELIAS, AD SKARIN, AT SUGARBAKER, DJ AF KIRN, DH LYNCH, TJ MENTZER, SJ LEE, TH STRAUSS, GM ELIAS, AD SKARIN, AT SUGARBAKER, DJ TI MULTIMODALITY THERAPY OF PATIENTS WITH STAGE-IIIA, N2 NON-SMALL-CELL LUNG-CANCER - IMPACT OF PREOPERATIVE CHEMOTHERAPY ON RESECTABILITY AND DOWNSTAGING SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID RADIATION-THERAPY; ONCOLOGY-GROUP; CARCINOMA; MEDIASTINOSCOPY; IRRADIATION AB To assess the effect of neoadjuvant platinum-based chemotherapy on resectability, stage of disease at resection, and patterns of recurrence and survival in patients with IIIA, N2 non-small-cell lung cancer, we examined the first 60 patients treated with neoadjuvant chemotherapy followed by attempted resection in our institution. Of 67 patients identified, 7 patients were ineligible because of comorbidities, 3 patients refused chemotherapy, and 1 consented but died before treatment. Fifty-six received neoadjuvant chemotherapy. Complications of chemotherapy were minor, with no deaths. Fifty-four patients had thoracotomy; 75% (n = 42) had complete resection and 25% (n = 14) had unresectable lesions. One postoperative death occurred (2%). Pathologic review of specimens and nodal groups revealed that 41% (n = 23) were downstaged, 39% (n = 22) remained stage IIIA, and 19% (n = 11) progressed. Squamous histologic type was predictive of resectability, 18 of 20 patients having resectable squamous cell tumors (p < 0.05). Actuarial survivals at 1 and 2 years were 74% and 52%, respectively. In patients with resectable tumors survivals at 1 and 2 years were 85% and 67%, respectively. For those with unresectable lesions, survivals were 43% and 14%. Relapse-free survivals at 1 and 2 years for patients with resectable lesions were 70% and 42%, respectively. Relapses were local in 25% (n = 4), at a distant site only in 50% (n = 8), combined local and distant in 25% (n = 4). Distant relapse occurred in the central nervous system only in 7 of 8 patients (88%). Complete resectability was highly predictive of improved survival (p < 0.0002). Weight loss did not affect resectability but was associated with decreased survival (p < 0.003). Neoadjuvant chemotherapy appears to improve resectability and to pathologically downstage N2 non-small-cell lung cancer from stage IIIA. Multiinstitutional randomized trials are needed to further demonstrate the efficacy of this approach. C1 BRIGHAM & WOMENS HOSP,DIV THORAC SURG,75 FRANCIS ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-19589] NR 20 TC 20 Z9 21 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD OCT PY 1993 VL 106 IS 4 BP 696 EP 702 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA MA733 UT WOS:A1993MA73300017 PM 8412265 ER PT J AU CIRESI, KF ANTHONY, JP HOFFMAN, WY BOWERSOX, JC REILLY, LM RAPP, JH AF CIRESI, KF ANTHONY, JP HOFFMAN, WY BOWERSOX, JC REILLY, LM RAPP, JH TI LIMB SALVAGE AND WOUND COVERAGE IN PATIENTS WITH LARGE ISCHEMIC ULCERS - A MULTIDISCIPLINARY APPROACH WITH REVASCULARIZATION AND FREE TISSUE TRANSFER SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID RANDOM-PATTERN FLAPS; LOWER-EXTREMITY; DISTAL REVASCULARIZATION; MAJOR AMPUTATIONS; MUSCLE FLAP; BYPASS; RECONSTRUCTION; PERONEAL; FOOT AB Purpose: Large ischemic wounds, particularly with exposed bone or tendons, may not heal even after successful revascularization. We have taken an aggressive approach for limb salvage that uses autogenous vein grafting and simultaneous microvascular free tissue transfer. Methods: In the past year, seven patients (average age 67 years; range 56 to 79) with ischemic disease and distal ulceration underwent revascularization for limb salvage and free tissue transfer. Each had a nonhealing wound (average size 80 cm2), present for 8.6 months (range 2 to 24 months). Simultaneous vein bypass and free tissue transfer was performed in four (57%) of the seven patients. Results: All flaps were initially viable; however, one was lost on day 4 because of hypotension and congestive heart failure. One patient with a successful flap died at 1 month of pneumonia. Minor wound complications were seen in four (57%) of seven patients. Five of the seven patients had the wounds heal completely and are ambulatory at an average follow up of 10 months. Conclusions: Our aggressive approach was successful in preserving limb length and function in 71% of our patients. We perform simultaneous procedures whenever possible to minimize operative and hospitalization times. We believe that this combined approach optimizes the treatment of ischemic limbs with large ulcers. C1 UNIV CALIF SAN FRANCISCO, SAN FRANCISCO VET AFFAIRS MED CTR, DIV PLAST & RECONSTRUCT SURG, SAN FRANCISCO, CA 94143 USA. UNIV CALIF SAN FRANCISCO, SAN FRANCISCO VET AFFAIRS MED CTR, DIV VASC SURG, SAN FRANCISCO, CA 94143 USA. NR 24 TC 32 Z9 32 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 OCT PY 1993 VL 18 IS 4 BP 648 EP 655 PG 8 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MB165 UT WOS:A1993MB16500012 PM 8411472 ER PT J AU SHERRY, B LI, XY TYLER, KL CULLEN, JM VIRGIN, HW AF SHERRY, B LI, XY TYLER, KL CULLEN, JM VIRGIN, HW TI LYMPHOCYTES PROTECT AGAINST AND ARE NOT REQUIRED FOR REOVIRUS-INDUCED MYOCARDITIS SO JOURNAL OF VIROLOGY LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; NATURAL-KILLER CELLS; MONOCLONAL-ANTIBODIES; VIRAL MYOCARDITIS; T-CELLS; MICE; VIRUS; PATHOGENESIS; COXSACKIEVIRUS-B3; INFECTION AB Many studies suggest that host lymphocytes are damaging, rather than protective, in virally induced myocarditis. We have investigated the role of lymphocyte-based immunity in murine myocarditis by using a myocarditic reovirus (reovirus serotype 3 8B), nonmyocarditic reoviruses, adoptive transfer experiments, and mice with severe combined immunodeficiency (SCID mice). Prior to infection, passive transfer of monoclonal antibodies specific for 8B capsid proteins protected neonatal mice against 8B-induced myocarditis, indicating that humoral immunity can protect against myocarditis. Some monoclonal antibodies acted by blocking viral spread to and/or replication in the heart. Passive transfer of reovirus-immune, but not naive, spleen cells prior to infection protected neonatal mice from 8B-induced myocarditis. Depletion of either CD4 or CD8 T cells resulted in increased viral titer in the heart but did not abrogate immune cell-mediated protection against myocardial injury. This shows that both CD4 and CD8 T cells can act independently to protect myocardial tissue from reovirus infection. In addition, reovirus 8B caused extensive myocarditis in SCID mice. This confirms a prior report (B. Sherry, F. J. Schoen, E. Wenske, and B. N. Fields, J. Virol. 63:4840-4849, 1989) that T cells are not required for reovirus-induced myocarditis and demonstrates for the first time that B cells are not required for reovirus-induced myocarditis. We used SCID mice and a panel of reoviruses to assess (i) the relationship between growth in the heart and myocardial damage and (ii) the possibility that nonmyocarditic reoviruses exhibit a myocarditic phenotype in the absence of functional lymphocytes. Growth in the heart was not the sole determinant of myocarditic potential in SCID mice. Although 8B induced myocarditis in SCID mice, no or minimal myocarditis was found in SCID mice infected with four reovirus strains previously shown (B. Sherry and B. N. Fields J. Virol. 63:4850-4856, 1989) to be nonmyocarditic or poorly myocarditic in normal neonatal mice. We conclude that (i) humoral immunity and cellular immunity are protective against, and not required for, reovirus-induced myocarditis and (ii) the potential to induce cardiac damage is a property of the virus independent of lymphocyte-based immunity. C1 DENVER VET AFFAIRS MED CTR,DEPT NEUROL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT NEUROL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT MICROBIOL IMMUNOL,DENVER,CO 80262. WASHINGTON UNIV,SCH MED,DEPT MED,DIV INFECT DIS,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PATHOL,DIV INFECT DIS,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT MOLEC MICROBIOL,DIV INFECT DIS,ST LOUIS,MO 63110. RP SHERRY, B (reprint author), N CAROLINA STATE UNIV,COLL VET MED,DEPT MICROBIOL PATHOL & PARASITOL,4700 HILLSBOROUGH ST,RALEIGH,NC 27606, USA. OI Tyler, Kenneth/0000-0003-3294-5888 FU NIAID NIH HHS [AI31250]; NINDS NIH HHS [2 P50 NS16998] NR 33 TC 48 Z9 52 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 OCT PY 1993 VL 67 IS 10 BP 6119 EP 6124 PG 6 WC Virology SC Virology GA LX120 UT WOS:A1993LX12000048 PM 8396673 ER PT J AU MOORE, JP SATTENTAU, QJ YOSHIYAMA, H THALI, M CHARLES, M SULLIVAN, N POON, SW FUNG, MS TRAINCARD, F PINKUS, M ROBEY, G ROBINSON, JE HO, DD SODROSKI, J AF MOORE, JP SATTENTAU, QJ YOSHIYAMA, H THALI, M CHARLES, M SULLIVAN, N POON, SW FUNG, MS TRAINCARD, F PINKUS, M ROBEY, G ROBINSON, JE HO, DD SODROSKI, J TI PROBING THE STRUCTURE OF THE V2-DOMAIN OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SURFACE GLYCOPROTEIN GP120 WITH A PANEL OF 8 MONOCLONAL-ANTIBODIES - HUMAN IMMUNE-RESPONSE TO THE V1-DOMAIN AND V2-DOMAIN SO JOURNAL OF VIROLOGY LA English DT Article ID PRINCIPAL NEUTRALIZING DETERMINANT; ENVELOPE GLYCOPROTEIN; CD4 BINDING; SOLUBLE CD4; CONFORMATIONAL-CHANGES; VARIABLE REGIONS; HIV-1 INFECTION; V3 LOOP; IDENTIFICATION; DOMAIN AB We have analyzed a panel of eight murine monoclonal antibodies (MAbs) that depend on the V2 domain for binding to human immunodeficiency virus type 1 (HIV-1) gp120. Each MAb is sensitive to amino acid changes within V2, and some are affected by substitutions elsewhere. With one exception, the MAbs were not reactive with peptides from the V2 region, or only poorly so. Hence their ability to bind recombinant strain IIIB gp120 depended on the preservation of native structure. Three MAbs cross-reacted with strain RF gp120, but only one cross-reacted with MN gp120, and none bound SF-2 gp120. Four MAbs neutralized HIV-1 IIIB with various potencies, and the one able to bind MN gp120 neutralized that virus. Peptide serology indicated that antibodies cross-reactive with the HxB2 VI and V2 regions are rarely present in HIV-1-positive sera, but the relatively conserved segment between the V1 and V2 loops was recognized by antibodies in a significant fraction of sera. Antibodies able to block the binding of V2 MAbs to IIIB or MN gp120 rarely exist in sera from HIV-1-infected humans; more common in these sera are antibodies that enhance the binding of V2 Mabs to gp120. This enhancement effect of HIV-1-positive sera can be mimicked by several human MAbs to different discontinuous gp120 epitopes. Soluble CD4 enhanced binding of one V2 MAb to oligomeric gp120 but not to monomeric gp120, perhaps by inducing conformational changes in the oligomer. C1 CTR IMMUNOL MARSEILLE LUMINY,F-13288 MARSEILLE,FRANCE. PASTEUR INST,HYBRIDOLABS,F-75724 PARIS,FRANCE. TANOX BIOSYST INC,HOUSTON,TX 77025. UNIV CONNECTICUT,DEPT PEDIAT,STORRS,CT 06030. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. ABBOTT LABS,DIV DIAGNOST,N CHICAGO,IL 60064. RP MOORE, JP (reprint author), NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10016, USA. RI Yoshiyama, Hironori/D-7902-2012 FU NIAID NIH HHS [AI 25542-05A1, P30 AI27742-04] NR 61 TC 107 Z9 107 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 OCT PY 1993 VL 67 IS 10 BP 6136 EP 6151 PG 16 WC Virology SC Virology GA LX120 UT WOS:A1993LX12000050 PM 7690418 ER PT J AU DORFMAN, T LUBAN, J GOFF, SP HASELTINE, WA GOTTLINGER, HG AF DORFMAN, T LUBAN, J GOFF, SP HASELTINE, WA GOTTLINGER, HG TI MAPPING OF FUNCTIONALLY IMPORTANT RESIDUES OF A CYSTEINE-HISTIDINE BOX IN THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 NUCLEOCAPSID PROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; STRANDED NUCLEIC-ACIDS; ZINC FINGER DOMAIN; BINDS METAL-IONS; CYS-HIS BOX; GENOMIC RNA; VIRAL-RNA; HIV-1; SEQUENCE; TRANSCRIPTION AB The human immunodeficiency virus type 1 (HIV-1) nucleocapsid protein contains two copies of a sequence motif, the cysteine-histidine box, that is conserved among retroviruses. To identify the functionally relevant positions of a cysteine-histidine box, each amino acid in the proximal copy of the motif was individually substituted by site-directed mutagenesis. Mutations at 5 of 14 positions abolished virus replication and reduced the viral RNA content of mutant particles to between 10 and 20% of parental levels. Mutations at other positions had either no or only a minor effect on virus replication and virion RNA content. In vitro binding of RNA to bacterially expressed mutant Pr55gag polyprotein correlated well with the effects of the mutations on particle-associated viral RNA levels. The two different copies of the motif in the HIV-1 nucleocapsid protein are not functionally equivalent, since the conversion of the proximal motif to an exact copy of the distal motif results in a defect in virus replication and a reduction in the viral RNA content of mutant particles. The simultaneous substitution of functionally relevant positions in both motifs led to a significant decline in gag protein export, indicating that the nucleocapsid domain of the gag precursor is also required for efficient assembly or release of the virion. C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV HUMAN RETROVIROL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. COLUMBIA UNIV COLL PHYS & SURG, DEPT MED, NEW YORK, NY 10032 USA. COLUMBIA UNIV COLL PHYS & SURG, DEPT BIOCHEM & MOLEC BIOPHYS, NEW YORK, NY 10032 USA. FU NCI NIH HHS [P30 CA06516]; NIAID NIH HHS [R01 AI29873, U01 AI24845] NR 48 TC 236 Z9 239 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X EI 1098-5514 J9 J VIROL JI J. Virol. PD OCT PY 1993 VL 67 IS 10 BP 6159 EP 6169 PG 11 WC Virology SC Virology GA LX120 UT WOS:A1993LX12000052 PM 8371356 ER PT J AU HERCZ, G PEI, Y GREENWOOD, C MANUEL, A SAIPHOO, C GOODMAN, WG SEGRE, GV FENTON, S SHERRARD, DJ AF HERCZ, G PEI, Y GREENWOOD, C MANUEL, A SAIPHOO, C GOODMAN, WG SEGRE, GV FENTON, S SHERRARD, DJ TI APLASTIC OSTEODYSTROPHY WITHOUT ALUMINUM - THE ROLE OF SUPPRESSED PARATHYROID FUNCTION SO KIDNEY INTERNATIONAL LA English DT Article ID CHRONIC RENAL-FAILURE; PERITONEAL-DIALYSIS PATIENTS; BONE-DISEASE; CALCIUM-CARBONATE; PHOSPHATE BINDER; HYPERCALCEMIA; PREVALENCE; DEPOSITION; POPULATION; HORMONE AB We evaluated 259 dialysis patients using serum parathyroid hormone (PTH, IRMA; normal range 1 to 5.5 pm or 10 to 55 pg/ml), the deferoxamine infusion test and iliac crest bone biopsy to determine the various forms of renal osteodystrophy and their risk factors. Although half of the biopsied patients had low turnover osteodystrophy, evidence of aluminum toxicity was present in only 1/3 of them. Additional risk factors for this bone lesion included treatment with peritoneal dialysis, ingestion of calcium carbonate, diabetes mellitus and advanced age. The PTH levels in patients with the aplastic lesion were significantly lower than in patients with normal or high bone turnover lesions [7.7 +/- 6.1 vs. 36.9 +/- 3.2 pm (77 +/- 61 vs. 369 +/- 32 pg/ml), P < 0.0001]. Aside from hypercalcemia, these patients were relatively asymptomatic. In a second study, 10 patients on peritoneal dialysis with the aplastic lesion had their dialysate calcium lowered from 1.62 to 1.0 mm. This resulted in a significant increase in PTH levels, from [3.7 +/- 0.8 to 10.6 +/- 1.9 pm (37 +/- 8 to 106 +/- 19 pg/ml), P < 0.001] which persisted over the nine-month observation period. In conclusion, the aplastic lesion is the most common form of renal osteodystrophy, with aluminum intoxication implicated in only 1/3 of the cases. In the remainder, factors identified include therapy with peritoneal dialysis using supraphysiological dialysate calcium, oral CaCO3 intake and diabetes mellitus. These factors may modulate their effect by lowering serum PTH to levels which are inadequate in maintaining normal bone turnover. The long-term sequelae of this non-aluminum related lesion remain to be defined. C1 UNIV TORONTO,WELLESLEY HOSP,TORONTO M4Y 1J3,ONTARIO,CANADA. UNIV WASHINGTON,VET ADM HOSP,SEATTLE,WA 98195. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 34 TC 251 Z9 253 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD OCT PY 1993 VL 44 IS 4 BP 860 EP 866 DI 10.1038/ki.1993.323 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA LX886 UT WOS:A1993LX88600025 PM 8258962 ER PT J AU FOX, JG STILLS, HF PASTER, BJ DEWHIRST, FE YAN, LL PALLEY, L PROSTAK, K AF FOX, JG STILLS, HF PASTER, BJ DEWHIRST, FE YAN, LL PALLEY, L PROSTAK, K TI ANTIGENIC SPECIFICITY AND MORPHOLOGIC CHARACTERISTICS OF CHLAMYDIA-TRACHOMATIS, STRAIN SFPD, ISOLATED FROM HAMSTERS WITH PROLIFERATIVE ILEITIS SO LABORATORY ANIMAL SCIENCE LA English DT Article ID MONOCLONAL-ANTIBODIES; INTRACELLULAR ANTIGEN; CAMPYLOBACTER-JEJUNI; SYRIAN-HAMSTERS; ENTERITIS; COLITIS; REPRODUCTION; PROCTITIS; FERRETS; AURATUS AB Profound diarrhea associated with proliferating intestinal cells containing intraepithelial campylobacter-like organisms (ICLO) occurs in a variety of mammalian hosts, particularly swine and hamsters. Recently, intracellular bacteria were isolated from proliferative intestinal tissue of hamsters and propagated in intestine cell line 407. Oral inoculation of hamsters with cell culture lysates containing these organisms reproduced the disease in susceptible hamsters. In the present study, an intracellular bacterium from the INT 407 cell line was shown by a variety of techniques to be a member of the genus Chlamydia and has been designated Chlamydia sp. strain SFPD. McCoy cells infected with Chlamydia sp. strain SFPD demonstrated bright fluorescent-stained intracytoplasmic inclusions when examined with fluorescein-labeled species-specific C. trachomatis monoclonal antibodies. The organism also reacted to fluorescein-labeled polyclonal but not monoclonal ICLO ''omega'' anti-sera. Ultrastructural examination of the Chlamydia sp. strain SFPD from McCoy cells revealed electrondense elementary bodies and a less electron-dense reticulate-like body that was circular, both features are consistent in morphology to developmental forms of Chlamydia and do not conform to ICLO morphology. Molecular studies, 16S ribosomal sequence analysis, and sequencing of the outer membrane protein confirmed that the isolate is a C. trachomatis closely related to the mouse pneumonitis strain of C. trachomatis. C1 FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02215. OHIO STATE UNIV,COLL VET MED,COLUMBUS,OH 43210. RP FOX, JG (reprint author), MIT,DIV COMPARAT MED,45-104,37 VASSAR ST,CAMBRIDGE,MA 02139, USA. FU NCRR NIH HHS [RR07036, RR01046]; NIDCR NIH HHS [DE04881] NR 37 TC 15 Z9 16 U1 0 U2 1 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI CORDOVA PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018 SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD OCT PY 1993 VL 43 IS 5 BP 405 EP 410 PG 6 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA MF111 UT WOS:A1993MF11100003 PM 7506316 ER PT J AU BENNETT, JM ANDERSEN, JW BEGG, CB GLICK, JH AF BENNETT, JM ANDERSEN, JW BEGG, CB GLICK, JH TI AGE AND HODGKINS-DISEASE - THE IMPACT OF COMPETING RISKS AND POSSIBLY SALVAGE THERAPY ON LONG-TERM SURVIVAL - AN ECOG STUDY SO LEUKEMIA RESEARCH LA English DT Article DE HODGKINS DISEASE; SALVAGE THERAPY; COMPETING RISKS ID RADIATION-THERAPY; CHEMOTHERAPY AB A detailed review of factors associated with survival was carried out in a cohort of 560 patients treated in two successive E.C.O.G. studies on advanced Hodgkin's disease. The study was undertaken to explore the impact of age on survival and to attempt to identify reasons for any observed differences. Data from two E.C.O.G. studies of patients with advanced Hodgkin's disease were examined separately and then pooled together. A special data request form was developed to capture additional information on treatments utilized for patients who were treated at relapse. The complete remission percentages were identical in both studies (72%) with no significant difference between the three age groupings (<40, 40-59, and >60 yr). This was true as well for disease-free survival. Nevertheless, overall survival was significantly better for the under aged 40 group and this difference was narrowed but not eliminated by competing risks. Our analysis of salvage therapy revealed a marginally significant difference in the CR% between the three groups, favoring the youngest cohort (