FN Thomson Reuters Web of Science™ VR 1.0 PT J AU STAINIER, D LEE, R FISHMAN, MC AF STAINIER, D LEE, R FISHMAN, MC TI ZEBRAFISH HEART DEVELOPMENT - PROSPECTS FOR GENETIC-ANALYSIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000628 ER PT J AU CANNON, SC AF CANNON, SC TI SODIUM-CHANNEL DEFECTS IN HUMAN NEUROMUSCULAR DISORDERS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 188 EP 188 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000638 ER PT J AU ARECECI, RJ KING, AAJ SIMON, MC ORKIN, SH WILSON, DB AF ARECECI, RJ KING, AAJ SIMON, MC ORKIN, SH WILSON, DB TI MOUSE GATA-4 - A RETINOIC ACID-INDUCIBLE GATA-BINDING TRANSCRIPTION FACTOR EXPRESSED IN HEART AND ENDODERMAL DERIVATIVES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,DIV PEDIAT HEMATOL ONCOL,ST LOUIS,MO 63110. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 191 EP 191 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000646 ER PT J AU MUNROE, DJ BRIC, E LOBBERT, R WHITTON, T STANTON, V BUCKLER, A HOUSMAN, DE AF MUNROE, DJ BRIC, E LOBBERT, R WHITTON, T STANTON, V BUCKLER, A HOUSMAN, DE TI PHYSICAL AND TRANSCRIPT MAPPING OF 11P15 - A STRATEGY FOR THE LOCALIZATION AND IDENTIFICATION OF THE GENE(S) RESPONSIBLE FOR THE LONG QT SYNDROME SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 201 EP 201 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000684 ER PT J AU CANNON, SC AF CANNON, SC TI SODIUM-CHANNEL DEFECTS IN HUMAN NEUROMUSCULAR DISORDERS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 244 EP 244 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000837 ER PT J AU LEWIS, S SCHWARZSCHILD, M DAUER, W HAMILL, L SYMES, A FINK, JS HYMAN, S AF LEWIS, S SCHWARZSCHILD, M DAUER, W HAMILL, L SYMES, A FINK, JS HYMAN, S TI LEUKEMIA INHIBITORY FACTOR (LIF) AND CILIARY NEUROTROPHIC FACTOR (CNTF) ACTIVATE P21-RAS IN A NEUROBLASTOMA CELL-LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 261 EP 261 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000901 ER PT J AU SEGAL, RA TAKAHASHI, H MCKAY, R STILES, C AF SEGAL, RA TAKAHASHI, H MCKAY, R STILES, C TI NEUROTROPHINS IN DEVELOPING CEREBELLUM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 269 EP 269 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000930 ER PT J AU SYMES, A FINK, JS AF SYMES, A FINK, JS TI IL6, CNTF, LIF AND ONCOSTATIN M INDUCE VIP MESSENGER-RNA THROUGH SIMILAR MOLECULAR MECHANISMS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 13 PY 1993 SU 17D BP 271 EP 271 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV880 UT WOS:A1993KV88000940 ER PT J AU ZHOU, SY SHOELSON, SE CHAUDHURI, M GISH, G PAWSON, T HASER, WG KING, F ROBERTS, T RATNOFSKY, S LECHLEIDER, RJ NEEL, BG BIRGE, RB FAJARDO, JE CHOU, MM HANAFUSA, H SCHAFFHAUSEN, B CANTLEY, LC AF ZHOU, SY SHOELSON, SE CHAUDHURI, M GISH, G PAWSON, T HASER, WG KING, F ROBERTS, T RATNOFSKY, S LECHLEIDER, RJ NEEL, BG BIRGE, RB FAJARDO, JE CHOU, MM HANAFUSA, H SCHAFFHAUSEN, B CANTLEY, LC TI SH2 DOMAINS RECOGNIZE SPECIFIC PHOSPHOPEPTIDE SEQUENCES SO CELL LA English DT Article ID MIDDLE-T-ANTIGEN; PHOSPHATIDYLINOSITOL KINASE-ACTIVITY; PROTEIN-TYROSINE KINASES; GROWTH-FACTOR RECEPTORS; SIGNAL TRANSDUCTION; BINDING; POLYOMAVIRUS; PP60C-SRC; GAP; SRC AB A phosphopeptide library was used to determine the sequence specificity of the peptide-binding sites of SH2 domains. One group of SH2 domains (Src, Fyn, Lck, Fgr, Abl, Crk, and Nck) preferred sequences with the general motif pTyr-hydrophilic-hydrophilic-Ile/Pro while another group (SH2 domains of p85, phospholipase C-gamma, and SHPTP2) selected the general motif pTyr-hydrophobic-X-hydrophobic. Individual members of these groups selected unique sequences, except the Src subfamily (Src, Fyn, Lck, and Fgr), which all selected the sequence pTyr-Glu-Glu-Ile. The variability in SH2 domain sequences at likely sites of contact provides a structural basis for the phosphopeptide selectivity of these families. Possible in vivo binding sites of the SH2 domains are discussed. C1 BETH ISRAEL HOSP, DEPT MED, BOSTON, MA 02215 USA. TUFTS UNIV, SCH MED, DEPT PHYSIOL, BOSTON, MA 02111 USA. BRIGHAM & WOMENS HOSP, DEPT MED, JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02115 USA. MT SINAI HOSP, SAMUEL LUNENFELD RES INST, DIV MOLEC & DEV BIOL, TORONTO M5G 1X5, ONTARIO, CANADA. BASF CORP, CAMBRIDGE, MA 02139 USA. ROCKEFELLER UNIV, NEW YORK, NY 10021 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV CELLULAR & MOLEC BIOL, BOSTON, MA 02115 USA. BETH ISRAEL HOSP, MOLEC MED UNIT, BOSTON, MA 02215 USA. TUFTS UNIV, SCH MED, DEPT BIOCHEM, BOSTON, MA 02111 USA. RP ZHOU, SY (reprint author), HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RI Pawson, Tony/E-4578-2013; Cantley, Lewis/D-1800-2014; Gish, Gerald/C-7228-2017 OI Cantley, Lewis/0000-0002-1298-7653; NR 41 TC 88 Z9 94 U1 1 U2 15 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 EI 1097-4172 J9 CELL JI Cell PD MAR 12 PY 1993 VL 72 IS 5 BP 767 EP 778 DI 10.1016/0092-8674(93)90404-E PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KR436 UT WOS:A1993KR43600012 ER PT J AU WAKSMAN, G SHOELSON, SE PANT, N COWBURN, D KURIYAN, J AF WAKSMAN, G SHOELSON, SE PANT, N COWBURN, D KURIYAN, J TI BINDING OF A HIGH-AFFINITY PHOSPHOTYROSYL PEPTIDE TO THE SRC SH2 DOMAIN - CRYSTAL-STRUCTURES OF THE COMPLEXED AND PEPTIDE-FREE FORMS SO CELL LA English DT Article ID SIGNAL TRANSDUCTION; PROTEIN; REFINEMENT AB The crystal structure of the Src SH2 domain complexed with a high affinity 11-residue phosphopeptide has been determined at 2.7 angstrom resolution by X-ray diffraction. The peptide binds in an extended conformation and makes primary interactions with the SH2 domain at six central residues: PQ(pY)EEI. The phosphotyrosine and the isoleucine are tightly bound by two well-defined pockets on the protein surface, resulting in a complex that resembles a two-pronged plug engaging a two-holed socket. The glutamate residues are in solvent-exposed environments in the vicinity of basic side chains of the SH2 domain, and the two N-terminal residues cap the phosphotyrosine-binding site. The crystal structure of Src SH2 in the absence of peptide has been determined at 2.5 angstrom resolution, and comparison with the structure of the high affinity complex reveals only localized and relatively small changes. C1 HOWARD HUGHES MED INST,NEW YORK,NY 10021. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. RP WAKSMAN, G (reprint author), ROCKEFELLER UNIV,NEW YORK,NY 10021, USA. RI Cowburn, David/A-8448-2008 NR 45 TC 649 Z9 659 U1 1 U2 8 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 12 PY 1993 VL 72 IS 5 BP 779 EP 790 DI 10.1016/0092-8674(93)90405-F PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KR436 UT WOS:A1993KR43600013 PM 7680960 ER PT J AU TROFATTER, JA MACCOLLIN, MM RUTTER, JL MURRELL, JR DUYAO, MP PARRY, DM ELDRIDGE, R KLEY, N MENON, AG PULASKI, K HAASE, VH AMBROSE, CM MUNROE, D BOVE, C HAINES, JL MARTUZA, RL MACDONALD, ME SEIZINGER, BR SHORT, MP BUCKLER, AJ GUSELLA, JF AF TROFATTER, JA MACCOLLIN, MM RUTTER, JL MURRELL, JR DUYAO, MP PARRY, DM ELDRIDGE, R KLEY, N MENON, AG PULASKI, K HAASE, VH AMBROSE, CM MUNROE, D BOVE, C HAINES, JL MARTUZA, RL MACDONALD, ME SEIZINGER, BR SHORT, MP BUCKLER, AJ GUSELLA, JF TI A NOVEL MOESIN-LIKE, EZRIN-LIKE, RADIXIN-LIKE GENE IS A CANDIDATE FOR THE NEUROFIBROMATOSIS-2 TUMOR SUPPRESSOR SO CELL LA English DT Article ID BILATERAL ACOUSTIC NEUROFIBROMATOSIS; PROTEIN-TYROSINE-PHOSPHATASE; TYPE-1 GENE; SEQUENCE HOMOLOGY; CDNA SEQUENCE; DNA MARKER; CHROMOSOME-22; CELLS; ASSOCIATION; CLONING AB Neurofibromatosis 2 (NF2) is a dominantly inherited disorder characterized by the occurrence of bilateral vestibular schwannomas and other central nervous system tumors including multiple meningiomas. Genetic linkage studies and investigations of both sporadic and familial tumors suggest that NF2 is caused by inactivation of a tumor suppressor gene in chromosome 22q12. We have identified a candidate gene for the NF2 tumor suppressor that has suffered nonoverlapping deletions in DNA from two independent NF2 families and alterations in meningiomas from two unrelated NF2 patients. The candidate gene encodes a 587 amino acid protein with striking similarity to several members of a family of proteins proposed to link cytoskeletal components with proteins in the cell membrane. The NF2 gene may therefore constitute a novel class of tumor suppressor gene. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. NCI,CLIN EPIDEMIOL BRANCH,BETHESDA,MD 20892. US PHS,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,ONCOL DRUG DISCOVERY,PRINCETON,NJ 08543. UNIV CINCINNATI,MED CTR,DEPT MOLEC GENET,CINCINNATI,OH 45267. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. GEORGETOWN UNIV,MED CTR,DEPT NEUROSURG,WASHINGTON,DC 20007. RP TROFATTER, JA (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129, USA. RI Haines, Jonathan/C-3374-2012; Haase, Volker Hans/A-6758-2013; OI Haase, Volker Hans/0000-0002-7051-8994; Rutter, Joni/0000-0002-6502-2361 FU NHGRI NIH HHS [HG00317, HG00672]; NINDS NIH HHS [NS24279] NR 73 TC 933 Z9 950 U1 0 U2 29 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 12 PY 1993 VL 72 IS 5 BP 791 EP 800 DI 10.1016/0092-8674(93)90406-G PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KR436 UT WOS:A1993KR43600014 PM 8453669 ER PT J AU CHOI, MJ FERNANDEZ, PC COUPAYEGERARD, B DANDREA, D SZERLIP, H KLEYMAN, TR AF CHOI, MJ FERNANDEZ, PC COUPAYEGERARD, B DANDREA, D SZERLIP, H KLEYMAN, TR TI TRIMETHOPRIM-INDUCED HYPERKALEMIA IN A PATIENT WITH AIDS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; TRANSTUBULAR POTASSIUM CONCENTRATION; IMMUNE-DEFICIENCY SYNDROME; NA+ CHANNEL; FROG-SKIN; THERAPY; SULFAMETHOXAZOLE; COMPLICATION; TRANSPORT; EVALUATE C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. UNIV PENN,DEPT MED,DIV RENAL & ELECTROLYTE,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. FU NIDDK NIH HHS [DK-07006] NR 29 TC 88 Z9 90 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 MAR 11 PY 1993 VL 328 IS 10 BP 703 EP 706 DI 10.1056/NEJM199303113281006 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA KQ861 UT WOS:A1993KQ86100006 PM 8433730 ER PT J AU COLE, DG BUCHBINDER, BR RICHARDSON, EP MARGOLIN, DH AF COLE, DG BUCHBINDER, BR RICHARDSON, EP MARGOLIN, DH TI A 67-YEAR-OLD MAN WITH MITRAL REGURGITATION AND AN ABRUPT ONSET OF ATAXIA AND FEVER - SUBACUTE BACTERIAL-ENDOCARDITIS, WITH MULTIPLE CEREBRAL EMBOLI AND CEREBRAL INFARCTS - MYCOTIC-ANEURYSM, LEFT MIDDLE CEREBRAL-ARTERY, RUPTURED, WITH FATAL INTRACEREBRAL AND SUBARACHNOID HEMORRHAGE - PARKINSONS-DISEASE, WITH NEURONAL DEGENERATION IN SUBSTANTIA-NIGRA (PARS COMPACTA) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID INFECTIVE ENDOCARDITIS; NEUROLOGIC COMPLICATIONS; STROKE REGISTRY; MANIFESTATIONS; MANAGEMENT; BRAIN C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP COLE, DG (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 53 TC 1 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 MAR 11 PY 1993 VL 328 IS 10 BP 717 EP 725 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA KQ861 UT WOS:A1993KQ86100009 ER PT J AU WEIR, GC AF WEIR, GC TI A DEFECTIVE BETA-CELL GLUCOSE SENSOR AS A CAUSE OF DIABETES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP WEIR, GC (reprint author), JOSLIN DIABET CTR,BOSTON,MA 02215, USA. NR 10 TC 10 Z9 10 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 MAR 11 PY 1993 VL 328 IS 10 BP 729 EP 731 DI 10.1056/NEJM199303113281012 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA KQ861 UT WOS:A1993KQ86100012 PM 8433735 ER PT J AU DUNN, JCY TOMPKINS, RG YARMUSH, ML AF DUNN, JCY TOMPKINS, RG YARMUSH, ML TI DYNAMICS OF TRANSCRIPTIONAL AND TRANSLATIONAL PROCESSES IN HEPATOCYTES CULTURED IN A COLLAGEN SANDWICH SO BIOTECHNOLOGY AND BIOENGINEERING LA English DT Note DE TRANSCRIPTION; TRANSLATION; MATHEMATICAL MODEL; PROTEIN SYNTHESIS ID GENE-EXPRESSION; MESSENGER-RNA; ALBUMIN; RAT; CONFIGURATION; LIVER AB A mathematical model which simulates the dynamic behavior of the hepatocytes cultured in a collagen sandwich is presented. Using several independently determined experimental parameters (e.g., albumin gene nuclear runoff activity, the level of albumin mRNA, and the albumin secretion rate), we have used this model to calculate the in vivo albumin gene transcriptional rate (0.27 molecules per second per hepatocyte), the half-life of albumin mRNA (3.3 days) in cultured hepatocytes, and the albumin polypeptide elongation rate (10 amino acids per second). In addition, the characteristic time constants for the transient increases in transcription (5 days) and in translation (10 days) were also obtained. These best-fit parameters were used to predict the rate of albumin secretion in rescued hepatocytes. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. NR 18 TC 5 Z9 5 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3592 J9 BIOTECHNOL BIOENG JI Biotechnol. Bioeng. PD MAR 5 PY 1993 VL 41 IS 5 BP 593 EP 598 DI 10.1002/bit.260410512 PG 6 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA KL591 UT WOS:A1993KL59100011 PM 18609591 ER PT J AU CANTIELLO, HF PRAT, AG BONVENTRE, JV CUNNINGHAM, CC HARTWIG, JH AUSIELLO, DA AF CANTIELLO, HF PRAT, AG BONVENTRE, JV CUNNINGHAM, CC HARTWIG, JH AUSIELLO, DA TI ACTIN-BINDING PROTEIN CONTRIBUTES TO CELL-VOLUME REGULATORY ION CHANNEL ACTIVATION IN MELANOMA-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID POTASSIUM CONDUCTANCE; APICAL MEMBRANE; BARIUM; CYTOSKELETON; INHIBITION; EPITHELIUM; TUBULES AB The cell volume regulatory response to a hypotonic stimulus is frequently initiated by activation of K+ and Cl- channels. We have characterized the hypotonic cell volume regulatory response of human melanoma cells devoid of actin-binding protein (ABP) and their genetically rescued counterpart transfected with the cDNA for ABP. ABP-deficient cells were unable to volume-regulate or activate K+ channels when exposed to a hypotonic stimulus. Genetic rescue with ABP resulted in recovery of both the cell volume regulatory response and the osmotically linked K+ channel activation. These data are consistent with a functional interaction between the actin cytoskeleton and osmotically sensitive ion transport. C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DIV EXPTL MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. NR 27 TC 124 Z9 127 U1 1 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 MAR 5 PY 1993 VL 268 IS 7 BP 4596 EP 4599 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KP884 UT WOS:A1993KP88400008 PM 8383118 ER PT J AU HALLAHAN, DE GIUS, D KUCHIBHOTLA, J SUKHATME, V KUFE, DW WEICHSELBAUM, RR AF HALLAHAN, DE GIUS, D KUCHIBHOTLA, J SUKHATME, V KUFE, DW WEICHSELBAUM, RR TI RADIATION SIGNALING MEDIATED BY JUN ACTIVATION FOLLOWING DISSOCIATION FROM A CELL TYPE-SPECIFIC REPRESSOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; IONIZING-RADIATION; BINDING-PROTEINS; GENE-EXPRESSION; FOS-PROTEIN; KAPPA-B; INHIBITOR; PHOSPHORYLATION; DOMAIN AB The promoter regions of several radiation-inducible genes contain AP-1 cis-acting regulatory elements that are dependent upon protein kinase C signaling. We analyzed nuclear protein from irradiated human tumor cell lines for binding to the AP-1 consensus sequence. The increase in nuclear protein binding following irradiation was specific for the AP-1 sequence and was reduced by antibodies to c-Jun and c-Fos. The AP-1 DNA binding sequence was found to regulate transcription in irradiated cells and mutation of the AP-1 site within the c-jun promoter abolished transcriptional induction by radiation. The gene encoding the chimeric transcription factor Gal4-Jun5-253, which includes the DNA binding region of Gal4 and the transcriptional regulatory region of c-Jun, was cotransfected with the reporter plasmid with Gal4 binding sequences (G5B-CAT). Transfection of RIT-3 and HeLa cells revealed that the regulatory region of Jun was sufficient to activate transcription following irradiation. Conversely, Hep G2 cells, which do not contain the cell type-specific Jun repressor, were not responsive to radiation-induced Jun activation. The c-Jun repressor was found to regulate Jun activation by experiments using the expression vector CMV-jun, which competes for Jun inhibitor and eliminates radiation-induction of Jun. We propose transcription factor dissociation from inhibitor proteins may participate in the initiation of cellular responses to ionizing radiation. C1 MICHAEL REESE MED CTR,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MOLEC GENET,CHICAGO,IL 60637. UNIV CHICAGO,DEPT CELL BIOL,CHICAGO,IL 60637. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. RP HALLAHAN, DE (reprint author), UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,5841 S MARYLAND AVE,BOX 442,CHICAGO,IL 60637, USA. FU NCI NIH HHS [CA37435, CA42596, CA41068] NR 33 TC 53 Z9 55 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 MAR 5 PY 1993 VL 268 IS 7 BP 4903 EP 4907 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KP884 UT WOS:A1993KP88400052 PM 8444868 ER PT J AU OFFRINGA, R BIERER, BE AF OFFRINGA, R BIERER, BE TI ASSOCIATION OF CD2 WITH TUBULIN - EVIDENCE FOR A ROLE OF THE CYTOSKELETON IN T-CELL ACTIVATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MICROTUBULE-ASSOCIATED PROTEINS; HUMAN LYMPHOCYTES-T; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; CYTOPLASMIC DOMAIN; BRAIN MICROTUBULES; MOLECULAR-CLONING; ANTIGEN RECEPTOR; BINDING PROTEIN; SURFACE AB In addition to the antigen-specific T cell receptor, a number of other T cell surface molecules contribute to T cell adhesion and activation. CD2 is a 50-kDa glycoprotein found on the surface of human T lymphocytes which plays a role in T cell adhesion and stimulation. The intracellular mechanisms by which CD2 functions are, however, not fully defined. Here we show that the T cell surface molecule CD2 physically interacts with tubulin. This interaction appears to involve the membrane-proximal part of the cytoplasmic domain of the CD2 molecule, suggesting that CD2 binds to the tubulin fraction previously shown to be present in membranes. Stimulation of T cells with activating pairs of anti-CD2 antibodies, capable of initiating lymphokine production and T cell proliferation, disrupts the CD2-tubulin complexes, suggesting that the dynamic interaction of CD2 with tubulin may play a role in T cell activation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,DANA 1610B,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 [AI28554] NR 44 TC 37 Z9 37 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 MAR 5 PY 1993 VL 268 IS 7 BP 4979 EP 4988 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KP884 UT WOS:A1993KP88400064 PM 8095265 ER PT J AU TAKAHASHI, H NAKADA, T PUISIEUX, I AF TAKAHASHI, H NAKADA, T PUISIEUX, I TI INHIBITION OF HUMAN COLON CANCER GROWTH BY ANTIBODY-DIRECTED HUMAN LAK CELLS IN SCID MICE SO SCIENCE LA English DT Article ID TUMOR-INFILTRATING LYMPHOCYTES; SEVERE COMBINED IMMUNODEFICIENCY; PERIPHERAL-BLOOD LYMPHOCYTES; ACTIVATED KILLER CELLS; MONOCLONAL-ANTIBODIES; RECOMBINANT INTERLEUKIN-2; METASTATIC MELANOMA; CYTO-TOXICITY; FC-RECEPTORS; MOUSE AB Advanced human colon cancer does not respond to lymphokine-activated killer (LAK) cells. In order to direct cytotoxic cells to the tumor, human LAK cells linked with antibodies to a tumor cell surface antigen were tested with established hepatic metastases in severe combined immunodeficient (SCID) mice. These cells had increased uptake into the tumor and suppression of tumor growth as compared with LAK cells alone, thereby improving the survival of tumor-bearing mice. Thus, tumor growth can be inhibited by targeted LAK cells, and SCID mice can be used to test the antitumor properties of human effector cells. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP TAKAHASHI, H (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA-35711, CA-57584] NR 41 TC 84 Z9 85 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 5 PY 1993 VL 259 IS 5100 BP 1460 EP 1463 DI 10.1126/science.8451642 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KP978 UT WOS:A1993KP97800038 PM 8451642 ER PT J AU ROSEN, DR SIDDIQUE, T PATTERSON, D FIGLEWICZ, DA SAPP, P HENTATI, A DONALDSON, D GOTO, J OREGAN, JP DENG, HX RAHMANI, Z KRIZUS, A MCKENNAYASEK, D CAYABYAB, A GASTON, SM BERGER, R TANZI, RE HALPERIN, JJ HERZFELDT, B VANDENBERGH, R HUNG, WY BIRD, T DENG, G MULDER, DW SMYTH, C LAING, NG SORIANO, E PERICAKVANCE, MA HAINES, J ROULEAU, GA GUSELLA, JS HORVITZ, HR BROWN, RH AF ROSEN, DR SIDDIQUE, T PATTERSON, D FIGLEWICZ, DA SAPP, P HENTATI, A DONALDSON, D GOTO, J OREGAN, JP DENG, HX RAHMANI, Z KRIZUS, A MCKENNAYASEK, D CAYABYAB, A GASTON, SM BERGER, R TANZI, RE HALPERIN, JJ HERZFELDT, B VANDENBERGH, R HUNG, WY BIRD, T DENG, G MULDER, DW SMYTH, C LAING, NG SORIANO, E PERICAKVANCE, MA HAINES, J ROULEAU, GA GUSELLA, JS HORVITZ, HR BROWN, RH TI MUTATIONS IN CU/ZN SUPEROXIDE-DISMUTASE GENE ARE ASSOCIATED WITH FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS SO NATURE LA English DT Article ID MOTOR NEURON DISEASE; DOWNS-SYNDROME; SACCHAROMYCES-CEREVISIAE; NEUROMUSCULAR-JUNCTION; ESCHERICHIA-COLI; LINKAGE ANALYSIS; TRANSGENIC MICE; MONOSOMY-21; RESOLUTION; PATHOLOGY AB AMYOTROPHIC lateral sclerosis (ALS) is a degenerative disorder of motor neurons in the cortex, brainstem and spinal cord1,2. Its cause is unknown and it is uniformly fatal, typically within five years3. About 10% of cases are inherited as an autosomal dominant trait, with high penetrance after the sixth decade4,5. In most instances, sporadic and autosomal dominant familial ALS (FALS) are clinically similar4,6,7. We have previously shown that in some but not all FALS pedigrees the disease is linked to a genetic defect on chromosome 21q (refs 8, 9). Here we report tight genetic linkage between FALS and a gene that encodes a cytosolic, Cu/Zn-binding superoxide dismutase (SOD1), a homodimeric metalloenzyme that catalyzes the dismutation of the toxic superoxide anion O2.- to O2 and H2O2 (ref. 10). Given this linkage and the potential role of free radical toxicity in other neurodenegerative disorders11, we investigated SOD1 as a candidate gene in FALS. We identified 11 different SOD1 missense mutations in 13 different FALS families. C1 MASSACHUSETTS GEN HOSP,DAY NEUROMUSCULAR RES LAB,ROOM 6627,MGH-E,BLDG 149,13TH ST,BOSTON,MA 02129. NORTHWESTERN UNIV,SCH MED,DEPT NEUROL,CHICAGO,IL 60611. ELEANOR ROOSEVELT INST CANC RES,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80206. MCGILL UNIV,CTR RES NEUROSCI,MONTREAL H3A 2T5,QUEBEC,CANADA. MONTREAL GEN HOSP,RES INST,MONTREAL H3G 1A4,QUEBEC,CANADA. MIT,DEPT BIOL,HOWARD HUGHES MED INST,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,GENET & AGING LAB,BOSTON,MA 02129. NORTHSHORE UNIV HOSP,DEPT NEUROL,MANHASSET,NY 11030. UNIV ZIEKENHUIZEN,DEPT NEUROL,B-3000 LOUVAIN,BELGIUM. UNIV WASHINGTON,SCH MED,DEPT NEUROL,SEATTLE,WA 98195. MAYO CLIN & MAYO FDN,DEPT NEUROL,ROCHESTER,MN 55905. AUSTRALIAN NEUROMUSCULAR RES INST,NEDLANDS,WA,AUSTRALIA. DUKE UNIV,MED CTR,DEPT MED NEUROL,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,MOLEC NEUROGENET LAB,BOSTON,MA 02129. RI Haines, Jonathan/C-3374-2012 NR 47 TC 4072 Z9 4162 U1 70 U2 357 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 4 PY 1993 VL 362 IS 6415 BP 59 EP 62 DI 10.1038/362059a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KP976 UT WOS:A1993KP97600059 PM 8446170 ER PT J AU ECK, MJ SHOELSON, SE HARRISON, SC AF ECK, MJ SHOELSON, SE HARRISON, SC TI RECOGNITION OF A HIGH-AFFINITY PHOSPHOTYROSYL PEPTIDE BY THE SRC HOMOLOGY-2 DOMAIN OF P56(LCK) SO NATURE LA English DT Article ID SIGNAL TRANSDUCTION; PDGF RECEPTOR; KINASE; PROTEINS; GENE AB THE Src homology-2 (SH2) domains are modules of about 100 amino-acid residues that are found in many intracellular signal-transduction proteins1,2. They bind phosphotyrosine-containing sequences with high affinity and specificity1-4, recognizing phosphotyrosine in the context of the immediately adjacent polypeptide sequence3-12. The protein p56lck (Lck) is a Src-like, lymphocyte-specific tyrosine kinase13-15. A phosphopeptide library screen has recently been used to deduce an 'optimal' binding sequence for the Lck SH2 domain16. There is selectivity for the residues Glu, Glu and Ile in the three positions C-terminal to the phosphotyrosine. An 11-residue phosphopeptide derived from the hamster polyoma middle-T antigen, EPQpYEEIPIYL, binds with an approximately 1 nM dissociation constant to the Lck SH2 (ref. 17), an affinity equivalent to that of the tightest known SH2-phosphopeptide complex. We report here the high-resolution crystallographic analysis of the Lck SH2 domain in complex with this phosphopeptide. Recent crystallographically derived structures of the Src SH2 domain in complex with low-affinity peptides18, which do not contain the EEI consensus, and NMR-derived structures of unliganded Abl (ref. 19) and p85 (ref. 20) SH2 domains have revealed the conserved fold of the SH2 domain and the properties of a phosphotyrosine binding pocket. Our high-affinity complex shows the presence of a second pocket for the residue (pY + 3) three positions C-terminal to the phosphotyrosine (pY). The peptide is anchored by insertion of the pY and pY + 3 side chains into their pockets and by a network of hydrogen bonds to the peptide main chain. In the low-affinity phosphopeptide/Src complexes18, the pY + 3 residues do not insert into the homologous binding pocket and the peptide main chain remains displaced from the surface of the domain. C1 CHILDRENS HOSP MED CTR,MOLEC MED LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. RP ECK, MJ (reprint author), CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 39 TC 462 Z9 465 U1 0 U2 7 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 4 PY 1993 VL 362 IS 6415 BP 87 EP 91 DI 10.1038/362087a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KP976 UT WOS:A1993KP97600068 PM 7680435 ER PT J AU SCHWARZSCHILD, M AF SCHWARZSCHILD, M TI IMAGES IN CLINICAL MEDICINE - NAIL IN THE BRAIN SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note RP SCHWARZSCHILD, M (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 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 MAR 4 PY 1993 VL 328 IS 9 BP 620 EP 620 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KP680 UT WOS:A1993KP68000005 ER PT J AU RICHARDSON, GS AF RICHARDSON, GS TI OVARIAN-CANCER SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID CARCINOMA RP RICHARDSON, GS (reprint author), MASSACHUSETTS GEN HOSP,VINCENT MEM GYNECOL SERV,BOSTON,MA 02114, USA. NR 9 TC 1 Z9 1 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 MAR 3 PY 1993 VL 269 IS 9 BP 1163 EP 1163 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KN611 UT WOS:A1993KN61100035 PM 8433473 ER PT J AU CHANG, AY KIM, K GLICK, J ANDERSON, T KARP, D JOHNSON, D AF CHANG, AY KIM, K GLICK, J ANDERSON, T KARP, D JOHNSON, D TI PHASE-II STUDY OF TAXOL, MERBARONE, AND PIROXANTRONE IN STAGE-IV NON-SMALL-CELL LUNG-CANCER - THE EASTERN COOPERATIVE ONCOLOGY GROUP RESULTS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ANTITUMOR AGENT; INVITRO; CHEMOTHERAPY; REGIMENS AB Background: Patients with metastatic (stage IV) non-small-cell lung cancer usually have a poor prognosis and disease refractory to chemotherapy. Three new agents-taxol, merbarone, and piroxantrone-have shown promising antitumor treatment in vitro and in animals. Taxol is an antimicrotubular agent that interferes with mitosis during cell division. Merbarone, a conjugate of thiobarbituric acid and aniline, is a topoisomerase II inhibitor, which thus inhibits DNA synthesis and tumor growth. Piroxantrone, an anthracenedione derivative, is a DNA intercalating agent that has shown potent antitumor activity in animal studies. Purpose: Our randomized phase 11 study was designed to evaluate the efficacy and toxicity of these agents in the treatment of stage IV metastatic non-small-cell lung cancer. Methods: Eligible patients (119) were randomly assigned to receive one of the three treatments given every 3 weeks: 250 mg/m2 taxol by a 24-hour intravenous infusion, 1000 mg/m2 merbarone by continuous intravenous infusion through a central catheter daily for 5 days, or 150 mg/m2 piroxantrone by intravenous infusion over 1 hour. Patients had received no chemotherapy. Response and toxicity were evaluated every 3 weeks. Results: Twenty-five patients were randomly assigned to receive taxol, 47 to receive merbarone, and 47 to receive piroxantrone. One of 44 assessable patients (2.3%) treated with piroxantrone had a complete response. Rates for partial response were 20.8% (five of 24 patients) and 5.7% (two of 35) for assessable patients treated with taxol or merbarone, respectively. One-year survival rates were 41.7%, 21.6%, and 22.6%, and median survival times were 24.1, 19.9, and 29.3 weeks for taxol, merbarone, and piroxantrone, respectively. These differences were not statistically significant, but this study was not designed to compare survival. In general, toxicity was manageable. With premedication, no anaphylaxis was observed with taxol. The most common toxic effects were leukopenia with taxol or piroxantrone treatment and thromboembolic complications with merbarone. Death directly related to treatment occurred in 4% (one patient), 11.4% (four), and 5% (two) of the assessable patients receiving taxol, merbarone, and piroxantrone, respectively. Cardiotoxicity and neurotoxicity occurred only occasionally in all three arms. Conclusion: On the basis of the response rate (20.8% partial response) and 1-year survival rate (41.7%), taxol is an active agent for the treatment of metastatic non-small-cell lung cancer. Merbarone and piroxantrone are relatively inactive. Implications: Further study of taxol is warranted. In future studies, taxol should be combined with other agents, and granulocyte colony-stimulating factor should be used to ameliorate myelosuppression. C1 VANDERBILT UNIV,DEPT MED,NASHVILLE,TN 37240. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. UNIV PENN,CTR CANC,DEPT MED,PHILADELPHIA,PA 19104. MED COLL WISCONSIN,DEPT MED,MILWAUKEE,WI 53226. TUFTS UNIV,NEW ENGLAND MED CTR HOSP,DEPT MED,BOSTON,MA 02111. RP CHANG, AY (reprint author), UNIV ROCHESTER,GENESSEE HOSP,CTR CANC,DEPT MED,DIV ONCOL HEMATOL,ROCHESTER,NY 14607, USA. FU NCI NIH HHS [CA-06594, CA-14548, CA-21115] NR 16 TC 435 Z9 441 U1 0 U2 4 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 MAR 3 PY 1993 VL 85 IS 5 BP 388 EP 394 DI 10.1093/jnci/85.5.388 PG 7 WC Oncology SC Oncology GA KN884 UT WOS:A1993KN88400015 PM 8094467 ER PT J AU DOUDNA, JA USMAN, N SZOSTAK, JW AF DOUDNA, JA USMAN, N SZOSTAK, JW TI RIBOZYME-CATALYZED PRIMER EXTENSION BY TRINUCLEOTIDES - A MODEL FOR THE RNA-CATALYZED REPLICATION OF RNA SO BIOCHEMISTRY LA English DT Article ID COMPLEMENTARY-STRAND RNA; GROUP-I INTRONS; CHEMICAL SYNTHESIS; TETRAHYMENA RIBOZYME; OLIGORIBONUCLEOTIDES; MISMATCHES; TEMPLATE; ORIGIN; WORLD; LIFE AB The existence of RNA enzymes that catalyze phosphodiester transfer reactions suggests that RNA-catalyzed RNA replication might be possible. Indeed, it has been shown that the Tetrahymena and sunY self-splicing introns will catalyze the template-directed ligation of RNA oligonucleotides (Doudna et al.,1989,1991). We have sought to develop a more general RNA replication system in which arbitrary template sequences could be copied by the assembly of a limited set of short of oligonucleotides. Here we examine the use of tetranucleotides as substrates for a primer-extension reaction in which the 5'-nucleoside of the tetranucleotide is the leaving group, and the primer is extended by the remaining three nucleotides. When the 5'-nucleoside is guanosine, the reaction is quite efficient, but a number of competing side reactions occur, in which inappropriate guanosine residues in the primer or the template occupy the guanosine binding site of the ribozyme. We have blocked these side reactions by using the guanosine analogue 2-aminopurine riboside (2AP) as the leaving group, in a reaction catalyzed by a mutant sunY ribozyme that binds efficiently to 2AP and not to guanosine. We have begun to address the issue of the fidelity of the primer-extension reaction by measuring reaction rates with a number of different triplet/template combinations. Our results provide the basis for the further development of an RNA-catalyzed RNA replication system using short oligonucleotide substrates with novel leaving groups. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 22 TC 31 Z9 31 U1 2 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 2 PY 1993 VL 32 IS 8 BP 2111 EP 2115 DI 10.1021/bi00059a032 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KP582 UT WOS:A1993KP58200032 PM 7680575 ER PT J AU NOZAKI, K FINKLESTEIN, SP BEAL, MF AF NOZAKI, K FINKLESTEIN, SP BEAL, MF TI DELAYED ADMINISTRATION OF BASIC FIBROBLAST GROWTH-FACTOR PROTECTS AGAINST N-METHYL-D-ASPARTATE NEUROTOXICITY IN NEONATAL RATS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE BFGF (BASIC FIBROBLAST GROWTH FACTOR); NMDA (N-METHYL-D-ASPARTATE); EXCITOTOXICITY (NEONATE); NEUROPROTECTION ID NEURONS; DEGENERATION AB Neuroprotective effects of basic fibroblast growth factor (bFGF) (200 mu/kg i.p.) were examined at different time points following intrastriatal injection of N-methyl-D-aspartate (NMDA) in seven-day-old rats. When administered 0.5 h before intrastriatal NMDA injection, 200 mug/kg of bFGF significantly reduced NMDA-induced lesion by 47% as compared with vehicle treatment. Posttreatment with the same dose of bFGF at 0, 0.5 or 1 h after NMDA injection also significantly reduced those lesions by 45, 35 or 26%, respectively, while no neuroprotective effects was observed when administered at 2 or 4 h after NMDA injection. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CNS GROWTH FACTOR RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,STROKE RES LAB,BOSTON,MA 02114. FU NIA NIH HHS [AG08207]; NINDS NIH HHS [NS10828, NS16367] NR 12 TC 29 Z9 29 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 2 PY 1993 VL 232 IS 2-3 BP 295 EP 297 DI 10.1016/0014-2999(93)90788-J PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KR639 UT WOS:A1993KR63900022 PM 8467865 ER PT J AU BUCHANAN, JR AF BUCHANAN, JR TI THE PAST AS PROLOGUE SO ACADEMIC MEDICINE LA English DT Article AB What has the Association of American Medical Colleges (AAMC) accomplished in the last 25 years in its efforts to advance medical education, biomedical research, and health delivery in this country? Can the AAMC's past accomplishments help predict how it will respond to future challenges? To answer these questions, the author traces in detail the recent history of the AAMC, focusing on the expansion of the association's role and constituencies and bow these and other changes were precipitated by recommendations in the AAMC's 1965 ''Coggeshall Report.'' He also recounts how the AAMC has responded to the pressures and needs of recent years (such as fostering an increase in the number of practicing physicians) and describes in detail the organization and functions of the AAMC's staff, with emphasis on its six divisions and the fact that many of the complex issues that confront the AAMC transcend the boundaries of governance councils and staff divisions and dictate that association policy be based on broad consensus. Looking ahead, he sees at least four important activities that the AAMC will continue to be involved with: fostering the education of more minority students; promoting health services research; finding an appropriate role in the evolution of health care reform; and addressing the need for academic medicine to be more socially responsive. The author concludes that the AAMC's highly regarded record, its organization, and its financial stability all indicate that it will do well as it tackles the issues on the horizon and others not yet in view. He urges members of the academic medicine community to support and become involved in the AAMC so that it can remain effective. RP BUCHANAN, JR (reprint author), MASSACHUSETTS GEN HOSP,10 N GROVE ST,BOSTON,MA 02114, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD MAR PY 1993 VL 68 IS 3 BP 173 EP 177 DI 10.1097/00001888-199303000-00001 PG 5 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA KT426 UT WOS:A1993KT42600001 PM 8447904 ER PT J AU CARR, P NOBLE, J FRIEDMAN, RH STARFIELD, B BLACK, C AF CARR, P NOBLE, J FRIEDMAN, RH STARFIELD, B BLACK, C TI CHOICES OF TRAINING-PROGRAMS AND CAREER PATHS BY WOMEN IN INTERNAL-MEDICINE SO ACADEMIC MEDICINE LA English DT Article ID GENDER DIFFERENCES; UNITED-STATES; SPECIALTY PREFERENCES; ATTITUDES; STUDENTS AB Purpose. To examine the choices of career paths of women in internal medicine, specifically to determine (1) whether women continue to prefer primary care practice more often than men do and (2) whether differences in career paths between men and women result from differences in the natures of the training programs they complete. Method. A database containing demographic, training, and clinical-practice information on 19,151 physicians (3,569 women and 15,582 men) who had been trained in internal medicine was constructed by merging data from the National Resident Matching Program matches in internal medicine for 1977-1982 with data from the 1985 American Medical Association Physician Masterfile, which contains physician practice profiles. Results. Similar percentages of the men and the women chose primary care residencies (8% versus 9%, ns) and trained in the 100 major medical centers (49% versus 50%, ns). The women more frequently trained in programs affiliated with medical schools in the top prestige quartile (38% versus 33%, p < .05). The attrition rates of residents who left their training for careers in other medical fields were the same for the men and the women (14%). Fewer women obtained board certification (74% versus 80%, p < .01). The women chose to practice general internal medicine more frequently than did the men (52 % versus 45%, p < .0001), regardless of the training program completed (primary care or traditional). Conclusion. The women pursued primary-care-oriented internal medicine to a significantly greater degree than did the men, regardless of the type of training program completed (primary care or traditional). C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. BOSTON CITY HOSP,GEN INTERNAL MED SECT,BOSTON,MA 02118. BOSTON UNIV,SCH MED,BOSTON,MA 02118. BOSTON UNIV HOSP,MED CTR,MED INFORMAT SYST UNIT,BOSTON,MA 02218. JOHNS HOPKINS UNIV,DIV HLTH POLICY,BALTIMORE,MD 21218. UNIV MANITOBA,FAC MED,DEPT COMMUNITY HLTH SCI,WINNIPEG R3T 2N2,MANITOBA,CANADA. RP CARR, P (reprint author), MASSACHUSETTS GEN HOSP,GEN MED UNIT,BULFINCH 1,FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HRSA 240-85-0048] NR 18 TC 11 Z9 11 U1 1 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD MAR PY 1993 VL 68 IS 3 BP 219 EP 223 DI 10.1097/00001888-199303000-00015 PG 5 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA KT426 UT WOS:A1993KT42600017 PM 8447918 ER PT J AU WALL, C PETROPOULOS, AE AF WALL, C PETROPOULOS, AE TI HUMAN VERTICAL EYE-MOVEMENT RESPONSES TO EARTH HORIZONTAL PITCH SO ACTA OTO-LARYNGOLOGICA LA English DT Article DE VESTIBULOOCULAR REFLEX; OTOLITHIC ORGANS; SCLERAL SEARCH COILS; OFF VERTICAL AXIS ROTATION ID VESTIBULO-OCULAR REFLEX; NYSTAGMUS; CAT; ASYMMETRY; GRAVITY; MONKEY; AXIS AB The vertical eye movements in humans produced in response to head-over-heels constant velocity pitch rotation about a horizontal axis resemble those from other species. At 60-degrees/s these are persistent and tend to have non-reversing slow components that are compensatory to the direction of rotation. In most, but not all subjects, the slow component velocity was well characterized by a rapid build-up followed by an exponential decay to a non-zero baseline. Super-imposed was a cyclic or modulation component whose frequency corresponded to the time for one revolution and whose maximum amplitude occurred during a specific head orientation. All response components (exponential decay, baseline and modulation) were larger during pitch backward compared to pitch forward runs. Decay time constants were shorter during the backward runs, thus, unlike left to right yaw axis rotation, pitch responses display significant asymmetries between paired forward and backward runs. RP WALL, C (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC00290] NR 20 TC 5 Z9 5 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6489 J9 ACTA OTO-LARYNGOL JI Acta Oto-Laryngol. PD MAR PY 1993 VL 113 IS 2 BP 113 EP 118 DI 10.3109/00016489309135777 PG 6 WC Otorhinolaryngology SC Otorhinolaryngology GA KU625 UT WOS:A1993KU62500001 PM 8475723 ER PT J AU PANDOLFI, F OLIVA, A SACCO, G POLIDORI, V LIBERATORE, D MEZZAROMA, I GIOVANNETTI, A KURNICK, JT AIUTI, F AF PANDOLFI, F OLIVA, A SACCO, G POLIDORI, V LIBERATORE, D MEZZAROMA, I GIOVANNETTI, A KURNICK, JT AIUTI, F TI FIBROBLAST-DERIVED FACTORS PRESERVE VIABILITY INVITRO OF MONONUCLEAR-CELLS ISOLATED FROM SUBJECTS WITH HIV-1 INFECTION SO AIDS LA English DT Article DE AIDS; HIV-1 INFECTION; CD4 LYMPHOCYTES; APOPTOSIS; FIBROBLASTS; FIBROBLAST-DERIVED FACTORS; CYTOKINES ID T-CELLS; APOPTOSIS; DEATH; LYMPHOCYTES; MECHANISM; SURVIVAL AB Peripheral blood mononuclear cells (PBMC) from HIV-infected subjects have an increased mortality rate (MR) when incubated in vitro for 3 days in a culture medium. We have previously shown that fibroblast-conditioned medium (FCM) can preserve viability, without significant activation, of human lymphocytes in vitro. We therefore tested the ability of two FCM and other factors to reduce spontaneous MR in HIV-positive PBMC. Methods: PBMC were cultured for 3 days in control medium and medium supplemented with FCM or recombinant cytokines [interleukin (IL)-2, IL-6, IL-7, granulocyte macrophage colony-stimulating factor]. Cells viable at day 3 were counted in a cytofluorimeter after staining with ethidium bromide. DNA was extracted from the cultures and evaluated for the presence of low molecular weight fragmentation. Results: The MR of PBMC from 51 HIV-positive subjects and from 21 healthy controls were 30.1 and 9.5%, respectively (P < 0.0001). The MR was higher in 40 patients with a CD4+ lymphocyte count < 400 x 10(6)/I than in subjects with a count > 400 x 10(6)/L (32.84 versus 20.96%; P = 0.047). IL-2 and FCM significantly reduced MR in HIV-positive subjects (MR: 17.8 and 20.4%; P: < 0.001 and 0.005, respectively). This effect was more evident in subjects with a CD4+ lymphocyte count < 400 x 10(6)/I and in subjects with negative p24 antigenaemia. Cellular proliferation accounts for increased survival in IL-2-supplemented cultures but not in those with FCM. DNA was extracted from fresh PBMC and cells cultured for 3 days for 22 HIV-positive cases. DNA degradation was documented and bands related to an apoptotic mechanism of death observed, especially in subjects with more advanced disease. Conclusions: Our data suggest that FCM inhibits accelerated cell death in vitro of PBMC isolated from HIV-positive patients. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP PANDOLFI, F (reprint author), UNIV ROMA LA SAPIENZA,DEPT ALLERGY & CLIN IMMUNOL,CATTEDRA IMMUNOL CLIN,VIALE UNIV 37,I-00185 ROME,ITALY. RI Giovannetti, Antonello/E-7736-2012 FU NCI NIH HHS [CA44324]; NIAMS NIH HHS [AR39993] NR 12 TC 23 Z9 23 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD MAR PY 1993 VL 7 IS 3 BP 323 EP 329 DI 10.1097/00002030-199303000-00003 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA KT079 UT WOS:A1993KT07900003 PM 8471193 ER PT J AU STERN, Y FOLSTEIN, M ALBERT, M RICHARDS, M MILLER, L BYLSMA, F LAFLECHE, G MARDER, K BELL, K SANO, M DEVANAND, D LORECK, D WOOTTEN, J BELLO, J AF STERN, Y FOLSTEIN, M ALBERT, M RICHARDS, M MILLER, L BYLSMA, F LAFLECHE, G MARDER, K BELL, K SANO, M DEVANAND, D LORECK, D WOOTTEN, J BELLO, J TI MULTICENTER STUDY OF PREDICTORS OF DISEASE COURSE IN ALZHEIMER-DISEASE (THE PREDICTORS STUDY) .1. STUDY DESIGN, COHORT DESCRIPTION, AND INTERSITE COMPARISONS SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article DE MULTICENTER STUDY; PREDICTORS OF DISEASE COURSE; DEMENTIA ID DEMENTIA; DEPRESSION; SCALE AB Clinicians should be able to provide the patient with Alzheimer disease (AD) and the family with an accurate prediction of what to expect, but the variability in the rate of disease progression precludes this. In several previous studies, specific clinical signs such as muscular rigidity, myoclonus, and hallucinations or delusions were associated with rapid progression to a more severe stage of dementia or death. The ''Predictors Study,'' a longitudinal study at three independent sites, was designed to develop a predictor model of the natural history of Alzheimer disease. The study was conducted at three study sites, New York, Baltimore, and Boston in a cohort of 224 patients with early probable AD. This article describes the design and implementation of the Predictors Study, and compares features of the study cohort at baseline across sites. Patients were all at the mild stage of disease at entry and were relatively comparable across sites. Extrapyramidal signs and delusions were common, but myoclonus was rarely observed. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT NEUROL,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT PSYCHIAT,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,SERGIEVSKY CTR,NEW YORK,NY 10032. JOHNS HOPKINS UNIV,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21218. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DIV NEURORADIOL,BRONX,NY 10461. FU NIA NIH HHS [AG07232, AG07370, AG08702] NR 24 TC 74 Z9 74 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD SPR PY 1993 VL 7 IS 1 BP 3 EP 21 DI 10.1097/00002093-199307010-00002 PG 19 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA KX083 UT WOS:A1993KX08300001 PM 8481224 ER PT J AU RICHARDS, M FOLSTEIN, M ALBERT, M MILLER, L BYLSMA, F LAFLECHE, G MARDER, K BELL, K SANO, M DEVANAND, D LORECK, D WOOTTEN, J STERN, Y AF RICHARDS, M FOLSTEIN, M ALBERT, M MILLER, L BYLSMA, F LAFLECHE, G MARDER, K BELL, K SANO, M DEVANAND, D LORECK, D WOOTTEN, J STERN, Y TI MULTICENTER STUDY OF PREDICTORS OF DISEASE COURSE IN ALZHEIMER-DISEASE (THE PREDICTORS STUDY) .2. NEUROLOGICAL, PSYCHIATRIC, AND DEMOGRAPHIC INFLUENCES ON BASE-LINE MEASURES OF DISEASE SEVERITY SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article DE MULTICENTER STUDY; PREDICTORS OF DISEASE COURSE; EXTRAPYRAMIDAL SIGNS ID EXTRAPYRAMIDAL SIGNS; DEMENTIA; EEG AB The ''Predictors Study'' is a prospective cohort study of the natural history of Alzheimer disease (AD), the aim of which is to identify milestones in disease progression and to develop a model to predict disease course in individual patients. The empirical background to this study is based on previous reports that the presence of extrapyramidal signs (EPS), myoclonus, and psychosis in AD may signify greater disease severity at any given stage and a more rapid course of the disease over time. The present analyses were conducted to determine whether these independent ''predictor'' variables were associated with greater disease severity at baseline within a new cohort of 224 mild AD patients recruited from three different medical centers (in New York, Baltimore, and Boston). Measures of disease severity were provided by the modified Mini-Mental State Examination (mMMSE) and the Blessed Dementia Rating Scale (BDRS), which measures functional capacity. Independent variables were EPS, delusions, and slowing of the posterior dominant EEG rhythm. The frequency of myoclonus and hallucinations was too low to permit adequate statistical assessment of their effects at this time. EPS and EEG slowing were associated with low mMMSE scores, whereas delusions were primarily associated with impaired functional capacity. These effects were independent of the influence of age and disease duration. These results indicate that the effects of these independent variables can be detected at mild stages of AD and that these effects can be generalized across different geographical regions. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT NEUROL,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT PSYCHIAT,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,GERTRUDE H SERGIEVSKY CTR,NEW YORK,NY 10032. JOHNS HOPKINS UNIV,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21218. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. FU NIA NIH HHS [AG07232, AG07370, AG08702] NR 28 TC 51 Z9 52 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD SPR PY 1993 VL 7 IS 1 BP 22 EP 32 DI 10.1097/00002093-199307010-00003 PG 11 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA KX083 UT WOS:A1993KX08300002 PM 8481223 ER PT J AU OCONNELL, JX ROSENBERG, AE AF OCONNELL, JX ROSENBERG, AE TI HISTIOCYTIC LYMPHADENITIS ASSOCIATED WITH A LARGE JOINT PROSTHESIS SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE JOINT PROSTHESIS; POLYETHYLENE; POLYMETHYLMETHACRYLATE; LYMPHADENOPATHY ID SILICONE LYMPHADENOPATHY; HIP-REPLACEMENT; LYMPH-NODES AB Distinctive microscopic findings in enlarged axillary lymph nodes removed during modified radical mastectomy in a 76-year-old woman with a previous ipsilateral total shoulder joint replacement are described. The sinuses of the lymph nodes were distended by numerous large macrophages that had abundant granular eosinophilic cytoplasm. Periodic acid-Schiff staining was positive, and polarization microscopy revealed birefringent particles of polyethylene. These findings were diagnostic of the reactive lymphadenopathy that is seen uncommonly in lymph nodes draining large joint prostheses. RP OCONNELL, JX (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 10 TC 18 Z9 18 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 MAR PY 1993 VL 99 IS 3 BP 314 EP 316 PG 3 WC Pathology SC Pathology GA KR561 UT WOS:A1993KR56100018 PM 8447293 ER PT J AU CUNNINGHAM, MJ ANONSEN, CK KINANE, B AF CUNNINGHAM, MJ ANONSEN, CK KINANE, B TI ACQUIRED LARYNGOMALACIA SECONDARY TO OBSTRUCTIVE ADENOTONSILLAR HYPERTROPHY SO AMERICAN JOURNAL OF OTOLARYNGOLOGY LA English DT Article RP CUNNINGHAM, MJ (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 4 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 MAR-APR PY 1993 VL 14 IS 2 BP 132 EP 136 DI 10.1016/0196-0709(93)90053-A PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA KR679 UT WOS:A1993KR67900011 PM 8484479 ER PT J AU KRADIN, RL XIA, W MCCARTHY, K SCHNEEBERGER, EE AF KRADIN, RL XIA, W MCCARTHY, K SCHNEEBERGER, EE TI FCR+/- SUBSETS OF IA+ PULMONARY DENDRITIC CELLS IN THE RAT DISPLAY DIFFERENCES IN THEIR ABILITIES TO PROVIDE ACCESSORY CO-STIMULATION FOR NAIVE (OX-22+) AND SENSITIZED (OX-22-) T-CELLS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; MONOCLONAL-ANTIBODY; LYMPHOCYTES-T; VASCULAR ENDOTHELIUM; BRAIN CAPILLARIES; LANGERHANS CELLS; MRC OX-43; LUNG; MACROPHAGES; REACTS AB A substantial body of evidence indicates that the primary sensitization of naive T cells to inhaled antigens occurs in the regional lymph nodes, whereas secondary responses may be generated directly within lung tissue. Ia+ pulmonary dendritic cells are widely distributed within the rat lung where they can participate in the induction of the immune response to inhaled antigens. Recently, two subsets of Ia+ pulmonary dendritic cells have been distinguished based on their expression of Fc receptors (FcR), but little is known concerning their abilities to support the responses of naive or sensitized T cells. In order to address this question, pulmonary FcR+/-dendritic cells have been purified from enzymatic digests of Lewis rat lungs, based on their differential binding to beat-aggregated immunoglobulin. The FcR+/- dendritic cell subsets differed with respect to their light microscopic appearance and in their expression of non-specific esterase. Only the FcR+ subset was able lo phagocytize latex beads and showed intracellular phagolysosomes by electron microscopy. Both of the FcR+/- subsets rapidly formed clusters with naive (OX-22+) and sensitized (OX-22-) T cells. However, the clusters yielded by the FcR+ subset were substantially smaller, possibly reflecting their diminished surface membrane expression of the intercellular adhesion molecule-1. The FcR+/- subsets were capable of presenting soluble and particulate antigens to OX-22- T cells. FcR+ cells were less effective than FcR- cells in promoting the proliferative response of OX-22+ T cells to concanavalin A and in the primary mixed leukocyte reaction. We conclude that the FcR+/- pulmonary dendritic cells differ in their abilities to support the responses of naive and sensitized T lymphocytes. This observation may have significance for how primary and secondary pulmonary cell-mediated immune responses are generated. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,COX BLDG 5,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-36781] NR 31 TC 15 Z9 15 U1 0 U2 0 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 MAR PY 1993 VL 142 IS 3 BP 811 EP 819 PG 9 WC Pathology SC Pathology GA KR805 UT WOS:A1993KR80500018 PM 8456942 ER PT J AU GLASS, WF KREISBERG, JI TROYER, DA AF GLASS, WF KREISBERG, JI TROYER, DA TI 2-CHAIN UROKINASE, RECEPTOR, AND TYPE-1 INHIBITOR IN CULTURED HUMAN MESANGIAL CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PLASMINOGEN ACTIVATOR; UROKINASE; THROMBIN; PLASMINOGEN ACTIVATOR INHIBITOR; AND PHOSPHOLIPASE-C ID FIBRO-SARCOMA CELLS; PLASMINOGEN-ACTIVATOR; GLYCOSYL-PHOSPHATIDYLINOSITOL; POLYACRYLAMIDE GELS; PHOSPHOLIPASE-C; PRO-UROKINASE; SHAPE CHANGE; PROTEINS; PROENZYME; ADHESION AB Urokinase-type plasminogen activator (u-PA), its receptor (u-PAR), and type 1 inhibitor (PAI-1) in cultured human mesangial cells were investigated. Treatment with phospholipase C (PLC) released plasminogen activators [with relative mol wt (M(r)) of 55,000 and 100,000] and u-PAR into the culture medium. By Western blot, both u-PA and PAI-1 were present in the M(r) 100,000 band. Since PAI-1 binds only active, two-chain u-PA (tcu-PA), formation of the M(r) 100,000 band reflects conversion of the single-chain, proenzyme form of u-PA (scu-PA) to tcu-PA. Immunofluorescence staining of whole cells demonstrated the presence of PAI-1, u-PA, and u-PAR. Immunofluorescence staining and Western blot analysis showed enrichment of PAI-1, u-PA, and u-PAR in a preparation of substratum-attached extracellular matrix and membrane proteins termed adhesion plaques. Using a chromogenic assay, we found that PAI-1 expression in adhesion plaques exceeded that of u-PA. We conclude that cultured human mesangial cells produce receptor-bound u-PA/PAI-1 complexes localized to adhesion plaques. C1 UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET HOSP,DEPT PATHOL,SAN ANTONIO,TX 78284. RP GLASS, WF (reprint author), UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL,BOX 214,CHARLOTTESVILLE,VA 22908, USA. FU NIDDK NIH HHS [DK-29787, DK-34234] NR 30 TC 14 Z9 14 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 MAR PY 1993 VL 264 IS 3 BP F532 EP F539 PN 2 PG 8 WC Physiology SC Physiology GA KV271 UT WOS:A1993KV27100092 PM 8384415 ER PT J AU SUN, XH MARTIN, V WEISS, RH KAYSEN, GA AF SUN, XH MARTIN, V WEISS, RH KAYSEN, GA TI SELECTIVE TRANSCRIPTIONAL AUGMENTATION OF HEPATIC GENE-EXPRESSION IN THE RAT WITH HEYMANN NEPHRITIS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE NEPHROTIC SYNDROME; COAGULATION; ACUTE PHASE PROTEINS; MESSENGER RIBONUCLEIC ACID; FIBRINOGEN; ALBUMIN; ALPHA-1-ACID GLYCOPROTEIN; RIBOSOMAL RIBONUCLEIC ACID ID NEPHROTIC SYNDROME; ALPHA-1-ACID GLYCOPROTEIN; LIPOPROTEIN METABOLISM; ALBUMIN; INFLAMMATION; FIBRINOGEN; RNA; SERUM; GLUCOCORTICOIDS; TRANSFERRIN AB The synthesis of albumin and other hepatic proteins, many regulated as part of the acute phase response, is increased in the nephrotic syndrome. It has been postulated that synthesis of all proteins secreted by the liver is increased by the same mechanism in the nephrotic syndrome. However, the observation that synthesis of some apolipoproteins is not increased suggests that only a specific group of proteins may be similarly regulated in nephrosis. We measured synthesis of albumin and of two acute phase proteins, fibrinogen and alpha1-acid glycoprotein (alpha1-AG), in rats with Heymann nephritis (HN), their mRNA concentration in liver, and the rate of transcription of their genes by hepatic nuclei. Albumin and fibrinogen mRNA levels almost doubled in HN, but alpha1-AG mRNA was unchanged. Ribosomal RNA (28S) concentration and transcription were also increased significantly in HN. Transcription of albumin and fibrinogen also increased twofold, but transcription of alpha1-AG was unchanged. Fibrinogen and albumin synthesis each increased more than fourfold in HN and correlated with one another. In contrast alpha1-AG synthesis only increased by 50% and did not correlate with albumin synthesis. Both albumin and alpha1-AG were lost in the urine of HN, and their plasma concentrations were reduced. Fibrinogen was not lost in the urine and its plasma concentration was significantly increased in HN. Synthesis of a group of proteins including both positive acute phase (fibrinogen) and negative acute phase (albumin) proteins is increased transcriptionally in the nephrotic syndrome. Synthesis of other proteins is increased posttranscriptionally. Therefore, a coordinated group of hepatic proteins is similarly regulated in HN, and this is not due to the acute phase response. Furthermore, neither the change in plasma concentration of a specific protein nor the possibility that protein is lost in urine determines whether its synthesis will be changed at the transcriptional level. C1 US DEPT VET AFFAIRS,NO CALIF SYST CLIN,BENECIA,CA 94510. UNIV CALIF DAVIS,SCH MED,DEPT MED,DIV NEPHROL,RENAL BIOCHEM LAB,DAVIS,CA 95616. FU NIDDK NIH HHS [1-RO1-DK-42297-01] NR 43 TC 20 Z9 20 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 MAR PY 1993 VL 264 IS 3 BP F441 EP F447 PN 2 PG 7 WC Physiology SC Physiology GA KV271 UT WOS:A1993KV27100079 PM 7681261 ER PT J AU SILVERMAN, JM SIEVER, LJ HORVATH, TB COCCARO, EF KLAR, H DAVIDSON, M PINKHAM, L APTER, SH MOHS, RC DAVIS, KL AF SILVERMAN, JM SIEVER, LJ HORVATH, TB COCCARO, EF KLAR, H DAVIDSON, M PINKHAM, L APTER, SH MOHS, RC DAVIS, KL TI SCHIZOPHRENIA-RELATED AND AFFECTIVE PERSONALITY-DISORDER TRAITS IN RELATIVES OF PROBANDS WITH SCHIZOPHRENIA AND PERSONALITY-DISORDERS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID BORDERLINE PERSONALITY; FAMILY HISTORY; SCHIZOTYPAL; TRANSMISSION; INTERVIEW; CRITERIA; VALIDITY AB Objective: The possible heterogeneity of the schizophrenia-related personality disorder traits associated with DSM-III criteria for schizotypal personality disorder was investigated using the family history method. A familial relationship to schizophrenia was hypothesized for schizophrenia-related personality disorder traits without coexisting affective personality disorder traits, pure schizophrenia-related personality disorder traits. Alternatively, a familial relationship with borderline personality disorder was hypothesized for schizophrenia-related personality disorder traits with comorbid affective personality disorder traits. Method: Criteria for schizophrenia-related and affective personality disorder traits were used to assess the 588 nonpsychotic first-degree relatives of SS chronic schizophrenic probands and 67 probands with personality disorders. The probands with one or more DSM-III personality disorders were categorized as having schizotypal personality disorder without borderline personality disorder (pure schizotypal personality disorder), borderline personality disorder without schizotypal personality disorder (pure borderline personality disorder), both disorders, or neither. Results: The morbid risk of all cases of schizophrenia-related personality disorder traits was higher in relatives of probands with schizophrenia and pure schizotypal personality disorder than in relatives of probands with neither schizotypal nor borderline personality disorder, however, it differed only slightly from that observed in the relatives of probands with both schizotypal and borderline personality disorders and pure borderline personality disorder. In contrast, the risk of pure schizophrenia-related personality disorder traits was higher in relatives of probands with schizophrenia and pure schizotypal personality disorder, while the risk of coexisting schizophrenia-related and affective personality disorder traits was lower in both of these groups than among the relatives of probands with both schizotypal and borderline personality disorders and pure borderline personality disorder. Conclusions: These results offer preliminary indications that schizotypal personality disorder features present without comorbid affective personality disorder traits may more specifically characterize the personality characteristics familially related to schizophrenia. Furthermore, they indicate that schizotypal personality disorder features as currently defined are found in relatives of patients other than those with schizophrenia or schizotypal personality disorder. C1 CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. RP SILVERMAN, JM (reprint author), BRONX VET ADM MED CTR,PSYCHIAT SERV 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIMH NIH HHS [MH-42827, MH-45212] NR 38 TC 37 Z9 38 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 1993 VL 150 IS 3 BP 435 EP 442 PG 8 WC Psychiatry SC Psychiatry GA KN845 UT WOS:A1993KN84500009 PM 8434659 ER PT J AU SCHNURR, PP FRIEDMAN, MJ ROSENBERG, SD AF SCHNURR, PP FRIEDMAN, MJ ROSENBERG, SD TI PREMILITARY MMPI SCORES AS PREDICTORS OF COMBAT-RELATED PTSD SYMPTOMS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID POSTTRAUMATIC-STRESS-DISORDER; VETERANS; SAMPLE AB Objective: The authors used data collected before military service to assess predictors of combat-related lifetime symptoms of posttraumatic stress disorder (PTSD). Method: The subjects were 131 male Vietnam and Vietnam-era veterans who bad taken the MMPI in college and who were interviewed as adults with the Structured Clinical Interview for DSM-III-R. Scores on the basic MMPI scales were used to predict combat exposure, lifetime history of any PTSD symptoms given exposure, and lifetime PTSD classification (symptoms only, subthreshold PTSD, or full PTSD). Results: Group means on the MMPI scales were within the normal range. No scale predicted combat exposure. Hypochondriasis, psychopathic deviate, masculinity-femininity, and paranoia scales predicted PTSD symptoms. Depression, hypomania, and social introversion predicted diagnostic classification among subjects with PTSD symptoms. The effects persisted when amount of combat exposure was controlled for. Conclusions: Premilitary personality can affect vulnerability to lifetime PTSD symptoms in men exposed to combat. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PSYCHIAT,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,US DEPT VET AFFAIRS,HANOVER,NH 03756. NR 15 TC 130 Z9 133 U1 1 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 MAR PY 1993 VL 150 IS 3 BP 479 EP 483 PG 5 WC Psychiatry SC Psychiatry GA KN845 UT WOS:A1993KN84500017 PM 8434666 ER PT J AU BARSKY, AJ CLEARY, PD SARNIE, MK KLERMAN, GL AF BARSKY, AJ CLEARY, PD SARNIE, MK KLERMAN, GL TI THE COURSE OF TRANSIENT HYPOCHONDRIASIS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID SELF-REPORT; SOMATOSENSORY AMPLIFICATION; VALIDITY; SYMPTOMS; ILLNESS; SCALE AB Objective: This study examined the longitudinal course of patients known to have had a previous episode of transient hypochondriasis. Method: Twenty-two transiently hypochondriacal patients and 24 nonhypochondriacal patients from the same general medical clinic were reexamined after an average of 22 months with the use of self-report questionnaires, structured diagnostic interviews, and medical record review. Results: The hypochondriacal patients continued to manifest significantly more hypochondriacal symptoms, more somatization, and more psychopathological symptoms at follow-up. They also reported significantly more amplification of bodily sensations and more functional disability and utilized more medical care. These differences persisted after control for differences in medical morbidity and marital status. Only one hypochondriacal patient, however, had a DSM-III-R diagnosis of hypochondriasis at follow-up. Multivariate analyses revealed that the only significant predictors of hypochondriacal symptoms at follow-up were hypochondriacal symptoms and the tendency to amplify bodily sensations at the baseline evaluation. Conclusions. Hypochondriacal symptoms appear to have some temporal stability: patients who experienced hypochondriacal episodes at the beginning of the study were significantly more hypochondriacal 2 years later than comparison patients. They were not, however, any more likely to develop DSM-III-R-defined hypochondriasis. Thus, hypochondriacal symptoms may be distinct from the axis I disorder. The data are also compatible with the hypothesis that preexisting amplification of bodily sensations is an important predictor of subsequent hypochondriacal symptoms. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT HLTH CARE POLICY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SOCIAL MED,BOSTON,MA 02115. CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. RP BARSKY, AJ (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,WARREN 631,FRUIT ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-40487] NR 27 TC 50 Z9 50 U1 1 U2 3 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 1993 VL 150 IS 3 BP 484 EP 488 PG 5 WC Psychiatry SC Psychiatry GA KN845 UT WOS:A1993KN84500018 PM 8434667 ER PT J AU HEBERT, JR HARRIS, DR SORENSEN, G STODDARD, AM HUNT, MK MORRIS, DH AF HEBERT, JR HARRIS, DR SORENSEN, G STODDARD, AM HUNT, MK MORRIS, DH TI A WORK-SITE NUTRITION INTERVENTION - ITS EFFECTS ON THE CONSUMPTION OF CANCER-RELATED NUTRIENTS SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID DIETARY-FAT; LUNG-CANCER; VITAMIN-C; CARCINOGENESIS; CAROTENOIDS; PREVENTION; RISK AB Objectives. In a work-site nutrition intervention targeting fat and fiber, we examined the intervention's effect on specific nutrients implicated in carcinogenesis, including trace metals, vitamins, and categories of fatty acids. The rationale was based on the association observed in a variety of epidemiologic studies between these nutrients and epithelial cancers. Methods. Data were taken from eight control companies and five intervention companies that fully implemented the Treatwell intervention. Analyses of variance were used preserving the study's nested design. Results. Significant intervention-related associations were observed for increased total vitamin A and carotene. Marginal intervention effects were observed for relative decreases in the percentage of calories from both saturated and monounsaturated fatty acids, a relatively smaller increase in the percentage of calories from polyunsaturated fatty acids, and an increase in the consumption of vitamin B6. Conclusions. Results indicate a broader effect of the intervention than on fat and fiber only. Increased intake of carotene, the single most important of these other nutrients, is plausibly related to a variety of eptihelial cancers. C1 UNIV MASSACHUSETTS,SCH PUBL HLTH,AMHERST,MA 01003. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV EPIDEMIOL & CONTROL,BOSTON,MA 02115. MAINSTREAM NUTR,WINNIPEG,MB,CANADA. RP HEBERT, JR (reprint author), UNIV MASSACHUTTS,SCH MED,DIV PREVENT & BEHAV MED,55 LAKE AVE N,WORCESTER,MA 01655, USA. OI Harris, Donald/0000-0002-8262-3716 FU NCI NIH HHS [5R01 CA46028] NR 39 TC 13 Z9 13 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 1993 VL 83 IS 3 BP 391 EP 394 DI 10.2105/AJPH.83.3.391 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KX085 UT WOS:A1993KX08500017 PM 8438978 ER PT J AU KOPANS, DB AF KOPANS, DB TI MAMMOGRAPHY - POSITIVE PREDICTIVE VALUE AND TRUE-POSITIVE BIOPSY RATE - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP KOPANS, DB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 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 MAR PY 1993 VL 160 IS 3 BP 660 EP 661 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KM935 UT WOS:A1993KM93500047 ER PT J AU JONES, EC CLEMENT, PB YOUNG, RH AF JONES, EC CLEMENT, PB YOUNG, RH TI INFLAMMATORY PSEUDOTUMOR OF THE URINARY-BLADDER - A CLINICOPATHOLOGICAL, IMMUNOHISTOCHEMICAL, ULTRASTRUCTURAL, AND FLOW CYTOMETRIC STUDY OF 13 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE URINARY BLADDER; INFLAMMATORY PSEUDOTUMOR; PSEUDOSARCOMA; PSEUDOSARCOMATOUS FIBROMYXOID TUMOR; MYOFIBROBLASTIC TUMOR ID PLASMA-CELL GRANULOMA; PSEUDOSARCOMATOUS LESIONS; NODULAR FASCIITIS; FIBROMYXOID TUMOR; CYTOKERATIN; PROLIFERATIONS; LEIOMYOSARCOMA; EXPRESSION; CARCINOMA; TRACT AB We report 13 cases of inflammatory pseudotumor of the urinary bladder in patients having no history of recent local trauma. The average age of the patients (eight females, five males) was 35.4 years (range, 19 to 60 years). Gross hematuria (nine of 13 cases) and recurrent cystitis (three of 13 cases) were the most common presentations. Cystoscopy and gross examination revealed either a polypoid intraluminal mass or a submucosal mural mass, ranging in size from 2 to 7 cm. The lesions were commonly gelatinous. Histological examination showed that the lesions consisted of spindle cells with tapering eosinophilic cytoplasm, typically widely separated in a vascular myxoid matrix with acute and chronic inflammatory cells. In four cases the lesions had more compact cellularity with areas of fibrosis and less myxoid change. The muscularis propria was involved in 10 cases, the perivesical fat in two cases. The spindle cells were immunoreactive for vimentin (10 of 10) and muscle-specific actin (10 of 10). A few cases exhibited immunoreactivity for smooth-muscle-specific actin (three of eight), cytokeratin (two of 10), desmin (two of nine), and epithelial membrane antigen (two of eight). Ultrastructural examination of four cases revealed myofibroblasts, fibroblasts, or a mixture of the two cell types. DNA content analysis by flow cytometry yielded diploid histograms (six of six). Clinical follow-up in all cases demonstrated no evidence of recurrence (mean follow-up, 25.8 months). The findings indicate that this lesion is a benign, likely inflammatory or reparative, mesenchymal lesion that can be recognized by its distinctive pathological features. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP JONES, EC (reprint author), UNIV BRITISH COLUMBIA,VANCOUVER GEN HOSP,DEPT PATHOL,855 W 12TH AVE,VANCOUVER V5Z 1M9,BC,CANADA. NR 34 TC 125 Z9 130 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAR PY 1993 VL 17 IS 3 BP 264 EP 274 DI 10.1097/00000478-199303000-00007 PG 11 WC Pathology; Surgery SC Pathology; Surgery GA KN937 UT WOS:A1993KN93700007 PM 8434707 ER PT J AU FROSTELL, CG BLOMQVIST, H HEDENSTIERNA, G LUNDBERG, J ZAPOL, WM AF FROSTELL, CG BLOMQVIST, H HEDENSTIERNA, G LUNDBERG, J ZAPOL, WM TI INHALED NITRIC-OXIDE SELECTIVELY REVERSES HUMAN HYPOXIC PULMONARY VASOCONSTRICTION WITHOUT CAUSING SYSTEMIC VASODILATION SO ANESTHESIOLOGY LA English DT Article DE ANESTHETICS, NITRIC OXIDE; HEART, VASCULAR PRESSURES; HORMONES, ENDOTHELIN; LUNG, VASCULAR RESISTANCE, HYPOXIA; MUSCLE, SMOOTH, ENDOTHELIUM-DERIVED RELAXING FACTOR ID ARTERIAL SMOOTH-MUSCLE; ENDOTHELIAL-CELLS; RELAXING FACTOR; NITROPRUSSIDE; RELAXATION; RELEASE; HYPERTENSION; ANIMALS; TISSUE; BLOOD AB Background: Nitric oxide (NO), an endothelium-derived relaxing factor, acts as a local vasodilator. The authors examined the effects of NO on pulmonary and systemic circulation in human volunteers. Methods: Nine healthy adults were studied awake while breathing 1) air, 2) 12% O2 in N2, 3) followed by the same mixture of O2 and N2 containing 40 ppm of NO. Pulmonary artery and radial artery pressures were monitored. Results: The Pa(O2) decreased from 106 +/- 4 (mean +/- standard error of the mean) while breathing air (21% O2) to 47 +/- 2 mmHg after 6 min of breathing 12% O2. Concomitantly, the pulmonary artery mean pressure (PAP) increased from 14.7 +/- 0.8 mmHg to 19.8 +/- 0.9 mmHg, and the cardiac output (CO) increased from 6.1 +/- 0.4 to 7.7 +/- 0.6 L/min. After adding 40 ppm NO to the inspired gas while maintaining the FI(O2) at 0.12, the PAP decreased (P < 0.01, by analysis of variance) to the level when breathing air while the Pa(O2) and Pa(CO2) were unchanged. The dilation (or recruitment) of pulmonary vessels produced by inhaling NO during hypoxia was not accompanied by any alteration in the systemic vascular resistance or mean arterial pressure (MAP). The authors also examined the effects of inhaling No while breathing air. Breathing 40 ppm NO in 21% O2 for 6 min produced no significant changes of PAP, CO, Pa(O2), MAP, or central venous pressure. Plasma endothelinlike immunoreactivity concentrations did not change either during hypoxia or hypoxia with NO inhalation. Conclusions. Inhalation of 40 ppm NO selectively induced pulmonary vasodilation and reversed hypoxic pulmonary vasoconstriction in healthy humans without causing systemic vasodilation. C1 UNIV HOSP UPPSALA,DEPT CLIN PHYSIOL,S-75185 UPPSALA,SWEDEN. DANDERYD HOSP,DEPT ANAESTHESIA & INTENS CARE,S-18288 DANDERYD,SWEDEN. KAROLINSKA INST,DEPT PHARMACOL,S-10401 STOCKHOLM 60,SWEDEN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-42397] NR 39 TC 321 Z9 323 U1 1 U2 6 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 1993 VL 78 IS 3 BP 427 EP 435 DI 10.1097/00000542-199303000-00005 PG 9 WC Anesthesiology SC Anesthesiology GA KR688 UT WOS:A1993KR68800004 PM 8457043 ER PT J AU MOLLER, JT PEDERSEN, T RASMUSSEN, LS JENSEN, PF PEDERSEN, BD RAVLO, O RASMUSSEN, NH ESPERSEN, K JOHANNESSEN, NW COOPER, JB GRAVENSTEIN, JS CHRAEMMERJORGENSEN, B WIBERGJORGENSEN, F DJERNES, M HESLET, L JOHANSEN, SH AF MOLLER, JT PEDERSEN, T RASMUSSEN, LS JENSEN, PF PEDERSEN, BD RAVLO, O RASMUSSEN, NH ESPERSEN, K JOHANNESSEN, NW COOPER, JB GRAVENSTEIN, JS CHRAEMMERJORGENSEN, B WIBERGJORGENSEN, F DJERNES, M HESLET, L JOHANSEN, SH TI RANDOMIZED EVALUATION OF PULSE OXIMETRY IN 20,802 PATIENTS .1. DESIGN, DEMOGRAPHY, PULSE OXIMETRY FAILURE RATE, AND OVERALL COMPLICATION RATE SO ANESTHESIOLOGY LA English DT Article DE ANESTHESIA, COMPLICATIONS; COMPLICATIONS, HYPOXEMIA; MYOCARDIAL ISCHEMIA; EQUIPMENT, FAILURE; PULSE OXIMETER; HYPOXIA; MONITORING, OXYGEN; PERIOPERATIVE; POSTOPERATIVE; OXYGEN, BLOOD LEVELS; RECOVERY; SAFETY ID GENERAL-ANESTHESIA; RISK-FACTORS; PREVENTION; MORBIDITY; MULTICENTER; STANDARDS AB Background. Although pulse oximetry is currently in widespread use, there are few data documenting improvement in patient outcome as a result of the use of oximetry. The authors describe the study design, patient demographic findings, data validation, pulse oximetry failure rate, and overall postoperative complication rates in the first large prospective randomized multicenter clinical trial on perioperative pulse oximetry monitoring. Methods. In five Danish hospitals, by random assignment, monitoring did or did not include pulse oximetry for patients 18 yr of age and older, whether scheduled for elective or emergency operations, or for regional or general anesthesia, except during cardiac and neurosurgical procedures. Operational definitions were established for perioperative events and postoperative complications. The data were collected preoperatively, during anesthesia, in the postanesthesia care unit, and until the day of discharge from the hospital or the seventh postoperative day. Results. Of 20,802 patients, 10,312 were assigned to the oximetry group and 10,490, to the control group. In general, the demographic data, patient factors, and anesthetic agents used were distributed evenly. A slight intergroup difference was found in the distribution of age, duration of surgery, some types of surgery, and some types of anesthesia. The total failure rate of the oximetry was 2.5%, but it increased to 7.2% in patients with American Society of Anesthesiologists physical status 4 (P < 0.00001). In 14.9% of the patients, one or more events occurred in the operating room and 13.5% in the postanesthesia care unit. The overall postoperative complication rate was 9.7%. The total rates of cardiovascular and respiratory complications were 2.78% and 3.50%, respectively. Within the first seven postoperative days, 0.47% of the patients died. Anesthesia was not thought to have been solely responsible for any death, but in 7 patients (1 per 3,365), it was a possible contributory factor. Conclusions. Despite the finding of a few significant intergroup differences, the randomization was well balanced with a high validity of data. The overall postoperative complication rate was similar to that in other recent morbidity and mortality studies. C1 UNIV COPENHAGEN,HERLEV HOSP,DEPT ANESTHESIA,DK-2730 HERLEV,DENMARK. GLOSTRUP CTY HOSP,DK-2600 GLOSTRUP,DENMARK. HILLEROD CENT HOSP,HILLEROD,DENMARK. ESBJERG CENT HOSP,ESBJERG,DENMARK. ODENSE HOSP,ODENSE,DENMARK. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV FLORIDA,COLL MED,DEPT ANESTHESIOL,GAINESVILLE,FL 32611. NR 23 TC 134 Z9 135 U1 0 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 1993 VL 78 IS 3 BP 436 EP 444 DI 10.1097/00000542-199303000-00006 PG 9 WC Anesthesiology SC Anesthesiology GA KR688 UT WOS:A1993KR68800005 PM 8457044 ER PT J AU MOLLER, JT JOHANNESSEN, NW ESPERSEN, K RAVLO, O PEDERSEN, BD JENSEN, PF RASMUSSEN, NH RASMUSSEN, LS PEDERSEN, T COOPER, JB GRAVENSTEIN, JS CHRAEMMERJORGENSEN, B DJERNES, M WIBERGJORGENSEN, F HESLET, L JOHANSEN, SH AF MOLLER, JT JOHANNESSEN, NW ESPERSEN, K RAVLO, O PEDERSEN, BD JENSEN, PF RASMUSSEN, NH RASMUSSEN, LS PEDERSEN, T COOPER, JB GRAVENSTEIN, JS CHRAEMMERJORGENSEN, B DJERNES, M WIBERGJORGENSEN, F HESLET, L JOHANSEN, SH TI RANDOMIZED EVALUATION OF PULSE OXIMETRY IN 20,802 PATIENTS .2. PERIOPERATIVE EVENTS AND POSTOPERATIVE COMPLICATIONS SO ANESTHESIOLOGY LA English DT Article DE COMPLICATIONS, HYPOXEMIA, INTRAOPERATIVE; POSTOPERATIVE; MONITORING OUTCOME, PULSE OXIMETRY; STUDY DESIGN, PROSPECTIVE, RANDOMIZED ID CLOSED CLAIMS ANALYSIS; ANESTHETIC MISHAPS; POTENTIAL ERRORS; HYPOXEMIA; PREVENTION; OBSERVER AB Background. The authors describe the effect of pulse oximetry monitoring on the frequency of unanticipated perioperative events, changes in patient care, and the rate of postoperative complications in a prospective randomized study. Methods. The study included 20,802 surgical patients in Denmark randomly assigned to be monitored or not with pulse oximetry in the operating room (OR) and postanesthesia care unit (PACU). Results. During anesthesia and in the PACU, significantly more patients in the oximetry group had at least one respiratory event than did the control patients. This was the result of a 19-fold increase in the incidence of diagnosed hypoxemia in the oximetry group than in the control group in both the OR and PACU (P < 0.00001). In the OR, cardiovascular events were observed in a similar number of patients in both groups, except myocardial ischemia (as defined by angina or ST-segment depression), which was detected in 12 patients in the oximetry group and in 26 patients in the control group (P < 0.03). Several changes in PACU care were observed in association with the use of pulse oximetry. These included higher flow rate of supplemental oxygen (P < 0.00001), increased use of supplemental oxygen at discharge (P < 0.00001), and increased use of naloxone (P < 0.02). The rate of changes in patient care as a consequence of the oximetry monitoring increased as the American Society of Anesthesiologists physical status worsened (P < 0.00001). One or more postoperative complications occurred in 10% of the patients in the oximetry group and in 9.4% in the control group (difference not significant). The two groups did not differ significantly in cardiovascular, respiratory, neurologic, or infectious complications. The duration of hospital stay was a median of 5 days in both groups (difference not significant). An equal number of in-hospital deaths were registered in the two groups. Questionnaires, completed by the anesthesiologists at the five participating departments, revealed that 18% of the anesthesiologists had experienced a situation in which a pulse oximeter helped to avoid a serious event or complication and that 80% of the anesthesiologists felt more secure when they used a pulse oximeter. Conclusions: This study demonstrated that pulse oximetry can improve the anesthesiologist's ability to detect hypoxemia and related events in the OR and PACU and that the use of the oximeter was associated with a significant decrease in the rate of myocardial ischemia. Although monitoring with pulse oximetry prompted a number of changes in patient care, a reduction in the overall rate of postoperative complications was not observed. C1 UNIV COPENHAGEN,HERLEV HOSP,DEPT ANESTHESIA,DK-2730 HERLEV,DENMARK. ESBJERG CENT HOSP,ESBJERG,DENMARK. ODENSE HOSP,ODENSE,DENMARK. GLOSTRUP CTY HOSP,DK-2600 GLOSTRUP,DENMARK. HILLEROD CENT HOSP,HILLEROD,DENMARK. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV FLORIDA,COLL MED,DEPT ANESTHESIOL,GAINESVILLE,FL 32611. OI Rasmussen, Lars/0000-0002-7480-3004 NR 24 TC 182 Z9 186 U1 1 U2 6 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 1993 VL 78 IS 3 BP 445 EP 453 DI 10.1097/00000542-199303000-00007 PG 9 WC Anesthesiology SC Anesthesiology GA KR688 UT WOS:A1993KR68800006 PM 8457045 ER PT J AU MONTGOMERY, WW SAMSON, MJ VARVARES, MA GOODMAN, ML AF MONTGOMERY, WW SAMSON, MJ VARVARES, MA GOODMAN, ML TI CUTANEOUS SQUAMOUS-CELL CARCINOMA OCCURRING IN A PECTORALIS MAJOR MYOCUTANEOUS FLAP - CASE-REPORT AND LITERATURE-REVIEW SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Review DE MOUTH NEOPLASMS; SQUAMOUS CELL CARCINOMA; SURGICAL FLAPS ID RECONSTRUCTION AB The pectoralis major myocutaneous flap is a reliable regional flap commonly used for the reconstruction of head and neck defects. We report a case of a squamous cell carcinoma that occurred on the cutaneous paddle of a pectoralis flap in a patient with previous chest wall lesions. The need for a careful history of previous chest wall cutaneous lesions is stressed in patients who are to undergo this type of reconstruction. C1 USN HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,PORTSMOUTH,VA. RP MONTGOMERY, WW (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 6 TC 5 Z9 5 U1 0 U2 1 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD MAR PY 1993 VL 102 IS 3 BP 206 EP 208 PN 1 PG 3 WC Otorhinolaryngology SC Otorhinolaryngology GA KT618 UT WOS:A1993KT61800007 PM 8457122 ER PT J AU AMERHAUSER, A MOELLEKEN, BRW MATHES, SJ GOODING, G GOLDSTEIN, R CALLEN, P FILLY, RA MAY, JW AF AMERHAUSER, A MOELLEKEN, BRW MATHES, SJ GOODING, G GOLDSTEIN, R CALLEN, P FILLY, RA MAY, JW TI COLOR FLOW ULTRASOUND FOR DELINEATING MICROSURGICAL VESSELS - A CLINICAL AND EXPERIMENTAL-STUDY SO ANNALS OF PLASTIC SURGERY LA English DT Article ID DOPPLER US; DUPLEX; HEMODYNAMICS; HYPERTENSION AB There is a need in plastic and reconstructive surgery for a method of monitoring flaps and replants pre- and postoperatively. This study evaluates color flow Doppler done as a monitoring technique for microvascular vessels. The capability of color flow ultrasound to monitor venous and arterial insufficiency and occlusion was studied by means of an experimental system in the Yucatan miniature swine model. A circulatory circuit in line with a magnetic flow probe is created. Measurements are made on the isolated hind limb of the animal. Color flow ultrasound is demonstrated to be a technique that is sensitive to venous and arterial insufficiency at flow rates as low as 3.0 ml/min. Characteristic waveform patterns are shown to predict arterial and venous insufficiency before they actually progress to occlusion. A clinical series of 25 postoperative patients is presented, consisting of volunteer studies as well as pre- and postoperative examinations of free flaps and replantations. Color flow ultrasound is shown to visualize a spectrum of pre- and postoperative microvascular conduits encountered in plastic and reconstructive surgery. C1 UNIV CALIF SAN FRANCISCO,DEPT SURG,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DIV PLAST RECONSTRUCT & HAND SURG,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 24 TC 33 Z9 33 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0148-7043 J9 ANN PLAS SURG JI Ann. Plast. Surg. PD MAR PY 1993 VL 30 IS 3 BP 193 EP 203 DI 10.1097/00000637-199303000-00001 PG 11 WC Surgery SC Surgery GA KR678 UT WOS:A1993KR67800001 PM 8494300 ER PT J AU RATTNER, DW FERGUSON, C WARSHAW, AL AF RATTNER, DW FERGUSON, C WARSHAW, AL TI FACTORS ASSOCIATED WITH SUCCESSFUL LAPAROSCOPIC CHOLECYSTECTOMY FOR ACUTE CHOLECYSTITIS SO ANNALS OF SURGERY LA English DT Article AB Objective This article determined which preoperative data correlated with successful completion of a laparoscopic cholecystectomy in patients with acute cholecystitis. Summary Background Data Although laparoscopic cholecystectomy is the procedure of choice in chronic cholecystitis, its use in acute cholecystitis may be associated with higher costs and complication rates. It is not known which patients with acute cholecystitis are likely to require conversion to open cholecystectomy based on preoperative data or if a cooling-off period with medical therapy can diminish inflammation and increase the chance of successful laparoscopic cholecystectomy. Methods All laparoscopic cholecystectomies done by the authors between 10/90 and 2/92 were reviewed. Data on cases of acute cholecystitis were prospectively collected on standardized data forms. Results Twenty of 281 laparoscopic cholecystectomies were done for acute cholecystitis; 7/20 patients with acute cholecystitis required conversion to open cholecystectomy compared with 6/281 patients undergoing elective operation for chronic cholecystitis. In patients with acute cholecystitis the interval from admission to cholecystectomy in the successful cases was 0.6 days vs. 5 days in the cases requiring conversion to open cholecystectomy (p = .01). Cases requiring conversion to open cholecystectomy also had higher WBC (14.0 vs. 9.0, p < .05). alkaline phosphatase (206 vs. 81, p < .02, and APACHE II scores (10.6 vs. 5.1, p < .05). Ultrasonographic findings such as gallbladder distention, wall thickness, and pericholecystic fluid did not correlate with the success of laparoscopic cholecystectomy. Patients converted from laparoscopic to open cholecystectomy required more operating room time (1 20 min vs. 87 min, p < .01) and more postop hospital days (6 vs. 2, p < .001). Conclusions Laparoscopic cholecystectomy for acute cholecystitis should be done immediately after the diagnosis is established because delaying surgery allows inflammation to become more intense, thus increasing the technical difficulty of laparoscopic cholecystectomy. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RATTNER, DW (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114, USA. NR 10 TC 172 Z9 177 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD MAR PY 1993 VL 217 IS 3 BP 233 EP 236 DI 10.1097/00000658-199303000-00003 PG 4 WC Surgery SC Surgery GA KT415 UT WOS:A1993KT41500004 PM 8452401 ER PT J AU AKINS, CW AF AKINS, CW TI SELECTION OF CARDIAC VALVULAR PROSTHESES SO ANNALS OF THORACIC SURGERY LA English DT Bibliography RP AKINS, CW (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD MAR PY 1993 VL 55 IS 3 BP 801 EP 802 PG 2 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA KT989 UT WOS:A1993KT98900052 PM 8452459 ER PT J AU COLLINS, LA MALANOSKI, GJ ELIOPOULOS, GM WENNERSTEIN, CB FERRARO, MJ MOELLERING, RC AF COLLINS, LA MALANOSKI, GJ ELIOPOULOS, GM WENNERSTEIN, CB FERRARO, MJ MOELLERING, RC TI INVITRO ACTIVITY OF RP59500, AN INJECTABLE STREPTOGRAMIN ANTIBIOTIC, AGAINST VANCOMYCIN-RESISTANT GRAM-POSITIVE ORGANISMS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID ENTEROCOCCI AB The in vitro activity of RP59500, a streptogramin antibiotic, against 146 clinical isolates of vancomycin-resistant gram-positive bacteria was examined. Five strains of the species Enterococcus casseliflavus and Enterococcus gallinarum, for which the MIC of vancomycin was 8 mug/ml, were also studied. Twenty-eight vancomycin-susceptible strains of Enterococcusfaecalis and Enterococcusfaecium were included for comparison. The drug was highly active against Leuconostoc spp., Lactobacillus spp., and Pediococcus spp. (MICs, less-than-or-equal-to 2 mug/ml). RP59500 was more active against vancomycin-susceptible strains of E. faecium than E. faecalis (MICs for 90% of the strains [MIC90s], 1.0 versus 32 mug/ml). Vancomycin-resistant strains of E. faecalis were as resistant to RP59500 as vancomycin-susceptible strains (MIC90, 32 mug/ml), but some vancomycin-resistant E. faecium strains were relatively more resistant to the new agent (MIC90, 16; MIC range, 0.5 to 32 mug/ml) than were vancomycin-susceptible organisms of this species. C1 NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 12 TC 105 Z9 105 U1 1 U2 2 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 MAR PY 1993 VL 37 IS 3 BP 598 EP 601 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA KP921 UT WOS:A1993KP92100034 PM 8460927 ER PT J AU SELINGER, M WALKER, KA PRESCOTT, TE DAVIS, RE AF SELINGER, M WALKER, KA PRESCOTT, TE DAVIS, RE TI A POSSIBLE EXPLANATION OF PROBLEM-SOLVING DEFICITS BASED ON RESOURCE-ALLOCATION THEORY SO APHASIOLOGY LA English DT Article ID INTELLIGENCE; APHASIA AB This investigation examined non-verbal problem-solving abilities. Two groups of visual-spatial puzzles were administered to 10 left-CVA patients, 10 right-CVA patients and 10 normal subjects. The puzzles were divided into named and unnamed groups to examine the effects of non-language stimuli on test performance. Results indicated significant differences, with right-CVA patients having the greatest difficulty on all puzzles, left-CVA patients having the greatest difficulty with unnamed puzzles and making errors on some named puzzles and normal subjects making significantly fewer errors but having a response pattern similar to the left-CVA patients. The findings imply that, in terms of resource allocation theory, when the task utilized the competence of the left hemisphere for naming in conjunction with the visual-spatial competence of the right hemisphere, each hemisphere's resources were utilized and scores on the puzzles increased. C1 NO MICHIGAN UNIV,MARQUETTE,MI 49855. RP SELINGER, M (reprint author), DENVER VAMC 126,1055 CLERMONT ST,DENVER,CO 80220, USA. NR 28 TC 3 Z9 3 U1 1 U2 1 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0268-7038 J9 APHASIOLOGY JI Aphasiology PD MAR-APR PY 1993 VL 7 IS 2 BP 165 EP 175 DI 10.1080/02687039308249504 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA KP793 UT WOS:A1993KP79300003 ER PT J AU HEGARTY, KA AF HEGARTY, KA TI SEEING VOICES - A JOURNEY INTO THE WORLD OF THE DEAF - SACKS,O SO APPLIED PSYCHOLINGUISTICS LA English DT Book Review RP HEGARTY, KA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD MAR PY 1993 VL 14 IS 1 BP 121 EP 124 DI 10.1017/S0142716400010171 PG 4 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA KZ432 UT WOS:A1993KZ43200006 ER PT J AU HODGSON, JM AF HODGSON, JM TI PHONOLOGICAL PROCESSES IN LITERACY - A TRIBUTE TO LIBERMAN,ISABELLE,Y. - BRADY,SA, SHANKWEILER,DP SO APPLIED PSYCHOLINGUISTICS LA English DT Book Review ID READ RP HODGSON, JM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 12 TC 1 Z9 1 U1 2 U2 5 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD MAR PY 1993 VL 14 IS 1 BP 127 EP 133 DI 10.1017/S0142716400010195 PG 7 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA KZ432 UT WOS:A1993KZ43200008 ER PT J AU LEVENTHAL, LC JAWORSKY, C WERTH, V AF LEVENTHAL, LC JAWORSKY, C WERTH, V TI AN ASYMPTOMATIC PENILE LESION - CIRCULAR INDURATED LYMPHANGITIS OF THE PENIS (CILP) WITH CONCURRENT SYPHILIS SO ARCHIVES OF DERMATOLOGY LA English DT Note RP LEVENTHAL, LC (reprint author), VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 11 TC 3 Z9 3 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAR PY 1993 VL 129 IS 3 BP 366 EP & DI 10.1001/archderm.129.3.366 PG 0 WC Dermatology SC Dermatology GA KR036 UT WOS:A1993KR03600019 PM 8447680 ER PT J AU MAHLER, ME AF MAHLER, ME TI SPECIFICITY OF THE UPGOING THUMB SO ARCHIVES OF NEUROLOGY LA English DT Letter RP MAHLER, ME (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROBEHAV UNIT,B111,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD MAR PY 1993 VL 50 IS 3 BP 239 EP 239 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA KQ120 UT WOS:A1993KQ12000002 PM 8442700 ER PT J AU LEE, PP YANG, JC SCHACHAT, AP AF LEE, PP YANG, JC SCHACHAT, AP TI IS INFORMED CONSENT NEEDED FOR FLUORESCEIN ANGIOGRAPHY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID CONTRAST-ENHANCED RADIOGRAPHY AB Fluorescein angiography is a common diagnostic procedure. Questions have been frequently raised as to whether explicit informed consent is needed for this procedure and what form such consent should take. Review of existing legal concepts indicates that the need for explicit consent varies from state to state, but that the trend is to require an explicit discussion of risks, benefits, and alternatives. Documentation of such information can adequately range from a brief, written notation in the patient's chart to a complete, separate form. C1 BROWN & WOOD,NEW YORK,NY. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. OI Lee, Paul/0000-0002-3338-136X NR 17 TC 4 Z9 4 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 MAR PY 1993 VL 111 IS 3 BP 327 EP 330 PG 4 WC Ophthalmology SC Ophthalmology GA KR446 UT WOS:A1993KR44600021 PM 8447740 ER PT J AU GUYER, DR TIEDEMAN, J YANNUZZI, LA SLAKTER, JS PARKE, D KELLEY, J TANG, RA MARMOR, M ABRAMS, G MILLER, JW GRAGOUDAS, ES AF GUYER, DR TIEDEMAN, J YANNUZZI, LA SLAKTER, JS PARKE, D KELLEY, J TANG, RA MARMOR, M ABRAMS, G MILLER, JW GRAGOUDAS, ES TI INTERFERON-ASSOCIATED RETINOPATHY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID LEUKOCYTE-A INTERFERON; COTTON-WOOL SPOTS; KAPOSIS SARCOMA; ALPHA-2 INTERFERON; THERAPY; INHIBITION; EYELASHES; ALFA-2A; DISEASE AB Interferon alfa is used to treat various systemic disorders and recently has been suggested as a possible treatment for choroidal neovascularization. We report 10 cases of retinal ischemia associated with the use of interferon alfa for various illnesses. The retinal findings include cotton-wool spot formation, capillary nonperfusion, arteriolar occlusion, and hemorrhage. The retinal complications may sometimes be reversible when treatment is stopped. Our findings emphasize the need to have patients who are receiving interferon alfa therapy monitored for these retinal complications, which may rarely be associated with permanent loss of vision secondary to closure of retinal capillaries. C1 DUKE UNIV,CTR EYE,DURHAM,NC 27706. UNIV OKLAHOMA,DEPT OPHTHALMOL,OKLAHOMA CITY,OK. GREATER BALTIMORE MD MED CTR,DEPT OPHTHALMOL,BALTIMORE,MD. UNIV TEXAS,SCH MED,DEPT OPHTHALMOL,HOUSTON,TX 77025. STANFORD UNIV,DEPT OPHTHALMOL,PALO ALTO,CA 94304. MED COLL WISCONSIN,DEPT OPHTHALMOL,MILWAUKEE,WI 53226. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RETINA SERV,BOSTON,MA 02114. RP GUYER, DR (reprint author), MANHATTAN EYE EAR & THROAT HOSP,RETINAL RES LAB,210 E 64TH ST,NEW YORK,NY 10021, USA. NR 41 TC 210 Z9 214 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAR PY 1993 VL 111 IS 3 BP 350 EP 356 PG 7 WC Ophthalmology SC Ophthalmology GA KR446 UT WOS:A1993KR44600026 PM 8447745 ER PT J AU PINS, MR ROSENTHAL, DI SPRINGFIELD, DS ROSENBERG, AE AF PINS, MR ROSENTHAL, DI SPRINGFIELD, DS ROSENBERG, AE TI FLORID EXTRAVASCULAR PAPILLARY ENDOTHELIAL HYPERPLASIA (MASSON PSEUDOANGIOSARCOMA) PRESENTING AS A SOFT-TISSUE SARCOMA SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID HEMANGIOENDOTHELIOMA; HEMANGIOMA; TUMOR AB Papillary endothelial hyperplasia (also known as Masson's pseudoangiosarcoma) is a hyperplastic proliferation of endothelial cells that is usually an incidental finding within thrombosed dilated blood vessels or vascular tumors. Rare extravascular forms occur and can histologically closely mimic angiosarcoma. We report a case of extravascular papillary endothelial hyperplasia that extensively involved a large, traumatic, deep soft-tissue hematoma in a 19-year-old man and clinically presented as a soft-tissue sarcoma. We also summarize characteristics of 314 cases of papillary endothelial hyperplasia reported in the literature and identify 13 likely cases of the rare extravascular form. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 36 TC 70 Z9 73 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD MAR PY 1993 VL 117 IS 3 BP 259 EP 263 PG 5 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA KQ558 UT WOS:A1993KQ55800008 PM 8442671 ER PT J AU WARSHAW, AL AF WARSHAW, AL TI RESTORATION, NOT PRESERVATION, OF GENERAL-SURGERY RESIDENCY SO ARCHIVES OF SURGERY LA English DT Editorial Material C1 MASSACHUSETTS EYE & EAR INFIRM, SURG SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT SURG, BOSTON, MA 02115 USA. NR 12 TC 15 Z9 15 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD MAR PY 1993 VL 128 IS 3 BP 265 EP 268 PG 4 WC Surgery SC Surgery GA KQ121 UT WOS:A1993KQ12100002 PM 8442680 ER PT J AU FREUND, RM SIEBERT, JW CABRERA, RC LONGAKER, MT EIDELMAN, Y ADZICK, NS GARG, HG AF FREUND, RM SIEBERT, JW CABRERA, RC LONGAKER, MT EIDELMAN, Y ADZICK, NS GARG, HG TI SERIAL QUANTITATION OF HYALURONAN AND SULFATED GLYCOSAMINOGLYCANS IN FETAL SHEEP SKIN SO BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL LA English DT Article ID HYPERTROPHIC SCAR; OPEN WOUNDS; ACID; PROTEOGLYCAN; FIBRONECTIN; FIBROBLASTS; DEPOSITION; INHIBITION; COLLAGEN; MODEL C1 UNIV CALIF SAN FRANCISCO,FETAL TREATMENT PROGRAM,SAN FRANCISCO,CA 94143. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA 02114. RP FREUND, RM (reprint author), NYU MED CTR,INST RECONSTRUCT PLAST SURG,NEW YORK,NY 10016, USA. NR 33 TC 10 Z9 13 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 MAR PY 1993 VL 29 IS 4 BP 773 EP 783 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KY075 UT WOS:A1993KY07500020 PM 8490582 ER PT J AU MILLER, JB EVERITT, EA SMITH, TH BLOCK, NE DOMINOV, JA AF MILLER, JB EVERITT, EA SMITH, TH BLOCK, NE DOMINOV, JA TI CELLULAR AND MOLECULAR DIVERSITY IN SKELETAL-MUSCLE DEVELOPMENT - NEWS FROM INVITRO AND INVIVO SO BIOESSAYS LA English DT Review ID REGULATORY FACTORS; CLONAL ANALYSIS; CHICK-EMBRYO; FIBER TYPES; JAW MUSCLE; EXPRESSION; CELLS; GENE; MYOSIN; MYOD1 AB Skeletal muscle formation is studied in vitro with myogenic cell lines and primary muscle cell cultures, and in vivo with embryos of several species. We review several of the notable advances obtained from studies of cultured cells, including the recognition of myoblast diversity, isolation of the MyoD family of muscle regulatory factors, and identification of promoter elements required for muscle-specific gene expression. These studies have led to the ideas that myoblast diversity underlies the formation of the multiple types of fast and slow muscle fibers, and that myogenesis is controlled by a combination of ubiquitous and muscle-specific transcriptional regulators that may be different for each gene. We further review some unexpected results that have been obtained when ideas from work in culture have been tested in developing animals. The studies in vivo point to additional molecular and cellular mechanisms that regulate muscle formation in the animal. C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP MILLER, JB (reprint author), MASSACHUSETTS GEN HOSP,NEUROMUSCULAR LAB,149 13TH ST,BOSTON,MA 02129, USA. NR 60 TC 37 Z9 40 U1 0 U2 4 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD MAR PY 1993 VL 15 IS 3 BP 191 EP 196 DI 10.1002/bies.950150308 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA KX035 UT WOS:A1993KX03500007 PM 8387785 ER PT J AU ELGENDY, HM NORMAN, ME KEATON, AR LAURENCIN, CT AF ELGENDY, HM NORMAN, ME KEATON, AR LAURENCIN, CT TI OSTEOBLAST-LIKE CELL (MC3T3-E1) PROLIFERATION ON BIOERODIBLE POLYMERS - AN APPROACH TOWARDS THE DEVELOPMENT OF A BONE BIOERODIBLE POLYMER COMPOSITE-MATERIAL SO BIOMATERIALS LA English DT Article DE OSTEOBLAST; HYDROXYAPATITE; BONE REPAIR; CELL POLYMER MATRIX ID DRUG-CARRIER MATRICES; IMPLANT MATERIALS; TISSUE REACTION; INVITRO; HYDROXYAPATITE; BIOCOMPATIBILITY; SUBSTRATA; LINE; POLYANHYDRIDES; DEGRADATION AB An osteogenic cell line (MC3T3-E1) was used to study the potential of bioerodible polymers and ceramics to support osteoblast growth for a proposed bone-polymer composite for skeletal tissue repair. MC3T3-E1 cells were seeded on to 50:50 poly(lactide-co-glycolide), hydroxyapatite, 50:50 hydroxyapatite/poly(lactide-co-glycolide), and the poly(anhydride), poly(bis(p-carboxyphenoxy) propane surfaces. Cell attachment and growth on these surfaces was found to be highest on poly(lactide-co-glycolide), the least on hydroxyapatite and hydroxyapatite/poly(lactide-co-glycolide) combinations gave intermediate values. The order of adhesion and growth of MC3T3-E1 cells on the polymer and ceramic systems was poly(lactide-co-glycolide) is greater than hydroxyapatite/poly(lactide-co-glycolide) which is greater than hydroxyapatite. Negligible growth was found on poly(bis(p-carboxyphenoxy) propane. High alkaline phosphatase activity for the cells grown on poly(lactide-co-glycolide) and hydroxyapatite/poly(lactide-co-glycolide) confirmed retention of the osteoblast phenotype. This in vitro evaluation suggests that poly(lactide-co-glycolide) and hydroxyapatite/poly(lactide-co-glycolide) combinations may be candidate biomaterials for the construction of a cell-polymer matrix for skeletal tissue regeneration. C1 MIT,HARVARD MIT DIV HLTH SCI & TECHNOL,BLDG 56,ROOM 141,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA 02114. OI Elgendy, Hoda/0000-0002-5573-7419 NR 49 TC 102 Z9 104 U1 0 U2 7 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0142-9612 J9 BIOMATERIALS JI Biomaterials PD MAR PY 1993 VL 14 IS 4 BP 263 EP 269 DI 10.1016/0142-9612(93)90116-J PG 7 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA KU449 UT WOS:A1993KU44900003 PM 8386557 ER PT J AU SKATES, SJ AF SKATES, SJ TI ON SECANT APPROXIMATIONS TO CUMULATIVE DISTRIBUTION-FUNCTIONS SO BIOMETRIKA LA English DT Article DE CUMULATIVE DISTRIBUTION FUNCTION; PEARSON TYPE-IV DISTRIBUTION; SECANT APPROXIMATION; SKEW-T DISTRIBUTION; TAIL PROBABILITY; UNIFORM ASYMPTOTIC EXPANSION ID LOG LIKELIHOOD RATIO; TAIL PROBABILITIES; MARGINAL DENSITIES AB We investigate the properties of an approximation, called the secant approximation, to the cumulative distribution function where the density is of a broad parametric class. Formulae for higher order terms are derived that give the approximation explicitly in terms of functions that define the density. In all cases examined, the first order secant approximation is monotonic and has the correct limits at both ends of the support, resulting in the important property that the approximation itself is a cumulative distribution function. We give conditions under which the approximation has bounded relative errors throughout the support. The superiority of the secant approximation is illustrated in the particular case of the skew t family of distributions, also known as Pearson's Type IV family. A collection of formulae useful for the systematic evaluation of these approximations is given in Appendix 2. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SKATES, SJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114, USA. NR 33 TC 7 Z9 8 U1 0 U2 2 PU BIOMETRIKA TRUST PI LONDON PA UNIV COLLEGE LONDON GOWER ST-BIOMETRIKA OFFICE, LONDON, ENGLAND WC1E 6BT SN 0006-3444 J9 BIOMETRIKA JI Biometrika PD MAR PY 1993 VL 80 IS 1 BP 223 EP 235 DI 10.2307/2336771 PG 13 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA KZ195 UT WOS:A1993KZ19500018 ER PT J AU RAINES, DE MILLER, KW AF RAINES, DE MILLER, KW TI THE ROLE OF CHARGE IN LIPID SELECTIVITY FOR THE NICOTINIC ACETYLCHOLINE-RECEPTOR SO BIOPHYSICAL JOURNAL LA English DT Article ID SPIN-LABEL; PROTEIN INTERACTIONS; MEMBRANES; BINDING; CHOLESTEROL; SPECIFICITY; DISPERSIONS AB The effect of salt and pH titration on the selectivity of spin-labeled analogues of phosphatidic acid, phosphatidylserine, phosphatidylcholine, and stearic acid for the nicotinic acetylcholine receptor (nAcChoR) reconstituted into dioleoylphosphatidylcholine was examined at 0-degrees-C using electron spin resonance spectroscopy. The order of selectivity at pH 7.4 and 0 mM NaCl was phosphatidylserine > stearic acid > phosphatidic acid > phosphatidylcholine. The addition up to 2 M NaCl or titration of pH from 5.0 to >9.0 did not alter the selectivity of the phospholipids for the nAcChoR. For stearic acid, conversely, titration of pH from 5.0 to 9.0 at 0 mM NaCl and titration of NaCl from 0 to 2 M at pH 9.0 both increased selectivity for the nAcChoR. It is concluded that electrostatic interactions do not account for the selectivity of the negatively charged phospholipids, phosphatidylserine, and phosphatidic acid for the nAcChoR. This is consistent with the known orientation of the transmembrane sequences M1 and M4, which predicts a balance in the number of negative and positive charges in the lipid-protein interface and suggests that the two positive charges on each M3 helix are not exposed to the lipid-protein interface. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIGMS NIH HHS [GM07592, GM15904] NR 21 TC 16 Z9 16 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD MAR PY 1993 VL 64 IS 3 BP 632 EP 641 PG 10 WC Biophysics SC Biophysics GA KR826 UT WOS:A1993KR82600008 PM 8386010 ER PT J AU SHIH, JP OGAWA, M AF SHIH, JP OGAWA, M TI MONOCLONAL-ANTIBODY J11D.2 RECOGNIZES CELL CYCLE-DORMANT, PRIMITIVE HEMATOPOIETIC PROGENITORS OF MICE SO BLOOD LA English DT Article ID DIFFERENTIATION ANTIGENS; STEM-CELLS; T-CELLS; COLONIES; IDENTIFICATION; CULTURE; ORIGIN C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. FU NIDDK NIH HHS [DK32294] NR 18 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1993 VL 81 IS 5 BP 1155 EP 1160 PG 6 WC Hematology SC Hematology GA KP977 UT WOS:A1993KP97700007 PM 8443377 ER PT J AU MIR, R ANDERSON, J STRAUCHEN, J NISSEN, NI COOPER, MR RAFLA, S CANELLOS, GP BLOOMFIELD, CD GOTTLIEB, AJ PETERSON, B BARCOS, M AF MIR, R ANDERSON, J STRAUCHEN, J NISSEN, NI COOPER, MR RAFLA, S CANELLOS, GP BLOOMFIELD, CD GOTTLIEB, AJ PETERSON, B BARCOS, M TI HODGKINS-DISEASE IN PATIENTS 60 YEARS OF AGE OR OLDER - HISTOLOGIC AND CLINICAL-FEATURES OF ADVANCED-STAGE DISEASE SO CANCER LA English DT Article DE HODGKIN DISEASE; NON-HODGKIN LYMPHOMA; CLASSIFICATION; AGE; ANATOMIC SITES; TREATMENT; SURVIVAL ID PROGNOSTIC FACTORS; SURVIVAL; CHEMOTHERAPY; PROCARBAZINE; RADIOTHERAPY; VINBLASTINE; COMBINATION; PREDNISONE; REMISSION; SUBTYPES AB Background. This article reviews the salient pathologic and clinical features of 171 patients with Stage III-IV disease who were 60 years of age or older who were treated on four Hodgkin disease (HD) protocols from 1969 to 1988. Methods. Pretherapy sections were reviewed centrally for correlation of the histologic classification with anatomic sites of involvement and survival. Results. The diagnosis of HD was confirmed in 114 (66.7%) patients. Non-Hodgkin lymphomas (NHL) and a miscellaneous non-HD group accounted for 52 (30.4%) and 5 (2.9%) of the cases. The overall median survival times of patients with Stage III-IV HD and NHL who were 60 years of age or older in the four protocols were not significantly different (1.5 versus 1.3 years, respectively; P = 0.28). There also was no significant correlation between the survival of these patients with HD and either the Rye classification, 19 specific histologic parameters, or the British National Lymphoma Investigation grading system for HDNS. In the last protocol, the 5-year survival rate of patients with HD who were 60 years of age or older was lower than that of patients 40-59 years of age or that of those younger than 40 years of age (31% versus 63% versus 79%, respectively, P < 0.0001). Patients with HD entered into the two most recent protocols showed lower incidences of involvement of cervical and iliac-inguinal-femoral lymph nodes and skin-subcutaneous tissues than the patients with NHL who were misdiagnosed as HD. Moreover, patients with Stage III-IV HD in the most recent protocol who were 60 years of age or older had lower rates of involvement of the cervical and mediastinal-hilar lymph nodes and a higher rate of involvement of the gastrointestinal tract than younger patients. Conclusions. Patients with Stage III-IV HD and NHL who are 60 years of age or older differ with respect to the rates of involvement of specific anatomic sites but not in survival when treated with HD protocols. In contrast, patients of different age groups with Stage III-IV HD disease differ with regard to the rates of involvement of anatomic sites and survival. C1 ROSWELL PK CANC INST,DEPT PATHOL,ELM & CARLTON ST,BUFFALO,NY 14263. LONG ISL JEWISH MED CTR,NEW HYDE PK,NY 11042. UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. MT SINAI HOSP,NEW YORK,NY. RIGSHOSP,DK-2100 COPENHAGEN,DENMARK. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC 27103. METHODIST HOSP,BROOKLYN,NY 11215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CANC & LEUKEMIA GRP B,LEBANON,NH. SUNY UPSTATE MED CTR,SYRACUSE,NY 13210. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. FU NCI NIH HHS [CA-04457, CA-11028, CA-03927] NR 51 TC 26 Z9 27 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 MAR 1 PY 1993 VL 71 IS 5 BP 1857 EP 1866 DI 10.1002/1097-0142(19930301)71:5<1857::AID-CNCR2820710524>3.0.CO;2-B PG 10 WC Oncology SC Oncology GA KP990 UT WOS:A1993KP99000023 PM 8448750 ER PT J AU HUTSON, PR TUTSCH, K SPRIGGS, D CHRISTIAN, M RAGO, R MUTCH, R WILDING, G AF HUTSON, PR TUTSCH, K SPRIGGS, D CHRISTIAN, M RAGO, R MUTCH, R WILDING, G TI EVIDENCE OF AN ABSORPTION PHASE AFTER SHORT INTRAVENOUS SURAMIN INFUSIONS SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE SURAMIN; ABSORPTION; PHARMACOKINETICS ID HEPARIN; PHARMACOKINETICS; THERAPY AB Suramin was given as an intravenous infusion to 16 cancer patients in a phase I trial. Individual pharmacokinetic parameters were calculated from a test dose given 1 week prior to the administration of a full-dose (350-700 mg/m2) regimen of 1-h loading and maintenance infusions. A distribution phase of 3.8 h was found. Plasma suramin concentrations were noted to increase following cessation of the intravenous test infusion in eight subjects. A model is proposed in which high-capacity, low-affinity binding of suramin to a shallow compartment adjacent to the intravascular space occurs rapidly during infusion, followed by absorption back into the measured blood pool with binding to plasma albumin. Despite the observable presence of this postinfusion peak shortly after the cessation of the brief suramin infusion, the pharmacokinetics of suramin were best characterized by a traditional two-compartment model. The dose-adjusted area under the concentration-time curve (AUC) increased with dose, supporting a hypothesis of sustained absorption of suramin to vascular endothelium but also raising the possibility of dose-dependent clearance. C1 UNIV WISCONSIN,DEPT HUMAN ONCOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,NCI,CTEP,DCT,MADISON,WI 53705. RP HUTSON, PR (reprint author), UNIV WISCONSIN,SCH PHARM,425 N CHARTER ST,MADISON,WI 53706, USA. FU NCI NIH HHS [N01-CM-07306, T32-CA09614]; NCRR NIH HHS [M01-RR03186] NR 20 TC 6 Z9 6 U1 0 U2 0 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 MAR PY 1993 VL 31 IS 6 BP 495 EP 499 DI 10.1007/BF00685042 PG 5 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA KT115 UT WOS:A1993KT11500013 PM 8453691 ER PT J AU BLUM, RH EDMONSON, J RYAN, L PELLETIER, L AF BLUM, RH EDMONSON, J RYAN, L PELLETIER, L TI EFFICACY OF IFOSFAMIDE IN COMBINATION WITH DOXORUBICIN FOR THE TREATMENT OF METASTATIC SOFT-TISSUE SARCOMA SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON IFOSFAMIDE IN THE TREATMENT OF SARCOMAS, AT THE 6TH EUROPEAN CONF ON CLINICAL ONCOLOGY AND CANCER NURSING CY OCT 27, 1991 CL FLORENCE, ITALY SP ASTA MEDICA DE IFOSFAMIDE; DOXORUBICIN; METASTATIC SOFT-TISSUE SARCOMA ID UNRESECTABLE SARCOMA; PHASE-II; MESNA AB On the basis of ifosfamide's demonstrated single-agent activity in adult soft-tissue sarcoma, the Eastern Cooperative Oncology Group (ECOG) tested whether ifosfamide would add to the efficacy of doxorubicin in a three-regimen, controlled phase III trial. Doxorubicin, ECOG's standard to which newer chemotherapeutic treatments are compared, was given at a dose of 80 mg/m2 every 3 weeks and was designated the control regimen. Ifosfamide was given at a dose of 3,750 mg/m2 on days 1 and 2 every 3 weeks in combination with 30 mg/m2 doxorubicin given each day for 2 days; additionally, mesna was given to counter the genitourinary toxicity associated with ifosfamide. A second experimental regimen consisted of doxorubicin (40 mg/m2), mitomycin (8 mg/m2), and cisplatin (60 mg/m2), all given intravenously on day 1, with repeated cycles being scheduled for day 21. Of the 279 adults with soft-tissue sarcoma who were entered in the study, 260 were analyzed. The overall response rate was 20% for doxorubicin, 34% for ifosfamide/doxorubicin, and 31% for doxorubicin/mitomycin/cisplatin, with the difference between the first two regimens being significant (P = 0.04). The median survival was 8.8, 11.5, and 9 months, respectively, for the three regimens. Myelosuppression, the predominant toxicity, occurred in 60%, 88%, and 58% of patients, respectively. C1 MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. DATA MANAGEMENT OFF,BROOKLINE,MA. RP BLUM, RH (reprint author), NYU MED CTR,KAPLAN CANC CTR,550 1ST AVE,NEW YORK,NY 10016, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 NR 8 TC 7 Z9 7 U1 0 U2 0 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 MAR PY 1993 VL 31 SU 2 BP S238 EP S240 PG 3 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA KW661 UT WOS:A1993KW66100016 PM 8453706 ER PT J AU TITUSERNSTOFF, L BARNHILL, RL DURAY, PH ERNSTOFF, MS KIRKWOOD, JM AF TITUSERNSTOFF, L BARNHILL, RL DURAY, PH ERNSTOFF, MS KIRKWOOD, JM TI DYSPLASTIC NEVI IN RELATION TO SUPERFICIAL SPREADING MELANOMA SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; MELANOCYTIC NEVI; RISK; ASSOCIATION; HISTORY AB The aim of the present study was to evaluate the frequency with which histologically confirmed dysplastic nevi are observed among patients with superficial spreading melanoma compared to patients with nodular melanoma. A pathology review of 117 new cases of first primary nonfamilial cutaneous melanoma identified 61 patients with superficial spreading melanoma and 19 with nodular melanoma. Study participants received a physician-conducted skin examination which included enumeration of clinically benign and atypical nevi and the surgical excision of the clinically most atypical nevus. Patients' dysplastic nevus status was established by histological review of the clinically most atypical nevus. A comparison based on the tumor subtypes showed that dysplastic nevi occur nearly four times more frequently among patients with a prior diagnosis of superficial spreading melanoma relative to nodular melanoma (odds ratio 3.6; P = 0.03). C1 DARTMOUTH COLL,DEPT COMMUNITY & FAMILY MED,HANOVER,NH 03755. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. PITTSBURGH CANC INST,PITTSBURGH,PA 15213. UNIV PITTSBURGH,SCH MED,DIV MED ONCOL,PITTSBURGH,PA 15213. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,HEMATOL & ONCOL SECT,HANOVER,NH 03756. RP TITUSERNSTOFF, L (reprint author), NORRIS COTTON CANC CTR,DARTMOUTH MED SCH,DEPT MED,HINMAN BOX 7927,HANOVER,NH 03755, USA. NR 25 TC 6 Z9 6 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD MAR-APR PY 1993 VL 2 IS 2 BP 99 EP 101 PG 3 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA KR070 UT WOS:A1993KR07000002 PM 8467253 ER PT J AU PIWNICAWORMS, D CHIU, ML BUDDING, M KRONAUGE, JF KRAMER, RA CROOP, JM AF PIWNICAWORMS, D CHIU, ML BUDDING, M KRONAUGE, JF KRAMER, RA CROOP, JM TI FUNCTIONAL IMAGING OF MULTIDRUG-RESISTANT P-GLYCOPROTEIN WITH AN ORGANOTECHNETIUM COMPLEX SO CANCER RESEARCH LA English DT Article ID HEXAKIS 2-METHOXYISOBUTYL ISONITRILE; MULTIPLE-DRUG RESISTANCE; CHICK MYOCARDIAL-CELLS; IMMUNOHISTOCHEMICAL DETECTION; HUMAN-TUMORS; GENE; EXPRESSION; ACCUMULATION; PERFUSION; KINETICS AB The multidrug-resistant P-glycoprotein (Pgp), a M(r) 170,000 plasma membrane protein encoded by the mammalian multidrug resistance gene (MDR1), appears to function as an energy-dependent efflux pump. Many of the drugs that interact with Pgp are lipophilic and cationic at physiological pH. We tested the hypothesis that the synthetic gamma-emitting organotechnetium complex, hexakis(2-methoxyisobutylisonitrile)technetium(I) ([Tc-99m]SESTAMIBI), a lipophilic cationic radiopharmaceutical, could be a suitable Pgp transport substrate capable of functional imaging of the MDR phenotype. The cellular pharmacological profile of [Tc-99m]SESTAMIBI transport was examined in Chinese hamster V79 lung fibroblasts and the 77A and LZ derivative cell lines which express modestly low, intermediate, and very high levels of Pgp, respectively. Steady-state contents of [Tc-99m]SESTAMIBI in V79, 77A, and LZ cells were 10.0 +/- 0.5 (SEM) (n = 9), 3.6 +/- 0.5 (n = 8), and 0.4 +/- 0.02 (n = 9) fmol.(mg protein)-1 (nM(o))-1, respectively, consistent with enhanced extrusion of the imaging agent by Pgp-enriched cells. Maximal doses (>100 muM) of the multidrug-resistant reversal agents verapamil and cyclosporin A enhanced [Tc-99m]SESTAMIBI accumulation in V79, 77A, and LZ cells by approximately 10-, 25-, and 200-fold, respectively. The median effective concentration values for tracer accumulation in the presence of verapamil in V79, 77A, and LZ cells were 4, 100, and 200 muM, and those for cyclosporin A were 0.9, 3, and >25 muM, respectively. Pgp-mediated [Tc-99m]SESTAMIBI transport occurred against its electrochemical gradient and was found to be ATP dependent displaying an apparent K(m) of 50 muM. Carrier-added [Tc-99]SESTAMIBI was 11- to 13-fold less toxic in multidrug-resistant cells, and inhibited photolabeling of Pgp by [I-125]iodoaryl azidoprazosin in a concentration-dependent manner; half-maximal displacement was observed at approximately 100- to 1000-fold molar excess [Tc-99m]SESTAMIBI. Exploiting the favorable gamma emission properties of Tc-99m, functional expression of Pgp was successfully imaged in human tumor xenographs in nude mice with pharmacologically inert tracer quantities of [Tc-99m]SESTAMIBI. Functional imaging with these organotechnetium complexes may provide a novel mechanism to rapidly characterize Pgp expression in human tumors in vivo, target reversal agents in vivo, and ultimately provide a means to direct patients to specific cancer therapies. C1 HARVARD UNIV,CHILDRENS HOSP,DANA FARBER CANC INST,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. AMER CYANAMID CO,LEDERLE LABS,PEARL RIVER,NY 10965. RP PIWNICAWORMS, D (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,DEPT RADIOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 011227, CA 48162]; NHLBI NIH HHS [HL 42966] NR 49 TC 420 Z9 428 U1 3 U2 8 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 MAR 1 PY 1993 VL 53 IS 5 BP 977 EP 984 PG 8 WC Oncology SC Oncology GA KN706 UT WOS:A1993KN70600008 PM 8094997 ER PT J AU HASS, R GUNJI, H HIRANO, M WEICHSELBAUM, R KUFE, D AF HASS, R GUNJI, H HIRANO, M WEICHSELBAUM, R KUFE, D TI PHORBOL ESTER-INDUCED MONOCYTIC DIFFERENTIATION IS ASSOCIATED WITH G(2) DELAY AND DOWN-REGULATION OF CDC25 EXPRESSION SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID MYELOID LEUKEMIC-CELLS; CONTROL GENE CDC2; FISSION YEAST; PROTEIN-KINASE; TYROSINE PHOSPHORYLATION; U937 CELLS; CYCLIN-B; M-PHASE; HUMAN HOMOLOG; C-FOS AB Treatment of human U-937 myeloid leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with growth arrest and induction of monocytic differentiation. The present results demonstrate that exposure of G1- or S phase-enriched U-937 cells to TPA was associated with delayed transition through G2-M and then exit from the cell cycle in the subsequent G0-G1 phase. In contrast, G2-M cells treated with TPA progressed through G1-S, were delayed in the next G2-M phase, and then entered a nonproliferative G0-G1 state. The effects of TPA on expression of cell cycle control genes demonstrated down-regulation of the cdc25 mitotic inducer during S-G2 progression. In order to investigate the role of cdc25 in the control of cell cycle progression, U-937 cells were stably transfected with an antisense cdc25 construct under control of a metallothionein-inducible promoter. Expression of this construct in G1 phase cells was associated with a significant delay in transition through S and G2-M phase. Similar results were obtained when G1 phase cells were incubated with a 14-base pair antisense cdc25 oligomer. Taken together, these results indicate that the cdc25 gene product is functionally associated with S-G2 transition of proliferating myeloid leukemia cells and that down-regulation of this gene by TPA is associated with G2-M delay. C1 UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. PRITZKER SCH MED,CHICAGO,IL 60637. RP HASS, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 FU NCI NIH HHS [CA42802] NR 55 TC 30 Z9 32 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD MAR PY 1993 VL 4 IS 3 BP 159 EP 166 PG 8 WC Cell Biology SC Cell Biology GA KT858 UT WOS:A1993KT85800003 PM 8466854 ER PT J AU MULLER, RT CALDWELL, RA HUNTER, JE AF MULLER, RT CALDWELL, RA HUNTER, JE TI CHILD PROVOCATIVENESS AND GENDER AS FACTORS CONTRIBUTING TO THE BLAMING OF VICTIMS OF PHYSICAL CHILD-ABUSE SO CHILD ABUSE & NEGLECT LA English DT Article DE CHILD ABUSE; VICTIM BLAME; RESPONSIBILITY ATTRIBUTIONS; SEX DIFFERENCES ID RAPE VICTIM; SELF-BLAME; ATTRACTIVENESS; RESPONSIBILITY; ATTRIBUTIONS; PERCEPTIONS; OBSERVER; SEX AB This study was an investigation of factors contributing to blame attributions directed toward victims of physical child abuse. The total sample consisted of 897 college undergraduates. Subjects read eight vignettes describing physically abusive parent-child interactions, and indicated their attributions of responsibility toward parent and child. We predicted that: (a) aggressively provocative children (compared to nonprovocative) would be ascribed greater blame; (b) male subjects would be more likely to blame the child; (c) in situations in which the abusive parent is male (compared to female), the child would be blamed more; and (d) male children (compared to females) would receive greater blame. The results supported all hypotheses. The data also suggested several interaction effects. Significance tests were supplemented with effect size analyses. C1 MICHIGAN STATE UNIV,E LANSING,MI 48824. RP MULLER, RT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,PSYCHOL OFF,BULFINCH 5,14 FRUIT ST,BOSTON,MA 02114, USA. NR 42 TC 21 Z9 21 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PD MAR-APR PY 1993 VL 17 IS 2 BP 249 EP 260 DI 10.1016/0145-2134(93)90044-6 PG 12 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA KV778 UT WOS:A1993KV77800006 PM 8472177 ER PT J AU BADIMON, JJ FUSTER, V CHESEBRO, JH BADIMON, L AF BADIMON, JJ FUSTER, V CHESEBRO, JH BADIMON, L TI CORONARY ATHEROSCLEROSIS - A MULTIFACTORIAL DISEASE SO CIRCULATION LA English DT Review DE ATHEROSCLEROSIS; ETHIOPATHOGENESIS; THROMBOSIS, PROGRESSION AND REGRESSION ID LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE CELLS; APOLIPOPROTEIN-A-I; EVANS-BLUE UPTAKE; ENHANCED MACROPHAGE DEGRADATION; ACUTE MYOCARDIAL-INFARCTION; RABBIT CAROTID-ARTERY; SUDDEN ISCHEMIC DEATH; ENDOTHELIAL-CELLS; HEART-DISEASE AB Background. Several of the theories on the pathogenesis of atherosclerosis may be integrated into a single multifactorial one. According to this theory, the most likely sequence of events involved in early atherosclerosis is vascular dysfunction and/or injury, monocyte recruitment and macrophage formation, lipid deposition, vascular smooth muscle cell proliferation (mitogenic factor mediated), and synthesis of extracellular matrix. The interaction of all these factors will configurate the typical characteristic of the atherosclerotic plaque. Methods and Results. Accumulating experimental and clinical data suggest two pathways in atherosclerotic progression. In some cases, the very slow process of the pathogenesis of early lesions may be significantly accelerated by means of thrombus formation and organization. Thrombosis is a key process in the pathogenesis of late atherogenesis and in the development of acute ischemic syndromes. Conclusions. The possibility of retarding human atherosclerosis or even inducing its regression is one of the present therapeutic challenges. Of the different approaches to this question, one approach aims at better control of risk factors, especially plasma lipid levels. Another approach attempts to enhance the removal of lipids from the arterial wall by increasing plasma high density lipoprotein levels. Each of these approaches, by acting on the lipid-rich plaques more prone to rupture, might prevent plaque progression and induce regression to prevent acute coronary events. A third approach, based on the key role of platelet thrombus formation in the conversion of chronic to acute events, would be the use of antithrombotic therapy. This last approach may partially prevent progression of the disease. C1 CSIC,CTR INVEST & DESARROLLO,CARDIOVASC RES LAB,BARCELONA,SPAIN. RP BADIMON, JJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,JACKSON BLDG,ROOM 1328,32 FRUIT ST,BOSTON,MA 02114, USA. RI BADIMON, LINA/O-4711-2014; Fuster, Valentin/H-4319-2015 OI BADIMON, LINA/0000-0002-9162-2459; Fuster, Valentin/0000-0002-9043-9986 NR 184 TC 155 Z9 160 U1 2 U2 8 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1993 VL 87 IS 3 SU S BP 3 EP 16 PG 14 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KR796 UT WOS:A1993KR79600003 ER PT J AU FISHER, DZ DISALVO, TG DEC, GW DESANCTIS, RW AF FISHER, DZ DISALVO, TG DEC, GW DESANCTIS, RW TI TRANSIENT LEFT-VENTRICULAR ANEURYSM IN A PATIENT WITH HYPERTROPHIC CARDIOMYOPATHY AND MYOCARDITIS SO CLINICAL CARDIOLOGY LA English DT Note DE HYPERTROPHIC CARDIOMYOPATHY; MYOCARDITIS; LEFT VENTRICULAR ANEURYSM ID DYSFUNCTION AB Left ventricular wall motion abnormalities, aneurysm formation, and progression to global hypokinesis have been described in patients with myocarditis and in patients with hypertrophic cardiomyopathy. We document a case of reversible aneurysm formation, cardiogenic shock, and complete recovery in a patient with myocarditis and hypertrophic cardiomyopathy. Pathophysiologic mechanisms of myocardial injury and recovery are discussed. C1 HARVARD UNIV,SCH MED,DEPT MED,CARDIAC UNIT,BOSTON,MA 02115. RP FISHER, DZ (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. NR 15 TC 2 Z9 2 U1 0 U2 0 PU CLINICAL CARDIOLOGY PUBL CO PI MAHWAH PA PO BOX 832, MAHWAH, NJ 07430-0832 SN 0160-9289 J9 CLIN CARDIOL JI Clin. Cardiol. PD MAR PY 1993 VL 16 IS 3 BP 253 EP 256 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KP992 UT WOS:A1993KP99200014 PM 8444000 ER PT J AU SOUKIASIAN, SH JAKOBIEC, FA NILES, JL PAVANLANGSTON, D AF SOUKIASIAN, SH JAKOBIEC, FA NILES, JL PAVANLANGSTON, D TI TRIMETHOPRIM SULFAMETHOXAZOLE FOR SCLERITIS ASSOCIATED WITH LIMITED WEGENERS GRANULOMATOSIS - USE OF HISTOPATHOLOGY AND ANTINEUTROPHIL CYTOPLASMIC ANTIBODY (ANCA) TEST SO CORNEA LA English DT Article DE ANTINEUTROPHIL CYTOPLASMIC ANTIBODY; SCLERITIS; TRIMETHOPRIM SULFAMETHOXAZOLE; WEGENERS GRANULOMATOSIS AB Ophthalmic involvement may be noted in less-than-or-equal 58% of Wegener's granulomatosis cases, scleritis being one of the most frequent and potentially devastating manifestations. Cytotoxic immunosuppressive drug therapy is effective treatment for this disorder but potentially highly toxic. Recent uncontrolled and anecdotal reports have suggested a possible therapeutic role for a much less toxic agent, trimethoprim/sulfamethoxazole, in limited Wegener's granulomatosis. We report a patient who had a conjunctival nodule and scleritis. Biopsy of the nodule suggested Wegener's granulomatosis, confirmed serologically with serum anti-neutrophil cytoplasmic antibody (ANCA) testing. Treatment with oral trimethoprim/sulfamethoxazole was successful. Clinical response was paralleled by normalization of serial anti-neutrophil cytoplasmic antibody titers. This case is the first well-documented ophthalmologic report of limited Wegener's granulomatosis responding to trimethoprim/sulfamethoxazole and adds to the body of literature suggesting a potential role for this drug in selected cases of limited Wegener's granulomatosis. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,CORNEA SERV,BOSTON,MA 02114. NR 0 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3740 J9 CORNEA JI Cornea PD MAR PY 1993 VL 12 IS 2 BP 174 EP 180 DI 10.1097/00003226-199303000-00015 PG 7 WC Ophthalmology SC Ophthalmology GA KN812 UT WOS:A1993KN81200015 PM 8500327 ER PT J AU REYNOLDS, AM RYAN, DP DOODY, DP AF REYNOLDS, AM RYAN, DP DOODY, DP TI PERMISSIVE HYPERCAPNIA AND PRESSURE-CONTROLLED VENTILATION AS TREATMENT OF SEVERE ADULT RESPIRATORY-DISTRESS SYNDROME IN A PEDIATRIC BURN PATIENT SO CRITICAL CARE MEDICINE LA English DT Article DE ADULT RESPIRATORY DISTRESS SYNDROME; INTERMITTENT POSITIVE-PRESSURE VENTILATION; HYPERCAPNIA; ANOXEMIA; PEDIATRICS; BURNS; CRITICAL CARE; PULMONARY EMERGENCIES; MECHANICAL VENTILATION ID LUNG-FUNCTION; FAILURE; MORTALITY; INJURY; CHILDREN; SURVIVAL; ECMO C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 18 TC 7 Z9 7 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 MAR PY 1993 VL 21 IS 3 BP 468 EP 471 DI 10.1097/00003246-199303000-00028 PG 4 WC Critical Care Medicine SC General & Internal Medicine GA KQ902 UT WOS:A1993KQ90200028 ER PT J AU COOK, RM MILLER, YE BUNN, PA AF COOK, RM MILLER, YE BUNN, PA TI SMALL-CELL LUNG-CANCER - ETIOLOGY, BIOLOGY, CLINICAL-FEATURES, STAGING, AND TREATMENT SO CURRENT PROBLEMS IN CANCER LA English DT Review ID MYC GENE FAMILY; GROWTH FACTOR-I; RETINOBLASTOMA SUSCEPTIBILITY GENE; NEURO-ENDOCRINE DIFFERENTIATION; CROSS-RESISTANT CHEMOTHERAPY; HIGH-DOSE CYCLOPHOSPHAMIDE; GASTRIN-RELEASING PEPTIDE; TUMOR SUPPRESSOR GENES; BOMBESIN-LIKE PEPTIDES; LONG-TERM SURVIVORS AB Lung cancer is the leading cause of cancer death in the United States. Small cell lung cancer (SCLC) accounts for 20% to 25% of all bronchogenic carcinoma and is associated with the poorest 5-year survival of all histologic types. SCLC differs in its etiologic, pathologic, biologic, and clinical features from non-SCLC, and these differences have translated to distinct approaches to its prevention and treatment. Compared with other histologic types of lung cancer, exposures to tobacco smoke, ionizing radiation, and chloromethyl ethers pose a substantially greater risk for development of SCLC. The histologic classification of SCLC has been revised to include three categories: (1) small cell carcinoma, (2) mixed small cell/large cell, and (3) combined small cell carcinoma. Ultrastructurally, SCLC displays a number of neuroendocrine features in common with pulmonary neuroendocrine cells, including dense core vesicles or neurosecretory granules. These dense core vesicles are associated with a variety of secretory products, cell surface antigens, and enzymes. The biology of SCLC is complex. The activation of a number of dominant proto-oncogenes and the inactivation of tumor suppressor genes in SCLC have been described. Dominant proto-oncogenes that have been found to be amplified or overexpressed in SCLC include the myc family, c-myb, c-kit, c-jun, and c-src. Altered expression of two tumor suppressor genes in SCLC, p53 and the retinoblastoma gene product, has been demonstrated. Cytogenetic and molecular evidence for chromosomal loss of 3p, 5q, 9p, 11p, 13q, and 17p in SCLC has intensified the search for other tumor suppressor genes with potential import in this malignancy. Bombesin/gastrin-releasing peptide, insulin-like growth factor 1, and transferrin have been identified as autocrine growth factors in SCLC, with a number of other peptides under active investigation. Several mechanisms of drug resistance in SCLC have been described, including gene amplification, the recently described overexpression of multi-drug resistance-related protein (MRP), and the expression of P-glycoprotein. The classic SCLC staging system has been supplanted by a revised TNM staging system where limited disease and extensive disease are equivalent to the TNM stages I through III and stage IV, respectively. Therapeutically, recent strategies have attained small improvements in survival but significant reductions in the toxicities of chemotherapeutic regimens. Presently, the overall 5-year survival for SCLC is 5% to 10%, with limited disease associated with a significantly higher survival rate. The present preferred therapeutic strategy for limited disease is four to six cycles of etoposide-cisplatin (EP)-based chemotherapy combined with concurrent or alternating radiotherapy. There is no overwhelming evidence that alternating chemotherapeutic regimens are superior to EP-based regimens. Maintenance chemotherapy is not recommended. It is reasonable to use a strategy of surgery followed by chemotherapy for the rare patient with stage I and II SCLC; however, surgery remains an experimental option for those with stage III disease after chemotherapy. Chemotherapy without radiotherapy is the cornerstone of palliative therapy for diose patients with SCLC who have extensive disease. New therapies on the horizon for SCLC include the camptothecin derivatives, mitotic spindle poisons such as taxol, and analogues of the vinca alkaloids. C1 UNIV COLORADO, HLTH SCI CTR, CTR CANC, DEPT MED, DIV MED ONCOL, DENVER, CO 80262 USA. DENVER VET AFFAIRS MED CTR, DENVER, CO USA. RP UNIV COLORADO, HLTH SCI CTR, CTR CANC, DEPT CHEM, DIV PULM SCI & CRIT CARE MED, DENVER, CO 80262 USA. NR 312 TC 19 Z9 20 U1 0 U2 4 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0147-0272 EI 1535-6345 J9 CURR PROB CANCER JI Curr. Probl. Cancer PD MAR-APR PY 1993 VL 17 IS 2 BP 71 EP 141 PG 71 WC Oncology SC Oncology GA LN068 UT WOS:A1993LN06800001 ER PT J AU SMITH, TH BLOCK, NE RHODES, SJ KONIECZNY, SF MILLER, JB AF SMITH, TH BLOCK, NE RHODES, SJ KONIECZNY, SF MILLER, JB TI A UNIQUE PATTERN OF EXPRESSION OF THE 4 MUSCLE REGULATORY FACTOR PROTEINS DISTINGUISHES SOMITIC FROM EMBRYONIC, FETAL AND NEWBORN MOUSE MYOGENIC CELLS SO DEVELOPMENT LA English DT Article DE MYOGENESIS; MYOBLASTS; MUSCLE REGULATORY FACTORS; SOMITES; MOUSE ID HEAVY-CHAIN ISOFORMS; LOOP-HELIX PROTEINS; BINDING-FACTOR; DNA-BINDING; GENE FAMILY; MYOD1; LINEAGE; DIFFERENTIATION; TRANSCRIPTION; FIBROBLASTS AB A unique pattern of expression of the four muscle regulatory factor (MRF) proteins was found to distinguish early somitic from embryonic, fetal and newborn limb myogenic cells in vitro. Expression of the myosin heavy chain (MHC), MyoD, myogenin, Myf-5, and MRF4 proteins was examined by immunocytochemistry in cultures of four distinct types of mouse myogenic cells: somitic (E8.5), embryonic (Ell.5), fetal (E16.5) and newborn limb. In embryonic, fetal and newborn cultures, the MRF proteins were expressed in generally similar patterns: MyoD was the first MRF expressed; MyoD and myogenin were expressed by more cells than Myf-5 or MRF4; and each of the four MRFs was found both in cells that expressed MHC and in cells that did not express MHC. In cultures of somitic cells, in contrast, Myf-5 was expressed first and by more cells than MyoD or myogenin; MRF4 was not detected; and the MRFs were never found to be coexpressed with MHC in the same cell. Thus, some somitic cells had the unexpected ability to maintain MHC expression in the absence of detectable MRF protein expression. The different myogenic programs of embryonic, fetal and newborn myogenic cells are not, therefore, a simple result of qualitatively different MRF expression patterns, whereas myogenesis by somitic cells does include a unique pattern of MRF expression. C1 MASSACHUSETTS GEN HOSP,NEUROMUSCULAR LAB,149 13TH ST,BOSTON,MA 02129. PURDUE UNIV,DEPT BIOL SCI,W LAFAYETTE,IN 47907. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. NR 56 TC 103 Z9 106 U1 2 U2 2 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD MAR PY 1993 VL 117 IS 3 BP 1125 EP 1133 PG 9 WC Developmental Biology SC Developmental Biology GA KY548 UT WOS:A1993KY54800025 PM 8391976 ER PT J AU KLEIN, RL LOPESVIRELLA, MF AF KLEIN, RL LOPESVIRELLA, MF TI METABOLISM BY HUMAN ENDOTHELIAL-CELLS OF VERY LOW-DENSITY-LIPOPROTEIN SUBFRACTIONS ISOLATED FROM TYPE-1 (INSULIN-DEPENDENT) DIABETIC-PATIENTS SO DIABETOLOGIA LA English DT Article DE ENDOTHELIAL CELLS; VERY LOW DENSITY LIPOPROTEIN SUBFRACTIONS; DIABETES-MELLITUS; ATHEROSCLEROSIS ID MONOCYTE-DERIVED MACROPHAGES; CHOLESTERYL ESTER SYNTHESIS; CULTURED HUMAN-FIBROBLASTS; APOLIPOPROTEIN-A-I; DEGRADATION; MELLITUS; RECEPTOR; BINDING; PLASMA; LDL AB The very low density lipoprotein (VLDL) fraction was isolated from 11 normolipidaemic Type 1 (insulin-dependent) diabetic patients in good to fair glycaemic control and from 11 age-, sex- and race-matched, non-diabetic, control subjects. The rate of receptor-mediated degradation by human endothelial cells was significantly greater (p < 0.02) for the total VLDL fraction isolated from diabetic patients compared to control subjects and averaged 1008 +/- 300 and 717 +/- 150 ng . mg cell protein-1 . 16 h-1, respectively. The total VLDL fraction was separated into three subfractions: VLDL-I, S(f) 100-400 (S(f) = Svedberg units); VLDL-II, S(f) 60-100; VLDL-III, S(f) 20-60. Rates of receptor-mediated degradation of VLDL-I and VLDL-II isolated from diabetic patients were significantly greater than the comparable subfraction isolated from control subjects and averaged 1023 +/- 279 vs 361 +/- 122 (p < 0.01) and 433 +/- 70 vs 294 +/- 70 ng . mg cell protein-1 . 16 h-1 (p < 0.03), respectively. Rates of receptor-mediated degradation of the V-III subfraction isolated from the two groups did not differ significantly There were no significant differences in the chemical composition or in the plasma concentrations of the VLDL subfractions isolated from diabetic patients compared to control subjects. There was a significant increase in the apoprotein E content of VLDL-I (p < 0.01) and VLDL-II (p < 0.05) isolated from diabetic patients. There was a significant increase in the ratio of apoprotein C compared to apoprotein E (p < 0.03) in VLDL-I isolated from control subjects compared to the diabetic patients. There were no significant differences in the apoprotein composition of VLDL-III isolated from the two groups. C1 MED UNIV S CAROLINA,RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,RES SERV,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. NR 50 TC 13 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD MAR PY 1993 VL 36 IS 3 BP 258 EP 264 DI 10.1007/BF00399960 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KN255 UT WOS:A1993KN25500016 PM 8462776 ER PT J AU ARCHER, GL AUGER, P DOERN, GV FERRARO, MJ FUCHS, PC JORGENSEN, JH LOW, DE MURRAY, PR RELLER, LB STRATTON, CW WENNERSTEN, CB MOELLERING, RC AF ARCHER, GL AUGER, P DOERN, GV FERRARO, MJ FUCHS, PC JORGENSEN, JH LOW, DE MURRAY, PR RELLER, LB STRATTON, CW WENNERSTEN, CB MOELLERING, RC TI RP-59500, A NEW STREPTOGRAMIN HIGHLY-ACTIVE AGAINST RECENT ISOLATES OF NORTH-AMERICAN STAPHYLOCOCCI SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Note ID PRISTINAMYCIN; STREPTOCOCCI AB To assess the potential clinical utility of RP 59500, 10 investigators from separate locations in the United States and Canada each tested approximately 200 current isolates of staphylococci (Staphylococcus aureus and coagulase-negative staphylococci) by a standard protocol. RP 59500 was highly active (MIC90 less-than-or-equal-to 2 mug/ml) against all strains, including those that were resistant to oxacillin, ciprofloxacin, erythromycin, and spiramycin. C1 NEW ENGLAND DEACONESS HOSP, DEPT MED, BOSTON, MA 02215 USA. DUKE UNIV, MED CTR, DURHAM, NC 27710 USA. VANDERBILT UNIV, MED CTR, NASHVILLE, TN 37240 USA. BARNES HOSP, ST LOUIS, MO 63110 USA. INST CARDIOL MONTREAL, MONTREAL H1T 1C8, QUEBEC, CANADA. MED CTR HOSP, SAN ANTONIO, TX USA. MT SINAI HOSP, TORONTO M5G 1X5, ONTARIO, CANADA. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, RICHMOND, VA 23298 USA. UNIV MASSACHUSETTS, MED CTR, WORCESTER, MA 01605 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. ST VINCENTS HOSP & MED CTR, PORTLAND, OR USA. RI Low, Donald/B-1726-2012 NR 8 TC 30 Z9 30 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0732-8893 EI 1879-0070 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD MAR-APR PY 1993 VL 16 IS 3 BP 223 EP 226 DI 10.1016/0732-8893(93)90113-L PG 4 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA KU723 UT WOS:A1993KU72300005 PM 8477576 ER PT J AU CRAIG, WA AF CRAIG, WA TI QUALITATIVE SUSCEPTIBILITY TESTS VERSUS QUANTITATIVE MIC TESTS SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Article ID INHIBITORY CONCENTRATION; ANTIMICROBIAL AGENTS; THERAPY; CIPROFLOXACIN; ANTIBIOTICS; BACTEREMIA; INFECTIONS; EFFICACY; ACCURACY; INVITRO AB Qualitative susceptibility categories show reasonable, but incomplete, correlation with therapeutic outcome. Studies using quantitative MIC tests have demonstrated that treatment failures within the susceptible category are associated with higher minimum inhibitory concentrations (MICs) than with therapeutic successes. Other trials have exhibited enhanced response for increasing ratios of a pharmacokinetic parameter to MIC (for example, peak level to MIC ratio for aminoglycosides). Dose-response studies in animal infection models also demonstrate an excellent correlation between the dose of drug required for a given response and the infecting organism MIC. These studies suggest that the use of quantitative MIC tests may enable more individualization of the therapeutic regimen, especially in regards to dose and dosing frequency, than provided by qualitative category susceptibility tests. However, there are only rare studies that have used MIC results or pharmacokinetic parameters to improve efficacy. Furthermore, these studies have not consistently documented enhanced clinical efficacy. MICs can also be used to reduce drug dosage and cost of antimicrobial therapy for very susceptible organisms. Additional studies are clearly needed to define the full potential of the quantitative MIC test result. C1 UNIV WISCONSIN,MADISON,WI 53706. RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 26 TC 25 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD MAR-APR PY 1993 VL 16 IS 3 BP 231 EP 236 DI 10.1016/0732-8893(93)90115-N PG 6 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA KU723 UT WOS:A1993KU72300007 PM 8477578 ER PT J AU FERRARO, MJ AF FERRARO, MJ TI THE ROLE OF THE CLINICAL MICROBIOLOGY LABORATORY AND THE CLINICAL PHARMACY IN THE MANAGEMENT OF INFECTIOUS-DISEASE (ASM, 1992) - CONCLUSIONS SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Editorial Material ID POSITIVE BLOOD CULTURES; COMPREHENSIVE ANALYSIS; 500 EPISODES; BACTEREMIA; FUNGEMIA; ADULTS RP FERRARO, MJ (reprint author), MASSACHUSETTS GEN HOSP,GRAY 5,FRUIT ST,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 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD MAR-APR PY 1993 VL 16 IS 3 BP 275 EP 276 DI 10.1016/0732-8893(93)90121-M PG 2 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA KU723 UT WOS:A1993KU72300013 ER PT J AU YANDELL, DW THOR, AD AF YANDELL, DW THOR, AD TI P53 ANALYSIS IN DIAGNOSTIC PATHOLOGY - BIOLOGIC IMPLICATIONS AND POSSIBLE CLINICAL-APPLICATIONS SO DIAGNOSTIC MOLECULAR PATHOLOGY LA English DT Editorial Material ID BREAST CANCERS; MUTATIONS; GENE; ACCUMULATION; CARCINOMAS; PROGNOSIS; PROTEIN C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. NR 21 TC 32 Z9 33 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1052-9551 J9 DIAGN MOL PATHOL JI Diagn. Mol. Pathol. PD MAR PY 1993 VL 2 IS 1 BP 1 EP 3 PG 3 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Pathology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Pathology GA MC148 UT WOS:A1993MC14800001 PM 8287220 ER PT J AU GANZINI, L WALSH, JR MILLAR, SB AF GANZINI, L WALSH, JR MILLAR, SB TI DRUG-INDUCED DEPRESSION IN THE AGED - WHAT CAN BE DONE SO DRUGS & AGING LA English DT Article ID BETA-BLOCKER THERAPY; PARKINSONS-DISEASE; ANTIHYPERTENSIVE DRUGS; SCHIZOPHRENIC-PATIENTS; HOSPITALIZED-PATIENTS; MEDICAL ILLNESS; HYPERTENSION; PROPRANOLOL; RESERPINE; SYMPTOMS AB Over 10% of medically ill elderly persons have concurrent major depression, and medical illness is the most influential stressor contributing to depression in old age. The contribution of prescribed medications to depression in the medically ill is poorly understood. Most information on drug-induced depression is derived from case reports; 43 classes of medications have been implicated, including reserpine, beta-blockers, levodopa, corticosteroids, and antipsychotics. However, large rigorously performed studies of some drugs, particularly antihypertensives, suggest that drug-induced depression is uncommon and idiosyncratic. There is no evidence that age is an independent risk factor for drug-induced depression. However, elderly persons are the largest consumers of prescribed drugs, and the burden of drug-induced depression is carried by the old. Because of the frequency of atypical presentations of mental disorders in the elderly, drug-induced depression is often misdiagnosed. Nevertheless, basic principles of geriatric medicine offer useful guidance to clinicians in evaluating the complex interrelationships between prescribed medications and depression. We recommend an approach that includes regular inquiry into the common symptoms of mood disorders, vigilance in assessing the contribution of drugs in their development, but scepticism in assessing a depressive episode as caused only by medication. C1 OREGON HLTH SCI UNIV,DEPT PSYCHIAT,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,GERONTOL SECT,PORTLAND,OR 97207. OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PHARM SERV,PORTLAND,OR 97207. RP GANZINI, L (reprint author), PORTLAND VET AFFAIRS MED CTR,PSYCHIAT SERV,116 A-P,POB 1034,PORTLAND,OR 97207, USA. NR 76 TC 13 Z9 14 U1 2 U2 2 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1170-229X J9 DRUG AGING JI Drugs Aging PD MAR-APR PY 1993 VL 3 IS 2 BP 147 EP 158 DI 10.2165/00002512-199303020-00005 PG 12 WC Geriatrics & Gerontology; Pharmacology & Pharmacy SC Geriatrics & Gerontology; Pharmacology & Pharmacy GA KV780 UT WOS:A1993KV78000005 PM 8477147 ER PT J AU CHEN, JZ TROUNSTINE, M KURAHARA, C YOUNG, F KUO, CC XU, Y LORING, JF ALT, FW HUSZAR, D AF CHEN, JZ TROUNSTINE, M KURAHARA, C YOUNG, F KUO, CC XU, Y LORING, JF ALT, FW HUSZAR, D TI B-CELL DEVELOPMENT IN MICE THAT LACK ONE OR BOTH IMMUNOGLOBULIN KAPPA-LIGHT CHAIN GENES SO EMBO JOURNAL LA English DT Article DE B-CELL DEVELOPMENT; GENE REARRANGEMENT; GENE TARGETING; KAPPA-DEFICIENT MICE; RS REARRANGEMENT ID PERIPHERAL LYMPHOID ORGANS; MURINE LEUKEMIA-VIRUS; LYMPHOCYTES-B; LAMBDA LOCUS; BONE-MARROW; STEM-CELLS; MOUSE; REARRANGEMENT; REGION; PROLIFERATION AB We have generated mice that lack the ability to produce immunoglobulin (Ig) chi light chains by targeted deletion of Jchi and Cchi gene segments and the intervening sequences in mouse embryonic stem cells. In wild type mice, approximately 95% of B cells express chi light chains and only approximately 5% express lambda light chains. Mice heterozygous for the JchiCchi deletion have approximately 2-fold more lambda+ B cells than wild-type littermates. Compared with normal mice, homozygous mutants for the JchiCchi deletion have about half the number of B cells in both the newly generated and the peripheral B cell compartments, and all of these B cells express lambda light chains in their Ig. Therefore, homozygous mutant mice appear to produce lambda-expressing cells at nearly 10 times the rate observed in normal mice. These findings demonstrate that chi gene assembly and/or expression is not a prerequisite for lambda gene assembly and expression. Furthermore, there is no detectable rearrangement of 3' chi RS sequences in lambda+ B cells of the homozygous mutant mice, thus rearrangements of these sequences, per se, is not required for lambda light chain gene assembly. We discuss these findings in the context of their implications for the control of Ig light chain gene rearrangement and potential applications of the mutant animals. C1 GENPHARM INT INC,297 N BERNARDO AVE,MT VIEW,CA 94043. HARVARD UNIV,DEPT GENET,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. OI Loring, Jeanne/0000-0001-6226-9767 FU NIAID NIH HHS [1 R43 AI32268-01]; PHS HHS [A.I.20047] NR 60 TC 134 Z9 135 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD MAR PY 1993 VL 12 IS 3 BP 821 EP 830 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KR539 UT WOS:A1993KR53900002 PM 8458340 ER PT J AU KEUTMANN, HT RUBIN, DA AF KEUTMANN, HT RUBIN, DA TI A SUBUNIT INTERACTION SITE IN HUMAN LUTEINIZING-HORMONE - IDENTIFICATION BY PHOTOAFFINITY CROSS-LINKING SO ENDOCRINOLOGY LA English DT Article ID HUMAN CHORIO-GONADOTROPIN; HUMAN CHORIOGONADOTROPIN-BETA; ALPHA-SUBUNIT; GLYCOPROTEIN HORMONES; RECEPTOR-BINDING; LUTROPIN; PEPTIDE; MUTAGENESIS; REGION; BENZOYLPHENYLALANINE AB The sites of noncovalent association between the alpha- (common) and beta- (hormone-specific) subunits in the glycoprotein hormones [LH, human CG (hCG), FSH, and TSH] remain to be completely defined. This information is essential to efforts to map the three-dimensional structure of the hormones and to help explain the stability of the hormone heterodimer in the circulation. Among numerous approaches that have been employed to identify these sites of subunit interaction, chemical or photoaffinity cross-linking has the advantage of identifying the complementary sites of contact on the respective subunits. We have used the stable photoaffinity ligand, L-benzoylphenylalanine (Bpa), to evaluate subunit interaction by the hLHbeta sequence (1-15). A peptide from this region of hCGbeta has been shown previously to inhibit subunit association. The H-3-labeled Bpa was incorporated into the peptide at position 8 (Trp) during solid-phase synthesis. After incubation with alpha under long-wavelength (366 nm) ultraviolet light, a Bpa-(1-15)-labeled alpha-fraction was isolated. Control experiments showed the binding to be covalent and specific to (1-15). Two other Bpa-labeled beta-fragments, the receptor-binding loop (38-57) and the (30-43) peptide containing the highly conserved CAGY sequence, did not cross-link. The site of contact in a was localized by peptide mapping and sequence analysis to the N-terminal fragment (18-33), most likely at Met-29 or Gly-30. Both the alpha- and beta-sites are adjacent to or overlapping receptor-binding regions. Subunit contact sites and receptor-binding segments may thus be oriented in close proximity to provide a multicomponent receptor-binding domain imparting full activity to the native hormone. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP KEUTMANN, HT (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114, USA. FU NICHD NIH HHS [HD-12851] NR 37 TC 20 Z9 20 U1 1 U2 2 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1993 VL 132 IS 3 BP 1305 EP 1312 DI 10.1210/en.132.3.1305 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KP290 UT WOS:A1993KP29000052 PM 7679977 ER PT J AU HALL, JE AF HALL, JE TI POLYCYSTIC OVARIAN DISEASE AS A NEUROENDOCRINE DISORDER OF THE FEMALE REPRODUCTIVE AXIS SO ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA LA English DT Article ID GONADOTROPIN-RELEASING-HORMONE; FOLLICLE-STIMULATING-HORMONE; HYPOTHALAMIC-PITUITARY AXIS; PULSATILE LUTEINIZING-HORMONE; HUMAN MENSTRUAL-CYCLE; SEX STEROID CONTROL; NORMAL WOMEN; PULSE FREQUENCY; DEFICIENT MEN; OVULATION INDUCTION C1 MASSACHUSETTS GEN HOSP,NATL CTR INFERTIL RES,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP HALL, JE (reprint author), MASSACHUSETTS GEN HOSP,REPROD ENDOCRINE UNIT,BHX-5,BOSTON,MA 02114, USA. NR 68 TC 19 Z9 19 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8529 J9 ENDOCRIN METAB CLIN JI Endocrinol. Metabol. Clin. North Amer. PD MAR PY 1993 VL 22 IS 1 BP 75 EP 92 PG 18 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LA544 UT WOS:A1993LA54400005 PM 8095452 ER PT J AU DADAMIO, L AWAD, KM REINHERZ, EL AF DADAMIO, L AWAD, KM REINHERZ, EL TI THYMIC AND PERIPHERAL APOPTOSIS OF ANTIGEN-SPECIFIC T-CELLS MIGHT COOPERATE IN ESTABLISHING SELF TOLERANCE SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE APOPTOSIS; MATURE THYMOCYTES; T-CELLS; PERIPHERAL DELETION; STAPHYLOCOCCAL ENTEROTOXIN-B (SEB) ID MAJOR HISTOCOMPATIBILITY COMPLEX; RECEPTOR TRANSGENIC MICE; STAPHYLOCOCCAL ENTEROTOXIN-B; NEGATIVE SELECTION; MONOCLONAL-ANTIBODIES; POSITIVE SELECTION; CLONAL ELIMINATION; GENE SEGMENTS; THYMOCYTES; DELETION AB Aside from CD4+CD8+ double-positive (DP) thymocytes, the subpopulations of T lineage cells affected by negative selection are unknown. To address whether this process occurs in more mature cell types, we have compared the responses of purified single-positive (SP) murine thymocytes and peripheral T cells to the superantigen staphylococcal enterotoxin B (SEB) utilizing as antigen-presenting cells (APC) a fibroblast cell line expressing transfected I-E(k) class II molecules. Whereas approximately 70% of SEB-reactive SP thymocytes, either CD4+ or CD8+, undergo programmed cell death (apoptosis) and, therefore, negative selection, CD4+ and CD8+ antigen-specific peripheral T cells are predominantly activated and proliferate to APC+ SEB. Thus, mature thymocytes and peripheral T cells, with identical patterns and levels of expression of CD4, CD8 and T cell receptor (TCR), are programmed to elicit different responses following TCR stimulation. Unexpectedly, however activation of peripheral T cells was preceded by deletion of a large fraction of Vbeta8+ T lymphocytes (SEB specific). This surprising phenomenon was also observed in in vivo studies: in fact, administration of SEB to adult mice resulted in depletion of the majority of antigen-specific T cells from the peripheral lymphoid tissues analyzed (lymph nodes and spleen). This depletion is the consequence of deletion as indicated by program cell death of Vbeta8+ T cells and is followed by proliferation of the remaining SEB-reactive T cells. Clonal elimination of peripheral T cells may represent a mechanism by which tolerance to self antigens never expressed in and/or exported to the thymus is achieved. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,IMMUNOBIOL LAB,BOSTON,MA 02115. RP DADAMIO, L (reprint author), PERUGIA UNIV,SCH MED,INST PHARMACOL,VIA GIOCHETTO,I-06100 PERUGIA,ITALY. FU NCI NIH HHS [CA49232]; NIAID NIH HHS [AI21226] NR 45 TC 54 Z9 55 U1 1 U2 3 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 MAR PY 1993 VL 23 IS 3 BP 747 EP 753 DI 10.1002/eji.1830230327 PG 7 WC Immunology SC Immunology GA KU075 UT WOS:A1993KU07500026 PM 8095461 ER PT J AU SACHS, DH SMITH, CV EMERY, DW LEGUERN, C BODINE, D NIENHUIS, A SYKES, M AF SACHS, DH SMITH, CV EMERY, DW LEGUERN, C BODINE, D NIENHUIS, A SYKES, M TI INDUCTION OF SPECIFIC TOLERANCE TO MHC-DISPARATE ALLOGRAFTS THROUGH GENETIC-ENGINEERING SO EXPERIMENTAL NEPHROLOGY LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON RENAL TRANSPLANT TOLERANCE : MOLECULAR MECHANISMS OF T-CELL REGULATION CY JUN 27, 1992 CL PARIS, FRANCE SP EXPTL NEPHROL, ROCHE PROD DE TOLERANCE; MHC; RETROVIRUS; BONE MARROW TRANSPLANTATION; MINIATURE SWINE; GENETIC ENGINEERING; CLASS-I ANTIGENS; CLASS-II ANTIGENS AB The potential for induction of transplantation tolerance through genetic engineering of allogeneic MHC genes is being studied in two animal models. The first system involves a congenic mouse strain combination differing by a single class I locus. Using a retroviral vector, cDNA encoding one allele of this locus was introduced into bone marrow of the congenic partner strain, and the transduced bone marrow was used to reconstitute autologous animals. Skin-grafting data indicate that this reconstitution led to tolerance for the allelic products of this class I locus. The second system involves similar manipulations of miniature swine bone marrow, with the goal of inducing to tolerance to class II antigens, since these antigens have been shown to be of overwhelming importance in determining the fate of vascularized allografts in this model. In vitro data in a bone marrow culture system indicate that an appropriate vector for this purpose has been produced. RP SACHS, DH (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 0 TC 18 Z9 18 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-7782 J9 EXP NEPHROL JI Exp. Nephrol. PD MAR-APR PY 1993 VL 1 IS 2 BP 128 EP 133 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA LU925 UT WOS:A1993LU92500009 PM 8081957 ER PT J AU BROUILLET, EP SHINOBU, L MCGARVEY, U HOCHBERG, F BEAL, MF AF BROUILLET, EP SHINOBU, L MCGARVEY, U HOCHBERG, F BEAL, MF TI MANGANESE INJECTION INTO THE RAT STRIATUM PRODUCES EXCITOTOXIC LESIONS BY IMPAIRING ENERGY-METABOLISM SO EXPERIMENTAL NEUROLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; D-ASPARTATE RECEPTOR; HUNTINGTONS-DISEASE; MAGNETIC-RESONANCE; QUINOLINIC ACID; RHESUS-MONKEY; BASAL GANGLIA; BRAIN; NEUROTOXICITY; NEURONS RP HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, NEUROL SERV, NEUROCHEM LAB, BOSTON, MA 02114 USA. RI Brouillet, Emmanuel/B-4784-2014 OI Brouillet, Emmanuel/0000-0001-6322-7403 FU NINDS NIH HHS [NS10828, NS16367] NR 43 TC 190 Z9 190 U1 0 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4886 EI 1090-2430 J9 EXP NEUROL JI Exp. Neurol. PD MAR PY 1993 VL 120 IS 1 BP 89 EP 94 DI 10.1006/exnr.1993.1042 PG 6 WC Neurosciences SC Neurosciences & Neurology GA KV145 UT WOS:A1993KV14500007 PM 8477830 ER PT J AU RYAN, CM SCHMIDT, J LEWANDROWSKI, K COMPTON, CC RATTNER, DW WARSHAW, AL TOMPKINS, RG AF RYAN, CM SCHMIDT, J LEWANDROWSKI, K COMPTON, CC RATTNER, DW WARSHAW, AL TOMPKINS, RG TI GUT MACROMOLECULAR PERMEABILITY IN PANCREATITIS CORRELATES WITH SEVERITY OF DISEASE IN RATS SO GASTROENTEROLOGY LA English DT Article ID STIMULATION; SEPSIS; CELL C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PATHOL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. FU NIGMS NIH HHS [GM 07035, GM 21700] NR 24 TC 82 Z9 86 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD MAR PY 1993 VL 104 IS 3 BP 890 EP 895 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KP448 UT WOS:A1993KP44800027 PM 8440440 ER PT J AU FERGUSON, DR PICHA, G WYLLIE, R GOFF, J KELSEY, P ROBERTSON, E SALWAN, F IANNUCCILLI, E WHITE, J MARSHALL, J KOZAREK, R AF FERGUSON, DR PICHA, G WYLLIE, R GOFF, J KELSEY, P ROBERTSON, E SALWAN, F IANNUCCILLI, E WHITE, J MARSHALL, J KOZAREK, R TI EARLY EXPERIENCES WITH THE PULLWIRE ONE-STEP BUTTON(R) (POSB) SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 APPL MED TECHNOL,INDEPENDENCE,OH. PAMA COMMUNITY GEN HOSP,PAMA,OH. RHODE ISL HOSP,PROVIDENCE,RI 02902. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ST LUKES GEN HOSP,SEATTLE,WA. VIRGINIA MASON MED CTR,SEATTLE,WA 98101. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD MAR-APR PY 1993 VL 39 IS 2 BP 250 EP 250 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LA057 UT WOS:A1993LA05700054 ER PT J AU SAVIDES, TJ SEE, JA JENSEN, DM JUTABHA, R MACHICADO, GA HIRABAYASHI, K AF SAVIDES, TJ SEE, JA JENSEN, DM JUTABHA, R MACHICADO, GA HIRABAYASHI, K TI EFFICACY OF SIMULTANEOUS BIOPSY AND COAGULATION WITH DIFFERENT FORCEPS IN A CANINE MODEL TO SIMULATE DIMINUTIVE POLYP REMOVAL SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, W LOS ANGELES VAMC, CURE, LOS ANGELES, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD MAR-APR PY 1993 VL 39 IS 2 BP 304 EP 304 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LA057 UT WOS:A1993LA05700267 ER PT J AU KATO, J MATSUSHIME, H HIEBERT, SW EWEN, ME SHERR, CJ AF KATO, J MATSUSHIME, H HIEBERT, SW EWEN, ME SHERR, CJ TI DIRECT BINDING OF CYCLIN-D TO THE RETINOBLASTOMA GENE-PRODUCT (PRB) AND PRB PHOSPHORYLATION BY THE CYCLIN D-DEPENDENT KINASE CDK4 SO GENES & DEVELOPMENT LA English DT Article DE G1 CYCLINS; D-TYPE CYCLINS; CYCLIN-DEPENDENT KINASES (CDKS); RETINOBLASTOMA GENE PRODUCT (PRB) ID E2F TRANSCRIPTION FACTOR; ADENOVIRUS E1A PROTEINS; LARGE T-ANTIGEN; CELL-CYCLE; SUSCEPTIBILITY GENE; ONCOGENE; CDC2; EXPRESSION; GLYCOPROTEINS; REGIONS AB The product (pRb) of the retinoblastoma gene (RB-1) prevents S-phase entry during the cell cycle, and inactivation of this growth-suppressive function is presumed to result from pRb hyperphosphorylation during late G1 phase. Complexes of the cyclin-dependent kinase, cdk4, and each of three different D-type cyclins, assembled in insect Sf9 cells, phosphorylated a pRb fusion protein in vitro at sites identical to those phosphorylated in human T cells. Only D-type cyclins activated cdk4 enzyme activity, whereas cyclins A, B1, and E did not. When Sf9 cells were coinfected with baculovirus vectors encoding human pRb and murine D-type cyclins, cyclins D2 and D3, but not D1, bound pRb with high stoichiometry in intact cells. Introduction of a vector encoding cdk4, together with those expressing pRb and D-type cyclins, induced pRb hyperphosphorylation and dissociation of cyclins D2 and D3, whereas expression of a kinase-defective cdk4 mutant in lieu of the wild-type catalytic subunit yielded ternary complexes. The transcription factor E2F-1 also bound to pRb in insect cells, and coexpression of cyclin D-cdk4 complexes, but neither subunit alone, triggered pRb phosphorylation and prevented its interaction with E2F-1. The D-type cyclins may play dual roles as cdk4 regulatory subunits and as adaptor proteins that physically target active enzyme complexes to particular substrates. C1 ST JUDE CHILDRENS RES HOSP, DEPT TUMOR CELL BIOL, MEMPHIS, TN 38105 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. ST JUDE CHILDRENS RES HOSP, HOWARD HUGHES MED INST, MEMPHIS, TN 38105 USA. FU NCI NIH HHS [CA-47064, CA-21765] NR 73 TC 1047 Z9 1059 U1 1 U2 19 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR PY 1993 VL 7 IS 3 BP 331 EP 342 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA KR218 UT WOS:A1993KR21800001 PM 8449399 ER PT J AU MACCOLLIN, M ROMANO, D BUDARF, M DENNY, C TROFATTER, J MENON, A ROULEAU, G FONTAINE, B EMANUEL, B GUSELLA, J AF MACCOLLIN, M ROMANO, D BUDARF, M DENNY, C TROFATTER, J MENON, A ROULEAU, G FONTAINE, B EMANUEL, B GUSELLA, J TI A SET OF STS ASSAYS TARGETING THE CHROMOSOME-22 PHYSICAL FRAMEWORK MARKERS SO GENOMICS LA English DT Note ID HUMAN DNA; GENE; ORGANIZATION; SEQUENCE; MAP C1 MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET LAB, BLDG 149, 13TH ST, BOSTON, MA 02129 USA. UNIV PENN, SCH MED, DEPT PEDIAT, PHILADELPHIA, PA 19104 USA. UNIV PENN, SCH MED, DEPT GENET, PHILADELPHIA, PA 19104 USA. CHILDRENS HOSP PHILADELPHIA, DIV HUMAN GENET & MOLEC BIOL, PHILADELPHIA, PA 19104 USA. UNIV CALIF LOS ANGELES, MED CTR, GWYNNE HAZEN CHERRY MEM LABS, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, MED CTR, JONSSON COMPREHENS CANC CTR, LOS ANGELES, CA 90024 USA. MCGILL UNIV, DEPT NEUROL NEUROSURG, MONTREAL H3A 2T5, QUEBEC, CANADA. MCGILL UNIV, CTR RES NEUROSCI, MONTREAL H3A 2T5, QUEBEC, CANADA. HOP LA PITIE SALPETRIERE, F-75651 PARIS 13, FRANCE. FU NHGRI NIH HHS [HG00317, HG00425]; NINDS NIH HHS [NS24279] NR 18 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD MAR PY 1993 VL 15 IS 3 BP 680 EP 683 DI 10.1006/geno.1993.1125 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KU531 UT WOS:A1993KU53100030 PM 8468063 ER PT J AU SCHERER, SW NEUFELD, EJ LIEVENS, PMJ ORKIN, SH KIM, J TSUI, LC AF SCHERER, SW NEUFELD, EJ LIEVENS, PMJ ORKIN, SH KIM, J TSUI, LC TI REGIONAL LOCALIZATION OF THE CCAAT DISPLACEMENT PROTEIN GENE (CUTL1) TO 7Q22 BY ANALYSIS OF SOMATIC-CELL HYBRIDS SO GENOMICS LA English DT Note ID CHROMOSOME-7; PROMOTER C1 HOSP SICK CHILDREN,DEPT GENET,555 UNIV AVE,TORONTO M5G 1X8,ONTARIO,CANADA. UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO M5S 1A1,ONTARIO,CANADA. CHILDRENS HOSP,DIV PEDIAT HEMATOL ONCOL,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HOWARD HUGHES MED INST,CAMBRIDGE,MA. RI Tsui, Lap-chee/A-1081-2010; Neufeld, Ellis/F-9331-2011; Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Scherer, Stephen /0000-0002-8326-1999 NR 9 TC 24 Z9 24 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR PY 1993 VL 15 IS 3 BP 695 EP 696 DI 10.1006/geno.1993.1130 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KU531 UT WOS:A1993KU53100035 PM 8468066 ER PT J AU ANDERSON, TI AF ANDERSON, TI TI SMALL AND UNFILLED PSYCHOTHERAPY GROUPS - UNDERSTANDING AND USING THEM EFFECTIVELY SO GROUP LA English DT Article AB Many open-ended psychotherapy groups have fewer than five members, and fewer than the number the therapist considers necessary for the group to be filled. This paper discusses the rationale for starting such groups and the special dynamics of running them. It then suggests strategies for the therapist to use in maximizing their therapeutic effectiveness. Suggestions are made for further research into the demographic and dynamic aspects of such groups. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 9 TC 0 Z9 0 U1 0 U2 0 PU HUMAN SCI PRESS INC PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 SN 0362-4021 J9 GROUP JI Group PD SPR PY 1993 VL 17 IS 1 BP 13 EP 20 DI 10.1007/BF01419600 PG 8 WC Psychology, Clinical SC Psychology GA LA498 UT WOS:A1993LA49800002 ER PT J AU GOFF, BA MUNTZ, HG BELL, DA WERTHEIM, I RICE, LW AF GOFF, BA MUNTZ, HG BELL, DA WERTHEIM, I RICE, LW TI HUMAN PAPILLOMAVIRUS TYPING IN PATIENTS WITH PAPANICOLAOU SMEARS SHOWING SQUAMOUS ATYPIA SO GYNECOLOGIC ONCOLOGY LA English DT Article ID DIFFERENT VIRAL TYPES; INTRAEPITHELIAL NEOPLASIA; CERVICAL CYTOLOGY; UTERINE CERVIX; CARCINOMA; CANCER; INFECTION; CELLS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP GOFF, BA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,VINCENT GYNECOL SERV,BOSTON,MA 02114, USA. NR 28 TC 12 Z9 12 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 MAR PY 1993 VL 48 IS 3 BP 384 EP 388 DI 10.1006/gyno.1993.1066 PG 5 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA KU912 UT WOS:A1993KU91200017 PM 8385061 ER PT J AU MCINTYRE, JA TAYLOR, CG TORRY, DS WAGENKNECHT, DR WILSON, J FAULK, WP AF MCINTYRE, JA TAYLOR, CG TORRY, DS WAGENKNECHT, DR WILSON, J FAULK, WP TI HEPARIN AND PREGNANCY IN WOMEN WITH A HISTORY OF REPEATED MISCARRIAGES SO HAEMOSTASIS LA English DT Article; Proceedings Paper CT 3RD NOVO NORDISK INTERNATIONAL SYMP ON THROMBOTIC DISORDERS CY SEP 30-OCT 01, 1992 CL COPENHAGEN, DENMARK SP NOVO NORDISK DE IMMUNOTHERAPY; RECURRENT ABORTION; INHIBITORS ID BETA-2-GLYCOPROTEIN-I APOLIPOPROTEIN-H; RECURRENT SPONTANEOUS-ABORTIONS; ANTIPHOSPHOLIPID ANTIBODIES; LEUKOCYTE TRANSFUSIONS; COAGULATION; PREVENTION; INHIBITOR; ANTIGENS; BINDING AB Many patients who experience recurrent spontaneous abortions (RSA) have high titered antibodies to trophoblast antigens and/or negatively charged phospholipids. Pregnancy success has been documented in some of these patients subsequent to heparin treatment. The effect of heparin on in vitro assays used to detect antibodies to phospholipids and trophoblast antigens has been investigated. We have found that complement-mediated detection of antibodies to trophoblast and lymphocyte antigens is inhibited by absorption of sera with solid-phase heparin. The data show that such inhibition involves an inhibitor and a heparin-sensitive regulator of the inhibitor. Heparin inhibits binding of antiphospholipid antibodies to phospholipids in solid-phase ELISA. The mechanism for this inhibition appears to involve an interaction between heparin and antibody to phospholipid. These findings reveal novel heparin-mediated reactions that bridge immunological and hematological interactions. The extent of heparin modulation of these antibody reactivities should be clarified in future clinical trials involving heparin treatment for RSA. C1 DEMBURY HOSP,DEPT HEMATOL,TUNBRIDGE WELLS,KENT,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,BOSTON,MA 02115. RP MCINTYRE, JA (reprint author), METHODIST HOSP INDIANA,CRTI,1701 N SENATE BLVD,INDIANAPOLIS,IN 46202, USA. NR 29 TC 29 Z9 29 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0147 J9 HAEMOSTASIS JI Haemostasis PD MAR PY 1993 VL 23 SU 1 BP 202 EP 211 PG 10 WC Hematology SC Hematology GA KU838 UT WOS:A1993KU83800028 PM 8495868 ER PT J AU TIMKO, C NGUYEN, ATQ WILLIFORD, WO MOOS, RH AF TIMKO, C NGUYEN, ATQ WILLIFORD, WO MOOS, RH TI QUALITY OF CARE AND OUTCOMES OF CHRONIC MENTALLY-ILL PATIENTS IN HOSPITALS AND NURSING-HOMES SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID RESIDENTIAL FACILITIES; INTEGRATION AB Quality of care in three types of facilities in which chronic mentally ill patients reside was examined to determine how it was related to patient functioning and to determine how patients' dependency on others for self-care moderated relationships between quality of care and patient functioning. Methods: Discriminant function analyses and multiple regression analyses were used to examine 12-month follow-up data from a Department of Veterans Affairs (VA) study of 294 chronic mentally ill patients in 52 community nursing homes, nine VA nursing home care units, and 43 VA hospital psychiatric units. Results: The three types of facilities were best differentiated by staff and resident characteristics and facility policies. Residents of community nursing homes were more impaired, and staff were less well trained, than in the VA facilities. The community nursing homes had less restrictive policies. Patients who lived in facilities that gave them more control over their daily lives and that had larger proportions of high-functioning patients reported more life satisfaction and vigor. Patients in facilities with more social and recreational activities reported less life satisfaction. The extent to which facility features were beneficial or harmful was related to patients' self-care dependency. Supportive physical features and living-assistance services tended to aid impaired residents, whereas more experienced staff and policies that promoted control by residents tended to aid independent residents. Conclusions: Program managers may need to tailor facility environments to patients' level of functioning to maximize beneficial effects. C1 VET ADM MED CTR,COOPERAT STUDIES PROGRAM,PERRY POINT,MD. STANFORD UNIV,MED CTR,STANFORD,CA 94305. RP TIMKO, C (reprint author), US DEPT VET AFFAIRS,CTR HLTH CARE EVALUAT,3801 MIRANDA AVE 152,PALO ALTO,CA 94304, USA. FU NIMH NIH HHS [MH28177] NR 29 TC 18 Z9 18 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD MAR PY 1993 VL 44 IS 3 BP 241 EP 246 PG 6 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA KP048 UT WOS:A1993KP04800007 PM 8444434 ER PT J AU ROSENBERG, AE OCONNELL, JX DICKERSIN, GR BHAN, AK AF ROSENBERG, AE OCONNELL, JX DICKERSIN, GR BHAN, AK TI EXPRESSION OF EPITHELIAL MARKERS IN MALIGNANT FIBROUS HISTIOCYTOMA OF THE MUSCULOSKELETAL SYSTEM - AN IMMUNOHISTOCHEMICAL AND ELECTRON-MICROSCOPIC STUDY SO HUMAN PATHOLOGY LA English DT Article DE MALIGNANT FIBROUS HISTIOCYTOMAS; ELECTRON MICROSCOPY; IMMUNOHISTOCHEMISTRY; KERATIN; EPITHELIAL MEMBRANE ANTIGEN ID SOFT-TISSUE SARCOMAS; SMOOTH-MUSCLE TUMORS; MEMBRANE ANTIGEN; CYTOKERATIN EXPRESSION; FIBROHISTIOCYTIC TUMORS; INTERMEDIATE FILAMENTS; MONOCLONAL-ANTIBODIES; SURGICAL PATHOLOGY; CELL CARCINOMA; NEOPLASMS RP ROSENBERG, AE (reprint author), MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,DEPT PATHOL,BOSTON,MA 02114, USA. NR 49 TC 49 Z9 51 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD MAR PY 1993 VL 24 IS 3 BP 284 EP 293 DI 10.1016/0046-8177(93)90039-J PG 10 WC Pathology SC Pathology GA KR936 UT WOS:A1993KR93600010 PM 7681032 ER PT J AU GHIKA, J WIEGNER, AW FANG, JJ DAVIES, L YOUNG, RR GROWDON, JH AF GHIKA, J WIEGNER, AW FANG, JJ DAVIES, L YOUNG, RR GROWDON, JH TI PORTABLE SYSTEM FOR QUANTIFYING MOTOR ABNORMALITIES IN PARKINSONS-DISEASE SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Article ID QUANTITATIVE-EVALUATION; ELASTIC PROPERTIES; INTENTION TREMOR; REACTION-TIME; MOVEMENTS; ELBOW; EXECUTION; RIGIDITY AB In order to quantify motor disabilities in Parkinson's disease (PD), we designed a compact, portable, neurophysiological system based upon a personal computer to measure tremor, bradykinesia, and muscle tone. Tremor was detected by solid state accelerometers and translated into a digital signal. The system displayed the root mean square displacements and frequency distribution of the tremor in the horizontal and vertical planes, along with a reconstructed graphic image of the displacement. Bradykinesia was measured using a panel that detects release and depression of switches in response to auditory and visual signals; the system calculated subjects' reaction times and movement times in milliseconds. Tone at the elbow was measured by strapping the upper extremity to a lightweight low-friction cradle and then passively moving the cradle with an instrumented handle. Signals representing torque and arm angle were processed by the computer and displayed in real time on the screen with stiffness as a mean slope in Nm/degree. In clinical tests, quantitative measures of tremor, movement time and rigidity were significantly abnormal in PD patients compared to control subjects. We conclude that this system is a convenient and accurate method to quantitate important aspects of the parkinsonian syndrome, and may be applied to quantitate other movement disorders. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. W ROXBURY VA MED CTR,BOSTON,MA. NR 53 TC 46 Z9 46 U1 0 U2 1 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0018-9294 J9 IEEE T BIO-MED ENG JI IEEE Trans. Biomed. Eng. PD MAR PY 1993 VL 40 IS 3 BP 276 EP 283 DI 10.1109/10.216411 PG 8 WC Engineering, Biomedical SC Engineering GA LH044 UT WOS:A1993LH04400008 PM 8335331 ER PT J AU ACHESON, DWK CALDERWOOD, SB BOYKO, SA LINCICOME, LL KANE, AV DONOHUEROLFE, A KEUSCH, GT AF ACHESON, DWK CALDERWOOD, SB BOYKO, SA LINCICOME, LL KANE, AV DONOHUEROLFE, A KEUSCH, GT TI COMPARISON OF SHIGA-LIKE TOXIN-I B-SUBUNIT EXPRESSION AND LOCALIZATION IN ESCHERICHIA-COLI AND VIBRIO-CHOLERAE BY USING TRC OR IRON-REGULATED PROMOTER SYSTEMS SO INFECTION AND IMMUNITY LA English DT Article ID SHIGELLA DIARRHEA; NUCLEOTIDE-SEQUENCE; PURIFICATION; PATHOGENESIS; GENES; ENTEROTOXIN; ANTIBODIES AB Shiga-like toxin I (SLT-1) B-subunit expression was examined by using the trc promoter in two different constructs, pSBC32 and pSBC54, in which 710 bp of DNA downstream of the B subunit in pSBC32 was deleted. The trc promoter in pSBC54 was replaced also with the SLT-I iron-regulated promoter to create a third plasmid, pSBC61. SLT-I B-subunit expression was examined from all three plasmids following transfer into Escherichia coli JM105 and the cholera toxin A-subunit gene deletion mutant Vibrio cholerae 0395-Nl. The SLT-I B subunit was expressed from all constructs. pSBC61 was regulated by elemental iron and produced equivalent amounts of SLT-1 B subunit from both E. coli and V. cholerae. In contrast to the cholera toxin B subunit, virtually all released into the medium, the SLT-I B subunit was predominantly cell associated in the pSBC61 constructs. Both pSBC32 and pSBC54 were inducible with isopropyl-beta-D-thiogalactopyranoside (IPTG) in the E. coli background but not the V. cholerae background; however, when E. coli cultures were allowed to grow for 24 h, the yield of SLT-I B subunit was not increased by IPTG induction. Both pSBC32 and -54 expressed more SLT-I B subunit in the V. cholerae host than in the E. coli host. Scale-up to a 9.9-liter fermentor culture of V. cholerae 0395 N1(pSBC32) resulted in the isolation of 220 mg of SLT-I B. The purified B subunit was identical, in terms of binding to Vero cells, stoichiometry after chemical cross-linking, and ability to inhibit cytotoxicity of intact Shiga toxin, to native SLT-I B subunit from E. coli O157:H7. C1 NEW ENGLAND MED CTR, CTR GASTROENTEROL RES ABSORPT & SECRETORY PROC, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, INFECT DIS UNIT, BOSTON, MA 02114 USA. RP ACHESON, DWK (reprint author), NEW ENGLAND MED CTR, DIV GEOG MED & INFECT DIS, BOSTON, MA 02111 USA. FU NIAID NIH HHS [AI-16242, AI-20253, AI-27329] NR 23 TC 24 Z9 24 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD MAR PY 1993 VL 61 IS 3 BP 1098 EP 1104 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KN097 UT WOS:A1993KN09700042 PM 8432592 ER PT J AU FINK, LM EIDT, JF JOHNSON, K COOK, JM COOK, CD MORSER, J MARLAR, R COLLINS, CL SCHAEFER, R XIE, SS HSU, SM HSU, PL AF FINK, LM EIDT, JF JOHNSON, K COOK, JM COOK, CD MORSER, J MARLAR, R COLLINS, CL SCHAEFER, R XIE, SS HSU, SM HSU, PL TI THROMBOMODULIN ACTIVITY AND LOCALIZATION SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE THROMBOMODULIN; VASCULAR INJURY; MESOTHELIOMA ID SMOOTH-MUSCLE CELLS; VEIN ENDOTHELIAL-CELLS; TUMOR-NECROSIS-FACTOR; RABBIT AORTA; CYCLIC-AMP; PROTEIN-C; EXPRESSION; MESOTHELIOMA; THROMBIN; ANTIGEN AB An overview on the properties, actions and localization of thrombomodulin (TM) in situations of tissue injury and in selected tumors is presented. The localization and activity of TM after injury to vascular endothelium shows that following balloon catheter denudation of the endothelium of the rabbit aorta, the activity and immunohistochemical staining is markedly reduced. The functional and antigenic levels approach the control levels approximately one week after the initial injury. The results suggest that the neointimal smooth muscle cells express TM. This phenotypic plasticity of the neointimal smooth muscle cells may be important in conferring thrombo-resistance to the lumenal lining cells of vessels after injury. Studies are also reviewed on the use of soluble recombinant TM to prevent thrombosis after ligature of vessels in an experimental model. Further characterization on the immunohistochemical distribution of TM in normal tissues and tumors shows that staining with a monoclonal anti TM antibody can be very useful in separating mesotheliomas from pulmonary adenocarcinomas. These studies may lead to insights concerning the role of TM in tissue-injury-repair and tissue differentiation. C1 VET AFFAIRS MED CTR, LITTLE ROCK, AR USA. UNIV ARKANSAS MED SCI HOSP, DEPT PATHOL, LITTLE ROCK, AR 72205 USA. BERLEX CORP, S SAN FRANCISCO, CA USA. DENVER VET AFFAIRS MED CTR, DENVER, CO USA. UNIV COLORADO, SCH MED, DEPT PATHOL, DENVER, CO 80202 USA. FU NCI NIH HHS [CA 4762] NR 48 TC 30 Z9 30 U1 1 U2 1 PU U B C PRESS PI BILBAO PA UNIV BASQUE COUNTRY, EDITORIAL SERVICES, PO BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PD MAR PY 1993 VL 37 IS 1 BP 221 EP 226 PG 6 WC Developmental Biology SC Developmental Biology GA KT670 UT WOS:A1993KT67000028 PM 8389578 ER PT J AU WIGGS, JL AF WIGGS, JL TI MOLECULAR-GENETICS AND OCULAR DISEASE SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Review RP WIGGS, JL (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP 1 EP 36 PG 36 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600002 PM 8325725 ER PT J AU CHEN, S MUKAI, S AF CHEN, S MUKAI, S TI GENETICS OF RETINOBLASTOMA SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP CHEN, S (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 2 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP 57 EP 65 DI 10.1097/00004397-199303320-00006 PG 9 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600005 PM 8325743 ER PT J AU NETLAND, PA WIGGS, JL DREYER, EB AF NETLAND, PA WIGGS, JL DREYER, EB TI INHERITANCE OF GLAUCOMA AND GENETIC-COUNSELING OF GLAUCOMA PATIENTS SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Review RP NETLAND, PA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA CONSULTAT SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 16 Z9 16 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP 101 EP 120 DI 10.1097/00004397-199303320-00011 PG 20 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600010 PM 8325726 ER PT J AU HAYNIE, GD MUKAI, S AF HAYNIE, GD MUKAI, S TI GENETIC-BASIS OF COLOR-VISION SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP HAYNIE, GD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP 141 EP 152 DI 10.1097/00004397-199303320-00014 PG 12 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600013 PM 8325729 ER PT J AU VOLPE, NJ LESSELL, S AF VOLPE, NJ LESSELL, S TI LEBER HEREDITARY OPTIC NEUROPATHY SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP VOLPE, NJ (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP 153 EP 168 DI 10.1097/00004397-199303320-00015 PG 16 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600014 PM 8325730 ER PT J AU SHOKRAVI, MT DRYJA, TP AF SHOKRAVI, MT DRYJA, TP TI RETINITIS-PIGMENTOSA AND THE RHODOPSIN GENE SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article C1 MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 6 Z9 6 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP 219 EP 228 DI 10.1097/00004397-199303320-00020 PG 10 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600019 PM 8325735 ER PT J AU JACOBS, DS DOHLMAN, CH AF JACOBS, DS DOHLMAN, CH TI IS KERATOCONUS GENETIC SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP JACOBS, DS (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 16 Z9 16 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP 249 EP 260 DI 10.1097/00004397-199303320-00023 PG 12 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600022 PM 8325738 ER PT J AU JAKOBIEC, FA LAMKIN, JC AF JAKOBIEC, FA LAMKIN, JC TI ADVANCES IN OPHTHALMIC GENETICS AND HERITABLE EYE DISEASES - PREFACE SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Editorial Material RP JAKOBIEC, FA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SPR PY 1993 VL 33 IS 2 BP R17 EP R18 PG 2 WC Ophthalmology SC Ophthalmology GA LF406 UT WOS:A1993LF40600001 ER PT J AU UEBERLA, K LU, YC CHUNG, E HASELTINE, WA AF UEBERLA, K LU, YC CHUNG, E HASELTINE, WA TI THE NF-KAPPA-B P65 PROMOTER SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE NF-KAPPA-B P65 PROMOTER ID SEQUENCES AB The promoter of the human gene encoding the p65 subunit of the transcription factor NF-kappaB was cloned and the nucleotide sequence determined. The p65 promoter lacks both TATA and CCAAT consensus sequences. The p65 promoter contains three consensus binding sites of the transcription factor SP1. In contrast to the promoter of the p50 subunit of NF-kappaB, no sequences predicted to bind NF-kappaB are present in the p65 promoter. Phorbol ester (PMA) and phytohemagglutinin (PHA) treatment of Jurkat cells did not activate the p65 promoter in transient transfection experiments. Using different deletion mutants of the p65 promoter, essential promoter elements were mapped. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,JF824,44 BINNEY ST,BOSTON,MA 02115. RI Uberla, Klaus/C-5676-2008 FU NCI NIH HHS [CA36974]; NIAID NIH HHS [AI28785, AI24845] NR 14 TC 50 Z9 50 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD MAR PY 1993 VL 6 IS 3 BP 227 EP 230 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KN542 UT WOS:A1993KN54200002 PM 8450395 ER PT J AU GAGLIANO, NJ EMANS, SJ WOODS, ER AF GAGLIANO, NJ EMANS, SJ WOODS, ER TI CHOLESTEROL SCREENING IN THE ADOLESCENT SO JOURNAL OF ADOLESCENT HEALTH LA English DT Article; Proceedings Paper CT MEETING OF THE SOC FOR ADOLESCENT MEDICINE CY MAR 22-25, 1990 CL ATLANTA, GA SP SOC ADOLESCENT MED DE CHOLESTEROL; ADOLESCENTS; HYPERCHOLESTEROLEMIA; CHOLESTEROL SCREENING; FAMILY HISTORY ID CORONARY HEART-DISEASE; RISK-FACTORS; ADULT HYPERCHOLESTEROLEMIA; FAMILY HISTORY; UNITED-STATES; CHILDHOOD; CHILDREN; STRATEGIES; MUSCATINE; THERAPY AB Guidelines for screening populations for hypercholesterolemia are controversial. In pediatric patients, screening has been targeted to those with a family history of hypercholesterolemia or early myocardial infarction. Because specific guidelines for adolescents have not been developed, we undertook a study of cholesterol screening in 224 consecutive patients (mean age, 14.8 +/- 2.2 years; range, 11-20 years). In this study, 33 (14.7%) adolescents had levels above 185 mg/dL; 71 (32.7%) of the patients reported a positive family history for early myocardial infarction or elevated lipids. A positive family history obtained from the adolescent patient had a 36% sensitivity, 69% specificity, 17% positive predictive value, and an 87% negative predictive value compared with elevated cholesterol level. A positive history reported by the parent had a 65% sensitivity, 46% specificity, 16% positive predictive value, and an 89% negative predictive value. A positive family history obtained from either parent or adolescent had a 45% sensitivity, 69% specificity, 19% positive predicative value, and 89% negative predictive value. Family history by the adolescent was significantly different from parental history (p < 0.001). Family history is a poor predictor for cholesterol level in adolescents. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DIV ADOLESCENT YOUNG ADULT MED,BOSTON,MA 02115. OI Emans, S. Jean/0000-0002-4535-7850 NR 37 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1054-139X J9 J ADOLESCENT HEALTH JI J. Adolesc. Health PD MAR PY 1993 VL 14 IS 2 BP 104 EP 108 DI 10.1016/1054-139X(93)90093-5 PG 5 WC Psychology, Developmental; Public, Environmental & Occupational Health; Pediatrics SC Psychology; Public, Environmental & Occupational Health; Pediatrics GA KV381 UT WOS:A1993KV38100007 PM 8476872 ER PT J AU SHAO, TC KONG, A MARAFELIA, P CUNNINGHAM, GR AF SHAO, TC KONG, A MARAFELIA, P CUNNINGHAM, GR TI EFFECTS OF FINASTERIDE ON THE RAT VENTRAL PROSTATE SO JOURNAL OF ANDROLOGY LA English DT Article DE THYMIDINE INCORPORATION; MESSENGER RNA PROSTATE IN; MESSENGER RNA; TRMP-2 ID 5-ALPHA-REDUCTASE INHIBITOR; GROWTH; CASTRATION; DNA; DIHYDROTESTOSTERONE; EXPRESSION; ANDROGENS AB The objectives of this study were to compare changes in the ventral prostate (VP) of young adult Sprague Dawley rats after 28 days of treatment with finasteride (F), a potent 5alpha-reductase inhibitor, with those caused by castration (Cx). VP concentrations of DHT were reduced to 20.2% and 6.6% of controls (1,947 +/- 207 pg/VP, mean +/- SE) by F (5 or 20 mg/kg/day) and to 2.6% of controls by Cx. VP weights were reduced 49% and 54% by F and 88% by Cx. DNA/VP fell 25% and 15% with F treatment and 72% after Cx, whereas RNA and protein/VP were reduced 37-51% by F and 91-93% by Cx. The RNA/DNA and the protein/DNA ratios fell to 30-36% of controls after F treatment and to 70% of controls after Cx. The mRNA concentrations of the C3 subunit of prostatein 28S ribosomal RNA fell after treatment with F (5 mg/kg/day) and after Cx, whereas the mRNA for TRPM-2, an androgen-suppressed protein associated with apoptosis, was increased only after castration. To examine further the effects of F on the rate of DNA synthesis, 7-day regressed adult rats were treated for 3 days with testosterone propionate +/-F, and incorporation of H-3-thymidine in minced ventral prostates was determined. F inhibited H-3-thymidine incorporation. We conclude that Cx causes a greater reduction in cell number/VP and a greater reduction in RNA and protein/cell than F and that the differences between F treatment and castration probably result from differences in prostatic concentrations of T. However, we cannot exclude the possibility that small differences in DHT contribute to these differences. C1 DEPT VET AFFAIRS MED CTR,MED & RES SERV,2002 HOLCOMBE BLVD,HOUSTON,TX 77030. BAYLOR COLL MED,HOUSTON,TX 77030. NR 29 TC 34 Z9 34 U1 0 U2 0 PU AMER SOC ANDROLOGY, INC PI LAWRENCE PA C/O ALLEN PRESS, INC PO BOX 368, LAWRENCE, KS 66044 SN 0196-3635 J9 J ANDROL JI J. Androl. PD MAR-APR PY 1993 VL 14 IS 2 BP 79 EP 86 PG 8 WC Andrology SC Endocrinology & Metabolism GA LB839 UT WOS:A1993LB83900002 PM 8390428 ER PT J AU VERTEL, BM WALTERS, LM GRIER, B MAINE, N GOETINCK, PF AF VERTEL, BM WALTERS, LM GRIER, B MAINE, N GOETINCK, PF TI NANOMELIC CHONDROCYTES SYNTHESIZE, BUT FAIL TO TRANSLOCATE, A TRUNCATED AGGRECAN PRECURSOR SO JOURNAL OF CELL SCIENCE LA English DT Article DE CARTILAGE; ENDOPLASMIC RETICULUM; PROTEOGLYCANS; INTRACELLULAR TRAFFICKING; MUTANTS ID PROTEOGLYCAN CORE PROTEIN; CHONDROITIN SULFATE PROTEOGLYCAN; ASIALOGLYCOPROTEIN RECEPTOR SUBUNITS; DEFECTIVE INTRACELLULAR-TRANSPORT; PRE-GOLGI DEGRADATION; VIRUS G-PROTEIN; ENDOPLASMIC-RETICULUM; MONOCLONAL-ANTIBODY; INFLUENZA HEMAGGLUTININ; CARTILAGE PROTEOGLYCANS AB Cartilage extracellular matrix (ECM) is composed primarily of type II collagen and large, link stabilized aggregates of hyaluronic acid and chondroitin sulfate proteoglycan (aggrecan). Maturation and function of these complex macromolecules are dependent upon sequential processing events which occur during their movements through specific subcellular compartments in the constituitive secretory pathway. Failure to complete these events successfully results in assembly of a defective ECM and may produce skeletal abnormalities. Nanomelia is a lethal genetic mutation of chickens characterized by shortened and malformed limbs. Previous biochemical studies have shown that cultured nanomelic chondrocytes synthesize a truncated aggrecan core protein precursor that disappears with time; however, the protein does not appear to be processed by the Golgi or secreted. The present study investigates the intracellular trafficking of the defective aggrecan precursor using immunofluorescence, immunoelectron microscopy and several inhibitors. Results indicate that nanomelic chondrocytes assemble an ECM that contains type II collagen, but lacks aggrecan. Instead, aggrecan precursor was localized intracellularly, within small cytoplasmic structures corresponding to extensions of the endoplasmic reticulum (ER). At no time were precursor molecules observed in the Golgi. In contrast, normal and nanomelic chondrocytes exhibited no difference in the intracellular or extracellular distribution of type II procollagen. Therefore, retention of the aggrecan precursor appears to be selective. Incubation of chondrocytes at 15-degrees-C resulted in the retention and accumulation of product in the ER. After a return to 37-degrees-C, translocation of the product to the Golgi was observed for normal, but not for nanomelic, chondrocytes, although the precursors disappeared with time. Ammonium chloride, an inhibitor of lysosomal function, had no effect on protein loss, suggesting that the precursor was removed by a non-lysosomal mechanism, possibly by ER-associated degradation. Based on these studies, we suggest that nanomelic chondrocytes are a useful model for examining cellular trafficking and sorting events and the processes by which abnormal products are targeted for retention or degradation. Further investigations should provide insight into the mechanisms underlying chondrodystrophies and other related diseases. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. RP VERTEL, BM (reprint author), UNIV HLTH SCI CHICAGO MED SCH,DEPT CELL BIOL & ANAT,3333 GREEN BAY RD,N CHICAGO,IL 60064, USA. FU NICHD NIH HHS [HD22016]; NIDDK NIH HHS [DK28433] NR 61 TC 47 Z9 47 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD MAR PY 1993 VL 104 BP 939 EP 948 PN 3 PG 10 WC Cell Biology SC Cell Biology GA KY983 UT WOS:A1993KY98300033 PM 8314884 ER PT J AU KRIAUCIUNAS, KM GOLDSTEIN, BJ LIPES, MA KAHN, CR AF KRIAUCIUNAS, KM GOLDSTEIN, BJ LIPES, MA KAHN, CR TI MODULATION OF EXPRESSION OF INSULIN AND IGF-I RECEPTOR BY EPSTEIN-BARR-VIRUS AND ITS GENE-PRODUCTS LMP AND EBNA-2 IN LYMPHOCYTE CELL-LINES SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; LEUKOCYTE ANTIGEN-DR; MESSENGER-RNA; BURKITTS-LYMPHOMA; B-CELLS; TRANSFORMED LYMPHOCYTES; CULTURED LYMPHOCYTES; RESISTANT PATIENT; DECREASED LEVELS; BINDING AB The receptors for insulin and insulin-like growth factor I (IGF-I) are two closely related integral membrane glycoproteins involved in signalling of cell growth and metabolism. We have used the unique paradigm of pairs of Burkitt lymphoma cell lines (BLO2, BL30, BL41) with or without Epstein-Barr Virus (EBV) infection and cells transfected with EBV-related genes to examine effects of EBV on expression of these receptors at the gene and protein functional level. in BL30 and BL41 cells, EBV infection increased surface insulin binding and total receptor number by 2- and 18-fold, respectively. By contrast, EBV infection decreased total IGF-I receptors by 29 to 87% in all three cell lines. In general, there was a correlation between total receptor concentration and the level of insulin or IGF-I receptor mRNAs, although in one cell line insulin binding increased while receptor mRNA levels decreased slightly, suggesting posttranslational effects. BL41 cells transfected with a vector expressing the EBV latent membrane protein (LMP) exhibited a 2.6- to 3.2-fold increase in insulin receptor expression, whereas cells transfected with EBNA-2 (one of the EBV nuclear antigens) alone exhibited no effect. However, EBNA-2 appears to be required for the EBV effect on insulin receptor expression since cells infected with a mutant virus, P3JHRI, which lacks the EBNA-2 gene failed to show an increase in insulin receptor number. These data indicate that EBV infection of lymphocytes increases expression of insulin receptors while simultaneously decreasing expression of IGF-I receptors. The magnitude and sometimes even the direction of change, depends on host cell factors. A maximal increase in insulin receptors appears to require the coordinate action of several of the EBV proteins including LMP and EBNA-2. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,DIV RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 31036, DK 36836] NR 55 TC 13 Z9 13 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD MAR PY 1993 VL 154 IS 3 BP 486 EP 495 DI 10.1002/jcp.1041540306 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA KP604 UT WOS:A1993KP60400005 PM 8382208 ER PT J AU NOZAKI, K FINKLESTEIN, SP BEAL, MF AF NOZAKI, K FINKLESTEIN, SP BEAL, MF TI BASIC FIBROBLAST GROWTH-FACTOR PROTECTS AGAINST HYPOXIA-ISCHEMIA AND NMDA NEUROTOXICITY IN NEONATAL RATS SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE BASIS FIBROBLAST GROWTH FACTOR; EXCITATORY AMINO ACID; HYPOXIA-ISCHEMIA; N-METHYL-D-ASPARTATE; NEONATE ID CENTRAL-NERVOUS-SYSTEM; FACTOR PROMOTES SURVIVAL; RECEPTOR MESSENGER-RNA; METHYL-D-ASPARTATE; GLUTAMATE NEUROTOXICITY; CHOLINERGIC NEURONS; HIPPOCAMPAL-NEURONS; NEURITE EXTENSION; CEREBRAL-PALSY; FGF-RECEPTOR AB Basic fibroblast growth factor (bFGF) is a polypeptide that promotes neuronal survival and blocks excitatory amino acid (EAA) neurotoxicity in vitro at very low concentrations. In the present study, we examined whether systemically administered bFGF could prevent neuronal damage induced by either EAAs or hypoxia-ischemia in vivo. Neuroprotective effects were examined in a neonatal model of hypoxia-ischemia (unilateral ligation of the carotid artery followed by exposure to 8% oxygen for 1.5 h) and following intrastriatal injection of N-methyl-D-aspartate (NMDA) in 7-day-old rats. Intra-peritoneal administration of a single dose of bFGF (50-300 mug/kg) 30 min before intrastriatal injection of NMDA showed a dose-dependent neuroprotective effect. Repeated doses of bFGF (100 mug/kg) both before and after intrastriatal NMDA injection produced a much greater significant protective effect than a single dose administered prior to the injection. Intraperitoneal injection of single dose of 100 mug/kg of bFGF 30 min before hypoxia-ischemia reduced neuronal damage by 38% (p = 0.14), while administration of bFGF at a dose of 100 mug/kg i.p. three times, 30 min before and 0 and 30 min after hypoxia-ischemia. significantly reduced neuronal damage by 64% (p = 0.004). Systemic administration of bFGF did not change body temperature for up to 3 h. These results show that systemic administration of bFGF can exert neuroprotective effects against both NMDA-induced excitotoxicity and hypoxia-ischemia in vivo. C1 MASSACHUSETTS GEN HOSP,NEUROCHEM LABS,NEUROL RES 4,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIA NIH HHS [AG08207]; NINDS NIH HHS [NS10828, NS16367] NR 68 TC 150 Z9 151 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD MAR PY 1993 VL 13 IS 2 BP 221 EP 228 PG 8 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA KM808 UT WOS:A1993KM80800006 PM 8436614 ER PT J AU SEIFER, DB MACLAUGHLIN, DT PENZIAS, AS BEHRMAN, HR ASMUNDSON, L DONAHOE, PK HANING, RV FLYNN, SD AF SEIFER, DB MACLAUGHLIN, DT PENZIAS, AS BEHRMAN, HR ASMUNDSON, L DONAHOE, PK HANING, RV FLYNN, SD TI GONADOTROPIN-RELEASING-HORMONE AGONIST-INDUCED DIFFERENCES IN GRANULOSA-CELL CYCLE KINETICS ARE ASSOCIATED WITH ALTERATIONS IN FOLLICULAR-FLUID MULLERIAN-INHIBITING SUBSTANCE AND ANDROGEN CONTENT SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HUMAN CORPUS-LUTEUM; OOCYTE MEIOSIS; BINDING-SITES; RAT; RECEPTORS; OVARIES; GROWTH AB We have previously shown that the proliferative index (PI), as determined by flow cytometry of luteinized granulosa cells obtained at oocyte retrieval, is greater in ovulation induction regimens which include the GnRH analog (GnRH-a) leuprolide acetate than those using human menopausal gonadotropin (hMG) only. Specific growth factors or intrafollicular hormones may contribute to this leuprolide acetate-induced difference in cell cycle kinetics. We examined whether differences in the PI of these granulosa cells are associated with the alterations of follicular fluid content of Mullerian-inhibiting substance (MIS) and other intrafollicular hormones including FSH, estradiol, progesterone, androstenedione, and testosterone. The control group consisted of follicular fluid obtained from 18 follicles from 4 women receiving hMG alone. The GnRH-a treated group consisted of follicular fluids obtained from 55 follicles aspirated from 18 women receiving GnRH-a in addition to hMG. One-way analysis of variance using log-transformed data and expressed as geometric means with 95% confidence intervals, demonstrated that the follicles from the control group had a significant 14-fold higher concentration of 2.46 ng/mL MIS, 95% CI (1.8-4.8) us. 0.18 ng/mL, 95% CI (0.13-0.24) P < 0.0005, a 3-fold higher concentration of 17.55 nmol/L androstenedione, 95% CI (14.620. 9) us. 5.76 nmol/L, 95% CI (3.1-10.5) P < 0.02, and a 1.5-fold higher concentration of 29.43 nmol/L testosterone 95% CI (22.5-38.14) vs. 19.3 nmol/L, 95% of CI (11.1-33.9) P < 0.01 than GnRH-a treated follicles, although the PI value in controls was half that of the GnRH-a group. These data demonstrate that GnRH-a induced differences in granulosa cell cycle kinetics are associated with alterations of MIS and androgen intrafollicular fluid content and suggest that MIS may be a mitotic inhibitor of human granulosa cells. C1 MASSACHUSETTS GEN HOSP, PEDIAT SURG RES LABS, BOSTON, MA 02114 USA. YALE UNIV, SCH MED, DEPT PATHOL, DIV REPROD ENDOCRINOL, NEW HAVEN, CT 06510 USA. RP SEIFER, DB (reprint author), BROWN UNIV, WOMEN & INFANTS HOSP, SCH MED, DEPT OBSTET & GYNECOL, DIV REPROD ENDOCRINOL, PROVIDENCE, RI 02905 USA. OI Seifer, David/0000-0003-3950-9341 FU FDA HHS [FD-R-000669-01]; NCI NIH HHS [CA 17393]; NIA NIH HHS [AG00566] NR 18 TC 45 Z9 50 U1 1 U2 2 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 MAR PY 1993 VL 76 IS 3 BP 711 EP 714 DI 10.1210/jc.76.3.711 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KQ341 UT WOS:A1993KQ34100033 PM 8445031 ER PT J AU GANZINI, L LEE, MA HEINTZ, RT BLOOM, JD AF GANZINI, L LEE, MA HEINTZ, RT BLOOM, JD TI IS THE PATIENT SELF-DETERMINATION ACT APPROPRIATE FOR ELDERLY PERSONS HOSPITALIZED FOR DEPRESSION SO JOURNAL OF CLINICAL ETHICS LA English DT Article ID LIFE; SUICIDE; CONSENT C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. DAMMASCH STATE HOSP,WILSONVILLE,OR. OREGON HLTH SCI UNIV,DEPT PSYCHIAT,PORTLAND,OR 97201. NR 23 TC 8 Z9 8 U1 2 U2 4 PU UNIV PUBL GROUP, INC PI FREDERICK PA 12 SOUTH MARKET ST, STE 301, FREDERICK, MD 21701 SN 1046-7890 J9 J CLIN ETHIC JI J. Clin. Ethics PD SPR PY 1993 VL 4 IS 1 BP 46 EP 50 PG 5 WC Ethics; Social Sciences, Biomedical SC Social Sciences - Other Topics; Biomedical Social Sciences GA LZ265 UT WOS:A1993LZ26500008 PM 8490219 ER PT J AU GANZINI, L LEE, MA AF GANZINI, L LEE, MA TI AUTHENTICITY, AUTONOMY, AND MENTAL-DISORDERS SO JOURNAL OF CLINICAL ETHICS LA English DT Article ID PATIENT C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NR 9 TC 4 Z9 4 U1 0 U2 0 PU UNIV PUBL GROUP, INC PI FREDERICK PA 12 SOUTH MARKET ST, STE 301, FREDERICK, MD 21701 SN 1046-7890 J9 J CLIN ETHIC JI J. Clin. Ethics PD SPR PY 1993 VL 4 IS 1 BP 58 EP 61 PG 4 WC Ethics; Social Sciences, Biomedical SC Social Sciences - Other Topics; Biomedical Social Sciences GA LZ265 UT WOS:A1993LZ26500011 PM 8490222 ER PT J AU MONTANA, E BONNERWEIR, S WEIR, GC AF MONTANA, E BONNERWEIR, S WEIR, GC TI BETA-CELL MASS AND GROWTH AFTER SYNGENEIC ISLET CELL TRANSPLANTATION IN NORMAL AND STREPTOZOCIN DIABETIC C57BL/6 MICE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE DIABETES; ENDOCRINE PANCREAS; INSULIN; ISLET OF LANGERHANS; BETA-CELL REPLICATION ID MOUSE PANCREATIC-ISLETS; OBESE-HYPERGLYCEMIC MICE; DEPANCREATIZED DOGS; ENDOCRINE FUNCTION; DNA-REPLICATION; GLUCOSE; RATS; KIDNEY; LIVER; ALLOGRAFTS AB In islet transplantation, nonimmunological factors such as limited growth capacity or increased death rate could reduce the beta cell mass in the graft and lead to failure of the transplant. We studied the evolution of beta cell replication and mass after transplantation of insufficient, minimally sufficient, or excessive islet tissue. Streptozocin diabetic C57BL/6 mice received 150 or 300 syngeneic islets under the kidney capsule and normal mice received 300 islets. In streptozocin diabetic mice 300 islets restored normoglycemia; beta cell replication in transplanted islets was similar to replication in normal pancreas and beta cell mass in the graft remained constant. In contrast, 150 islets were insufficient to achieve normoglycemia; beta cell replication was increased initially but not by 18 or 30 d despite persistent hyperglycemia, and beta cell mass felt progressively. When islets were transplanted into normal recipients, beta cell replication remained normal but beta cells underwent atrophy and mass in the graft was substantially reduced. Therefore, with a successful islet transplant, in diabetic mice beta cell replication and mass remain constant. In contrast, when insufficient islet tissue is transplanted an initial increase in beta cell replication can not compensate for a decline in beta cell mass. When excessive islet tissue is transplanted, beta cell mass is reduced despite normal beta cell replication. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. RP MONTANA, E (reprint author), NEW ENGLAND DEACONESS HOSP,JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK-36836, DK-35449] NR 48 TC 175 Z9 176 U1 0 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 MAR PY 1993 VL 91 IS 3 BP 780 EP 787 DI 10.1172/JCI116297 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KR461 UT WOS:A1993KR46100007 PM 8450059 ER PT J AU KIUCHI, K SHANNON, RP KOMAMURA, K COHEN, DJ BIANCHI, C HOMCY, CJ VATNER, SF VATNER, DE AF KIUCHI, K SHANNON, RP KOMAMURA, K COHEN, DJ BIANCHI, C HOMCY, CJ VATNER, SF VATNER, DE TI MYOCARDIAL BETA-ADRENERGIC-RECEPTOR FUNCTION DURING THE DEVELOPMENT OF PACING-INDUCED HEART-FAILURE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ADENYLYL CYCLASE; BETA-1-ADRENERGIC RECEPTORS; BETA-2-ADRENERGIC RECEPTORS; CONGESTIVE HEART FAILURE; NOREPINEPHRINE ID HUMAN VENTRICULAR MYOCARDIUM; ADENYLATE-CYCLASE SYSTEM; FAILING HUMAN-HEART; PLASMA NOREPINEPHRINE; DOWN-REGULATION; DILATED CARDIOMYOPATHY; NERVOUS-SYSTEM; G-PROTEIN; BINDING; DESENSITIZATION AB The development of pacing-induced heart failure was studied in chronically instrumented, conscious dogs paced at a rate of 240 beats / min for 1 d (n = 6), 1 wk (n = 6), and 3-4 wk (n = 7). Left ventricular (LV) dP/dt was decreased (P < 0.01 25) at 1 d, LV end-diastolic pressure and heart rate were increased (P < 0.0125) at 1 wk, but clinical signs of heart failure were only observed after 3-4 wk of pacing. Plasma norepinephrine rose (P < 0.0 1 25) after 1 d of pacing, whereas LV norepinephrine was reduced (P < 0.01 25) only after 3-4 wk of pacing. Both the fraction of beta-adrenergic receptors binding agonist with high affinity and adenylyl cyclase activity decreased (P < 0.0125) after 1 d of pacing. Total beta-adrenergic receptor density was not changed at any time point, but beta1-adrenergic receptor density was decreased (P < 0.0125) after 1 wk. the functional activity of the guanine nucleotide binding protein, G(s), was not reduced, but the G(ialpha2) isoform of the a subunit of the GTP-inhibitory protein rose after 3-4 wk of pacing. Thus, myocardial beta-adrenergic signal transduction undergoes change shortly (1 d) after the initiation of pacing, before heart failure develops. The mechanism of beta-adrenergic receptor dysfunction in pacing-induced heart failure is characterized initially by elevated plasma levels of catecholamines, uncoupling of beta-adrenergic receptors, and a defect in the adenylyl cyclase catalytic unit. Selective down-regulation of beta1-adrenergic receptors, increases in G(ialpha2), and decreases in myocardial catecholamine levels occur as later events. C1 NEW ENGLAND REG PRIMATE RES CTR, 1 PINE HILL DR, POB 9102, SOUTHBOROUGH, MA 01772 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, DEPT MED, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT PEDIAT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CARDIAC UNIT, BOSTON, MA 02114 USA. RI bianchi, cesario/H-6238-2012 FU NHLBI NIH HHS [HL-38070, HL-37404, HL-33107] NR 58 TC 152 Z9 155 U1 0 U2 5 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 MAR PY 1993 VL 91 IS 3 BP 907 EP 914 DI 10.1172/JCI116312 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KR461 UT WOS:A1993KR46100022 PM 8383704 ER PT J AU BYRD, TF HORWITZ, MA AF BYRD, TF HORWITZ, MA TI REGULATION OF TRANSFERRIN RECEPTOR EXPRESSION AND FERRITIN CONTENT IN HUMAN MONONUCLEAR PHAGOCYTES - COORDINATE UP-REGULATION BY IRON TRANSFERRIN AND DOWN-REGULATION BY INTERFERON-GAMMA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE IRON; MACROPHAGE; CYTOKINES; LEGIONELLA-PNEUMOPHILA; TUMOR NECROSIS FACTOR-ALPHA ID TUMOR NECROSIS FACTOR; HUMAN-MONOCYTES; MESSENGER-RNA; INTRACELLULAR MULTIPLICATION; LEGIONELLA-PNEUMOPHILA; HEAVY-CHAIN; PROTEIN; BINDING; MACROPHAGES; LYMPHOCYTES AB We have investigated the regulation of key human iron binding proteins in mononuclear phagocytes by IFNgamma and iron transferrin. In a previous study, we demonstrated that IFNgamma down-regulates the expression on human monocytes of transferrin receptors, the major source of iron for the cell. In the present study, we show that IFNgamma also downregulates the intracellular concentration of ferritin, the major iron storage protein in the cell. By radioimmunoassay, the mean ferritin content of nonactivated monocytes was 361+/-107 fg/monocyte (mean+/-SEM) whereas the mean ferritin content of IFNgamma-activated monocytes was 64+/-13 fg/monocyte, an 82% reduction with activation (P < 0.01, t test). Consistent with its downregulating effect on these iron proteins, IFNgamma treatment also results in decreased iron incorporation. IFNgamma-activated monocytes incorporated 33% less iron from Fe-59-transferrin than nonactivated monocytes (P < 0.05, t test). Gel filtration chromatography revealed that incorporated iron is located primarily in ferritin in both nonactivated and IFNgamma-activated monocytes. Ferritin in IFNgamma-activated monocytes is saturated with approximately three times as much Fe-59 as ferritin in nonactivated monocytes. We have also explored the effect of iron transferrin on transferrin receptor expression and intracellular ferritin content in human monocytes. We have found that iron transferrin markedly upregulates both transferrin receptor expression and intracellular ferritin content in both nonactivated (2.3- and 1.3-fold, respectively) and IFNgamma-activated (3.4- and 2.9-fold, respectively) monocytes. This study demonstrates that transferrin receptor expression and intracellular ferritin content in human monocytes is unidirectionally and coordinately upregulated by iron transferrin and unidirectionally and coordinately downregulated by IFNgamma. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,DIV INFECT DIS,LOS ANGELES,CA 90024. RP BYRD, TF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,DIV INFECT DIS,WILSHIRE & SAWTELLE,W-111F,BLDG 500,LOS ANGELES,CA 90073, USA. FU NCI NIH HHS [CA-16042]; NIAID NIH HHS [AI-22421, AI-28825] NR 40 TC 120 Z9 121 U1 0 U2 5 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 MAR PY 1993 VL 91 IS 3 BP 969 EP 976 DI 10.1172/JCI116318 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KR461 UT WOS:A1993KR46100028 PM 8450071 ER PT J AU LIANG, TJ MAKDISI, WJ SUN, S HASEGAWA, K YING, Z WANDS, JR WU, CH WU, GY AF LIANG, TJ MAKDISI, WJ SUN, S HASEGAWA, K YING, Z WANDS, JR WU, CH WU, GY TI TARGETED TRANSFECTION AND EXPRESSION OF HEPATITIS-B VIRAL-DNA IN HUMAN HEPATOMA-CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE HEPATITIS-B VIRUS; REPLICATION; TARGETED EXPRESSION; ASIALOGLYCOPROTEIN ID VIRUS-DNA; HBV-DNA; TRANSIENT EXPRESSION; NUDE-MICE; GENE; LINE; REPLICATION; RECEPTOR; INVITRO; SYSTEM AB A soluble DNA carrier system consisting of an asialoglycoprotein covalently linked to poly-L-lysine was used to bind DNA and deliver hepatitis B virus (HBV) DNA constructs to asialoglycoprotein receptor-positive human hepatoma cells. 4 d after transfection with surface or core gene expression constructs, HBsAg and HBeAg in the media were measured to be 16 ng/ml and 32 U/ml per 10(7) cells, respectively. Antigen production was completely inhibited by the addition of an excess of asialoorosomucoid. On the other hand, asialoglycoprotein receptor-negative human hepatoma cells, SK-Hep1, did not produce any viral antigens under identical conditions after incubation with HBV DNA complexed to a conjugate composed of asialoorosomucoid and poly-L-lysine. Using a complete HBV genome construct, HBsAg and HBeAg levels reached 16 ng/ml and 16 U/ml per 10(7) cells, respectively. Northern blots revealed characteristic HBV RNA transcripts including 3.5-, 2.4-, and 2.1-kb fragments. Intracellular and extracellular HBV DNA sequences including relaxed circular, linear and single stranded forms were detected by Southern blot hybridization. Finally, 42-nm Dane particles purified from the spent culture medium were visualized by electron microscopy. This study demonstrates that a targetable DNA carrier system can transfect HBV DNA in vitro resulting in the production of complete HBV virions. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. UNIV CONNECTICUT,SCH MED,DEPT MED,DIV GASTROENTEROL HEPATOL,FARMINGTON,CT 06032. RP LIANG, TJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,GASTROINTESTINAL UNIT,JACKSON 812,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-54524, CA-46801]; NIDDK NIH HHS [DK-01952] NR 27 TC 21 Z9 22 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 MAR PY 1993 VL 91 IS 3 BP 1241 EP 1246 DI 10.1172/JCI116287 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KR461 UT WOS:A1993KR46100063 PM 8383700 ER PT J AU KRAMER, J ROSEN, FS COLTEN, HR RAJCZY, K STRUNK, RC AF KRAMER, J ROSEN, FS COLTEN, HR RAJCZY, K STRUNK, RC TI TRANSINHIBITION OF C1 INHIBITOR SYNTHESIS IN TYPE-1 HEREDITARY ANGIONEUROTIC-EDEMA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE HEREDITARY ANGIONEUROTIC EDEMA; C1-INHIBITOR; SYNTHESIS; TRANSLATION; TRANSINHIBITION ID MOLECULAR-BASIS; C1-INHIBITOR; DEFICIENCY; DELETION; GENE AB To ascertain the mechanism for decreased synthesis of C1 inhibitor (C1 INH) in certain patients with the autosomal dominant disorder hereditary angioneurotic edema, we studied expression of C1 INH in fibroblasts in which the mutant and wild type mRNA and protein could be distinguished because of deletion of exon 7 (DELTA(Ex7)). In the HANE DELTA(Ex7) cells, the amount of wild type mRNA (2.1 kb) was expressed at 52+/-2% (n = 5) of normal, whereas the mutant mRNA was 17+/-1% (n = 5) of normal. Rates of synthesis of both wild type and mutant proteins (11+/-3 and 3+/-1% of normal, respectively) were lower than predicted from the mRNA levels. There was no evidence of increased Cl INH protein catabolism. These data indicate that there are multiple levels of control of C1 INH synthesis in type I hereditary angioneurotic edema. Pretranslational regulation results in < 50% of the mutant truncated 1.9-kb mRNA. In addition, translational regulation results in decreased synthesis of both wild type and mutant C1 INH proteins. These data suggest a transinhibition of wild type C1 INH translation by mutant mRNA and / or protein. C1 WASHINGTON UNIV,SCH MED,DEPT PEDIAT,400 S KINGSHIGHWAY,ST LOUIS,MO 63110. WASHINGTON UNIV,ST LOUIS CHILDRENS HOSP,DIV ALLERGY & PULM MED,ST LOUIS,MO 63110. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,F69I,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-37591]; NIAID NIH HHS [AI-24836]; NIDDK NIH HHS [DK-26609] NR 16 TC 47 Z9 47 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 MAR PY 1993 VL 91 IS 3 BP 1258 EP 1262 DI 10.1172/JCI116290 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KR461 UT WOS:A1993KR46100066 PM 8450054 ER PT J AU CHUI, L ALBRITTON, W PASTER, B MACLEAN, I MARUSYK, R AF CHUI, L ALBRITTON, W PASTER, B MACLEAN, I MARUSYK, R TI DEVELOPMENT OF THE POLYMERASE CHAIN-REACTION FOR DIAGNOSIS OF CHANCROID SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID GENITAL ULCER DISEASE; HEMOPHILUS-DUCREYI; MONOCLONAL-ANTIBODIES; HAEMOPHILUS-DUCREYI; CLINICAL-DIAGNOSIS; RIBOSOMAL DNA; AMPLIFICATION; VARIANTS; PROBES; MEDIA AB The published nucleotide sequences of the 16S rRNA gene of Haemophilus ducreyi were used to develop primer sets and probes for the diagnosis of chancroid by polymerase chain reaction (PCR) DNA amplification. One set of broad specificity primers yielded a 303-bp PCR product from all bacteria tested. Two 16-base probes internal to this sequence were species specific for H. ducreyi when tested with 12 species of the families Pasteurellaceae and Enterobacteriaceae. The two probes in combination with the broad specificity primers were 100% sensitive with 51 strains of H. ducreyi isolated from six continents over a 15-year period. The direct detection of H. ducreyi from 100 clinical specimens by PCR showed a sensitivity of 83 to 98% and a specificity of 51 to 67%, depending on the number of amplification cycles. C1 UNIV ALBERTA,PUBL HLTH PROVINCIAL LAB,EDMONTON T6G 2J2,AB,CANADA. FORSYTH DENT CTR,BOSTON,MA 02115. UNIV MANITOBA,DEPT MED MICROBIOL,WINNIPEG R3T 2N2,MANITOBA,CANADA. FU NIDCR NIH HHS [DE08303] NR 34 TC 23 Z9 24 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 MAR PY 1993 VL 31 IS 3 BP 659 EP 664 PG 6 WC Microbiology SC Microbiology GA KM810 UT WOS:A1993KM81000034 PM 8458959 ER PT J AU MATTIA, AR WALDRON, MA SIERRA, LS AF MATTIA, AR WALDRON, MA SIERRA, LS TI USE OF THE UV PARALENS ADAPTER AS AN ALTERNATIVE TO CONVENTIONAL FLUORESCENCE MICROSCOPY FOR DETECTION OF PNEUMOCYSTIS-CARINII IN DIRECT IMMUNOFLUORESCENT MONOCLONAL ANTIBODY-STAINED PULMONARY SPECIMENS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; BRONCHOALVEOLAR LAVAGE SPECIMENS; INDUCED SPUTUM; PNEUMONIA; DIAGNOSIS AB The UV ParaLens light microscope adapter offers a useful and cost-effective alternative to conventional fluorescence microscopy for Pneumocystis carinii identification, particularly in AIDS patients. In a blinded study, in which 153 pulmonary specimens were examined for P. carinii by direct immunofluorescence, 40 of 42 specimens positive by fluorescence microscopy were also positive by ParaLens. No false positives were observed. C1 MASSACHUSETTS GEN HOSP,MICROBIOL LAB,BOSTON,MA 02114. RP MATTIA, AR (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 13 TC 4 Z9 4 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 MAR PY 1993 VL 31 IS 3 BP 720 EP 721 PG 2 WC Microbiology SC Microbiology GA KM810 UT WOS:A1993KM81000049 PM 8458971 ER PT J AU HOOVER, HC BRANDHORST, JS PETERS, LC SURDYKE, MG TAKESHITA, Y MADARIAGA, J MUENZ, LR HANNA, MG AF HOOVER, HC BRANDHORST, JS PETERS, LC SURDYKE, MG TAKESHITA, Y MADARIAGA, J MUENZ, LR HANNA, MG TI ADJUVANT ACTIVE SPECIFIC IMMUNOTHERAPY FOR HUMAN COLORECTAL-CANCER - 6.5-YEAR MEDIAN FOLLOW-UP OF A PHASE-III PROSPECTIVELY RANDOMIZED TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID AUTOLOGOUS TUMOR-CELL; RADIATION-THERAPY; CARCINOMA; VACCINE; CHEMOTHERAPY; METASTASES; BCG; FLUOROURACIL; LEVAMISOLE; GENERATION C1 ORGANON TEKNIKA CORP,BIOTECHNOL RES INST,ROCKVILLE,MD. RP HOOVER, HC (reprint author), MASSACHUSETTS GEN HOSP,DIV SURG ONCOL,COX-1,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 45079] NR 26 TC 207 Z9 210 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR PY 1993 VL 11 IS 3 BP 390 EP 399 PG 10 WC Oncology SC Oncology GA KP404 UT WOS:A1993KP40400003 PM 8445413 ER PT J AU GROSSMAN, SA FINKELSTEIN, DM RUCKDESCHEL, JC TRUMP, DL MOYNIHAN, T ETTINGER, DS AF GROSSMAN, SA FINKELSTEIN, DM RUCKDESCHEL, JC TRUMP, DL MOYNIHAN, T ETTINGER, DS TI RANDOMIZED PROSPECTIVE COMPARISON OF INTRAVENTRICULAR METHOTREXATE AND THIOTEPA IN PATIENTS WITH PREVIOUSLY UNTREATED NEOPLASTIC MENINGITIS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LEPTOMENINGEAL METASTASES; MENINGEAL CARCINOMATOSIS; NEUROTOXICITY; DIAGNOSIS; LEUKEMIA; TUMORS; FLOW C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNION UNIV,ALBANY,NY 12208. UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI 53706. RP GROSSMAN, SA (reprint author), JOHNS HOPKINS UNIV HOSP,CTR ONCOL,600 N WOLFE ST,BALTIMORE,MD 21205, USA. FU NCI NIH HHS [CA 06596, CA 16116, CA 23318] NR 27 TC 178 Z9 180 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 MAR PY 1993 VL 11 IS 3 BP 561 EP 569 PG 9 WC Oncology SC Oncology GA KP404 UT WOS:A1993KP40400026 PM 8445432 ER PT J AU GELBER, RD GOLDHIRSCH, A COATES, AS AF GELBER, RD GOLDHIRSCH, A COATES, AS TI ADJUVANT THERAPY FOR BREAST-CANCER - UNDERSTANDING THE OVERVIEW SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CLINICAL-TRIALS C1 OSPED CIVICO,INT BREAST CANC STUDY GRP,LUGANO,SWITZERLAND. ROYAL PRINCE ALFRED HOSP,DEPT MED ONCOL,AUSTRALIAN & NEW ZEALAND BREAST CANC TRIALS GRP,CAMPERDOWN,NSW 2050,AUSTRALIA. RP GELBER, RD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,IBCSG,CTR STAT,44 BINNEY ST,BOSTON,MA 02115, USA. NR 12 TC 32 Z9 32 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 MAR PY 1993 VL 11 IS 3 BP 580 EP 585 PG 6 WC Oncology SC Oncology GA KP404 UT WOS:A1993KP40400028 PM 8445434 ER PT J AU HOOVER, HC AF HOOVER, HC TI VACCINE ADJUVANT THERAPY FOR COLORECTAL-CANCER - VERY DRAMATIC OR HO-HUM - RESPONSE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter RP HOOVER, HC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR PY 1993 VL 11 IS 3 BP 586 EP 586 PG 1 WC Oncology SC Oncology GA KP404 UT WOS:A1993KP40400029 PM 8445435 ER PT J AU DUMOULIN, CL STEINBERG, FL YUCEL, EK DARROW, RD AF DUMOULIN, CL STEINBERG, FL YUCEL, EK DARROW, RD TI REDUCTION OF ARTIFACTS FROM BREATHING AND PERISTALSIS IN PHASE-CONTRAST MRA OF THE CHEST AND ABDOMEN SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Note DE ARTIFACTS; MAGNETIC RESONANCE ANGIOGRAPHY; MAGNETIC RESONANCE IMAGING, TECHNIQUES; CHEST; ABDOMEN ID MAGNETIC-RESONANCE ANGIOGRAPHY AB Strategies for the acquisition of temporally resolved phase-contrast angiography are described and demonstrated. Projections are acquired through the entire thickness of the subject permitting excitation geometries to be independent of image orientation. Minimal delays are used between the acquisition of oppositely flow-encoded data resulting in fewer artifacts from movement of nominally stationary tissue. A protocol that suppresses artifacts from both peristalsis and breathing is presented for the aortic arch and iliac arteries. C1 ROXAN RADIOL GRP,BEVERLY HILLS,CA. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP DUMOULIN, CL (reprint author), GE,CORP RES & DEV,POB 8,SCHENECTADY,NY 12301, USA. NR 14 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD MAR-APR PY 1993 VL 17 IS 2 BP 328 EP 332 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KT176 UT WOS:A1993KT17600031 PM 8454766 ER PT J AU WANG, CY STASHENKO, P AF WANG, CY STASHENKO, P TI CHARACTERIZATION OF BONE-RESORBING ACTIVITY IN HUMAN PERIAPICAL LESIONS SO JOURNAL OF ENDODONTICS LA English DT Article ID TUMOR-NECROSIS-FACTOR; PERIODONTAL-DISEASE; RESORPTION; INTERLEUKIN-1-BETA; PROSTAGLANDIN-E2; CYTOKINES; INVITRO; TISSUE AB Extracts of human periapical granulomas were tested for the presence of bone-resorbing activity. All granulomas (10 of 10) contained low but significant levels of bone-resorbing activity, ranging from 2.1 to 4.9% treatment - % control/mg specific Ca-45 release, as determined by the fetal rat long bone assay. Healthy periodontal ligament and dental pulp had no significant resorbing activity. In characterization studies, the resorbing activity in an extract pool was unaffected by the presence of polymyxin B, indicating an active moiety distinct from lipopolysaccharide. Resorbing activity was also unaffected by heating to 56-degrees-C for 30 min, but was completely abolished by proteinase K treatment or heating to 70-degrees-C, indicating that activity was largely protein mediated. Fast performance liquid chromatography gel filtration studies demonstrated that activity could be resolved to two major peaks, Of M(r) 30,000 to 60,000 (I), and 15,000 to 20,000 (II), with a minor peak present at <1,000 (III). Peak III was identified as prostaglandin E2 by radioimmunoassay. In inhibition studies, virtually all of the resorbing activity present was inhibited by anti-interleukin 1beta (69%) and anti-tumor necrosis factor beta (66%) antisera, whereas anti-interleukin 1alpha and antitumor necrosis factor a had no effect. Treatment with the cyclo-oxygenase inhibitor indomethacin also reduced activity by 74%. Taken together, these data demonstrate that most bone-resorbing activity present in chronic human periapical lesions is attributable to the action of resorptive cytokines interleukin 1beta and tumor necrosis factor beta, acting via both indomethac-independent and independent pathways. This activity may function to prevent reparative bone formation in the face of ongoing infection within the root canal system. C1 FORSYTH DENT CTR,DEPT IMMUNOL,140 FENWAY,BOSTON,MA 02115. FU NIDCR NIH HHS [DE-09018] NR 20 TC 45 Z9 51 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0099-2399 J9 J ENDODONT JI J. Endod. PD MAR PY 1993 VL 19 IS 3 BP 107 EP 111 DI 10.1016/S0099-2399(06)80503-0 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KP607 UT WOS:A1993KP60700001 PM 8509747 ER PT J AU NISHIKAWA, K GUO, YJ MIYASAKA, M TAMATANI, T COLLINS, AB SY, MS MCCLUSKEY, RT ANDRES, G AF NISHIKAWA, K GUO, YJ MIYASAKA, M TAMATANI, T COLLINS, AB SY, MS MCCLUSKEY, RT ANDRES, G TI ANTIBODIES TO INTERCELLULAR-ADHESION MOLECULE-1 LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 PREVENT CRESCENT FORMATION IN RAT AUTOIMMUNE GLOMERULONEPHRITIS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS; GOODPASTURE ANTIGEN; MONOCLONAL-ANTIBODY; NEPHRITIS; GLOMERULI; MACROPHAGE; RABBIT; INVIVO AB In patients with glomerulonephritis widespread crescents are associated with a poor prognosis. Crescent formation appears to depend on the migration of mononuclear cells into Bowman's space, and therefore the interaction between leukocytes and glomerular endothelium may be a critical event in the genesis of crescents. We performed the present study to determine the effects of mouse monoclonal antibodies to the adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function-associated antigen 1 (LFA-1) in a model of crescentic glomerulonephritis in Wistar-Kyoto rats, induced by immunization with bovine glomerular basement membrane (GBM). By 10-14 d after immunization, the rats had developed circulating anti-GBM antibodies, reactive with the alpha3 chain of type IV collagen (the Goodpasture antigen), accompanied by proteinuria, accumulation of rat immunoglobulin (Ig)G in the GBM, increased expression of ICAM-1 by glomerular endothelial cells, infiltration of glomerular tufts with LFA-1+ T cells and monocyte/macrophages, and early crescents. At 5 wk all rats had diffuse fibrocellular crescents, glomerular sclerosis, and tubulointerstitial damage. All rats developed severe renal insufficiency and died by 5 or 6 wk. The administration of monoclonal antibodies to rat ICAM-1 and LFA-1 markedly decreased the severity of the renal disease. In a group of rats injected three times a week with the monoclonal antibodies, from 2 d before immunization with GBM to day 14, glomerular abnormalities and proteinuria were virtually absent at day 14; even at 5 wk glomerular disease was quite mild, with only slight crescent formation and with only a mild decrease in renal function. When treatment was continued until 5 wk, the beneficial effects were even more marked, with virtual absence of crescents and with preservation of normal renal function. In a group of rats in which treatment was initiated on clay 14, shortly after the appearance of glomerular abnormalities, progression of the disease was appreciably retarded, and the decrease in renal function was inhibited. The kidneys of rats treated from days -2 to 14 with antibodies to ICAM-1 and LFA-1 showed bright linear staining for rat IgG along the GBM, which did not differ in intensity from that seen in untreated rats. Furthermore, the titers of anti-GBM antibodies at 2 wk in treated rats were not lower than that seen in most of the untreated rats. There was, however, moderate reduction of anti-GBM antibodies at 5 wk in the treated rats. In addition, in rats in which treatment was started after onset of the disease, the titers of anti-GBM antibodies did not decrease, although the progression of disease was inhibited. We conclude that the preventive or therapeutic effects of antibodies to ICAM-1 and LFA-1 in rat anti-GBM glomerulonephritis probably resulted mainly from interference with interaction between leukocytes and activated glomerular endothelium, although reduction in the autoimmune response may have contributed to the beneficial effects. The results raise the possibility that similar treatment might be used to limit the progression of glomerular damage in human crescentic glomerulonephritis. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. TOKYO METROPOLITAN INST MED SCI,DEPT IMMUNOL,TOKYO 113,JAPAN. FU NIDDK NIH HHS [DK-36807] NR 36 TC 206 Z9 207 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD MAR 1 PY 1993 VL 177 IS 3 BP 667 EP 677 DI 10.1084/jem.177.3.667 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KN886 UT WOS:A1993KN88600010 PM 8094735 ER PT J AU KANSAS, GS LEY, K MUNRO, JM TEDDER, TF AF KANSAS, GS LEY, K MUNRO, JM TEDDER, TF TI REGULATION OF LEUKOCYTE ROLLING AND ADHESION TO HIGH ENDOTHELIAL VENULES THROUGH THE CYTOPLASMIC DOMAIN OF L-SELECTIN SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID LYMPHOCYTE HOMING RECEPTOR; INTEGRIN BETA-1; EVOLUTIONARY CONSERVATION; MESENTERIC VENULES; CELL-INTERACTION; HUMAN HOMOLOG; MOLECULE-1; MIGRATION; PROTEINS; SUBUNIT AB L-selectin (leukocyte adhesion molecule 1/MEL-14), a member of the selectin family of cell adhesion molecules, mediates leukocyte rolling and leukocyte adhesion to endothelium at sites of inflammation. In addition, L-selectin mediates the binding of lymphocytes to high endothelial venules (HEV) of peripheral lymph nodes. The strong amino acid sequence conservation of the cytoplasmic domain of L-selectin between humans and mice suggests an important role for this region. Deletion of the COOH-terminal 11 amino acids from the approximately 17 amino acid cytoplasmic domain of L-selectin eliminated binding of lymphocytes to HEV in the in vitro frozen section assay, and also abolished leukocyte rolling in vivo in exteriorized rat mesenteric venules, but did not alter the lectin activity of L-selectin. Pretreatment of cells with cytochalasin B, which disrupts actin microfilaments, also abolished adhesion without affecting carbohydrate recognition. Therefore, the cytoplasmic domain of L-selectin regulates leukocyte adhesion to endothelium independent of ligand recognition, by controlling cytoskeletal interactions and/or receptor avidity. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FREE UNIV BERLIN,INST PHYSIOL,BERLIN 33,GERMANY. RP KANSAS, GS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,D714,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-54464] NR 39 TC 197 Z9 199 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 MAR 1 PY 1993 VL 177 IS 3 BP 833 EP 838 DI 10.1084/jem.177.3.833 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KN886 UT WOS:A1993KN88600026 PM 7679710 ER PT J AU HERIAN, AM TAYLOR, SL BUSH, RK AF HERIAN, AM TAYLOR, SL BUSH, RK TI ALLERGENIC REACTIVITY OF VARIOUS SOYBEAN PRODUCTS AS DETERMINED BY RAST INHIBITION SO JOURNAL OF FOOD SCIENCE LA English DT Article DE SOYBEAN; ALLERGENICITY; ANTIGENS; ANTIBODIES ID FOOD HYPERSENSITIVITY; SOY; PROTEINS; INFANTS; OIL AB Allergenic reactivity of soybean products (sprouts-Sp, tempeh-T, tofu-To, miso-M, mold hydrolyzed soy sauce-MHS, acid-hydrolyzed soy sauce-AHS, and hydrolyzed vegetable protein-HVP) was determined using RAST inhibition. All products inhibited binding of serum IgE from a pool of soy-allergic adults to raw soybean extract bound to microcrystalline cellulose, showing competitive inhibition with increasing protein. M,T, To and MHS showed competitive inhibition only at much higher protein concentrations, suggesting fermentation may alter or destroy allergenic epitopes. Selective destruction of epitopes was seen for MHS, To, and possibly M and T where inhibition curve slopes were not identical to intact material. Probably protein(s) with antigens common to raw soybean survived during processing of HVP and germination of sprouts. Based on RAST inhibition, these products are potentially hazardous to soybean-allergic individuals. C1 UNIV NEBRASKA,DEPT FOOD SCI & TECHNOL,LINCOLN,NE 68583. UNIV NEBRASKA,CTR FOOD PROC,LINCOLN,NE 68583. UNIV WISCONSIN,DEPT FOOD MICROBIOL & TOXICOL,FOOD RES INST,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,CTR CLIN SCI,DEPT MED,MADISON,WI 53792. NR 16 TC 46 Z9 53 U1 0 U2 8 PU INST FOOD TECHNOLOGISTS PI CHICAGO PA SUITE 300 221 N LASALLE ST, CHICAGO, IL 60601-1291 SN 0022-1147 J9 J FOOD SCI JI J. Food Sci. PD MAR-APR PY 1993 VL 58 IS 2 BP 385 EP 388 DI 10.1111/j.1365-2621.1993.tb04281.x PG 4 WC Food Science & Technology SC Food Science & Technology GA LV597 UT WOS:A1993LV59700038 ER PT J AU FREEDMAN, AS RHYNHART, K NOJIMA, Y SVAHN, J ELISEO, L BENJAMIN, CD MORIMOTO, C VIVIER, E AF FREEDMAN, AS RHYNHART, K NOJIMA, Y SVAHN, J ELISEO, L BENJAMIN, CD MORIMOTO, C VIVIER, E TI STIMULATION OF PROTEIN TYROSINE PHOSPHORYLATION IN HUMAN B-CELLS AFTER LIGATION OF THE BETA-1 INTEGRIN VLA-4 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN LYMPHOCYTES-B; CLASS-II MOLECULES; T-CELL; ADHESION MOLECULE-1; ANTIGEN RECEPTOR; MEMBRANE IMMUNOGLOBULIN; MONOCLONAL-ANTIBODY; SIGNAL TRANSDUCTION; ENDOTHELIAL-CELLS; CD4+ LYMPHOCYTES AB B lymphocytes express several adhesion molecules that are involved in cell-cell and cell-extracellular matrix interactions. The alpha4beta1 integrin VLA-4, expressed on pre-B and mature/activated B cells, mediates adhesion of these cells to its two ligands, VCAM-1 and fibronectin. Recent evidence suggests that VLA-4 is involved in T lymphocyte activation; however, relatively little is known of the role of VLA-4 in B cell differentiation. To begin to assess the potential involvement of VLA-4 in B cell activation, we have examined the effect of ligation of VLA-4 on protein tyrosine phosphorylation in B cells. We found that cross-linking of VLA-4 by either mAb or natural ligands (i.e., VCAM-1 and the FN-40 cleavage fragment of fibronectin) induced the tyrosine phosphorylation of a 110-kDa protein in a human pre-B cell line (Nalm-6), an EBV-transformed B cell line (SB), and normal tonsillar B cells. These findings suggest that VLA-4 can activate a tyrosine kinase in B cells and B cell lines. These signals may be involved in the subsequent differentiation of pre-B and mature B cells within specific microenvironments where VLA-4 mediated adhesion is operational. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. BIOGEN,CAMBRIDGE,MA 02142. RP FREEDMAN, AS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-55207]; NIAID NIH HHS [AI-12069]; NIAMS NIH HHS [AR-33713] NR 67 TC 77 Z9 77 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 1993 VL 150 IS 5 BP 1645 EP 1652 PG 8 WC Immunology SC Immunology GA KN532 UT WOS:A1993KN53200001 PM 7679689 ER PT J AU ROBERTSON, MJ MANLEY, TJ DONAHUE, C LEVINE, H RITZ, J AF ROBERTSON, MJ MANLEY, TJ DONAHUE, C LEVINE, H RITZ, J TI COSTIMULATORY SIGNALS ARE REQUIRED FOR OPTIMAL PROLIFERATION OF HUMAN NATURAL-KILLER-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NECROSIS FACTOR-ALPHA; BLOOD NK CELLS; INTERLEUKIN-2 RECEPTOR; IL-2 RECEPTOR; TYROSINE PHOSPHORYLATION; HUMAN-LYMPHOCYTES; T-CELLS; ACTIVATION ANTIGENS; STIMULATORY FACTOR; LYMPHOKINE GENES AB CD56dim NK cells, which comprise approximately 90% of human peripheral blood NK cells, respond to IL-2 with cytokine production, up-regulation of functionally relevant surface molecules, and augmented cytolytic activity. Nevertheless, CD56dim NK cells proliferate poorly in response to IL-2 alone. We found that other NK cell mitogens, including IL-4, IL-7, and IL-12, also induced little proliferation of CD56dim NK cells. Indeed, IL-2 stimulated at least 10-fold more NK cell proliferation than did IL-4, IL-7, or IL-12. In contrast, leukocyte-conditioned medium (LCM) induced two-to threefold greater proliferation of CD56dim NK cells than did optimal concentrations of IL-2. Although the calcium ionophore ionomycin did not stimulate proliferation by itself, it markedly augmented LCM-induced proliferation of CD56dim NK cells. Proliferation in response to either LCM alone or LCM together with ionomycin was almost completely abrogated by anti-IL-2R antibodies. Thus, IL-2 appears to be necessary but not sufficient for optimal proliferation of CD56dim NK cells. LCM-induced proliferation of ionomycin-activated CD56dim NK cells was inhibited 24% by anti-IL-1 heteroantisera and 57% by anti-TNF antisera; a combination of both antisera inhibited proliferation by 73%. Furthermore, although rIL-1 and TNF did not induce proliferation by themselves, both cytokines could augment IL-2-induced proliferation of resting or ionomycin-activated NK cells. Hence IL-1 and TNF do not appear to be primary NK cell mitogens, but rather accessory factors that can enhance IL-2-dependent NK cell proliferation. Stimulation through CD2 or CD16 Ag did not enhance LCM-induced NK cell proliferation. However, stimulation with NK-sensitive K562 cells strongly augmented CD56dim NK cell proliferation to LCM or to IL-2, IL-1, and TNF in combination. NK-resistant Daudi cells did not promote the proliferation of highly purified NK cells. Thus, NK cell proliferation may be enhanced by triggering through putative receptors for natural killing, and ionomycin may mimic such triggering. Although IL-2 by itself can induce NK cell proliferation, most NK cells resemble T and B lymphocytes in that they require multiple signals for optimal proliferation. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ROBERTSON, MJ (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 [CA-41619] NR 55 TC 90 Z9 90 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 1993 VL 150 IS 5 BP 1705 EP 1714 PG 10 WC Immunology SC Immunology GA KN532 UT WOS:A1993KN53200007 PM 7679691 ER PT J AU ZWEERINK, HJ GAMMON, MC UTZ, U SAUMA, SY HARRER, T HAWKINS, JC JOHNSON, RP SIROTINA, A HERMES, JD WALKER, BD BIDDISON, WE AF ZWEERINK, HJ GAMMON, MC UTZ, U SAUMA, SY HARRER, T HAWKINS, JC JOHNSON, RP SIROTINA, A HERMES, JD WALKER, BD BIDDISON, WE TI PRESENTATION OF ENDOGENOUS PEPTIDES TO MHC CLASS I-RESTRICTED CYTOTOXIC LYMPHOCYTES-T IN TRANSPORT DELETION MUTANT T2-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; HLA-B ANTIGENS; MONOCLONAL-ANTIBODY; VIRAL PEPTIDE; CELLS; GENE; EXPRESSION; SEQUENCE; HLA-B27; REGION AB The ability of minigene-encoded viral peptide epitopes to be presented by class I molecules in the absence of MHC-encoded transporters has been evaluated in mutant T2 cells. These cells have a large deletion in the class II MHC region that includes the known transporter protein for antigenic peptides and proteasome genes and they are defective in presenting viral epitopes to CTL. T2 cells that express minigenes encoding the influenza virus matrix peptide 58-66 (GILGFVFTL) and two HTLV 1 Tax peptides 11-19 (LLFGYPVYV) and 12-19 were lysed by HLA-A2-restricted peptide-specific CTL. Minigene expression of a HLA-A2-restricted HIV reverse transcriptase peptide 476-484 (ILKEPVHGV) with three charged residues sensitized T2 cells poorly for lysis by HIV-specific CTL unless the peptide was preceded by an endoplasmic reticulum translocation signal sequence. Expression of an influenza virus nucleoprotein peptide 383-391 (SRYWAIRTR) with three charged arginine residues did sensitize HLA-B27+ T2 cells for lysis by peptide-specific CTL. These and other results with endogenously expressed peptide analogs in which hydrophobic and charged amino acids were interchanged demonstrate that antigenic peptides can be translocated from the cytoplasm into the class I Ag presentation pathway independent of MHC-encoded transporters; and that peptide hydrophobicity appears not to be a major determinant in selecting peptides for this alternate pathway. C1 NINCDS,NEUROIMMUNOL BRANCH,MOLEC IMMUNOL SECT,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ZWEERINK, HJ (reprint author), MERCK SHARP & DOHME LTD,DEPT AUTOIMMUNE DIS RES,RAHWAY,NJ 07065, USA. NR 45 TC 96 Z9 97 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 MAR 1 PY 1993 VL 150 IS 5 BP 1763 EP 1771 PG 9 WC Immunology SC Immunology GA KN532 UT WOS:A1993KN53200013 PM 7679694 ER PT J AU PARHAMISEREN, B KUSSIE, PH STRONG, RK MARGOLIES, MN AF PARHAMISEREN, B KUSSIE, PH STRONG, RK MARGOLIES, MN TI CONSERVATION OF BINDING-SITE GEOMETRY AMONG P-AZOPHENYLARSONATE-SPECIFIC ANTIBODIES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTI-ARSONATE IDIOTYPE; ARS-A ANTIBODIES; JUNCTIONAL DIVERSITY; DIRECTED MUTAGENESIS; VARIABLE REGION; 3-DIMENSIONAL STRUCTURE; IMMUNE-RESPONSE; SOMATIC MUTATIONS; GENETIC-BASIS; AFFINITY AB Murine A/J anti-p-azophenylarsonate mAb that express a dominant cross-reactive Id are encoded by a single set of germ-line V(H) and V(L) region genes. The crystal structure of the Fab of antibody 36-71, which uses this canonical set of genes but is somatically mutated, was previously determined. An Fab 36-71:phenylarsonate complex was modeled, identifying amino acid side chains that were proposed as contact residues to hapten. The remarkable conservation of these residues among canonical anti-p-azophenylarsonate antibodies suggested that the overall binding site geometry was maintained among somatically mutated antiarsonate monoclonal antibodies. To test this hypothesis, we used the germ-line-encoded antibody 36-65 to construct mutant antibodies, using oligonucleotide-directed mutagenesis, which differed only at the putative H chain hapten-contacting residues, and measured their hapten binding. A framework residue at H chain position 47 involved in a hydrogen bond network with CDR residues was also mutated. Substitution of several amino acids at each position permitted evaluation of the stereochemical requirements for binding. The results indicate the importance of aromatic stacking of two H chain tyrosine residues against the phenyl ring of the hapten in maintaining affinity, as well as strict complementarity at H chain position 35. The results are consistent with the crystal model of the combining site, and provide further evidence for conservation of the three-dimensional binding site motif among antiarsonate antibodies that bear a dominant heritable Id. C1 CALTECH, PASADENA, CA 92115 USA. MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. FU NCI NIH HHS [R01-CA24432] NR 39 TC 24 Z9 24 U1 1 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 MAR 1 PY 1993 VL 150 IS 5 BP 1829 EP 1837 PG 9 WC Immunology SC Immunology GA KN532 UT WOS:A1993KN53200020 PM 8436818 ER PT J AU BHATT, SM LAURETANO, A CABELLOS, C HALPIN, C LEVINE, RA XU, WZ NADOL, JB TUOMANEN, E AF BHATT, SM LAURETANO, A CABELLOS, C HALPIN, C LEVINE, RA XU, WZ NADOL, JB TUOMANEN, E TI PROGRESSION OF HEARING-LOSS IN EXPERIMENTAL PNEUMOCOCCAL MENINGITIS - CORRELATION WITH CEREBROSPINAL-FLUID CYTOCHEMISTRY SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID INFLUENZAE TYPE-B; CHILDHOOD BACTERIAL-MENINGITIS; AUDITORY EVOKED-POTENTIALS; THERAPY; CHILDREN; IMPAIRMENT; SEQUELA; INFANTS; COCHLEA AB The development of hearing loss and concomitant cerebrospinal fluid (CSF) cytochemical changes in a model of pneumococcal meningitis were examined. Rabbits were injected intracisternally with 10(5) pneumococci. Auditory evoked potentials to clicks and to 10- and 1-kHz tone bursts were recorded hourly; CSF was analyzed every 4 h. Sensorineural hearing loss developed in all animals beginning 12 h after infection and progressed to severe deafness. The onset of hearing loss was preceded by a CSF leukocytosis of >2000 cells/muL and elevation of CSF protein and lactate concentrations to less-than-or-equal-to 1 mg/mL. Temporal bone histopathology showed pneumococci and leukocytes extending from the CSF to the perilymph via the cochlear aqueduct. Hearing loss can develop early in the course of meningitis and is preceded by the abrupt onset of inflammatory changes in CSF. Progression of hearing loss is rapid and proceeds from cochlear base to apex in parallel with the degree of inflammation. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT LARYNGOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT NEUROL,BOSTON,MA 02114. FU NIAID NIH HHS [AI-27938]; NIDCD NIH HHS [DC-00119] NR 38 TC 55 Z9 56 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAR PY 1993 VL 167 IS 3 BP 675 EP 683 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KN152 UT WOS:A1993KN15200021 PM 8440938 ER PT J AU DUNCAN, LM BERWICK, M BRUIJN, JA BYERS, HR MIHM, MC BARNHILL, RL AF DUNCAN, LM BERWICK, M BRUIJN, JA BYERS, HR MIHM, MC BARNHILL, RL TI HISTOPATHOLOGIC RECOGNITION AND GRADING OF DYSPLASTIC MELANOCYTIC NEVI - AN INTEROBSERVER AGREEMENT STUDY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID MALIGNANT-MELANOMA; CUTANEOUS MELANOMA; PRECURSOR LESIONS; RISK; DIAGNOSIS; PHENOTYPE; MARKERS; ATYPIA AB Before the controversies surrounding dysplastic melanocytic nevi are resolved, dermatopathologists must be able to reliably distinguish dysplastic nevi from common acquired nevi and malignant melanoma. To establish whether grading of melanocytic dysplasia has any biologic relevance, dermatopathologists must be able to consistently recognize two or more grades of atypia. We studied the concordance among five dermatopathologists for recognition and grading of 60 nevomelanocytic lesions. Ten cases from each of the following categories of melanocytic proliferation were retrieved from the Massachusetts General Hospital files: 1) common melanocytic nevi, 2) melanocytic nevi with features of dysplastic nevi, 3) dysplastic nevi with slight cytologic atypia, 4) dysplastic nevi with moderate cytologic atypia, 5) dysplastic nevi with severe cytologic atypia, and 6) primary malignant melanoma. The slides were reviewed independently; no discussion of diagnostic criteria preceded the review. Overall concordance for diagnosing dysplastic nevi was 77%, with a kappa statistic of 0.55-0.84. Furthermore, in grading dysplastic nevi, experienced dermatopathologists had a concordance ranging from 35% to 58% (kappa value 0.38-0.47). Those with less experience in grading dysplastic nevi had a concordance of 16-65% (kappa value 0.05-0.24). The five observers in this study reliably distinguished dysplastic nevi from common acquired nevi and malignant melanoma. Further refinement of the criteria for grading of nevomelanocytic dysplasia and experience in grading are critical for accuracy in subcategorization of dysplastic nevi. Consistent, reproducible subcategorization of dysplastic nevi is a requisite before the issue of biologic or prognostic relevance of grading (dysplastic nevi) can be addressed. This study supports the validity of existing criteria for the diagnosis of dysplastic nevi because the problems in diagnosis were at the limits of the spectrum, namely, discrimination of slightly atypical dysplastic nevi from common nevi and severely atypical dysplastic nevi from radial growth phase melanoma. C1 LAB PATHOL,LEIDEN,NETHERLANDS. CANC PREVENT RES INST,NEW YORK,NY. MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. RI Berwick, Marianne/E-9608-2010; Duncan, Lyn/E-9878-2013 NR 35 TC 62 Z9 62 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAR PY 1993 VL 100 IS 3 BP S318 EP S321 DI 10.1038/jid.1993.55 PG 4 WC Dermatology SC Dermatology GA KR121 UT WOS:A1993KR12100034 PM 8440913 ER PT J AU KIRCHHAUSEN, T STAUNTON, DE SPRINGER, TA AF KIRCHHAUSEN, T STAUNTON, DE SPRINGER, TA TI LOCATION OF THE DOMAINS OF ICAM-1 BY IMMUNOLABELING AND SINGLE-MOLECULE ELECTRON-MICROSCOPY SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE STRUCTURE; ADHESION RECEPTORS; EPITOPE MAPPING; ICAM-1 ID INTERCELLULAR-ADHESION MOLECULE-1; IMMUNE-SYSTEM; RHINOVIRUS; RECEPTOR; BINDING; LFA-1 AB Intercellular adhesion molecule 1 (ICAM-1), a member of the immunoglobulin gene superfamily, is a cell surface glycoprotein with an extracellular domain comprising five immunoglobulin-like domains. Soluble ICAM-1, a recombinant protein truncated at the transmembrane domain, has a rod-like shape, 19 nm long overall, with a characteristic bend 7.6 nm from one end of the molecule. Because the link between domain D2 and domain D3 is proline rich, it has been proposed that the short arm contains domains D1 and D2 and the long arm contains domains D3-D5. We used single-molecule electron microscopy of soluble ICAM-1 decorated with monoclonal antibodies specific for domains D1 and D4 to show that the bend instead lies between domains D3 and D4. Therefore, the short arm lies closer to the plasma membrane, whereas the long arm, containing all the known ligand binding sites on ICAM-1, is positioned toward the target cell surface. C1 HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP KIRCHHAUSEN, T (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,200 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA31798] NR 13 TC 39 Z9 40 U1 0 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD MAR PY 1993 VL 53 IS 3 BP 342 EP 346 PG 5 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA KV986 UT WOS:A1993KV98600018 PM 8095966 ER PT J AU BONVENTRE, JV KOROSHETZ, WJ AF BONVENTRE, JV KOROSHETZ, WJ TI PHOSPHOLIPASE-A(2) (PLA(2)) ACTIVITY IN GERBIL BRAIN - CHARACTERIZATION OF CYTOSOLIC AND MEMBRANE-ASSOCIATED FORMS AND EFFECTS OF ISCHEMIA AND REPERFUSION ON ENZYMATIC-ACTIVITY SO JOURNAL OF LIPID MEDIATORS LA English DT Article DE PHOSPHOLIPASES; PHOSPHOLIPIDS; CALCIUM; FATTY ACIDS; STROKE; MITOCHONDRIA; MICROSOMES ID LONG-TERM POTENTIATION; PROTEIN-KINASE-C; FREE FATTY-ACIDS; PLATELET-ACTIVATING-FACTOR; TRANSIENT CEREBRAL-ISCHEMIA; ARACHIDONIC-ACID; RAT-BRAIN; QUISQUALATE RECEPTORS; LIPOXYGENASE METABOLITES; CALCIUM-CONCENTRATION AB Phospholipases A2 comprise a family of enzymes that hydrolyze the acyl bond at the sn-2 position of phospholipids to generate free fatty acids and lysophospholipids. In the central nervous system products of PLA2 regulate neurotransmission. In addition, the lysophospholipids, free fatty acids, eicosanoids, platelet activating factor and reactive oxygen species, generated by enhanced PLA2 activity and arachidonic acid metabolism, may be responsible for many destructive cellular processes in neuronal tissue. There are interactions between glutamate and PLA2 and its products which suggest that PLA2 activity plays an important role in excitotoxic neuronal cell injury associated with ischemia. Our laboratory has demonstrated that multiple forms of Ca2+-dependent PLA2 are present in the gerbil brain. These forms differ from previously described forms and from each other. After ischemia and reperfusion, cytosolic, mitochondrial/synaptosomal and microsomal PLA2 enzymatic activities are enhanced. These stable modifications of enzymatic activity cannot be explained by a direct effect of Ca2+ alone and our data suggest that regulatory influences other than Ca2+ may play an important role in PLA2 activation and mediation of cellular injury after an ischemic insult. C1 MASSACHUSETTS GEN HOSP, MED SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROL SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT NEUROL, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK 39773]; NINDS NIH HHS [NS 10828] NR 88 TC 50 Z9 50 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8319 J9 J LIPID MEDIATOR JI J. Lipid Mediat. PD MAR-APR PY 1993 VL 6 IS 1-3 BP 457 EP 471 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LE580 UT WOS:A1993LE58000055 PM 8358004 ER PT J AU WRAY, SH AF WRAY, SH TI THE MANAGEMENT OF ACUTE VISUAL FAILURE SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID ISCHEMIC OPTIC NEUROPATHY; RETINAL ARTERY-OCCLUSION; SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTIPHOSPHOLIPID ANTIBODIES; CLINICAL PROFILE; NATURAL-HISTORY; DISEASE RP WRAY, SH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROVISUAL DISORDERS UNIT,BOSTON,MA 02114, USA. NR 62 TC 15 Z9 16 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD MAR PY 1993 VL 56 IS 3 BP 234 EP 240 DI 10.1136/jnnp.56.3.234 PG 7 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA KR145 UT WOS:A1993KR14500003 PM 8459237 ER PT J AU MOSKOWITZ, MA NOZAKI, K KRAIG, RP AF MOSKOWITZ, MA NOZAKI, K KRAIG, RP TI NEOCORTICAL SPREADING DEPRESSION PROVOKES THE EXPRESSION OF C-FOS PROTEIN-LIKE IMMUNOREACTIVITY WITHIN TRIGEMINAL NUCLEUS CAUDALIS VIA TRIGEMINOVASCULAR MECHANISMS SO JOURNAL OF NEUROSCIENCE LA English DT Article DE C-FOS IMMUNOREACTIVITY; SPREADING DEPRESSION (SD); TRIGEMINOVASCULAR MECHANISMS; TRIGEMINAL NUCLEUS CAUDALIS (TNC); SUMATRIPTAN; MIGRAINE; MENINGES ID MIDDLE CEREBRAL-ARTERY; GENE-RELATED PEPTIDE; SUBSTANCE-P; BLOOD-VESSELS; NERVOUS-SYSTEM; DORSAL HORN; SPINAL-CORD; RAT; BRAIN; STIMULATION AB The effects of neocortical spreading depression (SD) on the expression of immunoreactive c-fos protein were examined within the superficial laminae of trigeminal nucleus caudalis (TNC), a brainstem region processing nociceptive information. KCl was microinjected into the left parietal cortex at 9 min intervals over 1 hr, and SD was detected by a shift in interstitial DC potential within adjacent frontal cortex. The stained cells in lower brainstem and upper cervical spinal cord were counted on both sides after tissues were sectioned (50 mum) and processed for c-fos protein-like immunoreactivity (LI) using a rabbit polyclonal antiserum. C-fos protein-LI was visualized in the ventrolateral TNC, chiefly in laminae I and IIo and predominantly within spinal segment C1-2 (e. g., 1.5 to 4.5 mm from obex) ipsilaterally. SD significantly increased cell staining within ipsilateral TNC. The ratio of cells in laminae I and IIo on the left: right sides was 1.32 +/- 0.13 after 1 m KCl, as compared to 1.06 +/- 0.05 in control animals receiving 1 m NaCl instead of KCl microinjections (p < 0.01). The ratio was reduced to an insignificant difference after chronic surgical transection of meningeal afferents and recurrent SD (1.09 +/- 0.11). Pretreatment with intravenous sumatriptan, a 5-HT1-like receptor agonist that selectively blocks meningeal C-fibers and attenuates c-fos protein-LI within TNC after noxious meningeal stimulation, also reduced the ratio to an insignificant difference (1.10 +/-0.09). Sumatriptan or chronic surgical transection of meningeal afferents, however, did not reduce the ability of KCl microinjections to induce SD. On the other hand, combined hyperoxia and hypercapnia not only reduced the number of evoked SDs from 6.3 +/- 1.0 to 2.5 +/- 1.2 after 0.15 m KCl microinjection, but also significantly (p < 0.01) reduced associated c-fos protein-LI in TNC. These data indicate that multiple neocortical SDs activate cells within TNC. The increase in c-fos protein-LI, observed predominantly ipsilaterally, was probably mediated by SD-induced stimulation of ipsilaterally projecting unmyelinated C-fibers innervating the meninges. If true, this is the first report demonstrating that neurophysiological events within cerebral cortex can activate brainstem regions involved in the processing of nociceptive information via trigeminovascular mechanisms. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROSURG SERV,BOSTON,MA 02114. UNIV CHICAGO,DEPT NEUROL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT PHARMACOL & PHYSIOL SCI,CHICAGO,IL 60637. RP MOSKOWITZ, MA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,NEUROSURG SERV,BOSTON,MA 02114, USA. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [R01 NS019108, NS-19108, NS21558, R01 NS019108-23] NR 70 TC 233 Z9 236 U1 1 U2 2 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD MAR PY 1993 VL 13 IS 3 BP 1167 EP 1177 PG 11 WC Neurosciences SC Neurosciences & Neurology GA KP711 UT WOS:A1993KP71100026 PM 8382735 ER PT J AU MAXWELL, M GALANOPOULOS, T NEVILLEGOLDEN, J ANTONIADES, HN AF MAXWELL, M GALANOPOULOS, T NEVILLEGOLDEN, J ANTONIADES, HN TI EXPRESSION OF ANDROGEN AND PROGESTERONE RECEPTORS IN PRIMARY HUMAN MENINGIOMAS SO JOURNAL OF NEUROSURGERY LA English DT Article DE HORMONE RECEPTOR; MENINGIOMA; GENE EXPRESSION; PROTOONCOGENE; EPIDERMAL GROWTH FACTOR ID EPIDERMAL GROWTH-FACTOR; STEROID-HORMONE RECEPTORS; BREAST CANCER-CELLS; PRIMARY HUMAN ASTROCYTOMAS; ESTROGEN-RECEPTOR; COMPLEMENTARY-DNA; BINDING-ACTIVITY; MESSENGER-RNA; MCF-7 CELLS; FACTOR PDGF AB Meningiomas are common brain tumors that show a predilection for females and become more aggressive during pregnancy and menses. The existence of gender-specific hormone receptors in meningiomas has long been a matter of controversy; the recent cloning of androgen, estrogen, and progesterone receptors has facilitated their direct evaluation. The authors have demonstrated the expression of androgen and progesterone receptor messenger ribonucleic acid and protein product in nine primary human meningiomas by Northern blot analysis. Cellular localization was achieved by in situ hybridization analysis. Estrogen receptor expression was not detected. Normal adult meninges were shown to express very low levels of both androgen and progesterone receptors. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. UNIV OXFORD,RADCLIFFE INFIRM,DEPT NEUROPATHOL,OXFORD OX2 6HE,ENGLAND. CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. FU NCI NIH HHS [CA-09382, CA-30101]; NHLBI NIH HHS [HL-29583] NR 61 TC 61 Z9 62 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 MAR PY 1993 VL 78 IS 3 BP 456 EP 462 DI 10.3171/jns.1993.78.3.0456 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA KN936 UT WOS:A1993KN93600013 PM 8433149 ER PT J AU TAKAMIYA, Y FRIEDLANDER, RM BREM, H MALICK, A MARTUZA, RL AF TAKAMIYA, Y FRIEDLANDER, RM BREM, H MALICK, A MARTUZA, RL TI INHIBITION OF ANGIOGENESIS AND GROWTH OF HUMAN NERVE-SHEATH TUMORS BY AGM-1470 SO JOURNAL OF NEUROSURGERY LA English DT Article DE ANGIOGENESIS; AGM-1470; NERVE-SHEATH TUMOR; SCHWANNOMA; NEUROFIBROMATOSIS; NEUROFIBROMA; NEUROFIBROSARCOMA ID BILATERAL ACOUSTIC NEUROFIBROMATOSIS; SUBRENAL CAPSULE; NEUROFIBROSARCOMA; FUMAGILLIN; NEUROMAS; ANALOGS; CELLS; MOUSE AB The effectiveness of AGM-1470, a potent, fungal-derived inhibitor of angiogenesis, in suppressing the neovascularization and growth of human Schwann cell tumors was tested in six schwannomas, seven neurofibromas, and one neurofibrosarcoma. Tumor fragments from surgical specimens were implanted into the subrenal capsule of 348 nude mice (nu/nu). Seven days after implantation, the tumors were measured and vascularity was graded. The animals were then randomly assigned to one of two groups, to receive either saline (control group) or systemic AGM-1470 treatment. After 2 to 6 weeks of treatment, tumor size and degree of vascularity were recorded. In the six different schwannomas implanted into 138 mice, the average vascular grade in the control group after 2 weeks of treatment increased from 2.2 to 3.2 (+1.0), while in the AGM-1470-treated group it decreased from 2.2 to 1.7 (-0.5) (p < 0.01). In the seven different neurofibromas implanted into 158 mice, the change in the average vascular grade in control and AGM-1470-treated animals was +0.5 and -1.0, respectively (p < 0.01). In the one neurofibrosarcoma implanted into 52 mice, the change in average vascular grade in each group during the 6-week treatment period was +1.9 and -1.0, respectively (p < 0.01). Neurofibrosarcoma growth after 6 weeks of AGM-1470 treatment was only 8.5% of the growth found in the control animals (p < 0.01). This study determined that AGM-1470 is effective in inhibiting angiogenesis and the growth of human nerve-sheath tumors. C1 GEORGETOWN UNIV,MED CTR,DEPT NEUROSURG,3800 RESERVOIR RD NW,WASHINGTON,DC 20007. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG ONCOL LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,NEUROSURG SERV,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Friedlander, Robert/A-2845-2016 OI Friedlander, Robert/0000-0003-4423-9219 NR 34 TC 89 Z9 89 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 MAR PY 1993 VL 78 IS 3 BP 470 EP 476 DI 10.3171/jns.1993.78.3.0470 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA KN936 UT WOS:A1993KN93600015 PM 8433151 ER PT J AU OGILVY, CS OJEMANN, RG AF OGILVY, CS OJEMANN, RG TI POSTERIOR-FOSSA CRANIOTOMY FOR LESIONS OF THE CEREBELLOPONTINE ANGLE - TECHNICAL NOTE SO JOURNAL OF NEUROSURGERY LA English DT Note DE CEREBELLOPONTINE ANGLE; CRANIOTOMY; OPERATIVE EXPOSURE; SURGICAL TECHNIQUE; INSTRUMENTATION AB A safe technique is described for performing a lateral posterior fossa craniotomy to gain access to the cerebellopontine angle. The method makes use of currently available high-speed air drills. Thus, it is possible to replace the removed bone at the conclusion of the procedure and to re-establish normal tissue planes while providing rigid protection to the posterior fossa. RP OGILVY, CS (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 15 Z9 16 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 MAR PY 1993 VL 78 IS 3 BP 508 EP 509 DI 10.3171/jns.1993.78.3.0508 PG 2 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA KN936 UT WOS:A1993KN93600023 PM 8433159 ER PT J AU LAURENCIN, CT GERHART, T WITSCHGER, P SATCHER, R DOMB, A ROSENBERG, AE HANFF, P EDSBERG, L HAYES, W LANGER, R AF LAURENCIN, CT GERHART, T WITSCHGER, P SATCHER, R DOMB, A ROSENBERG, AE HANFF, P EDSBERG, L HAYES, W LANGER, R TI BIOERODIBLE POLYANHYDRIDES FOR ANTIBIOTIC DRUG DELIVERY - INVIVO OSTEOMYELITIS TREATMENT IN A RAT MODEL SYSTEM SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article ID BIOCOMPATIBILITY; CARRIER AB Acute and chronic osteomyelitis can be difficult to treat by conventional means. Current methods of treatment involve the use of systemic antibiotics, the local implantation of non-degradable drug carriers, and surgical debridement. Each method has specific drawbacks. We report on the use of a new controlled release system utilizing gentamicin and bioerodible, biocompatible polymers (polyanhydrides) designed for drug delivery applications for the treatment of clinical osteomyelitis. We compared this system's ability to reduce bacterial levels in infected bone with that of conventional non-degradable delivery systems based on polymethylmethacrylate (PMMA) and gentamicin. Polyanhydride copolymers of bis-carboxyphenoxypropane and sebacic acid P loaded with gentamicin sulfate and PMMA/gentamicin matrices were implanted in the long bones of Sprague-Dawley rats infected with a strain of Staphylococcus aureus. After 3 weeks of implantation, the polymeric delivery devices were removed and quantitative cultures were used to determine bacterial levels in bone. The polyanhydride/gentamicin matrices demonstrated significant degradation over the 3 week implantation period. Levels of bacteria, measured in colony forming units, were significantly lower in bone implanted with the polyanhydride/gentamicin release system than in long bones of control animals without an implant (p < 0.01), of animals with a polyanhydride polymer implant alone (p < 0.01), and of animals with a PMMA/gentamicin implant (p = 0.03). Bioerodible polyanhydrides show promise as a new treatment modality for infections in bone. C1 HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,BLDG E25 342,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT ORTHOPAED SURG,ORTHOPAED BIOMECH LAB,BOSTON,MA 02215. HEBREW UNIV JERUSALEM,FAC MED,SCH PHARM,JERUSALEM,ISRAEL. MIT,DEPT CHEM ENGN,CAMBRIDGE,MA 02139. FU NIAMS NIH HHS [AR 41972] NR 33 TC 82 Z9 83 U1 0 U2 5 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 MAR PY 1993 VL 11 IS 2 BP 256 EP 262 DI 10.1002/jor.1100110213 PG 7 WC Orthopedics SC Orthopedics GA LA753 UT WOS:A1993LA75300011 PM 8483038 ER PT J AU GUSTAFSON, ML LEE, MM ASMUNDSON, L MACLAUGHLIN, DT DONAHOE, PK AF GUSTAFSON, ML LEE, MM ASMUNDSON, L MACLAUGHLIN, DT DONAHOE, PK TI MULLERIAN INHIBITING SUBSTANCE IN THE DIAGNOSIS AND MANAGEMENT OF INTERSEX AND GONADAL ABNORMALITIES SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article; Proceedings Paper CT 23RD ANNUAL MEETING OF THE AMERICAN PEDIATRIC SURGICAL ASSOC CY MAY 13-16, 1992 CL COLORADO SPRINGS, CO SP AMER PEDIAT SURG ASSOC DE MULLERIAN INHIBITING SUBSTANCE; INTERSEX ANOMALIES ID GRANULOSA-CELL TUMORS; CLINICOPATHOLOGIC ANALYSIS; TRUE HERMAPHRODITISM; OOCYTE MEIOSIS; DUCT SYNDROME; ADULT-RAT; DYSGENESIS; MARKER; FETAL; OVARY C1 MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,WARREN 10,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV PEDIAT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. OI Lee, Mary/0000-0002-7204-4884 FU NCI NIH HHS [CA17393]; NICHD NIH HHS [HD07396]; PHS HHS [F32 H007435 02] NR 25 TC 35 Z9 38 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 MAR PY 1993 VL 28 IS 3 BP 439 EP 444 DI 10.1016/0022-3468(93)90245-G PG 6 WC Pediatrics; Surgery SC Pediatrics; Surgery GA KR551 UT WOS:A1993KR55100027 PM 8468660 ER PT J AU SUEN, HC CATLIN, EA RYAN, DP WAIN, JC DONAHOE, PK AF SUEN, HC CATLIN, EA RYAN, DP WAIN, JC DONAHOE, PK TI BIOCHEMICAL IMMATURITY OF LUNGS IN CONGENITAL DIAPHRAGMATIC-HERNIA SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article; Proceedings Paper CT 23RD ANNUAL MEETING OF THE AMERICAN PEDIATRIC SURGICAL ASSOC CY MAY 13-16, 1992 CL COLORADO SPRINGS, CO SP AMER PEDIAT SURG ASSOC DE CONGENITAL DIAPHRAGMATIC HERNIA; NITROFEN; FETAL LUNG DEVELOPMENT ID MULLERIAN INHIBITING SUBSTANCE; FETAL-RAT LUNG; DISATURATED PHOSPHATIDYLCHOLINE; HYPOPLASIA; DIAGNOSIS; REPAIR C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT SURG,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV NEONATAL & PEDIAT INTENS CARE,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LABS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 31 TC 101 Z9 103 U1 1 U2 2 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 MAR PY 1993 VL 28 IS 3 BP 471 EP 477 DI 10.1016/0022-3468(93)90250-O PG 7 WC Pediatrics; Surgery SC Pediatrics; Surgery GA KR551 UT WOS:A1993KR55100032 PM 8468664 ER PT J AU NORMAN, D BLAIS, MA HERZOG, D AF NORMAN, D BLAIS, MA HERZOG, D TI PERSONALITY-CHARACTERISTICS OF EATING-DISORDERED PATIENTS AS IDENTIFIED BY THE MILLON CLINICAL MULTIAXIAL INVENTORY SO JOURNAL OF PERSONALITY DISORDERS LA English DT Article ID DSM-III; AXIS-II; BULIMIA; MCMI; NERVOSA AB The Millon Clinical Multiaxial Inventory (MCMI) was used to determine the overall prevalence of personality disorders and profile characteristics in three groups of eating-disordered patients (17 anorexics, 58 bulimics, and 12 patients who met criteria for both bulimia and anorexia [bulimics with anorexia]). Eighty-four percent of all subjects were diagnosed as having a personality disorder according to the MCMI (BR > 84). Frequency data were used to compare the personality characteristics of the three groups. Bulimic subjects had significantly higher frequencies of dependent and histrionic MCMI personality disorder diagnoses and a significantly lower rate of schizoid personality disorder diagnoses than the other two groups. The anorexics and bulimics with anorexia evidenced higher frequency of avoidant MCMI personality diagnoses than did the bulimics. The results are discussed in terms of their clinical implications and directions for future research. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NORMAN, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,8 BULFINCH,BOSTON,MA 02114, USA. NR 26 TC 19 Z9 19 U1 0 U2 1 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0885-579X J9 J PERS DISORD JI J. Pers. Disord. PD SPR PY 1993 VL 7 IS 1 BP 1 EP 9 PG 9 WC Psychiatry SC Psychiatry GA KX677 UT WOS:A1993KX67700001 ER PT J AU KALUS, O BERNSTEIN, DP SIEVER, LJ AF KALUS, O BERNSTEIN, DP SIEVER, LJ TI SCHIZOID PERSONALITY-DISORDER - A REVIEW OF CURRENT STATUS AND IMPLICATIONS FOR DSM-IV SO JOURNAL OF PERSONALITY DISORDERS LA English DT Article ID AXIS-II; OUTPATIENT POPULATION; CRITERIA; SCHIZOPHRENIA; BORDERLINE; DIAGNOSIS; COMMUNITY; GENETICS; AVOIDANT AB Schizoid personality disorder (SZD) is one of three Diagnostic and Statistical Manual of Mental Disorders, 3rd edition, revised (DSM-III-R) ''odd cluster'' personality disorders (including schizotypal personality disorder [SPD] and paranoid personality disorder [PPD]) characterized by phenomenological similarities to schizophrenia. SZD is distinguished from the other two personality disorders by the prominence of social, interpersonal, and affective deficits (i.e., ''negative symptoms'') in the absence of psychoticlike cognitive/perceptual distortions. Despite a rich and extensive clinical and theoretical tradition regarding the schizoid character, its pre-DSM-III status was handicapped by considerable heterogeneity and lack of clear operationalized criteria for the disorder. The architects of DSM-III attempted to subdivide and sharpen the boundaries of this heterogeneous area by the addition of SPD and PPD within the odd cluster, and the avoidant personality disorder (AVD) within the ''anxious'' cluster. The narrowing of the SZD diagnosis by reassignment into these additional diagnoses, however, raises additional questions on the location of its diagnostic boundaries, and even whether the diagnosis remains a valid and separate entity. Evidence of extensive criteria overlap and comorbidity with other personality disorders are of particular concern in this regard. The low prevalence rates of DSM-III SZD further complicate attempts at addressing these issues empirically. Although modifications of the diagnostic criteria in DSM-III-R appear to have increased the sensitivity and prevalence of the diagnosis, the scarcity of empirical data on either DSM-III or DSM-III-R SZD remains a significantly limiting factor in resolving these concerns. C1 BRONX VET ADM MED CTR,BRONX,NY. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. NR 40 TC 13 Z9 13 U1 1 U2 4 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0885-579X J9 J PERS DISORD JI J. Pers. Disord. PD SPR PY 1993 VL 7 IS 1 BP 43 EP 52 PG 10 WC Psychiatry SC Psychiatry GA KX677 UT WOS:A1993KX67700006 ER PT J AU BERNSTEIN, DP USEDA, D SIEVER, LJ AF BERNSTEIN, DP USEDA, D SIEVER, LJ TI PARANOID PERSONALITY-DISORDER - REVIEW OF THE LITERATURE AND RECOMMENDATIONS FOR DSM-IV SO JOURNAL OF PERSONALITY DISORDERS LA English DT Article ID AXIS-II; OUTPATIENT POPULATION; SCHIZOPHRENIA; BORDERLINE; PSYCHOSIS; RELATIVES; PROBANDS; CRITERIA AB Since the time of Kraepelin (1921), the defining feature of paranoid personality disorder (PPD) has been considered to be a pervasive and unwarranted mistrust of others. Other clinical characteristics that have figured prominently in the descriptive literature on this disorder are the paranoid individual's hypersensitivity to criticism (Cameron, 1943, 1963; Kretschmer, 1925), antagonism and aggressiveness (Schneider, 1923; Sheldon, 1940; Sheldon & Stevens, 1942), rigidity (Shapiro, 1965), hyper-vigilence (Cameron, 1963; Shapiro, 1965), and excessive need for autonomy (Millon, 1969, 1981). This body of clinical literature formed the basis of the diagnostic criteria for PPD that were incorporated in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III). The DSM-III required that patients meet three criteria for suspiciousness, two for hypersensitivity, and two for restricted affectivity, in order to receive a diagnosis of PPD. In the DSM-III-R, the grouping of diagnostic criteria into sets was replaced by a truly polythetic system in which no single feature (or group of features) was required and any combination of four of seven criteria was sufficient for a PPD diagnosis. In this report, some of the major nosological issues concerning PPD are raised and addressed in light of current research findings. Particular emphasis is placed on research pertaining to the development of diagnostic criteria for PPD in the DSM-IV. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP BERNSTEIN, DP (reprint author), BRONX VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 49 TC 6 Z9 6 U1 2 U2 5 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0885-579X J9 J PERS DISORD JI J. Pers. Disord. PD SPR PY 1993 VL 7 IS 1 BP 53 EP 62 PG 10 WC Psychiatry SC Psychiatry GA KX677 UT WOS:A1993KX67700007 ER PT J AU WILENS, TE BIEDERMAN, J SPENCER, T GEIST, DE AF WILENS, TE BIEDERMAN, J SPENCER, T GEIST, DE TI A RETROSPECTIVE STUDY OF SERUM LEVELS AND ELECTROCARDIOGRAPHIC EFFECTS OF NORTRIPTYLINE IN CHILDREN AND ADOLESCENTS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE PEDIATRIC; ECG; NORTRIPTYLINE; PHARMACOKINETICS ID ATTENTION DEFICIT DISORDER; PLASMA-LEVELS; DEPRESSED CHILDREN; TRICYCLIC ANTIDEPRESSANT; CLINICAL-RESPONSE; MAJOR DEPRESSION; SUDDEN-DEATH; IMIPRAMINE; DESIPRAMINE; PLACEBO AB Objective: We retrospectively evaluated a large pediatric population treated with nortriptyline (NT) in an outpatient psychopharmacology clinic to assess pharmacokinetic and electrocardiographic (EKG) effects. Methods: A systematic search revealed 82 children and adolescents treated naturalistically with NT. All patients with available EKGs and serum NT levels were included in the series with the exception of those receiving concomitant antipsychotic agents. Forty-three percent of subjects were receiving medications in addition to NT. Results: Patients received an average (+/-SE) NT dose of 2.0 +/- 0.1 mg/kg yielding mean serum NT levels of 105.5 +/- 7.4 ng/mL. There was a linear relationship of NT dose (mg/kg) to serum NT levels (r = 0.50, p < 0.0001). NT treatment resulted in small increases in heart rate, and PR, QRS, and QTc intervals (all ps < 0.01), of similar magnitude in children and adolescents. Individuals with the highest baseline EKG indices had the least amount of change in those indices with NT treatment. There were only a few statistically significant associations between NT dose or serum NT levels and EKG parameters. NT treatment was significantly associated with the onset of asymptomatic sinus tachycardia (heart rate > 100 beats per minute), and prolongation of the EKG QRS (> 100 msec) and QTc (> 440 msec) intervals. Conclusions: These findings suggest: (1) NT has a predictable dose to level relationship, (2) the effect of NT on the EKG in this age group is mild and similar to that reported with other tricyclic antidepressants, and (3) there are few age-specific differences in NT-induced EKG changes. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WILENS, TE (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,PEDIAT PSYCHOPHARMACOL UNIT,ACC 725,BOSTON,MA 02114, USA. FU NIMH NIH HHS [R01MH-41314] NR 50 TC 14 Z9 14 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 MAR PY 1993 VL 32 IS 2 BP 270 EP 277 DI 10.1097/00004583-199303000-00006 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KN981 UT WOS:A1993KN98100006 PM 8444754 ER PT J AU BIEDERMAN, J FARAONE, SV MILBERGER, S DOYLE, A AF BIEDERMAN, J FARAONE, SV MILBERGER, S DOYLE, A TI DIAGNOSES OF ATTENTION-DEFICIT HYPERACTIVITY DISORDER FROM PARENT REPORTS PREDICT DIAGNOSES BASED ON TEACHER REPORTS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ATTENTION DEFICIT DISORDER; PARENT; TEACHER; CONGRUENCE ID CHILD AB Objective: For DSM-III attention deficit disorder (ADD), it was previously reported that, when a parent report leads to a diagnosis of ADD, it is highly likely that the teacher report will also be positive. This report seeks to generalize that finding to DSM-III-R attention-deficit hyperactivity disorder (ADHD). Method: In a population of 34 children meeting clinical criteria for DSM-III-R ADHD, parents and teachers independently responded to questions about individual ADHD symptoms. Results: Correlations between parents and teachers for individual symptoms were low to moderate; however, there was a 77% probability that the teacher report would result in a positive diagnosis given a positive parent diagnosis. This probability increased to 88% if ''broad'' teacher diagnoses of ADHD, defined by 35% of the 14 DSM-III-R symptoms, were included. Conclusions: In clinically-referred children, a clinical diagnosis of ADHD based on parent report is likely to be corroborated by a teacher report. C1 MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BROCKTON W ROXBURY VET ADM MED CTR,RES SERV,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 9 TC 46 Z9 47 U1 2 U2 3 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 MAR PY 1993 VL 32 IS 2 BP 315 EP 317 DI 10.1097/00004583-199303000-00011 PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KN981 UT WOS:A1993KN98100012 PM 8444759 ER PT J AU WILENS, TE BIEDERMAN, J GEIST, DE STEINGARD, R SPENCER, T AF WILENS, TE BIEDERMAN, J GEIST, DE STEINGARD, R SPENCER, T TI NORTRIPTYLINE IN THE TREATMENT OF ADHD - A CHART REVIEW OF 58 CASES SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE NORTRIPTYLINE; SERUM NORTRIPTYLINE LEVELS; ATTENTION DEFICIT HYPERACTIVITY DISORDER; COMORBIDITY ID ATTENTION DEFICIT DISORDER; PLASMA-LEVEL DESIGN; DOUBLE-BLIND; DEPRESSED CHILDREN; TRICYCLIC ANTIDEPRESSANTS; HYPERACTIVE-CHILDREN; IMIPRAMINE; ADOLESCENTS; METHYLPHENIDATE; DESIPRAMINE AB Objective: The potential benefit of the tricyclic antidepressant medication, nortriptyline (NT), in the treatment of children and adolescents with attention deficit hyperactivity disorder (ADHD) was evaluated. Method: A systematic search was conducted from a computerized data base of all clinic patients in an outpatient pediatric psychopharmacology unit treated with NT for ADHD. The records of the 58 subjects identified (37 children and 21 adolescents) were reviewed for overall response, dose, serum levels, and adverse effects. Results: Ninety-seven percent of the identified subjects had failed to respond to an average of four previous medication trials, 84% had at least one comorbid diagnosis with ADHD, and 47% were receiving at least one concurrent medication. NT doses ranged from 0.4 to 4.5 mg/kg (XBAR +/- SD = 2.0 +/- 1.0 mg/kg) and subjects received NT from 0.4 to 57.9 months (11.9 +/- 14.0 months). Overall, 76% of subjects were considered to have a moderate to marked improvement by an independent rater, which was corroborated by their clinicians. There was no association between response and age, rate of comorbidity, number of previous medication trials, or concurrent pharmacotherapy (all p NS). Although there were no overall differences in serum NT levels between responders and nonresponders, significantly more patients within the suggested therapeutic range in adults of 50 to 150 ng/ml were classified as ''markedly improved'' than those outside this range (68% versus 35%, p < 0.03). Mild adverse effects were reported in 20 subjects (34%). Conclusions: These findings suggest that NT may be an effective well-tolerated agent for ADHD children and adolescents. Additional controlled investigations utilizing NT for ADHD should be undertaken C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP WILENS, TE (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,PEDIAT PSYCHOPHARMACOL UNIT,ACC 725,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-41314] NR 45 TC 59 Z9 59 U1 4 U2 10 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 MAR PY 1993 VL 32 IS 2 BP 343 EP 349 DI 10.1097/00004583-199303000-00015 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KN981 UT WOS:A1993KN98100017 PM 8444763 ER PT J AU STEINGARD, R BIEDERMAN, J SPENCER, T WILENS, T GONZALEZ, A AF STEINGARD, R BIEDERMAN, J SPENCER, T WILENS, T GONZALEZ, A TI COMPARISON OF CLONIDINE RESPONSE IN THE TREATMENT OF ATTENTION-DEFICIT HYPERACTIVITY DISORDER WITH AND WITHOUT COMORBID TIC DISORDERS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE CLONIDINE; ATTENTION-DEFICIT HYPERACTIVITY DISORDER; TIC DISORDERS; TOURETTES SYNDROME ID LA-TOURETTES SYNDROME; METHYLPHENIDATE; PLACEBO AB Objective: Clonidine has been suggested as an alternative pharmacotherapy for patients with attention-deficit hyperactivity disorder (ADHD) and comorbid tic disorders. To examine the efficacy of clonidine in this population of children, the use of clonidine in the treatment of children with ADHD with and without comorbid tic disorders was examined in a retrospective chart review of 54 children over a 4-year period. Method: Treatment was administered openly to these patients in a Pediatric Psychopharmacology Clinic, and response was assessed using clinical global improvement measures. Results: Clonidine treatment resulted in improvement in both the ADHD (39/54; 72%) and tic symptoms (18/24; 75%) groups. The findings suggested that the children with ADHD with comorbid tic disorders (23/24; 96%) have a more frequent positive behavioral response to clonidine than children with ADHD without comorbid tic disorders (16/30; 53%). Conclusions: This report provides further support of a role for clonidine in the treatment of children with ADHD, particularly for those with comorbid tic disorders. C1 MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL CLIN,BOSTON,MA 02114. RP STEINGARD, R (reprint author), CHILDRENS HOSP MED CTR,DIV PSYCHOPHARMACOL,FEGAN 8,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 16 TC 69 Z9 71 U1 0 U2 2 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 MAR PY 1993 VL 32 IS 2 BP 350 EP 353 DI 10.1097/00004583-199303000-00016 PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KN981 UT WOS:A1993KN98100018 PM 8444764 ER PT J AU SPENCER, T BIEDERMAN, J KERMAN, K STEINGARD, R WILENS, T AF SPENCER, T BIEDERMAN, J KERMAN, K STEINGARD, R WILENS, T TI DESIPRAMINE TREATMENT OF CHILDREN WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER AND TIC DISORDER OR TOURETTES-SYNDROME SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE DESIPRAMINE; TOURETTES SYNDROME; ATTENTION-DEFICIT HYPERACTIVITY DISORDER ID SUDDEN-DEATH; IMIPRAMINE; GILLES; ADOLESCENTS; PLASMA; METHYLPHENIDATE; DEPRESSION; STIMULANTS; CLONIDINE; ADD AB Objective: As many as 50% of patients with Tourette's syndrome (TS) also meet diagnostic criteria for attention-deficit hyperactivity disorder (ADHD). Since antipsychotics are of limited value in controlling the symptoms of ADHD and stimulants can exacerbate tics, alternative treatments are direly needed. The purpose of this study was the examination of the efficacy of desipramine (DMI) in the treatment of pediatric patients with chronic tic disorder (CTD; TS or chronic motor tics) + attention-deficit hyperactivity disorder (ADHD). Method: All pediatric patients with the diagnosis of CTD that were treated with DMI were ascertained from retrospective systematic chart reviews of a psychopharmacology clinic and a neurology service specialized in movement disorders. Results: Of the 33 identified patients, 30 had comorbid CTD + ADHD and three had CTD alone. In all, 82% had significant improvement in CTD symptomatology and 80% significantly improved ADHD symptoms without major adverse effects over an average follow-up period of 16 months. Conclusions: Although the conclusions from this retrospective report can be seen as preliminary only until replicated in a controlled investigation, the magnitude and persistence of the response is encouraging and suggest a therapeutic role for DMI in the treatment of CTD + ADHD patients. C1 RHODE ISL HOSP,PEDIAT MOVEMENT DISORDERS CLIN,PROVIDENCE,RI 02902. BROWN UNIV,PROVIDENCE,RI 02912. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,PEDIAT PSYCHOPHARMACOL CLIN,BOSTON,MA 02115. RP SPENCER, T (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,FRUIT ST,BOSTON,MA 02114, USA. NR 54 TC 44 Z9 45 U1 2 U2 4 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 MAR PY 1993 VL 32 IS 2 BP 354 EP 360 DI 10.1097/00004583-199303000-00017 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KN981 UT WOS:A1993KN98100019 PM 8444765 ER PT J AU NIDORF, SM SIU, SC GALAMBOS, G WEYMAN, AE PICARD, MH AF NIDORF, SM SIU, SC GALAMBOS, G WEYMAN, AE PICARD, MH TI BENEFIT OF LATE CORONARY REPERFUSION ON VENTRICULAR MORPHOLOGY AND FUNCTION AFTER MYOCARDIAL-INFARCTION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY; EARLY RECOVERY; SURVIVAL; DYSFUNCTION; VOLUME; SIZE; THERAPY; DETERMINANT; IMPROVEMENT; ANGIOPLASTY AB Objectives. This study was designed to examine the relation between the timing and adequacy of perfusion of the infarct bed and changes in ventricular size and the extent of abnormal wall motion after acute myocardial infarction. Methods. A validated echocardiographic mapping technique was used to measure the left ventricular endocardial surface area index and the extent of abnormal wall motion over a 3-month period in 91 patients who had either 1) no anterograde or collateral flow to the infarct bed (n = 14), 2) only collateral flow to the infarct bed (n = 18), 3) restoration of anterograde flow to the infarct bed within hours of chest pain (early [n = 43]), or 4) restoration of anterograde flow to the infarct bed within a mean of 5 days after acute myocardial infarction (late [n = 16]). Results. Over the follow-up period, a progressive and significant increase in endocardial surface area index was observed only in the group of patients without anterograde or collateral flow to the infarct bed (entry 64 +/- 3.4 cm2/m2 vs. 3 months 75.9 +/-6.4 cm2/m2, p < 0.005). In contrast, a progressive reduction in the extent of abnormal wall motion was evident in the group of patients in whom anterograde flow to the infarct bed was restored within hours (entry 26.7 +/- 2.5 CM2 vs. 3 months 11.8 +/- 2.9 cm2, p < 0.001) or days (entry 22.1 +/- 3.6 CM2 vs. 3 months 11.8 +/-3.3 CM2, p < 0. 001) of coronary occlusion. Multiple stepwise linear regression analysis confirmed that by 3 months, 1) ventricular size was independently related to endocardial surface area index and abnormal wall motion at entry (p < 0.0001) and to the change in abnormal wall motion over the follow-up period (p < 0.0001), and 2) the change in abnormal wall motion was related to the presence of anterograde flow to the infarct bed (p < 0.0001) independent of the timing of reperfusion, infarct site or the extent of abnormal wall motion on admission. Conclusions. After myocardial infarction, the process of ventricular remodeling is influenced by changes in the extent of abnormal wall motion, which in turn are related to the adequacy rather than the timing of perfusion of the infarct bed. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NIDORF, SM (reprint author), MASSACHUSETTS GEN HOSP,NONINVAS CARDIAC LAB,CARDIAC UNIT,FOUNDERS HOUSE 8,BOSTON,MA 02114, USA. OI Picard, Michael/0000-0002-9264-3243 NR 41 TC 71 Z9 72 U1 2 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1993 VL 21 IS 3 BP 683 EP 691 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KP177 UT WOS:A1993KP17700018 PM 8436750 ER PT J AU HANDSCHUMACHER, MD LETHOR, JP SIU, SC MELE, D RIVERA, JM PICARD, MH WEYMAN, AE LEVINE, RA AF HANDSCHUMACHER, MD LETHOR, JP SIU, SC MELE, D RIVERA, JM PICARD, MH WEYMAN, AE LEVINE, RA TI A NEW INTEGRATED SYSTEM FOR 3-DIMENSIONAL ECHOCARDIOGRAPHIC RECONSTRUCTION - DEVELOPMENT AND VALIDATION FOR VENTRICULAR VOLUME WITH APPLICATION IN HUMAN-SUBJECTS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID TWO-DIMENSIONAL ECHOCARDIOGRAMS; CARDIAC-OUTPUT; MITRAL REGURGITATION; REAL-TIME; DOPPLER ECHOCARDIOGRAPHY; CLINICAL VALIDATION; ULTRASOUND IMAGES; ORIFICE METHOD; STROKE VOLUME; VALVE AB Objectives. The purpose of this study was to improve three-dimensional echocardiographic reconstruction by developing an automated mechanism for integrating spark gap locating data with corresponding images in real time and to validate use of this mechanism for the measurement of left ventricular volume. Background. Initial approaches to three-dimensional echocardiographic reconstruction were often limited by inefficient reconstructive processes requiring manual coordination of two-dimensional images and corresponding spatial locating data. Methods. In this system, a single computer overlays the binary-encoded positional data on the two-dimensional echocardiographic image, which is then recorded on videotape. The same system allows images to be digitized, traced, analyzed and displayed in three dimensions. This system was validated by using it to reconstruct 11 ventricular phantoms (19 to 271 ml) and 11 gel-filled excised ventricles (21 to 236 ml) imaged in intersecting long- and short-axis views and by apical rotation. To measure cavity volume, a surface was generated by an algorithm that takes advantage of the full three-dimensional data set. Results. Reconstructed cavity volumes agreed well with actual values: y = 0.96x + 2.2 for the ventricular phantoms in long- and short-axis views (r = 0.99, SEE = 2.7 ml); y = 0.95x + 2.9 for the phantoms, reconstructed by apical rotation (r = 0.99, SEE = 2.7 ml); and y = 0.99x + 0.11 ml for the excised ventricles (reconstructed in long- and short-axis views; r = 0.99, SEE = 5.9 ml). The mean difference between three-dimensional and actual volumes was 3% of the mean (3.0 ml) for the phantoms and 6% (4.6 ml) for the excised ventricles. Observer variability was 2.3% for the phantoms and 5.6% for the excised ventricles. Application to 14 normal subjects demonstrated feasibility of left ventricular reconstruction, which provided values for stroke volume that agreed well with an independent Doppler measure (y = 0.97x + 0.94; r = 0.95, SEE = 3.2 ml), with an observer variability of 4.9% (2.4 ml). Conclusions. A system has therefore been developed that automatically integrates locating and imaging data in no more time than the component two-dimensional echocardiographic scans. This system can accurately reconstruct ventricular volumes in vitro over a wide range and is feasible in vivo, thus laying the foundation for further applications. It has increased the efficiency of three-dimensional reconstruction and enhanced our ability to address clinical and research questions with this technique. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC ULTRASOUND LAB,FOUNDERS HOUSE 8,BOSTON,MA 02114. RI rivera, miguel/D-5026-2014 FU NHLBI NIH HHS [HL-07535, HL-38176] NR 39 TC 128 Z9 128 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1993 VL 21 IS 3 BP 743 EP 753 PG 11 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KP177 UT WOS:A1993KP17700025 PM 8436757 ER PT J AU HUTTER, AM AF HUTTER, AM TI A PRESCRIPTION FOR THE ACC HEALTH-POLICY PROCESS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material RP HUTTER, AM (reprint author), MASSACHUSETTS GEN HOSP,ACC BLDG,SUITE 467,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1993 VL 21 IS 3 BP 842 EP 843 PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KP177 UT WOS:A1993KP17700037 PM 8436767 ER PT J AU BUCHNER, DM HORNBROOK, MC KUTNER, NG TINETTI, ME ORY, MG MULROW, CD SCHECHTMAN, KB GERETY, MB FIATARONE, MA WOLF, SL ROSSITER, J ARFKEN, C KANTEN, K LIPSITZ, LA SATTIN, RW DENINO, LA AF BUCHNER, DM HORNBROOK, MC KUTNER, NG TINETTI, ME ORY, MG MULROW, CD SCHECHTMAN, KB GERETY, MB FIATARONE, MA WOLF, SL ROSSITER, J ARFKEN, C KANTEN, K LIPSITZ, LA SATTIN, RW DENINO, LA TI DEVELOPMENT OF THE COMMON DATA-BASE FOR THE FICSIT TRIALS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID MINI-MENTAL STATE; SELF-EFFICACY; RISK-FACTORS; FALLS; COMMUNITY; BALANCE; SCALE; FEAR AB The eight FICSIT (Frailty and Injuries: Cooperative Studies of Intervention Techniques) sites test different intervention strategies in selected target groups of older adults. To compare the relative potential of these interventions to reduce frailty and fall-related injuries, all sites share certain descriptive (risk-adjustment) measures and outcome measures. This article describes the shared measures, which are referred to as the FICSIT Common Data Base (CDB). The description is divided into four sections according to the four FICSIT committees responsible for the CDB: (1) psychosocial health and demographic measures; (2) physical health measures; (3) fall-related measures; and (4) cost and cost-effectiveness measures. Because the structure of the FICSIT trial is unusual, the CDB should expedite secondary analyses of various research questions dealing with frailty and falls. C1 SEATTLE VA MED CTR,HLTH SERV RES & DEV FIELD PROGRAM,SEATTLE,WA. AUDIE L MURPHY VET AFFAIRS HOSP,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX. TUFTS UNIV,HEBREW REHABIL CTR AGED,USDA,HUMAN NUTR RES CTR AGING,BOSTON,MA 02111. EMORY UNIV,SCH MED,DEPT REHABIL MED,ATLANTA,GA 30322. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. NIA,DIV BEHAV & SOCIAL RES,BETHESDA,MD 20892. KAISER PERMANENTE,CTR HLTH RES,NW REG,PORTLAND,OR. WASHINGTON UNIV,SCH MED,DIV BIOSTAT,ST LOUIS,MO 63110. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,DIV AGING,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DIV GERONTOL,BOSTON,MA 02115. CTR DIS CONTROL,DIV INJURY CONTROL,ATLANTA,GA 30333. OREGON HLTH SCI UNIV,DEPT COMMUNITY HLTH CARE SYST,PORTLAND,OR 97201. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. RP BUCHNER, DM (reprint author), UNIV WASHINGTON,DEPT HLTH SERV SC37,SEATTLE,WA 98195, USA. RI Wolf, Steven/F-6588-2010; OI Wolf, Steven/0000-0002-9446-8995; Miller, J Philip/0000-0003-4568-6846 FU NIA NIH HHS [U01-AG09087, U01-AG09089, U01-AG09117] NR 35 TC 226 Z9 234 U1 12 U2 17 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAR PY 1993 VL 41 IS 3 BP 297 EP 308 PG 12 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA KP998 UT WOS:A1993KP99800017 PM 8440854 ER PT J AU MULROW, CD GERETY, MB KANTEN, D DENINO, LA CORNELL, JE AF MULROW, CD GERETY, MB KANTEN, D DENINO, LA CORNELL, JE TI EFFECTS OF PHYSICAL THERAPY ON FUNCTIONAL STATUS OF NURSING-HOME RESIDENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article AB Nursing home residents typically have decreased functional and physical status and high health care utilization and costs. This randomized trial evaluates whether physical therapy is beneficial for frail debilitated long-stay residents of nursing homes. Subjects are recruited from a cohort of academic and community nursing home residents who have resided in the nursing home for greater than 3 months and are over age 60 and dependent in at least two activities of daily living. Subjects randomized to the intervention group receive one-on-one physical therapy sessions three times weekly for 4 months, while control group subjects receive structured social visits three times weekly to control for potential Hawthorne effects. Physical therapy sessions generally last 30 minutes and consist of functional activity and general conditioning exercises; these exercises are individually tailored to the subject's level of physical and functional disability. Prime outcome variables are physical function assessed by an observer-administered, performance-based instrument and self-perceived health status assessed by the Sickness Impact Profile. Health care utilization and associated costs are calculated for the following areas: the nursing home, hospitalizations, out-patient visits and procedures, medications, and the intervention. A cost-effectiveness ratio dividing incremental health care utilization and physical therapy intervention costs by the observed improvement in physical function is calculated. It is expected that results of this study can be used to help determine whether long-stay nursing home residents should be eligible for physical therapy. C1 GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [AGO9117] NR 10 TC 21 Z9 21 U1 3 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAR PY 1993 VL 41 IS 3 BP 326 EP 328 PG 3 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA KP998 UT WOS:A1993KP99800021 PM 8440858 ER PT J AU MITCHELL, JD LEE, R GARAN, H RUSKIN, JN TORCHIANA, DF VLAHAKES, GJ AF MITCHELL, JD LEE, R GARAN, H RUSKIN, JN TORCHIANA, DF VLAHAKES, GJ TI EXPERIENCE WITH AN IMPLANTABLE TIERED THERAPY DEVICE INCORPORATING ANTITACHYCARDIA PACING AND CARDIOVERTER DEFIBRILLATOR THERAPY SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID MALIGNANT VENTRICULAR ARRHYTHMIAS; SHOCK THERAPY; TACHYCARDIA; EFFICACY; FIBRILLATION; TERMINATION; SURVIVAL; TACHYARRHYTHMIAS; DETERMINANTS; WAVEFORMS AB The implantable cardioverter-defibrillator provides an alternative therapy for medically refractory ventricular tachyarrhythmias in patients who are not candidates for ventricular operations or in whom these operations have failed. Currently, however, available devices have limitations. In this report we describe our experience with a programmable, tiered therapy device with anti-ventricular tachyarrhythmia pacing and VVI pacing capabilities (Cadence V-100, Ventritex Inc, Sunnyvale, Calif.). This device offers certain advantages compared with conventional implantable cardioverter-defibrillators: (1) tiered, anti-ventricular tachyarrhythmia therapy incorporating programmable, rate-adaptive burst pacing in addition to energy-programmable cardioversion/defibrillation, (2) biphasic cardioversion/defibrillation waveforms, resulting in lower defibrillation thresholds, (3) the ability to abort therapy for nonsustained ventricular tachyarrhythmias, (4) electrogram storage of detected events for later retrieval and analysis, (5) noninvasive, device-generated programmed stimulation for system testing, and (6) backup VVI pacing capability. Forty patients (aged 14 to 79 years) with ventricular tachyarrhythmias refractory to medical therapy received this device. The mean left ventricular ejection fraction was 33 % +/- 16 %. Preoperative electrophysiologic testing revealed inducible monomorphic ventricular tachyarrhythmia responsive to rapid ventricular pacing in 36 patients (90 %). An extrapericardial two-patch configuration was used with either epicardial screw-in or bipolar endocardial sensing/pacing wires. No operative mortality and no device-related infection occurred. During a follow-up period of 16 +/- 7 months (range 3 to 30 months), 38 patients remained active with the implanted device; one patient died of congestive heart failure 4 months after implantation, and the system was explanted in one patient who underwent cardiac transplantation. In 33 patients a total of 1815 ventricular tachyarrhythmias were detected that resulted in therapy. Rate-adaptive burst pacing was used as the initial therapy in 1470 episodes and was successful in 1352 instances (92 %). Pacing-induced ventricular tachyarrhythmia acceleration occurred in 4 % of episodes. The remaining ventricular tachyarrhythmia episodes were treated with cardioversion. In 18 patients (45 %) cardioversion therapy was aborted after spontaneous termination of ventricular tachyarrhythmia. This device may be advantageous for patients with ventricular tachyarrhythmias treated by implantable cardioverter-defibrillator in whom (1) the ventricular tachyarrhythmia can be terminated with burst pacing, thus avoiding shocks, (2) frequent runs of nonsustained ventricular tachyarrhythmia occur, and reconfirmation of the presence of ventricular tachyarrhythmia is desirable to avoid unnecessary therapy, (3) electrogram retrieval can guide future therapy, and (4) VVI pacing may be needed for bradycardia, particularly after cardioversion. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,CARDIAC SURG UNIT,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 30 TC 4 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD MAR PY 1993 VL 105 IS 3 BP 453 EP 463 PG 11 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA KR715 UT WOS:A1993KR71500010 PM 8445925 ER PT J AU MCGUIRE, KL CURTISS, VE LARSON, EL HASELTINE, WA AF MCGUIRE, KL CURTISS, VE LARSON, EL HASELTINE, WA TI INFLUENCE OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE-1 TAX AND REX ON INTERLEUKIN-2 GENE-EXPRESSION SO JOURNAL OF VIROLOGY LA English DT Article ID RNA RESPONSE ELEMENTS; HTLV-I REX; NUCLEAR PROTEINS; CHLORAMPHENICOL ACETYLTRANSFERASE; TRANSCRIPTIONAL ACTIVATOR; REGULATORY PROTEINS; CYCLOSPORINE-A; LYMPHOCYTES-T; MESSENGER-RNA; RECEPTOR AB The X region of human T-cell leukemia virus type I (HTLV-I) encodes two proteins that regulate viral gene expression. The tax protein is the product of the transactivator gene and has been shown to up-regulate the expression of some cellular genes controlling T-cell replication, including that of the interleukin-2 (IL-2) T-cell growth hormone and the alpha chain of its receptor (IL-2R). Several studies have shown that tar transactivation of the IL-2R alpha-chain promoter is mediated by binding sites for the transcriptional activator NF-KB, and this mechanism has also been implicated in the tax activation of IL-2 promoter activity. The rex gene product of HTLV-I regulates viral protein production by influencing mRNA expression and has been implicated in the stabilization of IL-2R alpha-chain mRNA. In the present studies, the ability of the tax and rex proteins to transactivate IL-2 gene expression has been reinvestigated. The ability of the tax protein to transactivate IL-2 promoter activity appears, at least in part, to be mediated by the recognition sequence for a DNA-binding complex known as CD28RC. Consistent with this hypothesis is the observation that tar-mediated activation of IL-2 gene expression is resistant to the immunosuppressive affects of cyclosporin A, a property postulated for the CD28RC binding complex. Unexpectedly, this tax-mediated up-regulation of IL-2 expression is synergized by the presence of the rex protein. These findings demonstrate that transactivation of IL-2 gene expression by tar is augmented by mechanisms distinct from NF-kappaB and raise the possibility that rex, as well as tar, contributes to the oncogenic capability of HTLV-I by altering the expression of the IL-2 gene in T cells infected with this retrovirus. C1 SAN DIEGO STATE UNIV,COLL SCI,INST MOLEC BIOL,SAN DIEGO,CA 92182. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. RP MCGUIRE, KL (reprint author), SAN DIEGO STATE UNIV,COLL SCI,DEPT BIOL,SAN DIEGO,CA 92182, USA. FU NCI NIH HHS [CA53382-01A1] NR 48 TC 55 Z9 55 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1993 VL 67 IS 3 BP 1590 EP 1599 PG 10 WC Virology SC Virology GA KM613 UT WOS:A1993KM61300053 PM 8382312 ER PT J AU ZAZOPOULOS, E HASELTINE, WA AF ZAZOPOULOS, E HASELTINE, WA TI DISULFIDE BOND FORMATION IN THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 NEF PROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID MUTATIONAL ANALYSIS; NUCLEOTIDE-SEQUENCE; AIDS VIRUS; GENE; REPLICATION; REGION; HIV-1; LAV; DNA AB Substitution of alanine for cysteine residues of the human immunodeficiency virus type 1 LAI (BRU) and ELI Nef proteins was used to determine pairing of the cysteine residues present in each protein. The results show that under nonreducing conditions, alternative pairing of the cysteines occurs. The preferred pairing of cysteine residues of the LAI and ELI proteins differs. In the experimental system used, viruses carrying the ELI nef allele are found to express Nef proteins which accelerate virus replication. Mutation in critical cysteine residues of the protein reduce the rate of virus replication. In the same system, viruses harboring the LAI nef allele fail to replicate. These observations raise the possibility that differences in the observed biological activity of nef alleles may be attributed, at least in part, to differences in the secondary structure of the proteins. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [P30 CA06516]; NIAID NIH HHS [P30 AI28691, U01 AI24845] NR 19 TC 24 Z9 24 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 MAR PY 1993 VL 67 IS 3 BP 1676 EP 1680 PG 5 WC Virology SC Virology GA KM613 UT WOS:A1993KM61300065 PM 8437238 ER PT J AU HSU, HC YANG, K KHARBANDA, S CLINTON, S DATTA, R STONE, RM AF HSU, HC YANG, K KHARBANDA, S CLINTON, S DATTA, R STONE, RM TI ALL-TRANS RETINOIC ACID INDUCES MONOCYTE GROWTH-FACTOR RECEPTOR (C-FMS) GENE-EXPRESSION IN HL-60 LEUKEMIA-CELLS SO LEUKEMIA LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; TUMOR NECROSIS FACTOR; PROTEIN KINASE-C; DIFFERENTIATION THERAPY; LINE HL-60; ONCOGENE; TRANSLOCATION; RNA AB All-trans-retinoic (ATRA) treatment of patients with acute promyelocytic leukemia results in differentiation of the malignant cells and a high complete remission rate. ATRA treatment induced granulocytic differentiation in HL-60 cells as assessed by nitro-blue tetrazolium (NBT) reduction, but had no effect on non-specific esterase (NSE) staining, as expected in cells maturing along the monocytic lineage. However, our results demonstrate that ATRA (0.1-10 mum) induces expression of the c-fms (monocyte colony-stimulating factor receptor) gene in HL-60 cells. This effect was detectable after 2 days and expression was maximal at 5 days. Similar results were obtained during treatment with cis-retinoic acid (CRA), hexamethylene bisacetamide (HMBA), or dimethyl sulfoxide (DMSO). The results also demonstrate that ATRA-induced c-fms expression is potentiated by exposure to tumor necrosis factor alpha (TNFalpha) or dibutyryl cyclic adenosine monophosphate (cAMP). The induction of c-fms transcripts by ATRA is associated with induction of M-CSF-binding ability, suggesting cell surface expression of the monocyte growth factor receptor. Our results indicate that retinoic acid can induce features of both monocytic and granulocytic differentiation in HL-60 cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [CA42802, CA34283, K08-CA-01352] NR 25 TC 16 Z9 16 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD MAR PY 1993 VL 7 IS 3 BP 458 EP 462 PG 5 WC Oncology; Hematology SC Oncology; Hematology GA KT680 UT WOS:A1993KT68000017 PM 8445950 ER PT J AU CHOR, PJ GAUM, LD YOUNG, RH AF CHOR, PJ GAUM, LD YOUNG, RH TI CLEAR CELL ADENOCARCINOMA OF THE URINARY-BLADDER - REPORT OF A CASE OF PROBABLE MULLERIAN ORIGIN SO MODERN PATHOLOGY LA English DT Article DE URINARY BLADDER; ENDOMETRIOSIS; CLEAR CELL ADENOCARCINOMA ID ENDOMETRIOSIS; URETHRA AB A 35-yr-old woman with a history of endometriosis and several recent episodes of hematuria was found to have an exophytic tumor arising from the mucosa of the posterior bladder wall. Microscopic examination showed a typical clear cell adenocarcinoma with a predominant tubulo-cystic pattern. A radical cystectomy was performed. Pathologic examination showed no residual tumor, but grossly visible intramural cysts at the site of the tumor had features of endometriosis on microscopic examination, strongly suggesting that the clear cell adenocarcinoma arose from endometriosis and was of mullerian derivation. Only one other adenocarcinoma of the bladder, an endometrioid adenocarcinoma, has had a probable mullerian origin. Although rare, these cases indicate that some vesical adenocarcinomas are of mullerian type. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. ST JOHNS MERCY MED CTR,DEPT PATHOL,ST LOUIS,MO 63141. ST JOHNS MERCY MED CTR,DEPT UROL,ST LOUIS,MO 63141. NR 18 TC 30 Z9 32 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD MAR PY 1993 VL 6 IS 2 BP 225 EP 228 PG 4 WC Pathology SC Pathology GA KV283 UT WOS:A1993KV28300023 PM 8483895 ER PT J AU SHIRAKAWA, F SAITO, K BONAGURA, CA GALSON, DL FENTON, MJ WEBB, AC AURON, PE AF SHIRAKAWA, F SAITO, K BONAGURA, CA GALSON, DL FENTON, MJ WEBB, AC AURON, PE TI THE HUMAN PROINTERLEUKIN-1-BETA GENE REQUIRES DNA-SEQUENCES BOTH PROXIMAL AND DISTAL TO THE TRANSCRIPTION START SITE FOR TISSUE-SPECIFIC INDUCTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID REGULATED EXPRESSION; INDUCIBLE ENHANCER; NUCLEAR FACTOR; LONG ARM; INTERLEUKIN-1; C/EBP; CELLS; VIRUS; CHROMOSOME-2; PROTEINS AB In these studies, we have identified DNA sequences and specific protein interactions necessary for transcriptional regulation of the human prointerleukin 1beta (proIL-1beta) gene. A cell-type-independent lipopolysaccharide (LPS)-responsive enhancer element located between -3757 and -2729 bp upstream from the transcription start site (cap site) consisted of at least six discrete subregions which were essential to the maximal induction by LPS in transfected monocytes. The enhancer also appeared to mediate phorbol myristate acetate induction in monocytes and IL-1 responsiveness in fibroblasts. Deletion and base substitution mutations along with DNA binding studies demonstrated that the enhancer contained a minimum of three functional protein binding sequences, two of which appeared to be important for gene induction. One of the essential proteins which bound to the enhancer was similar or identical to members of the C/EBP family of transcription factors required for both IL-1- and LPS-specific induction of the IL-6 gene (i.e., the NF-IL6 proteins). When ligated to the proIL-1beta cap site-proximal region (located between -131 to +12), both the proIL-1beta and the simian virus 40 enhancer elements functioned more efficiently in monocytes than in HeLa cells, which are not normally competent for IL-1beta expression. When ligated to the murine c-fos promoter, however, the proIL-1beta enhancer was inducible in phorbol myristate acetate-stimulated HeLa cells, suggesting the existence of a proIL-1beta promoter-proximal requirement for tissue specificity. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. EVANS DEPT CLIN RES,BOSTON,MA 02118. WELLESLEY COLL,DEPT BIOL SCI,WELLESLEY,MA 02181. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RI Galson, Deborah/E-9370-2010 OI Galson, Deborah/0000-0002-2045-8807 FU NIAID NIH HHS [AI27850]; NIAMS NIH HHS [AR-03564] NR 52 TC 161 Z9 162 U1 0 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1993 VL 13 IS 3 BP 1332 EP 1344 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN579 UT WOS:A1993KN57900003 PM 8441379 ER PT J AU FELDER, S ZHOU, M HU, P URENA, J ULLRICH, A CHAUDHURI, M WHITE, M SHOELSON, SE SCHLESSINGER, J AF FELDER, S ZHOU, M HU, P URENA, J ULLRICH, A CHAUDHURI, M WHITE, M SHOELSON, SE SCHLESSINGER, J TI SH2 DOMAINS EXHIBIT HIGH-AFFINITY BINDING TO TYROSINE-PHOSPHORYLATED PEPTIDES YET ALSO EXHIBIT RAPID DISSOCIATION AND EXCHANGE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SRC HOMOLOGY REGION-2; CYTOPLASMIC SIGNALING PROTEINS; GROWTH-FACTOR RECEPTORS; PHOSPHOLIPASE C-II; EGF RECEPTOR; PHOSPHATIDYLINOSITOL-3 KINASE; REGULATES INTERACTIONS; PDGF RECEPTOR; TRANSDUCTION; SUBSTRATE AB src homology 2 (SH2) domains of intracellular signaling molecules such as phospholipase C-gamma and phosphatidylinositol 3'-kinase-associated protein p85 represent recognition motifs for specific phosphotyrosine-containing regions on activated growth factor receptors. The binding of SH2 domains to activated growth factor receptors controls the interaction with signaling molecules and the regulation of their activities. In this report, we describe the kinetic parameters and binding affinities of SH2 domains of p85 toward short phosphotyrosine-containing peptides with the amino acid sequence motif YMXM, derived from a major insulin receptor substrate, IRS-1, by using real time biospecific interaction analysis (BIAcore). Associations were specific and of very high affinity, with dissociation constants of 0.3 to 3 nM, between phosphopeptides and the two separate SH2 domains contained within p85. Nonphosphorylated peptides showed no measurable binding, and the interactions were specific for the primary sequence very close to the phosphotyrosine residue. Moreover, the interactions between phosphopeptides and SH2 domains of other signaling molecules were of much lower affinity. Interestingly, the binding of the SH2 domains to the tyrosine-phosphorylated peptides was of high affinity as a result of a very high on rate, of 3 x 10(7) to 40 x 10(7)/M/s; at the same time, the rate of dissociation, of 0.11 to 0.19/s, was rapid, allowing for rapid exchange of associating proteins with the tyrosine phosphorylation sites. C1 NYU MED CTR,DEPT PHARMACOL,550 1ST AVE,NEW YORK,NY 10016. SELECTIDE CORP,DEPT PHARMACOL,TUCSON,AZ 85737. HARVARD UNIV,BRIGHAM & WOMENS HOSP,JOSLIN DIABETES CTR,DEPT MED,RES DIV,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MAX PLANCK INST BIOCHEM,W-8033 MARTINSRIED,GERMANY. OI Hu, Patrick/0000-0002-5611-8062 NR 47 TC 173 Z9 174 U1 1 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1993 VL 13 IS 3 BP 1449 EP 1455 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN579 UT WOS:A1993KN57900016 PM 7680095 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 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; TRANSCRIPTION FACTOR E2F; ADENOVIRUS E1A PROTEINS; CELL-CYCLE; MOUSE FIBROBLASTS; DNA-BINDING; EXPRESSION; INVITRO; TRANSACTIVATION; TRANSFORMATION AB Enhanced expression of genes involved in nucleotide biosynthesis, such as dihydrofolate reductase (DHFR), is a hallmark of entrance into the DNA synthesis (S) phase of the mammalian cell cycle. To investigate the regulated expression of the DHFR gene, we stimulated serum-starved NIH 3T3 cells to synchronously reenter the cell cycle. Our previous results show that a cis-acting element at the site of DHFR transcription initiation is necessary for serum regulation. Recently, this element has been demonstrated to bind the cloned transcription factor E2F. In this study, we focused on the role of E2F in the growth regulation of DHFR. We demonstrated that a single E2F site, in the absence or presence of other promoter elements, was sufficient for growth-regulated promoter activity. Next, we showed that the increase in DHFR mRNA at the G1/S-phase boundary required protein synthesis, raising the possibility that a protein(s) lacking in serum-starved cells is required for DHFR transcription. We found that, similar to DHFR mRNA expression, levels of murine E2F1 mRNA were low in serum-starved cells and increased at the G1/S-phase boundary in a protein synthesis-dependent manner. Furthermore, in a cotransfection experiment, expression of human E2F1 stimulated the DHFR promoter 22-fold in serum-starved cells. We suggest that E2F1 way be the key protein required for DHFR transcription that is absent in serum-starved cells. Expression of E2F also abolished the serum-stimulated regulation of the DHFR promoter and resulted in transcription patterns similar to those seen with expression of the adenoviral oncoprotein EIA. In summary, we provide evidence for the importance of E2F in the growth regulation of DHFR and suggest that alterations in the levels of E2F may have severe consequences in the control of cellular proliferation. C1 UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706. HARVARD UNIV,SCH MED,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA07175, CA09135, CA45240] NR 56 TC 299 Z9 300 U1 1 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1993 VL 13 IS 3 BP 1610 EP 1618 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN579 UT WOS:A1993KN57900034 PM 8441401 ER PT J AU CARPENTER, CL AUGER, KR DUCKWORTH, BC HOU, WM SCHAFFHAUSEN, B CANTLEY, LC AF CARPENTER, CL AUGER, KR DUCKWORTH, BC HOU, WM SCHAFFHAUSEN, B CANTLEY, LC TI A TIGHTLY ASSOCIATED SERINE THREONINE PROTEIN-KINASE REGULATES PHOSPHOINOSITIDE 3-KINASE ACTIVITY SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID I PHOSPHATIDYLINOSITOL KINASE; RECEPTOR TYROSINE KINASES; MIDDLE-T-ANTIGEN; SIGNAL TRANSDUCTION; BETA-RECEPTOR; CELLS; TRANSFORMATION; PP60C-SRC; PHOSPHORYLATION; PURIFICATION AB We identified a serine/threonine protein kinase that is associated with and phosphorylates phosphoinositide 3-kinase (PtdIns 3-kinase). The serine kinase phosphorylates both the 85- and 110-kDa subunits of PtdIns 3-kinase and purifies with it from rat liver and immunoprecipitates with antibodies raised to the 85-kDa subunit. Tryptic phosphopeptide maps indicate that p85 from polyomavirus middle T-transformed cells is phosphorylated in vivo at three sites phosphorylated in vitro by the associated serine kinase. The 85-kDa subunit of PtdIns 3-kinase is phosphorylated in vitro on serine at a stoichiometry of approximately 1 mol of phosphate per mol of p85. This phosphorylation results in a three- to sevenfold decrease in PtdIns 3-kinase activity. Dephosphorylation with protein phosphatase 2A reverses the inhibition. This suggests that the association of protein phosphatase 2A with middle T antigen may function to activate PtdIns 3-kinase. C1 BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MOLEC & CELLULAR PHYSIOL,BOSTON,MA 02115. TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02111. RP CARPENTER, CL (reprint author), BETH ISRAEL HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02215, USA. RI Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 FU NCI NIH HHS [CA 34722]; NIGMS NIH HHS [GM 36624, GM 41890, R01 GM041890] NR 39 TC 216 Z9 216 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1993 VL 13 IS 3 BP 1657 EP 1665 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN579 UT WOS:A1993KN57900039 PM 8382773 ER PT J AU WITZGALL, R OLEARY, E GESSNER, R OUELLETTE, AJ BONVENTRE, JV AF WITZGALL, R OLEARY, E GESSNER, R OUELLETTE, AJ BONVENTRE, JV TI KID-1, A PUTATIVE RENAL TRANSCRIPTION FACTOR - REGULATION DURING ONTOGENY AND IN RESPONSE TO ISCHEMIA AND TOXIC INJURY SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DEPENDENT PROTEIN-KINASE; ZINC FINGER GENE; CATALYTIC SUBUNIT; MOUSE KIDNEY; C-FOS; EXPRESSION; SEQUENCES; FAMILY; DNA; DIFFERENTIATION AB We have identified a new putative transcription factor from the rat kidney, termed Kid-1 (for kidney, ischemia and developmentally regulated gene 1). Kid-1 belongs to the C2H2 class of zinc finger genes. Its mRNA accumulates with age in postnatal renal development and is detected predominantly in the kidney. Kid-1 mRNA levels decline after renal injury secondary to ischemia or folic acid administration, two insults which result in epithelial cell dedifferentiation, followed by regenerative hyperplasia and differentiation. The low expression of Kid-1 early in postnatal development, and when renal tissue is recovering after injury, suggests that the gene product is involved in establishment of a differentiated phenotype and/or regulation of the proliferative response. The deduced protein contains 13 C2H2 zinc fingers at the COOH end in groups of 4 and 9 separated by a 32-amino-acid spacer. There are consensus sites for phosphorylation in the NH2 terminus non-zinc finger region as well as in the spacer region between zinc fingers 4 and 5. A region of the deduced protein shares extensive homology with a catalytic region of Raf kinases, a feature shared only with TFIIE among transcription factors. To determine whether Kid-1 can modulate transcription, a chimeric construct encoding the Kid-1 non-zinc finger region (sense or antisense) and the DNA-binding region of GAL4 was transfected into COS and LLC-PK1 cells together with a chloramphenicol acetyltransferase (CAT) reporter plasmid containing GAL4 binding sites, driven by either a minimal promoter or a simian virus 40 enhancer. CAT activity was markedly inhibited in cells transfected with the sense construct compared with the activity in cells transfected with the antisense construct. To our knowledge, this pattern of developmental regulation, kidney expression, and regulation of transcription is unique among the C2H2 class of zinc finger-containing DNA-binding proteins. C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 38452, DK 12769, DK 39773] NR 57 TC 97 Z9 98 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1993 VL 13 IS 3 BP 1933 EP 1942 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN579 UT WOS:A1993KN57900068 PM 8382778 ER PT J AU DEFRANCO, C DAMON, DH ENDOH, M WAGNER, JA AF DEFRANCO, C DAMON, DH ENDOH, M WAGNER, JA TI NERVE GROWTH-FACTOR INDUCES TRANSCRIPTION OF NGFIA THROUGH COMPLEX REGULATORY ELEMENTS THAT ARE ALSO SENSITIVE TO SERUM AND PHORBOL 12-MYRISTATE 13-ACETATE SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID C-FOS GENE; PROTEIN KINASE-C; SWISS 3T3 CELLS; PC12 CELLS; NEURITE OUTGROWTH; RESPONSE ELEMENT; CYCLIC-AMP; 12-O-TETRADECANOYL PHORBOL-13-ACETATE; MESSENGER-RNAS; BINDING-SITE AB The expression of NGFIA (also known as egr1, zif268, TIS8, krox24, and d2) is rapidly and transiently increased by nerve growth factor (NGF) in PC12 cells. The 5'-region of this gene includes four serum response elements (SREs), a cAMP-like response element, an AP1-like response element, and an SP1-binding site. From deletion analysis of chloramphenicol acetyltransferase reporter constructs, we have established that the first 106 basepairs 5' of the transcriptional start site are sufficient for induction of NGFIA by NGF in PC12 cells; deletion beyond this point results in dramatically reduced induction of the gene. Using defined mutations in the NGFIA promoter and NGFIA-thymidine kinase hybrid promoters, we have defined three elements (SRE1, SRE2, and AP1-like) in the first 106 basepairs of upstream DNA, each of which contributes to induction of NGFIA by NGF. Cooperation by two of these elements (i.e. the two SREs or one SRE and the AP1-like element) is sufficient to confer transcriptional induction by NGF, but the combination of all three elements increased induction by NGF more effectively than a pair of elements. This suggests that the response of NGFIA to NGF is mediated by a cis-acting sequence that is composed of at least three distinct elements. An oligonucleotide composed of SRE1 and SRE2 that can confer the ability for NGF induction to heterologous promoter constructs complexes with proteins in PC12 cell nuclear extracts, but the protein-DNA complexes do not appear to be altered by NGF treatment, as measured by DNA mobility shift assays. We have also established that the regulatory region of NGFIA that mediates NGF induction also mediates the induction by serum and phorbol 12-myristate 13-acetate, suggesting that multiple signal transduction pathways must converge on these sequences to regulate the expression of this gene. C1 HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV PEDIAT ONCOL, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA-0936, CA-22427] NR 64 TC 49 Z9 49 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD MAR PY 1993 VL 7 IS 3 BP 365 EP 379 DI 10.1210/me.7.3.365 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KU730 UT WOS:A1993KU73000006 PM 8483478 ER PT J AU NEAR, RI MUDGETTHUNTER, M NOVOTNY, J BRUCCOLERI, R NG, SC AF NEAR, RI MUDGETTHUNTER, M NOVOTNY, J BRUCCOLERI, R NG, SC TI CHARACTERIZATION OF AN ANTIDIGOXIN ANTIBODY-BINDING SITE BY SITE-DIRECTED INVITRO MUTAGENESIS SO MOLECULAR IMMUNOLOGY LA English DT Article ID 3-DIMENSIONAL STRUCTURE; IDIOTYPE FAMILY; MUTATIONS; COMPLEX; HEAVY; GENES; SET AB In vitro mutagenesis and immunoglobulin gene transfection were used to investigate the binding site of a monoclonal antibody, 2610, that binds to digoxin, a cardiac glycoside. A computer model was generated in order to select sites in the complementarity determining regions (CDR) that would participate in binding. Residues in the CDR segments were chosen that possess high solvent exposure and were located in a putative cleft. The cloned heavy and light chain variable regions were subjected to in vitro mutagenesis at these sites. The mutated variable regions in M13 were then subcloned into expression vectors and transfected. The affinities and specificity binding properties of the resultant expressed antibodies were measured. Many of the mutants of the putative contact residues showed significant but not major alterations of binding properties. Since most of the residues in the binding site are non-polar and aromatic and since many of the mutations resulted in only modest binding changes, we theorize that much of the high affinity binding (> 10(9)/M) is the cumulation of many weak interactions, arising from dispersion forces and hydrophobic effects in the pocket. Preliminary mutagenesis of two L chain positions proposed to bind to the lactone end of digoxin have larger binding effects. Specificity studies show that the mutants more frequently possess altered binding to the lactone ring of digoxin that altered binding to other digoxin moieties. The data are most suggestive of a model in which lactone is at the bottom of a binding pocket, followed by the steroid nucleus and then by the sugar moiety extruding out of the pocket. The binding information may be useful in understanding the immune response to large, hydrophobic haptens. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ 08543. RP NEAR, RI (reprint author), MASSACHUSETTS GEN HOSP,CELLULAR & MOLEC RES LAB,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL19259] NR 29 TC 14 Z9 14 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD MAR PY 1993 VL 30 IS 4 BP 369 EP 377 DI 10.1016/0161-5890(93)90066-K PG 9 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA KT203 UT WOS:A1993KT20300005 PM 8455637 ER PT J AU SIEGEL, RE AF SIEGEL, RE TI CLINICAL CORRELATES OF PATHOLOGICAL FINDINGS - CASE 1 SO MOUNT SINAI JOURNAL OF MEDICINE LA English DT Article ID PULMONARY MICROVASCULAR CYTOLOGY; LYMPHANGITIC CARCINOMATOSIS; COR-PULMONALE; TUMOR EMBOLI; DIAGNOSIS; LUNG; CANCER C1 BRONX VET AFFAIRS MED CTR,MED INTENS CARE UNIT,BRONX,NY 10468. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. RP SIEGEL, RE (reprint author), BRONX VET AFFAIRS MED CTR,PULM SECT,BRONX,NY 10468, USA. NR 14 TC 0 Z9 0 U1 0 U2 0 PU MOUNT SINAI HOSPITAL PI NEW YORK PA BOX 1094 ONE GUSTAVE L LEVY PLACE ATTN: CIRCULATION ASST, NEW YORK, NY 10029-6574 SN 0027-2507 J9 MT SINAI J MED JI Mt. Sinai J. Med. PD MAR PY 1993 VL 60 IS 2 BP 121 EP 126 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA KT909 UT WOS:A1993KT90900006 PM 8469243 ER PT J AU BREAKEFIELD, XO AF BREAKEFIELD, XO TI GENE DELIVERY INTO THE BRAIN USING VIRUS VECTORS SO NATURE GENETICS LA English DT Editorial Material ID GLIOMA C1 HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RP BREAKEFIELD, XO (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,MOLEC NEUROGENET UNIT,BOSTON,MA 02114, USA. NR 20 TC 52 Z9 52 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 MAR PY 1993 VL 3 IS 3 BP 187 EP 189 DI 10.1038/ng0393-187 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA KP790 UT WOS:A1993KP79000002 PM 8485570 ER PT J AU KAJIWARA, K SANDBERG, MA BERSON, EL DRYJA, TP AF KAJIWARA, K SANDBERG, MA BERSON, EL DRYJA, TP TI A NULL MUTATION IN THE HUMAN PERIPHERIN RDS GENE IN A FAMILY WITH AUTOSOMAL DOMINANT RETINITIS PUNCTATA ALBESCENS SO NATURE GENETICS LA English DT Article ID HUMAN RETINAL DEGENERATION; SLOW RDS; GEL-ELECTROPHORESIS; RHODOPSIN MUTATIONS; MESSENGER-RNA; PIGMENTOSA; IDENTIFICATION; POLYMORPHISMS; NUCLEOTIDE; SEQUENCE AB The murine rds (retinal degeneration slow) allele is a semidominant null allele that causes photoreceptor degeneration. The wild-type sequence at the rds locus encodes a photoreceptor disc membrane protein named peripherin/RDS. Mutations in the homologous human peripherin/RDS gene can cause autosomal dominant retinitis pigmentosa, but these are missense mutations or deletions of single codons. No obvious null alleles have been reported in humans, so that the human phenotype corresponding to rds is as yet unknown. Here we report a 2-basepair deletion in codon 25 of the human gene in a family with autosomal dominant retinitis punctata albescens, suggesting that this disease, rather than retinitis pigmentosa, is the comparable human phenotype. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [EY08683, EY00169] NR 32 TC 145 Z9 149 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 MAR PY 1993 VL 3 IS 3 BP 208 EP 212 DI 10.1038/ng0393-208 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA KP790 UT WOS:A1993KP79000008 PM 8485575 ER PT J AU GASSER, T FAHN, S BREAKEFIELD, XO AF GASSER, T FAHN, S BREAKEFIELD, XO TI GENETICS OF THE IDIOPATHIC DYSTONIAS SO NERVENHEILKUNDE LA German DT Article DE DYSTONIA; MOVEMENT DISORDERS; GENETICS ID TORSION DYSTONIA; DOMINANT INHERITANCE; MYOCLONIC DYSTONIA; 9Q32-34; JEWS AB Recent advances in the molecular genetic analysis of the idiopathic torsion dystonias (ITD) have provided considerable improvement of our understanding of these diseases. The localization of a causative gene for early-onset generalized ITD on chromosome 9q34 (DYT1) in Ashkenazi-Jewish and non-Jewish families have helped to delineate the phenotypic spectrum of the mutation and made improved genetic counselling possible. Mutations in at least two other genes can cause dystonia: one on the X-chromosome and at least one, possibly several other, so far unmapped, autosomal genes. The role of genetic factors as a cause of the prevalent focal dystonias of adult onset will have to be elucidated by further genetic studies. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT NEUROL,DYSTONIA CLIN RES CTR,NEW YORK,NY 10032. RP GASSER, T (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA 02129, USA. NR 30 TC 1 Z9 1 U1 1 U2 1 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0722-1541 J9 NERVENHEILKUNDE JI Nervenheilkunde PD MAR PY 1993 VL 12 IS 2 BP 75 EP 79 PG 5 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KT551 UT WOS:A1993KT55100005 ER PT J AU KISCHKA, U MANDIR, AS GHIKA, J GROWDON, JH AF KISCHKA, U MANDIR, AS GHIKA, J GROWDON, JH TI ELECTROPHYSIOLOGIC DETECTION OF EXTRAPYRAMIDAL MOTOR SIGNS IN ALZHEIMERS-DISEASE SO NEUROLOGY LA English DT Article ID PARKINSONS-DISEASE; DEMENTIA; DIAGNOSIS; SEVERITY AB We applied quantitative methods to measure extrapyramidal signs in 50 Alzheimer's disease (AD) patients and 40 age-matched control subjects. We measured tremor using accelerometers, bradykinesia using computer-detected reaction times (RTs) and movement times (MTs), and rigidity using a strain gauge linked to a movable arm rest. We excluded subjects with a clinical diagnosis of Parkinson's disease and subjects who required antiparkinsonian, neuroleptic, or anxiolytic medications. Aside from rigidity in two patients, there were no extrapyramidal signs on clinical examination. Based on electrophysiologic measures, however, there was a significant increase in muscle tone (p < 0.001), RT (p < 0.01), and MT (p < 0.03) in AD patients as a group compared with control subjects. Within the AD group, muscle tone and MTs increased across clinical stages of dementia severity (p < 0.05). Tremor frequency and amplitude were normal in AD subjects. These data indicate that quantitative neurophysiologic measures are superior to conventional clinical examinations in detecting extrapyramidal signs in AD. The pathologic substrates of extrapyramidal signs in AD are uncertain but seem to be linked to the degenerative AD process. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,ACC 830,BOSTON,MA 02114. UNIV HEIDELBERG,W-6900 HEIDELBERG,GERMANY. EMORY UNIV,SCH MED,ATLANTA,GA 30322. SERV NEUROL,LAUSANNE,SWITZERLAND. FU NIA NIH HHS [P50 AG05134] NR 26 TC 28 Z9 28 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1993 VL 43 IS 3 BP 500 EP 505 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA KT215 UT WOS:A1993KT21500008 PM 8450990 ER PT J AU HARDIMAN, O FAUSTMAN, D LI, X SKLAR, RM BROWN, RH AF HARDIMAN, O FAUSTMAN, D LI, X SKLAR, RM BROWN, RH TI EXPRESSION OF MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS IN CULTURES OF CLONALLY DERIVED HUMAN MYOBLASTS SO NEUROLOGY LA English DT Article ID CLASS-II ANTIGENS; SKELETAL-MUSCLE; HLA-DR; MYOGENESIS; CELLS; MODULATION; DISORDERS; SURFACE; GAMMA; THY-1 AB We examined class I and class II HLA antigen expression by flow cytometry in clonal cultures derived from normal human skeletal muscle biopsies. Both HLA class I and class II antigens were constitutively expressed in all clones studied. By altering the constituents of the culture medium, we could modulate the expression of HLA class II but not HLA class I antigens. We noted heterogeneity in the expression of HLA class II antigens among different clones; an increased expression was associated with an increased propensity of myoblasts to fuse. These findings indicate that normal aneurally cultured myoblasts may express both HLA class I and class II antigens, that this expression may be modulated by in vitro agents, and that the presence of these antigens may relate to the process of in vitro myoblast fusion. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CECIL B DAY LAB NEUROMUSCULAR RES,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIABET UNIT,IMMUNOBIOL LAB,BOSTON,MA 02114. FU PHS HHS [R01 00787-05] NR 22 TC 11 Z9 12 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 MAR PY 1993 VL 43 IS 3 BP 604 EP 608 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA KT215 UT WOS:A1993KT21500027 PM 8451007 ER PT J AU CATANIA, MV HOLLINGSWORTH, Z PENNEY, JB YOUNG, AB AF CATANIA, MV HOLLINGSWORTH, Z PENNEY, JB YOUNG, AB TI QUISQUALATE RESOLVES 2 DISTINCT METABOTROPIC [H-3] GLUTAMATE BINDING-SITES SO NEUROREPORT LA English DT Article DE METABOTROPIC; RECEPTORS; SUBTYPES; QUISQUALATE; T-ACPD ID AMINO-ACID RECEPTOR; GLUTAMATE RECEPTOR; RAT-BRAIN; EXPRESSION AB METABOTROPIC receptor subtypes have been proposed based on pharmacological, signal transduction and cDNA sequence data. We assessed potential metabotropic binding site subtypes with in vitro quantitative [H-3]glutamate autoradiography in adult rat brains in the presence of saturating concentrations of N-methyl-D-aspartate (NMDA) and (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA). Quisqualate (QUIS) competition curves resolved two differentially distributed binding sites (K(Ihigh) = 17 nM; K(Ilow) = 62 muM). Trans-1-amino-cyclopentane-1,3-dicarboxylic acid (t-ACPD) and 1S,3R-ACPD displaced [H-3]glutamate binding both in the absence and presence of a quisqualate concentration (2.5 muM) that saturates the high affinity sites, suggesting that both sites are linked to metabotropic receptors. We conclude that two metabotropic binding sites with different distributions and pharmacological profiles can be detected with selective [H-3]glutamate binding assays. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,KENNEDY 9,FRUIT ST,BOSTON,MA 02114. RI Catania, Maria Vincenza/E-2627-2017 OI Catania, Maria Vincenza/0000-0002-9329-8517 FU NINDS NIH HHS [NS 19613] NR 21 TC 21 Z9 21 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAR PY 1993 VL 4 IS 3 BP 311 EP 313 DI 10.1097/00001756-199303000-00021 PG 3 WC Neurosciences SC Neurosciences & Neurology GA KT661 UT WOS:A1993KT66100021 PM 7682857 ER PT J AU ZHAO, JL SASTRY, SM SPERDUTO, RD CHEW, EY REMALEY, NA YANNUZZI, LA SORENSON, JA SEDDON, JM GRAGOUDAS, ES PULIAFITO, CA BURTON, TC FARBER, MD BLAIR, N STELMACK, T AXELROD, A HALLER, J PUSIN, S CASSEL, G SEIGEL, D SPERDUTO, RD HILLER, R CHEW, E TAMBOLI, A MILLER, DT SOWELL, AL GUNTER, EW DUNN, M AF ZHAO, JL SASTRY, SM SPERDUTO, RD CHEW, EY REMALEY, NA YANNUZZI, LA SORENSON, JA SEDDON, JM GRAGOUDAS, ES PULIAFITO, CA BURTON, TC FARBER, MD BLAIR, N STELMACK, T AXELROD, A HALLER, J PUSIN, S CASSEL, G SEIGEL, D SPERDUTO, RD HILLER, R CHEW, E TAMBOLI, A MILLER, DT SOWELL, AL GUNTER, EW DUNN, M TI ARTERIOVENOUS CROSSING PATTERNS IN BRANCH RETINAL VEIN OCCLUSION SO OPHTHALMOLOGY LA English DT Article AB Purpose: The study was designed to evaluate the relative anatomic position of the crossing vessels at the site of occlusion in eyes with branch retinal vein occlusion (BRVO). Methods: Fundus photographs of 106 eyes (104 patients) with recent BRVO from the Eye Disease Case-Control Study were used to examine the relative position of artery and vein at occluded crossings. Three separate comparison groups were formed by identifying corresponding arteriovenous crossings for each occluded crossing in: (1) the ipsilateral but opposite vessel arcade within eyes affected by BRVO; (2) the same quadrant in unaffected eyes of BRVO patients; and (3) the same quadrant in eyes of patients without BRVO, matched by age, sex, and race with the BRVO patients. Results: The site of obstruction of the branch vein was an arteriovenous crossing in all affected eyes. In 99% of eyes with BRVO, the artery was located anterior to the vein at the obstructed site. In the three comparison groups, the artery was anterior to the vein in 62%, 61%, and 54% of the crossings, respectively, yielding statistically significant differences for each group of control crossings compared with BRVO crossings (P < 0.001). Conclusion: Finding the vein to be consistently between the more rigid artery and the retina at almost all arteriovenous crossings affected by BRVO suggests a possible role for mechanical obstruction in the pathogenesis of BRVO. C1 NEI,DEPT HLTH & HUMAN SERV,BIOMETRY & EPIDEMIOL PROGRAM,BLDG 31,6A24,BETHESDA,MD 20892. MANHATTAN EYE EAR & THROAT HOSP,NEW YORK,NY 10021. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. MED COLL WISCONSIN,MILWAUKEE,WI 53226. ORKAND CORP,CTR COORDINATING,SILVER SPRING,MD. UNIV ILLINOIS,CHICAGO,IL 60680. JOHNS HOPKINS UNIV HOSP,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. CTR DIS CONTROL,CTR ENVIRONM HLTH & HYG CONTROL,DIV ENVIRONM HLTH LAB SCI,ATLANTA,GA 30333. FU Intramural NIH HHS [Z99 EY999999] NR 11 TC 81 Z9 87 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAR PY 1993 VL 100 IS 3 BP 423 EP 428 PG 6 WC Ophthalmology SC Ophthalmology GA KT500 UT WOS:A1993KT50000030 PM 8460014 ER PT J AU YOUNG, RH AF YOUNG, RH TI TUBULO-PAPILLARY ADENOMA (SO-CALLED NEPHROGENIC ADENOMA) ARISING IN THE RENAL PELVIS - CRITICAL COMMENTARY SO PATHOLOGY RESEARCH AND PRACTICE LA English DT Letter RP YOUNG, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0344-0338 J9 PATHOL RES PRACT JI Pathol. Res. Pract. PD MAR PY 1993 VL 189 IS 2 BP 226 EP 226 PG 1 WC Pathology SC Pathology GA KY676 UT WOS:A1993KY67600019 ER PT J AU GIA, O MOBILIO, S PALUMBO, M PATHAK, MA AF GIA, O MOBILIO, S PALUMBO, M PATHAK, MA TI BENZO-PSORALEN AND TETRAHYDROBENZO-PSORALEN CONGENERS - DNA-BINDING AND PHOTOBIOLOGICAL PROPERTIES SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID PHOTOREACTION AB Four new benzo- and tetrahydrobenzo-psoralens have been examined in their reversible interaction toward DNA and in their DNA-photobinding properties. These compounds were also examined for their ability to produce singlet oxygen and in vivo skin photosensitization reaction. Fluorescence and equilibrium dialysis measurements show that the complexation ability of benzoderivatives is remarkably high. Binding is less effective in the case of the tetrahydrocongeners. All compounds photoreact quite effectively to DNA. The photoadducts were obtained by enzymatic hydrolysis of drug-modified DNA and were characterized by high performance liquid chromatographic elution techniques. The 3,4 position represents the unique photoreactive site for benzopsoralens. Denaturation-renaturation experiments confirm that the benzoderivatives are purely monofunctional, while the tetrahydrocongeners form interstrand cross-links, even though to a remarkably lesser extent than 8-methoxypsoralen (8-MOP). The new compounds, in the presence of long-wavelength ultraviolet radiation, are very moderately effective in forming reactive oxygen species; they are ineffective in promoting oxidation of tyrosine and 3-(3,4-dihydroxyphenyl)alanine to dopachrome and melanin. Skin photosensitizing experiments on guinea pigs indicate that benzo- and tetrahydrobenzopsoralen derivatives are almost devoid of any phototoxic effects. Thus, this class of compounds appears to be interesting for the development of new, less phototoxic chemotherapeutic agents that interact with DNA better than 8-MOP. C1 UNIV PADUA,CNR,CTR STUDIO CHIM FARMACO & PROD BIOL ATT,DEPT PHARMACEUT SCI,I-35131 PADUA,ITALY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 26 TC 30 Z9 30 U1 1 U2 2 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD MAR PY 1993 VL 57 IS 3 BP 497 EP 503 DI 10.1111/j.1751-1097.1993.tb02325.x PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KT699 UT WOS:A1993KT69900017 PM 8475185 ER PT J AU ENOCHS, WS NILGES, MJ SWARTZ, HM AF ENOCHS, WS NILGES, MJ SWARTZ, HM TI A STANDARDIZED TEST FOR THE IDENTIFICATION AND CHARACTERIZATION OF MELANINS USING ELECTRON-PARAMAGNETIC-RESONANCE (EPR) SPECTROSCOPY SO PIGMENT CELL RESEARCH LA English DT Article DE MELANINS; PIGMENTS; PIGMENTATION; MELANOMA; ELECTRON PARAMAGNETIC RESONANCE SPECTROSCOPY; TEST ID NATURAL MELANINS AB Melanins are complex, incompletely understood polymeric pigments that historically have been difficult to investigate with common chemical, histochemical, and physico-chemical techniques. Because these pigments uniquely contain a stable population of organic free radicals, electron paramagnetic resonance (EPR) spectroscopy is a particularly effective method for studying them, and a set of qualitative EPR criteria has been established for their identification. However, a number of practical problems have arisen in applying these criteria to identify and characterize unknown pigments in relatively scarce pathological specimens, indicating that a standardized approach is needed. As reported here, a standardized EPR test for melanin based on the EPR criteria has been developed, guided by the requirements that it be sensitive, accurate, simple, and easy to interpret. It has been evaluated using the well-characterized synthetic melanin prepared by alkaline autooxidation of 5,6-dihydroxyphenylalanine (Dopa) and initially applied to the identification and characterization of an unknown pigment purified from an unusual malignant lung tumor. C1 UNIV ILLINOIS,COLL MED,URBANA,IL 61801. MASSACHUSETTS GEN HOSP,MRPP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,HANOVER,NH 03756. FU NCI NIH HHS [5 T32 CA 09067]; NCRR NIH HHS [RR 01811] NR 21 TC 82 Z9 84 U1 1 U2 10 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0893-5785 J9 PIGM CELL RES JI Pigm. Cell. Res. PD MAR PY 1993 VL 6 IS 2 BP 91 EP 99 DI 10.1111/j.1600-0749.1993.tb00587.x PG 9 WC Cell Biology; Dermatology SC Cell Biology; Dermatology GA LD176 UT WOS:A1993LD17600004 PM 8391699 ER PT J AU LI, CJ ZHANG, LJ DEZUBE, BJ CRUMPACKER, CS PARDEE, AB AF LI, CJ ZHANG, LJ DEZUBE, BJ CRUMPACKER, CS PARDEE, AB TI 3 INHIBITORS OF TYPE-1 HUMAN-IMMUNODEFICIENCY-VIRUS LONG TERMINAL REPEAT-DIRECTED GENE-EXPRESSION AND VIRUS-REPLICATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID TUMOR NECROSIS FACTOR; TOPOISOMERASE-I; HIV-1 REPLICATION; BETA-LAPACHONE; FACTOR-ALPHA; T-CELLS; ACTIVATION; TOXICITY; INVITRO AB Transcription of type 1 human immunodeficiency virus (HIV-1) provirus is governed by the viral long terminal repeat (LTR). Drugs can block HIV-1 replication by inhibiting activity of its LTR. We report that topotecan, beta-lapachone, and curcumin are potent and selective inhibitors of HIV-1 LTR-directed gene expression, at concentrations that have minor effects on cells. At these concentrations, each drug inhibited p24 antigen production in cells either acutely or chronically infected with HIV-1. Their target is transcriptional function of the LTR. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV INFECT DIS,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02215. RP LI, CJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 50608]; NIAID NIH HHS [AI 29173, AI 62534] NR 27 TC 175 Z9 183 U1 0 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 1 PY 1993 VL 90 IS 5 BP 1839 EP 1842 DI 10.1073/pnas.90.5.1839 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KP979 UT WOS:A1993KP97900044 PM 8446597 ER PT J AU BUSCIGLIO, J GABUZDA, DH MATSUDAIRA, P YANKNER, BA AF BUSCIGLIO, J GABUZDA, DH MATSUDAIRA, P YANKNER, BA TI GENERATION OF BETA-AMYLOID IN THE SECRETORY PATHWAY IN NEURONAL AND NONNEURONAL CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AMYLOID PRECURSOR PROTEIN; GOLGI COMPLEX; LYSOSOME; ASTROCYTE; ALZHEIMER DISEASE ID ALZHEIMERS-DISEASE; PROTEIN; PRECURSOR; PEPTIDE; IDENTIFICATION; AGGREGATION; CLEAVAGE; DEPOSITS; TANGLES; PLAQUES AB The cellular mechanism underlying the generation of beta-amyloid in Alzheimer disease and its relationship to the normal metabolism of the amyloid precursor protein are unknown. In this report, we show that 3- and 4-kDa peptides derived from amyloid precursor protein are normally secreted. Epitope mapping and radiolabel sequence analysis suggest that the 4-kDa peptide is closely related to full-length beta-amyloid and the 3-kDa species is a heterogeneous set of peptides truncated at the beta-amyloid N terminus. The beta-amyloid peptides are secreted in parallel with amyloid precursor protein. Inhibitors of Golgi processing inhibit secretion of beta-amyloid peptides, whereas lysosomal inhibitors have no effect. The secretion of beta-amyloid-related peptides occurs in a wide variety of cell types, but which peptides are produced and their absolute levels are dependent on cell type. Human astrocytes generated higher levels of beta-amyloid than any other cell type examined. These results suggest that beta-amyloid is generated in the secretory pathway and provide evidence that glial cells are a major source of beta-amyloid production in the brain. C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,ENDERS 260,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MIT,WHITEHEAD INST BIOMED RES,DEPT BIOL,CAMBRIDGE,MA 02142. RI Matsudaira, Paul/H-1475-2012 OI Matsudaira, Paul/0000-0002-8399-3276 FU NIA NIH HHS [AG09229]; NINDS NIH HHS [NS30352] NR 33 TC 494 Z9 504 U1 5 U2 19 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 1 PY 1993 VL 90 IS 5 BP 2092 EP 2096 DI 10.1073/pnas.90.5.2092 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KP979 UT WOS:A1993KP97900096 PM 8446635 ER PT J AU WOODY, G SCHUCKIT, M WEINRIEB, R YU, E AF WOODY, G SCHUCKIT, M WEINRIEB, R YU, E TI A REVIEW OF THE SUBSTANCE USE DISORDERS SECTION OF THE DSM-IV SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID ALCOHOL DEPENDENCE C1 SAN DIEGO VET AFFAIRS MED CTR,SAN DIEGO,CA. UNIV PENN,ADDICT TREATMENT & RES CTR,PHILADELPHIA,PA 19104. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. RP WOODY, G (reprint author), PHILADELPHIA VET AFFAIRS MED CTR,BLDG 7,39TH & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [DA 05186]; NIMH NIH HHS [MH 47200] NR 6 TC 9 Z9 9 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0193-953X J9 PSYCHIAT CLIN N AM JI Psychiatr. Clin. North Amer. PD MAR PY 1993 VL 16 IS 1 BP 21 EP 32 PG 12 WC Psychiatry SC Psychiatry GA KZ893 UT WOS:A1993KZ89300004 PM 8456046 ER PT J AU WEDDINGTON, WW AF WEDDINGTON, WW TI COCAINE - DIAGNOSIS AND TREATMENT SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID INTERPERSONAL PSYCHOTHERAPY; RELAPSE PREVENTION; LONG-TERM; ABUSERS; ABSTINENCE; TRIAL RP WEDDINGTON, WW (reprint author), VET AFFAIRS MED CTR,DEPT PSYCHIAT 116,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 32 TC 9 Z9 9 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0193-953X J9 PSYCHIAT CLIN N AM JI Psychiatr. Clin. North Amer. PD MAR PY 1993 VL 16 IS 1 BP 87 EP 95 PG 9 WC Psychiatry SC Psychiatry GA KZ893 UT WOS:A1993KZ89300009 PM 8456049 ER PT J AU BLACKER, D TSUANG, MT AF BLACKER, D TSUANG, MT TI UNIPOLAR RELATIVES IN BIPOLAR PEDIGREES - ARE THEY BIPOLAR SO PSYCHIATRIC GENETICS LA English DT Article DE BIPOLAR DISORDER; CASENESS INDEX; LINKAGE ANALYSIS; PEDIGREE STUDIES; UNIPOLAR DISORDER ID MANIC-DEPRESSIVE ILLNESS; AFFECTIVE-DISORDERS; MAJOR DEPRESSION; PSYCHIATRIC-DISORDERS; GENETIC TRANSMISSION; DIAGNOSTIC CRITERIA; LINKAGE ANALYSIS; X-CHROMOSOME; FAMILY; RELIABILITY AB The ambiguous status of unipolar relatives in the pedigrees of bipolar probands has long plagued investigators, and may have contributed significantly to the difficulties replicating linkage findings for bipolar disorder. We present here a conceptual model, based on a selective review of family and course data, and use it to quantify this problem, concluding that 65-74% of the unipolar relatives of bipolars must be bipolar from the genetic point of view. We then offer a set of predictions for the characteristics of UP individuals who are ''genetically bipolar'', and suggest that these characteristics should lead to differences between UP relatives of BPs and other UP groups. Such differences could then be combined to form a caseness index that would rank unipolar relatives by the chances that they are ''genetically bipolar'', and could serve as Ott's measure of certainty that weights the contribution of individual unipolar relatives in a linkage analysis. We conclude with a review of the implications of this model for the unipolar-bipolar distinction and the potential benefits and limitations of this approach to classification in linkage analyses of bipolar and other psychiatric disorders. C1 HARVARD UNIV,SCH PUBL HLTH,PROGRAM PSYCHIAT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. BROCKTON VA MED CTR,BROCKTON,MA. NR 68 TC 39 Z9 39 U1 2 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8829 J9 PSYCHIATR GENET JI Psychiatr. Genet. PD SPR PY 1993 VL 3 IS 1 BP 5 EP 16 DI 10.1097/00041444-199321000-00002 PG 12 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA KU639 UT WOS:A1993KU63900002 ER PT J AU HAMBURG, P AF HAMBURG, P TI PREOEDIPAL ARTICULATIONS - CLINICAL REFLECTIONS ON KRISTEVA AND IRIGARAY SO PSYCHOANALYTIC REVIEW LA English DT Article RP HAMBURG, P (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WALL 805,BOSTON,MA 02114, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2836 J9 PSYCHOANAL REV PD SPR PY 1993 VL 80 IS 1 BP 135 EP 150 PG 16 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA LC521 UT WOS:A1993LC52100007 PM 8316605 ER PT J AU SURMAN, OS AF SURMAN, OS TI POSSIBLE IMMUNOLOGICAL EFFECTS OF PSYCHOTROPIC MEDICATION SO PSYCHOSOMATICS LA English DT Article ID DELAYED-TYPE HYPERSENSITIVITY; ORGAN-TRANSPLANTATION; DEPRESSION; LITHIUM; CYCLOSPORINE; REJECTION; MODULATOR; SYSTEM AB Psychoactive drugs provide an essential intervention in the care of organ transplant recipients, yet little is known of their effect on immunological function. Human and animal data on immunological effects of neuroleptic (e.g., haloperidol, phenothiazines) and antidepressant agents (e.g., tricyclic antidepressants,fluoxetine) lead to conflicting hypotheses. Lithium carbonate acts through the phosphoinositide system and has a bipolar effect on neuronal activity. Lithium is known to have immune-enhancing properties and is difficult to administer in the peritransplant period but nonetheless deserves study for possible beneficial effects on allograft function. C1 MASSACHUSETTS GEN HOSP,TRANSPLANT UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. NR 27 TC 16 Z9 16 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 MAR-APR PY 1993 VL 34 IS 2 BP 139 EP 143 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA KP461 UT WOS:A1993KP46100006 PM 8456156 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI MEDICAL PSYCHIATRIC PRACTICE, VOL 1 - STOUDEMIRE,A, FOGEL,BS SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP GREENBERG, DB (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, 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 MAR-APR PY 1993 VL 34 IS 2 BP 188 EP 189 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA KP461 UT WOS:A1993KP46100016 ER PT J AU SCHOUTEN, R AF SCHOUTEN, R TI MENTAL DISABILITY LAW - A PRIMER, 4TH EDITION - ZUCKERMAN,D, CHARMANTZ,M SO PSYCHOSOMATICS LA English DT Book Review RP SCHOUTEN, R (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 1 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD MAR-APR PY 1993 VL 34 IS 2 BP 190 EP 190 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA KP461 UT WOS:A1993KP46100018 ER PT J AU SCOTT, JA PALMER, EL AF SCOTT, JA PALMER, EL TI NEURAL NETWORK ANALYSIS OF VENTILATION-PERFUSION LUNG SCANS SO RADIOLOGY LA English DT Article DE COMPUTERS, DIAGNOSTIC AID; COMPUTERS, NEURAL NETWORK; EMBOLISM, PULMONARY; LUNG, PERFUSION; LUNG, VENTILATION; RADIONUCLIDE IMAGING, TECHNOLOGY ID RADIOLOGIC-DIAGNOSIS AB A neural network model was constructed to interpret ventilation-perfusion (V/Q) lung scans. This model was trained with data from 100 consecutive V/Q scans with pulmonary angiographic correlation. The network was constructed from 28 input parameters that described various standard V/Q findings, which were fed into a single hidden layer that contained 10-20 nodes. The network output indicated the percentage probability of pulmonary embolism for each set of findings on V/Q scans. This network was then used to classify 28 new scans; the resultant classifications were compared with the rankings of an experienced observer who read the scans without knowledge of the correlative angiographic data. The network with 15 hidden nodes outperformed the experienced observer in prediction of the likelihood of pulmonary embolism in the 28-case test set (P = .039). The neural network has several advantages over current algorithms for interpretation of V/Q scans, including the ability to synthesize many variables into a single conclusion and to learn, or modify itself, at exposure to additional data. RP SCOTT, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 10 TC 50 Z9 50 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD MAR PY 1993 VL 186 IS 3 BP 661 EP 664 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KN053 UT WOS:A1993KN05300009 PM 8430170 ER PT J AU STACEYCLEAR, A MCCARTHY, KA HALL, DA PILESPELLMAN, E WHITE, G HULKA, CA WHITMAN, GJ HALPERN, EF KOPANS, DB AF STACEYCLEAR, A MCCARTHY, KA HALL, DA PILESPELLMAN, E WHITE, G HULKA, CA WHITMAN, GJ HALPERN, EF KOPANS, DB TI MAMMOGRAPHICALLY DETECTED BREAST-CANCER - LOCATION IN WOMEN UNDER 50 YEARS OLD SO RADIOLOGY LA English DT Article DE BREAST NEOPLASMS, LOCALIZATION; BREAST NEOPLASMS, RADIOGRAPHY; BREAST RADIOGRAPHY AB The mammograms of 86 women under the age of 50 years with mammographically detected cancers were reviewed. Sixty-three of these cancers (73%) were found at the periphery of the breast as defined by a zone 1 cm wide beneath the subcutaneous fat or anterior to the retromammary fat. This finding is likely due to the geometric configuration of the breast. If the breast is hemispheric, then more than 50% of the volume of breast tissue lies within this zone in a large percentage of women. Furthermore, the contrasting adjacent fat likely improves the ability to perceive an abnormality. Interaction of the terminal ducts with chemicals contained within or produced by the fat is a much less likely reason for the high percentage of cancers in this zone. Radiologists should be aware of this phenomenon and pay particular attention to this zone. C1 MASSACHUSETTS GEN HOSP,DEPT SURG ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 7 TC 17 Z9 17 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD MAR PY 1993 VL 186 IS 3 BP 677 EP 680 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KN053 UT WOS:A1993KN05300012 PM 8381550 ER PT J AU RABITO, CA FANT, LST WALTMAN, AC AF RABITO, CA FANT, LST WALTMAN, AC TI RENAL-FUNCTION IN PATIENTS AT RISK OF CONTRAST MATERIAL INDUCED ACUTE-RENAL-FAILURE - NONINVASIVE, REAL-TIME MONITORING SO RADIOLOGY LA English DT Article DE ANGIOGRAPHY, COMPLICATIONS; CONTRAST MEDIA, TOXICITY; DIETHYLENETRIAMINEPENTAACETIC ACID (DTPA); KIDNEY, FAILURE; KIDNEY, RADIONUCLIDE STUDY ID ANGIOGRAPHY; PYELOGRAPHY AB Real-time changes in renal function were studied in a group of 20 patients at risk of contrast-material-induced acute renal failure during different angiographic procedures. Renal function was evaluated with an ambulatory renal monitor (ARM) after a single injection of the glomerular filtration agent technetium-99m diethylenetriaminepentaacetic acid (DTPA). The ARM was used to continuously monitor the clearance of Tc-99m DTPA activity from the extracellular space in the arm of the patient during angiography. A one-compartment model was used to calculate on-line the rate constant for clearance of Tc-99m DTPA from the extracellular space. Changes in the rate constant were compared with changes in plasma creatinine level measured 1-4 days after angiography. The results showed that the ARM measured rapid changes in renal function during angiography with a resolution time of 5-10 minutes in patients with normal to moderately decreased renal function and 15-20 minutes in patients with severe renal dysfunction. The sensitivity of this technique was superior to that of plasma creatinine level analysis. C1 MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RABITO, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,100 FRUIT ST,BOSTON,MA 02114, USA. NR 21 TC 13 Z9 13 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD MAR PY 1993 VL 186 IS 3 BP 851 EP 854 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KN053 UT WOS:A1993KN05300040 PM 8430198 ER PT J AU HILDEBRANDT, N SOKOL, SM AF HILDEBRANDT, N SOKOL, SM TI IMPLICIT SUBLEXICAL PHONOLOGICAL PROCESSING IN AN ACQUIRED DYSLEXIC PATIENT SO READING AND WRITING LA English DT Article DE ACQUIRED DYSLEXIA; DEEP DYSLEXIA; IMPLICIT PROCESSING; SPELLING REGULARITY; SUBLEXICAL PHONOLOGICAL PROCESSING ID WORD IDENTIFICATION; TIME-COURSE; SOUND; RECOGNITION; DECISION; ALEXIA AB We report a case study of an acquired dyslexic subject, who on tasks standardly used to assess acquired dyslexia showed no evidence of having any access to sublexical phonological information. However, on a lexical decision task, he showed normal effects of spelling regularity for low-frequency words. Since this effect is typically attributed to the use of sublexical phonological information in word recognition, it appears that sublexical phonological processing is occurring for this subject. The spelling regularity effect is discussed with respect to models of written word recognition and to acquired dyslexia. It is suggested that the reason for the discrepancy in test results may be that the types of explicit tasks previously used in the neuropsychological literature on dyslexia, which require conscious awareness of phonological representations, are not sensitive to implicit processing. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HILDEBRANDT, N (reprint author), MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,VINCENT BURNHAM 830,FRUIT ST,BOSTON,MA 02114, USA. NR 52 TC 16 Z9 16 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0922-4777 J9 READ WRIT JI Read. Writ. PD MAR PY 1993 VL 5 IS 1 BP 43 EP 68 DI 10.1007/BF01026918 PG 26 WC Education & Educational Research; Psychology, Educational SC Education & Educational Research; Psychology GA KP567 UT WOS:A1993KP56700004 ER PT J AU SCHREINER, MS LEKSELL, LG GOBRAN, SR HOFFMAN, EA SCHERER, PW NEUFELD, GR AF SCHREINER, MS LEKSELL, LG GOBRAN, SR HOFFMAN, EA SCHERER, PW NEUFELD, GR TI MICROEMBOLI REDUCE PHASE-III SLOPES OF CO-2 AND INVERT PHASE-III SLOPES OF INFUSED SF6 SO RESPIRATION PHYSIOLOGY LA English DT Article DE DEAD SPACE, PULMONARY EMBOLIZATION; EXPIROGRAM, CO2; GAS EXCHANGE, PULMONARY EMBOLIZATION; GAS MIXING, INTRAPULMONARY; MAMMALS, GOAT; PULMONARY BLOOD FLOW, EMBOLIZATION ID SINGLE-BREATH WASHOUT; HEAVY-WATER; DOG LUNGS; PULMONARY; MODEL; CO2; HE AB We investigated the effect of increasing doses of intravenously infused glass microspheres (mean diameter 125 mum) on gas exchange in anesthetized, heparinized, mechanically ventilated goats (VT = 16-18 ml/kg). Breath-by-breath CO2 expirograms were collected using a computerized system (Study A) during the infusion of a total of 15 g of microspheres. We found a 50% decrease in extravascular lung water by indicator dilution with a corresponding doubling of alveolar dead space (VDalv). Airways deadspace (VDaw) decreased by 13 ml (10%) and mean normalized phase III slope for CO2 decreased from 0.23 to -0.08 L-1 becoming negative in 3 of 5 animals. In a second study (Study B), simultaneous breath-by-breath CO2 and infused SF6 expirograms were collected using an infrared CO2 analyzer and a mass spectrometer. Under baseline conditions VDaw for CO2 was smaller than for SF6 and the ratio of the phase III slope for SF6 to the phase III slope for CO2 was 1.39. Following embolization there were no differences in VDaw between the two gases, however, the phase III slope for CO2 became either slightly negative or extremely flat, while the phase III slope for SF6 became negative in 73% of the breaths ( -0.17 L-1, P < 0.05). Negative phase III slopes have been predicted by a single path model when blood flow is confined to the most mouthward generations of the acinus (Schwardt et al., Ann. Biomed. Engin, 19: 679-697, 1991). The agreement between the numerical model and the experimental data is consistent with a serial distribution of blood flow within the acinus. C1 PHILADELPHIA VA MED CTR,DEPT ANESTHESIA,38TH ST & WOODLAND AVE,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT ANESTHESIA,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT RADIOL,PHILADELPHIA,PA 19104. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA. UNIV PENN,SCH ENGN & APPL SCI,DEPT BIOENGN,PHILADELPHIA,PA 19104. FU NHLBI NIH HHS [HL-33891] NR 30 TC 18 Z9 18 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0034-5687 J9 RESP PHYSIOL JI Respir. Physiol. PD MAR PY 1993 VL 91 IS 2-3 BP 137 EP 154 DI 10.1016/0034-5687(93)90095-R PG 18 WC Physiology; Respiratory System SC Physiology; Respiratory System GA KR630 UT WOS:A1993KR63000001 PM 8469840 ER PT J AU MUELLER, PR DAWSON, SL AF MUELLER, PR DAWSON, SL TI PROVINCIALISM SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Editorial Material RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0739-9529 J9 SEMIN INTERVENT RAD JI Semin. Interv. Radiol. PD MAR PY 1993 VL 10 IS 1 BP U1 EP U1 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KR298 UT WOS:A1993KR29800001 ER PT J AU HAMBERG, LM MACFARLANE, R TASDEMIROGLU, E BOCCALINI, P HUNTER, GJ BELLIVEAU, JW MOSKOWITZ, MA ROSEN, BR AF HAMBERG, LM MACFARLANE, R TASDEMIROGLU, E BOCCALINI, P HUNTER, GJ BELLIVEAU, JW MOSKOWITZ, MA ROSEN, BR TI MEASUREMENT OF CEREBROVASCULAR CHANGES IN CATS AFTER TRANSIENT ISCHEMIA USING DYNAMIC MAGNETIC-RESONANCE-IMAGING SO STROKE LA English DT Article DE CEREBRAL BLOOD FLOW; CEREBRAL BLOOD VOLUME; CEREBRAL ISCHEMIA; HEMODYNAMICS; MAGNETIC RESONANCE IMAGING; CATS ID CEREBRAL BLOOD-FLOW; ULTRAFAST COMPUTED-TOMOGRAPHY; SUSCEPTIBILITY; CONTRAST; VOLUME; DIFFUSION; HYPEREMIA; NMR AB Background and Purpose: Hemodynamic changes associated with acute ischemia cannot be measured with conventional nuclear magnetic resonance imaging. In this study, we used dynamic susceptibility-contrast magnetic resonance imaging to measure the changes in vascular transit time and relative cerebral blood volume in a feline occlusion-reperfusion model. Methods: Dynamic susceptibility-contrast measurements were obtained before and during 10 minutes of global cerebral ischemia and for up to 3 hours after the onset of reperfusion. A cerebral blood flow index was calculated from the vascular transit time and relative cerebral blood volume measurements. Functional maps were constructed to demonstrate the regional hemodynamic differences resulting from the induced ischemia. Results: During the early phase after reperfusion, both the relative cerebral blood volume and blood flow index rose sharply, followed by a fall to near-basal levels at 45 minutes (1 x control and 1.3 x control, respectively). Thereafter, the volume rose slowly, whereas the How index continued to drop. At 3 hours, cerebral blood volume had reached 1.6 times its control value, whereas the flow index had returned to its base value. Conclusions: The hemodynamic behavior we observed in our model reflects the independent responses of the cerebral blood volume and flow index to ischemic insult. Measurements acquired by our method were consistent with the temporal behavior reported in previous radionuclide studies. Susceptibility-contrast nuclear magnetic resonance tomographic imaging proved to be valuable in detecting and quantifying both immediate and subsequent changes in the hemodynamic state of the ischemic and hyperemic feline brain. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,STROKE RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HAMBERG, LM (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,13TH ST,BLDG 149,2ND FLOOR,BOSTON,MA 02129, USA. RI Moskowitz, Michael/D-9916-2011 FU NCI NIH HHS [R01-CA40303]; NHLBI NIH HHS [R01-HL39810]; NINDS NIH HHS [NS-10828] NR 33 TC 102 Z9 102 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD MAR PY 1993 VL 24 IS 3 BP 444 EP 451 PG 8 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA KP501 UT WOS:A1993KP50100024 PM 8446981 ER PT J AU MEYER, JS TERAYAMA, Y TAKASHIMA, S OBARA, K WEATHERS, S AF MEYER, JS TERAYAMA, Y TAKASHIMA, S OBARA, K WEATHERS, S TI DENSITOMETRIC COMPARISONS OF POLIO-ARAIOSIS AND LEUKOARAIOSIS AMONG PATIENTS WITH ISCHEMIC VASCULAR DEMENTIA AND NORMAL VOLUNTEERS SO STROKE LA English DT Meeting Abstract C1 DEPT VET AFFAIRS MED CTR,HOUSTON,TX. BAYLOR COLL MED,HOUSTON,TX 77030. 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 MAR PY 1993 VL 24 IS 3 BP 511 EP 511 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA KP501 UT WOS:A1993KP50100093 ER PT J AU TERAYAMA, Y MEYER, JS KAWAMURA, J WEATHERS, S AF TERAYAMA, Y MEYER, JS KAWAMURA, J WEATHERS, S TI COGNITIVE RECOVERY CORRELATES WITH WHITE-MATTER RESTITUTION AFTER HEAD-INJURY SO SURGICAL NEUROLOGY LA English DT Article DE HEAD INJURY; COGNITION; WHITE-MATTER INTEGRITY; CEREBRAL BLOOD FLOW ID CEREBRAL BLOOD-FLOW; NORMAL-PRESSURE HYDROCEPHALUS; ENHANCED COMPUTED-TOMOGRAPHY; MULTI-INFARCT DEMENTIA; VASCULAR DEMENTIA; LESIONS; SCANS; CT AB Longitudinal measurements of local cerebral perfusion (LCBF) and local partition coefficients (Llambda) using xenon-enhanced computed tomography were examined in six patients who had suffered from head injury at a mean age of 30 +/- 9.3 years. They were selected from a larger group with head injury because all were observed longitudinally to make excellent cognitive recovery some years after acute cerebral trauma. Results were compared with similar longitudinal measurements made in six age-matched neurologically normal volunteers. In the index group, cognitive test scores were reduced at the time of the first LCBP measurement but significantly improved to normal at the time of the second. The mean interval between measurements was 2.7 +/- 0.7 years. At the time of the first measurement, all six patients exhibited abnormal volumes of white matter with reduced Hounsfield numbers and LCBF and Llambda values. Abnormalities in volume of white matter and LCBF and Llambda values improved to normal at the time of the second measurement. Perfusion values for frontal cortex, putamen, and thalamus were still slightly reduced but also improved toward normal between measurements. Cognitive recovery correlated best with restoration of white matter integrity, suggesting that following head injury, cognitive impairments may be associated with temporary disconnections of corticothalamic projection systems. C1 BAYLOR COLL MED,DEPT NEUROL,BLDG 7,ROOM 225,2002 HOLCOMBE BLVD,HOUSTON,TX 77030. DEPT VET AFFAIRS MED CTR,RADIOL SERV,HOUSTON,TX. DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,HOUSTON,TX. BAYLOR COLL MED,DEPT RADIOL,HOUSTON,TX 77030. NR 35 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0090-3019 J9 SURG NEUROL JI Surg. Neurol. PD MAR PY 1993 VL 39 IS 3 BP 177 EP 186 DI 10.1016/0090-3019(93)90179-5 PG 10 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA KV341 UT WOS:A1993KV34100001 PM 8456379 ER PT J AU BARRETT, BB ANDERSEN, JW ANDERSON, KC AF BARRETT, BB ANDERSEN, JW ANDERSON, KC TI STRATEGIES FOR THE AVOIDANCE OF BACTERIAL-CONTAMINATION OF BLOOD COMPONENTS SO TRANSFUSION LA English DT Article ID ROOM-TEMPERATURE; PLATELET TRANSFUSIONS; APHERESIS PLATELETS; WHITE CELLS; SEPSIS; STERILITY; PRODUCTS; CENTRIFUGATION; PROLIFERATION; STORAGE AB Gram staining and bacterial culturing methods were used to determine the incidence of bacterial contamination of cellular blood components at the time of transfusion reactions. Over a 5-year period, 2208 (4.3%) of 51,278 transfusions were complicated by reactions. Overall bacterial contamination occurred in 5 (0.03%) of 17,928 transfusions of single-donor apheresis platelets, 1 (0.14%) of 712 transfusions of pooled random-donor platelet concentrates, 1 (0.003%) of 31,385 transfusions of red cells, and 0 of 1253 transfusions of fresh-frozen plasma. Gram staining done at the time of positive cultures was positive in three of six cases. Although six of seven recipients of contaminated components suffered no clinical sequelae, contaminated transfusions may have been a contributing cause of death in one case. Attempts were made to avoid the transfusion of contaminated cellular blood components by performing routine bacterial cultures: 0 of 341 quality control cultures were positive. To avoid the transfusion of contaminated platelets by identifying bacteria, Gram staining was performed in all single-donor apheresis platelet units collected on open systems and daily in platelets stored >48 hours: 8 (0.15%) of 5334 smears done on 3829 platelet units were interpreted as positive, and those units were not transfused, but only two of eight units were culture positive. These studies suggest that bacterial contamination can result in adverse clinical sequelae in transfusion recipients and that both culturing and Gram staining are poor methods of screening for contaminated units. More sensitive and specific methods of generalized screening for bacterial contamination are needed. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,BLOOD COMPONENT LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 29 TC 127 Z9 129 U1 0 U2 2 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD MAR PY 1993 VL 33 IS 3 BP 228 EP 233 DI 10.1046/j.1537-2995.1993.33393174449.x PG 6 WC Hematology SC Hematology GA KQ447 UT WOS:A1993KQ44700010 PM 8438224 ER PT J AU COMPTON, CC AF COMPTON, CC TI WOUND-HEALING POTENTIAL OF CULTURED EPITHELIUM SO WOUNDS-A COMPENDIUM OF CLINICAL RESEARCH AND PRACTICE LA English DT Article; Proceedings Paper CT CLINICAL AND RESEARCH SYMP ON INNOVATIVE TECHNOLOGIES AND WOUND HEALING CY OCT 01-03, 1992 CL GRAD HOSP, PHILADELPHIA, PA SP GRAD HOSP, WOUND CARE CTR HO GRAD HOSP AB Cultured epithelial autografts (CEAU) represent a lifesaving technique for providing rapid, permanent wound coverage and skin replacement in massive burns. This therapy, initiated only 10 years ago, is now used in burn treatment worldwide and is part of standard burn therapy in over 80% of the burn units in the U.S.A. Moreover, recognition of the wound healing promotional capabilities of cultured keratinocytes (whether autologous or allogeneic) has lead to their use solely for this purpose in the treatment of many other types of disease and injury, dramatically increasing the scope of their clinical application over the past decade. This article is a review of our studies on the biological effects of cultured epithelial grafts on wound healing in treated patients and represents a presentation given at a 1992 symposium on Innovative Technologies in Wound Care in Philadelphia, PA sponsored by the Graduate Hospital Wound Care Center. RP COMPTON, CC (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,15 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 21 Z9 22 U1 0 U2 1 PU HEALTH MANAGEMENT PUBLICATIONSINC PI WAYNE PA 950 WEST VALLEY RD, STE 2800, WAYNE, PA 19087 SN 1044-7946 J9 WOUNDS JI Wounds-Compend. Clin. Res. Pract. PD MAR-APR PY 1993 VL 5 IS 2 BP 97 EP 111 PG 15 WC Dermatology; Surgery SC Dermatology; Surgery GA KW655 UT WOS:A1993KW65500009 ER PT J AU SASAKI, Y ZHANG, XF NISHIYAMA, M AVRUCH, J WANDS, JR AF SASAKI, Y ZHANG, XF NISHIYAMA, M AVRUCH, J WANDS, JR TI EXPRESSION AND PHOSPHORYLATION OF INSULIN-RECEPTOR SUBSTRATE-1 DURING RAT-LIVER REGENERATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID EPIDERMAL GROWTH-FACTOR; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; KINASE; AUTOPHOSPHORYLATION; ACTIVATION; ONCOGENES; PROTEINS; BLOOD AB Insulin has been shown to be important for normal liver regeneration to occur. The mechanisms whereby insulin may exert its effects on hepatocyte growth, however, are still unknown. The rat and human insulin receptor substrate 1 (IRS-1) is a specific target molecule for the insulin receptor beta subunit kinase and will bind to signal transducing molecules containing Src homology 2 domains through its multiple tyrosyl phosphorylation (TP) sites. This investigation examined how IRS-1 may be involved in insulin action during hepatocyte growth induced by two-thirds partial hepatectomy. The TP of IRS-1 was strikingly enhanced prior to the major wave of hepatocyte DNA synthesis at 24 h; IRS-1 protein and mRNA expression increased in parallel to a lesser extent after partial hepatectomy. TP of insulin receptor beta subunit, which enhances its kinase activity toward IRS-1, was increased in association with TP of IRS-1. Finally, phosphatidylinositol 3-kinase, one of signal transducing molecules containing Src homology 2 domains, was associated with IRS-1 following TP in vivo. These observations suggest that IRS-1 protein may play an important role in transmitting the insulin signal to intracellular regulators involved in hepatocyte growth. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,149 13TH ST,7TH FLOOR,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIABET UNIT,BOSTON,MA 02129. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02666, AA-08169] NR 33 TC 57 Z9 57 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 3805 EP 3808 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300003 PM 8382678 ER PT J AU MOORE, SEH SPIRO, RG AF MOORE, SEH SPIRO, RG TI INHIBITION OF GLUCOSE TRIMMING BY CASTANOSPERMINE RESULTS IN RAPID DEGRADATION OF UNASSEMBLED MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I MOLECULES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID N-LINKED OLIGOSACCHARIDES; ALPHA-D-MANNOSIDASE; ASIALOGLYCOPROTEIN RECEPTOR SUBUNITS; PRE-GOLGI DEGRADATION; ENDOPLASMIC-RETICULUM; RAT-LIVER; 1-DEOXYNOJIRIMYCIN; GLYCOPROTEINS; CLEAVAGE; ANTIGEN AB The CMT-cK(d)1 cell line provides a system for studying the initial processing steps of N-linked oligosaccharides as these cells have been shown to produce major histocompatibility complex (MHC) class I molecules which, due to a defect in assembly, recycle between the endoplasmic reticulum and a pre-Golgi compartment, failing to reach the cell surface (Hsu, V. W., Yuan, L. C., Nuchtern, J. G., Lippincott-Schwartz, J., Hammerling, G. J., and Klausner, R. D. (1991) Nature 352, 441-444). In the present study we observed that when the MHC class I heavy chain of these CMT cells was pulse-radiolabeled with [S-35]methionine in the presence of the glucosidase inhibitor, castanospermine (CST), it underwent a rapid degradation during a 60-min chase, in contrast to control cells in which it remained stable during that period. The CST-promoted instability of the MHC molecule appeared to be specific, as it did not occur when 1-deoxymannojirimycin, an inhibitor of mannosidase, was added to the cells. Although endomannosidase was found to be present in the CMT cells, the electrophoretic mobility of the MHC heavy chain produced in the presence of CST indicated that deglucosylation through the alternate route provided by this enzyme did not occur. Furthermore, gamma-interferon did not prevent the rapid disappearance of the MHC molecule, although it brought about entry of this glycoprotein into the secretory pathway in cells incubated without CST. The results of our studies suggest that retention of glucose on N-linked oligosaccharides may under certain circumstances provide a signal for pre-Golgi protein degradation. C1 JOSLIN DIABET CTR,ELLIOTT P JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK17477] NR 27 TC 72 Z9 73 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 3809 EP 3812 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300004 PM 8440676 ER PT J AU HOLTZMAN, EJ KINANE, TB WEST, K SOPER, BW KARGA, H AUSIELLO, DA ERCOLANI, L AF HOLTZMAN, EJ KINANE, TB WEST, K SOPER, BW KARGA, H AUSIELLO, DA ERCOLANI, L TI TRANSCRIPTIONAL REGULATION OF G-PROTEIN-ALPHA-I SUBUNIT GENES IN LLC-PK1 RENAL-CELLS AND CHARACTERIZATION OF THE PORCINE G-ALPHA-I-3 GENE PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MURINE SARCOMA-VIRUS; MESSENGER-RNA LEVELS; GTP-BINDING PROTEIN; PERTUSSIS TOXIN; MAMMALIAN-CELLS; SIGNAL TRANSDUCTION; ADENYLATE-CYCLASE; EPITHELIAL-CELLS; DNA METHYLATION; NA+ CHANNELS AB Heterotrimeric guanine nucleotide-binding proteins (G-proteins) function as signal transducers for a variety of hormone-coupled enzyme and ion transport systems in eukaryotic cells. The expression of pertussis toxin-sensitive G-proteins (G(i)) which couple their cognate receptors and effectors are regulated by cell cycle-dependent events in porcine LLC-PK1 renal epithelial cells. Galpha(i-2) and Galpha(i-3) isoforms are detected in these cells, and like Galpha(i-2) (Holtzman, E. J., Soper, B. W., Stow, L. L., Ausiello, D. A., and Ercolani, L. (1991) J. Biol. Chem. 266, 1763-1771), we now demonstrate that Galpha(i-3) mRNA and protein is coordinately expressed in these cells during differentiation. To gain further insights into these events, the porcine Galpha(i-3) gene minimal promoter was characterized and found 67 base pairs upstream from the major transcription start site. The 56-base pair minimal promoter lacked TATAAA and GC boxes but did contain a sequence GGAAGTG conserved in both the human and porcine gene that could potentially bind an adenovirus E4TF1 transcription factor. In cells stably transfected with Galpha(i-2) or Galpha(i-3) gene 5'-flanking sequences fused to firefly luciferase cDNA reporter, temporal 10-15-fold transcriptional activation of both genes occurred before cellular polarization. Utilizing mobility shift assays which compared nuclear extracts from cells before and after cell polarization, a motif in the 5' region of the gene promoter GTACTTCCGCT was identified that bound an induced nuclear protein complex during transcriptional activation. In polarized cells complemented with the human glucocorticoid receptor, dexamethasone decreased Galpha(i-2) but increased Galpha(i-3) basal transcription and mRNA content 3-fold. These studies demonstrate that both Galpha(i) genes are dynamically regulated in LLC-PK1 cells by both growth, differentiation, and hormone signals. C1 MASSACHUSETTS GEN HOSP E,RENAL UNIT,8TH FLOOR,149 13TH ST,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NIDDK NIH HHS [DK 42543] NR 70 TC 21 Z9 21 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 3964 EP 3975 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300027 PM 8440688 ER PT J AU SHOELSON, SE LEE, JS LYNCH, CS BACKER, JM PILCH, PF AF SHOELSON, SE LEE, JS LYNCH, CS BACKER, JM PILCH, PF TI BPA(B25) INSULINS - PHOTOACTIVATABLE ANALOGS THAT QUANTITATIVELY CROSS-LINK, RADIOLABEL, AND ACTIVATE THE INSULIN-RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MUTANT HUMAN INSULIN; BIOLOGICAL-ACTIVITY; PLASMA-MEMBRANE; BINDING-SITE; SUBUNIT STRUCTURE; PROTEIN DESIGN; SELECTIVE H-2; SIDE-CHAIN; MAIN CHAIN; ASSIGNMENT AB Benzoylphenylalanine (Bpa), a photoactivatable amino acid was incorporated into the 25 position of the insulin B-chain by a combination of chemical synthesis and enzymatic semisynthesis. Bpa(B25) insulin binds specifically to the insulin receptor with an affinity almost-equal-to 40% that of native insulin. Addition of biotin or epsilon-amino-hexanoic acid-iminobiotin at the epsilon-Lys(B29) position to form Bpa(B25),B29epsilon-biotinyl (BBpa) or Bpa(B25),B29epsilon-(Aha-iminobiotin) analogues had little adverse effect on receptor binding affinity and provided a convenient handle for affinity purification, gel shift assays, and blotting of cross-linked complexes with avidin. The analogues were readily I-125-iodinated with the majority of I-125 being incorporated at the Tyr(A14) position; the monoiodo-A14 derivative was easily separated from other forms by high performance liquid chromatography. Photolysis of a complex of the insulin receptor and either Bpa(B25) insulin or [I-125]iodo-Tyr(A14),Bpa(B25) insulin yields a covalent insulin-receptor complex. The efficiency of cross-linking with these reagents was unusually high, ranging from 60 to 100%. Furthermore, cross-linking to the insulin receptor results in kinase activation in vitro, and in intact cells insulin receptor phosphorylation and internalization were both activated. Notably, even at saturating concentrations one molecule of Bpa(B25) insulin covalently cross-linked each alpha2beta2 receptor, demonstrating that holoreceptor activation occurs with one high affinity insulin binding site occupied and, if a second insulin binds with lower affinity it must be in a different orientation. Bpa insulin analogues form a new class of photoaffinity reagents which facilitate studies relating insulin-insulin receptor structure and function. C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. RP SHOELSON, SE (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK36836, R01 DK36424, R01 DK43123] NR 63 TC 61 Z9 62 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 4085 EP 4091 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300045 PM 8382690 ER PT J AU LEE, JS OHARE, T PILCH, PF SHOELSON, SE AF LEE, JS OHARE, T PILCH, PF SHOELSON, SE TI INSULIN-RECEPTOR AUTOPHOSPHORYLATION OCCURS ASYMMETRICALLY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSINE KINASE-ACTIVITY; STRUCTURAL BASIS; LIGAND-BINDING; CYTOPLASMIC DOMAIN; HEPATOMA-CELLS; HUMAN-PLACENTA; HIGH-AFFINITY; BETA-SUBUNIT; PHOSPHORYLATION; REGION AB The unoccupied insulin receptor is a structurally symmetric, disulfide-linked dimer, comprising two alphabeta halves, each with a potential insulin binding alpha subunit and a kinase active beta subunit. In the accompanying paper (Shoelson, S. E., Lee, J., Lynch, C. S., Backer, J. M., and Pilch, P. F. (1993) J. Biol. Chem. 268, 4085-4091), we described the utility of a novel insulin analogue, L-benzoylphenylalanine(B25),B29epsilon-biotin insulin (BBpa insulin)1 as a probe for receptor behavior, and we determined that binding and cross-linking of one BBpa insulin molecule could fully stimulate insulin receptor autophosphorylation. Here we use this analogue to determine the symmetry of the autophosphorylation reaction. The alphabeta half-receptor that does not covalently couple to BBpa insulin incorporates 50% more orthophosphate than the alphabeta half that becomes coupled to the insulin analogue. Phosphopeptide mapping of each receptor half shows minimal differences in the phosphorylation sites or their relative contribution to the phosphate content of each half. The kinetics of P-32 incorporation into each receptor half are essentially identical over a 10-20-min time course. Phosphopeptide mapping analysis reveals that the phosphate incorporation patterns do not change between the two alphabeta half-receptor forms (BBpa insulin-linked and unlinked, respectively) at different time points or concentrations of ATP ranging from 12 to 200 muM. Based on these and other data, we propose a model of insulin receptor activation whereby binding of one insulin molecule can trigger autophosphorylation in an asymmetric fashion. C1 BOSTON UNIV,SCH MED,DEPT BIOCHEM,80 E CONCORD ST,BOSTON,MA 02118. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. FU NIDDK NIH HHS [DK36424, DK36836, DK43123] NR 44 TC 51 Z9 53 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 4092 EP 4098 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300046 PM 8440700 ER PT J AU AJCHENBAUM, F ANDO, K DECAPRIO, JA GRIFFIN, JD AF AJCHENBAUM, F ANDO, K DECAPRIO, JA GRIFFIN, JD TI INDEPENDENT REGULATION OF HUMAN D-TYPE CYCLIN GENE-EXPRESSION DURING G1-PHASE IN PRIMARY HUMAN LYMPHOCYTES-T SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; CDC2 PROTEIN-KINASE; CELL-CYCLE; MESSENGER-RNA; ACTIVATION; PRODUCT; YEAST; PROLIFERATION; PHOSPHORYLATION; PROGRESSION AB Cyclins and cyclin-dependent kinases are critically involved in controlling cell cycle progression in virtually all cells. The recent identification of candidate G1 cyclins in mammalian cells has been a major advance in this field, but the exact functions of these cyclins are unknown. The expression of three D-type cyclins (D1, D2, and D3) was investigated in primary human T lymphocytes as these cells were induced to leave G0, traverse G1, and enter S phase by T cell-specific mitogens. G0 phase T cells expressed low levels of cyclin D2, but not cyclin D3. Treatment of these cells with phytohemagglutinin and 12-O-tetradecanoylphorbol-13-acetate in the presence of fetal calf serum resulted in rapid induction of cyclin D2 RNA in early G1 and slower induction of cyclin D3 in late G1. Cyclin D1 was not detected in T cells under any condition tested. Treatment of T cells with hydroxyurea to arrest cells at G1/S did not block induction of either D2 or D3. However, arrest of cells in mid G1 with deferoxamine blocked D3 expression without affecting D2. Cyclosporin A blocked the induction of both cyclin D2 and D3. Polyclonal antisera were prepared in rabbits against both cyclin D2 and cyclin D3 glutathione S-transferase fusion proteins and used to examine cyclin D2 and D3 proteins in [S-35]methionine-labeled T cells. Protein levels were found to correlate closely with RNA levels for both cyclins. No detectable histone HI kinase activity could be precipitated with either cyclin. However, several cellular proteins were observed to coprecipitate with the cyclins, including several proteins that were observed to associate only with D3. These results indicate that striking differences exist in the induction and regulation of two candidate G1 cyclins in human T cells and suggest that these cyclins could participate in multiple cell cycle check-points during G0, G1, or S phase. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV NEOPLAST DIS MECHANISMS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 41 TC 253 Z9 257 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 4113 EP 4119 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300049 PM 8382693 ER PT J AU RHODES, CJ THORNE, BA LINCOLN, B NIELSEN, E HUTTON, JC THOMAS, G AF RHODES, CJ THORNE, BA LINCOLN, B NIELSEN, E HUTTON, JC THOMAS, G TI PROCESSING OF PROOPIOMELANOCORTIN BY INSULIN SECRETORY GRANULE PROINSULIN PROCESSING ENDOPEPTIDASES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOUSE PROOPIOMELANOCORTIN; PRO-OPIOMELANOCORTIN; MAMMALIAN-CELLS; ATT20 CELLS; PROHORMONE; CDNA; YEAST; KEX2; EXPRESSION; PROALBUMIN AB A lysed preparation of isolated insulin secretory granules efficiently cleaved murine proopiomelanocortin (mPOMC) at physiologically important Lys-Arg processing sites. This processing was mostly attributed to an activity that co-eluted with the proinsulin processing type-II endopeptidase from anion exchange chromatography (Lys-Arg-directed; Davidson, H. W., Rhodes, C. J., and Hutton, J. C. (1988) Nature 333, 93-96). The principal peptide hormone products generated by the insulin secretory granule lysate were identified by specific radioimmunoassay and NH2-terminal microsequencing analysis of high performance liquid chromatography-separated products as alpha-melanocyte-stimulating hormone, corticotropin-like intermediate, gamma-lipotropin, beta-endorphin-(1-31), 18-kDa NH2-terminal fragment and, to a lesser extent, adrenocorticotrophin and beta-lipotropin. This processing had an acidic pH optimum (pH 5-5.5) and was Ca2+-dependent (K0.5 activation = 5-80 muM). With increasing Ca2+ concentrations there was an increase in the extent to which mPOMC was processed. The in vitro processing of mPOMC by the insulin secretory granule endopeptidase activity reported here is in excellent agreement with the in vivo processing of this prohormone by a combination of PC2 and PC3, candidates of prohormone endpeptidase, in gene transfer studies with cells that express the regulated secretory pathway (Thomas, L., Leduc, R., Thorne, B. A., Smeekens, S. S., Steiner, D. F., and Thomas, G. (1991) Proc. Natl. Acad. Sci. U. S. A. 88, 5297-5301). C1 NOVO NORDISK,NOVO ALLE 28800,DENMARK. OREGON HLTH SCI UNIV,VOLLUM INST,PORTLAND,OR 97201. UNIV CAMBRIDGE,ADDENBROOKES HOSP,DEPT CLIN BIOCHEM,CAMBRIDGE CB2 2QR,ENGLAND. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RHODES, CJ (reprint author), BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,EP JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02115, USA. FU NCRR NIH HHS [BRGS07RR05673]; NIDDK NIH HHS [DK37274, R01 DK037274, DK36836, P30 DK036836]; Wellcome Trust NR 49 TC 21 Z9 21 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 4267 EP 4275 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300067 PM 8382698 ER PT J AU ALARCON, C LINCOLN, B RHODES, CJ AF ALARCON, C LINCOLN, B RHODES, CJ TI THE BIOSYNTHESIS OF THE SUBTILISIN-RELATED PROPROTEIN CONVERTASE PC3, BUT NOT THAT OF THE PC2 CONVERTASE, IS REGULATED BY GLUCOSE IN PARALLEL TO PROINSULIN BIOSYNTHESIS IN RAT PANCREATIC-ISLETS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INSULIN-SECRETORY-GRANULE; MESSENGER-RNA; TRANSLATIONAL CONTROL; COORDINATE REGULATION; BETA-CELL; PROTEINS; KEX2; CDNA; FURIN; IDENTIFICATION AB The biosynthesis of proinsulin is specifically stimulated by glucose in the pancreatic beta-cell, and this, in turn, places an increased demand on the mechanism for proinsulin to insulin conversion. Proteolytic proinsulin processing is catalyzed by two endopeptidases putatively identified as the subtilisin-related PC2 and PC3 convertases (Bennett, D. L., Bailyes, E. M., Nielson, E., Guest, P. C., Rutherford, N. G., Arden, S. D., and Hutton, J. C. (1992) J. Biol. Chem. 267, 15229-15236; Bailyes, E. M., Shennan, K. I. J., Seal, A. J., Smeekens, S. P., Steiner, D. F., Hutton, J. C., and Docherty, K. (1992) Biochem. J. 285, 391-394). In this study, we demonstrate in isolated rat pancreatic islets that the biosynthesis of PC3 was specifically stimulated by glucose relatively parallel to that of proinsulin. In contrast, however, PC2 biosynthesis was not glucose-regulated. The stimulation of PC3 and proinsulin biosynthesis was observed above a threshold of 4 mM glucose and reached a maximum (about 7-10-fold) above 10 mM glucose concentrations. Glucose stimulation for PC3 and proinsulin biosynthesis was rapid (occurring within 20 min and reaching a maximum by 60 min) and was not affected by the additional presence of actinomycin D, suggesting regulation predominately at the translational level. Moreover, the intracellular signals for glucose-stimulated PC3 and proinsulin biosynthesis appeared to be similar, requiring the metabolism of glucose. PC3 has been implicated as the key endopeptidase in proinsulin to insulin conversion, in that it is the enzyme which preferentially initiates the process (Rhodes, C. J., Lincoln, B., and Shoelson, S. E. (1992) J. Biol. Chem. 267, 22719-22727). We suggest that co-ordinate stimulation of PC3 biosynthesis, along with that of its proinsulin substrate, elucidates an additional control point by which the mechanism of proprotein processing might be regulated. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,EP JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCRR NIH HHS [BRGS07RR05673]; NIDDK NIH HHS [DK36836] NR 42 TC 135 Z9 135 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1993 VL 268 IS 6 BP 4276 EP 4280 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN533 UT WOS:A1993KN53300068 PM 8440711 ER PT J AU GORDON, LI HARRINGTON, D ANDERSEN, J AF GORDON, LI HARRINGTON, D ANDERSEN, J TI CHOP VERSUS M-BACOD IN NON-HODGKINS-LYMPHOMA - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP GORDON, LI (reprint author), NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 25 PY 1993 VL 328 IS 8 BP 581 EP 581 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KP053 UT WOS:A1993KP05300017 ER PT J AU AGUAYO, SM MILLER, YE KING, TE AF AGUAYO, SM MILLER, YE KING, TE TI IDIOPATHIC HYPERPLASIA OF PULMONARY NEUROENDOCRINE CELLS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID PEPTIDES; SMOKERS C1 DENVER VET AFFAIRS MED CTR,DENVER,CO 80220. NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO 80206. RP AGUAYO, SM (reprint author), ATLANTA VET AFFAIRS MED CTR,DECATUR,GA 30033, USA. NR 5 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 FEB 25 PY 1993 VL 328 IS 8 BP 582 EP 582 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KP053 UT WOS:A1993KP05300019 ER PT J AU QUINN, DA HALES, CA THOMPSON, BT TERRIN, ML AF QUINN, DA HALES, CA THOMPSON, BT TERRIN, ML TI SUBSELECTING PATIENTS AT RISK FOR PULMONARY-EMBOLISM - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MARYLAND MED RES INST,BALTIMORE,MD. RP QUINN, DA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 24 PY 1993 VL 269 IS 8 BP 987 EP 987 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KM603 UT WOS:A1993KM60300014 ER PT J AU BERK, DA YUAN, F LEUNIG, M JAIN, RK AF BERK, DA YUAN, F LEUNIG, M JAIN, RK TI MEASUREMENT OF MACROMOLECULAR DIFFUSION IN THE INTERSTITIAL SPACE OF A HUMAN TUMOR XENOGRAFT SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114. RI Berk, David/A-4863-2012 OI Berk, David/0000-0002-3855-6886 NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A878 EP A878 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97502064 ER PT J AU FILHO, IPT LEUNIG, M YUAN, F INTAGLIETTA, M JAIN, RK AF FILHO, IPT LEUNIG, M YUAN, F INTAGLIETTA, M JAIN, RK TI INTRAVASCULAR AND INTERSTITIUM PO2 MEASUREMENTS IN HUMAN TUMOR XENOGRAFTS AND IN NORMAL-TISSUES BY QUENCH PHOSPHORESCENCE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,DEPT AMES BIOENGN,LA JOLLA,CA 92093. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A905 EP A905 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97502228 ER PT J AU KANSAS, GS TEDDER, TF AF KANSAS, GS TEDDER, TF TI DOMAINS OF SELECTINS CONTROLLING CELL-ADHESION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A640 EP A640 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97500702 ER PT J AU LAMANCA, J MCCULLY, K HENSON, D SILAGE, DA SWEENEY, HL LEVINE, S AF LAMANCA, J MCCULLY, K HENSON, D SILAGE, DA SWEENEY, HL LEVINE, S TI EFFECT OF PHOSPHOCREATINE (PCR) DEPLETION ON EXERCISE CAPACITY (EC) OF THE INTACT RAT SO FASEB JOURNAL LA English DT Meeting Abstract C1 PHILADELPHIA VA MED CTR,BREATHING DISORDERS PROGRAM,PHILADELPHIA,PA. MED COLL PENN,PHILADELPHIA,PA 19129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A610 EP A610 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97500529 ER PT J AU LEE, I BOUCHER, Y ZLOTECKI, R JAIN, RK AF LEE, I BOUCHER, Y ZLOTECKI, R JAIN, RK TI TUMOR INTERSTITIAL FLUID PRESSURE IS INVERSELY RELATED WITH INTRATUMOR PO2 AND/OR PH SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT CENT HEMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A892 EP A892 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97502147 ER PT J AU LEUNIG, M YUAN, F BERK, DA MENGER, MD BOUCHER, Y MESSMER, K JAIN, RK AF LEUNIG, M YUAN, F BERK, DA MENGER, MD BOUCHER, Y MESSMER, K JAIN, RK TI CHARACTERIZATION OF MICROCIRCULATION AND TRANSPORT IN A HUMAN TUMOR XENOGRAFT SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114. UNIV MUNICH,INST SURG RES,W-8000 MUNICH 70,GERMANY. RI Berk, David/A-4863-2012 OI Berk, David/0000-0002-3855-6886 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A892 EP A892 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97502149 ER PT J AU LIEBER, CS LEO, MA ROBINS, S DECARLI, LM AF LIEBER, CS LEO, MA ROBINS, S DECARLI, LM TI ETHANOL DECREASES HEPATIC PHOSPHATIDYL METHYLTRANSFERASE ACTIVITY WHEREAS PHOSPHATIDYLCHOLINE INCREASES IT, WITH PROTECTION AGAINST CIRRHOSIS SO FASEB JOURNAL LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,CTR ALCOHOL RES & TREATMENT,LIVER DIS & NUTR SECT,BRONX,NY 10468. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. BOSTON VA MED CTR,BOSTON,MA 02130. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A842 EP A842 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97501856 ER PT J AU LUSCINSKAS, FW KANSAS, GS DING, H TEDDER, TF GIMBRONE, MA AF LUSCINSKAS, FW KANSAS, GS DING, H TEDDER, TF GIMBRONE, MA TI HUMAN MONOCYTES ROLL AND ATTACH TO INTERLEUKIN-4-ACTIVATED ENDOTHELIUM UNDER PHYSIOLOGICAL LEVELS OF FLOW SO FASEB JOURNAL LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DIV VASC RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A639 EP A639 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97500695 ER PT J AU MARTIN, GR JAIN, RK AF MARTIN, GR JAIN, RK TI PERIVASCULAR PH GRADIENTS IN NORMAL AND TUMOR-TISSUE MEASURED BY FRIM SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A894 EP A894 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97502164 ER PT J AU MELDER, RJ JAIN, RK AF MELDER, RJ JAIN, RK TI INCREASED PMN-ENDOTHELIAL ADHESION WITH HYPOXIA SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT CENT HEMATOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A895 EP A895 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97502167 ER PT J AU NANJI, AA ZHAO, S SADRZADEH, SMH KHETTRY, U WAXMAN, DJ AF NANJI, AA ZHAO, S SADRZADEH, SMH KHETTRY, U WAXMAN, DJ TI RELATIONSHIP BETWEEN CYTOCHROME-P450-2E1 INDUCTION AND SEVERITY OF LIVER-INJURY AND BLOOD-ALCOHOL LEVELS IN EXPERIMENTAL ALCOHOLIC LIVER-DISEASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A842 EP A842 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97501853 ER PT J AU QUINN, DA DAHLBERG, CGW THOMPSON, BT JOSEPH, PM BONVENTRE, JV HALES, CA AF QUINN, DA DAHLBERG, CGW THOMPSON, BT JOSEPH, PM BONVENTRE, JV HALES, CA TI STIMULATION BY PLATELET DERIVED GROWTH-FACTOR (PDGF) AND EPIDERMAL GROWTH-FACTOR (EGF) OF THE NA+/H+ EXCHANGER IN RELATION TO CELL-PROLIFERATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,PULM CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A544 EP A544 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97500146 ER PT J AU SOTOARAPE, I BEAGLE, J BURTON, M KAZEMI, H AF SOTOARAPE, I BEAGLE, J BURTON, M KAZEMI, H TI ROLE OF CENTRAL Y-AMINOBUTYRIC ACID (GABA) IN THE HYPOXIC VENTILATORY RESPONSE IN THE RAT SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A632 EP A632 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97500653 ER PT J AU TREPPO, S YU, X HALES, CA VENEGAS, JG AF TREPPO, S YU, X HALES, CA VENEGAS, JG TI PULMONARY PERFUSION AND ARTERIAL TRANSIT-TIME DISTRIBUTION USING PET SO FASEB JOURNAL 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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 23 PY 1993 VL 7 IS 4 BP A790 EP A790 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP975 UT WOS:A1993KP97501558 ER PT J AU ANDRADE, F BRASSARD, JM ANZUETO, A MAXWELL, LC LEVINE, SM LAWRENCE, RA JENKINSON, SG AF ANDRADE, F BRASSARD, JM ANZUETO, A MAXWELL, LC LEVINE, SM LAWRENCE, RA JENKINSON, SG TI EFFECTS OF RESISTIVE BREATHING IN RAT DIAPHRAGM (DPH) FUNCTION AFTER NORMOBARIC HYPEROXIA SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,SAN ANTONIO,TX 78284. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A222 EP A222 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97401284 ER PT J AU ANTONIADES, HN GALANOPOULOS, T NEVILLEGOLDEN, J KIRITSY, C LYNCH, SE AF ANTONIADES, HN GALANOPOULOS, T NEVILLEGOLDEN, J KIRITSY, C LYNCH, SE TI LOCALIZED EXPRESSION OF GROWTH-FACTORS AND RECEPTORS AT THE SITE OF INJURY SO FASEB JOURNAL LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA 02115. INST MOLEC BIOL,WORCESTER,MA 01605. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A37 EP A37 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97400208 ER PT J AU BERK, DA YUAN, F LEUNIG, M JAIN, RK AF BERK, DA YUAN, F LEUNIG, M JAIN, RK TI INTERSTITIAL DIFFUSION AND CONVECTION OF MACROMOLECULES IN A HUMAN TUMOR XENOGRAFT SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. RI Berk, David/A-4863-2012 OI Berk, David/0000-0002-3855-6886 NR 1 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A241 EP A241 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97401392 ER PT J AU BURTON, MD JOHNSON, DC HITZIG, B AF BURTON, MD JOHNSON, DC HITZIG, B TI VIABILITY OF THE ISOLATED BRAIN-STEM SPINAL PREPARATION BY 31P MRS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A459 EP A459 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97402658 ER PT J AU CASTILLO, L CHAPMAN, T YU, Y BURKE, J YOUNG, V AF CASTILLO, L CHAPMAN, T YU, Y BURKE, J YOUNG, V TI ARGININE AND CITRULLINE METABOLISM IN RELATION TO AN ARGININE-FREE INTAKE IN HEALTHY-YOUNG MEN SO FASEB JOURNAL LA English DT Meeting Abstract C1 MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A71 EP A71 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97400407 ER PT J AU CHOUDHURY, GG BISWAS, P GRANDALIANO, G ABBOUD, HE AF CHOUDHURY, GG BISWAS, P GRANDALIANO, G ABBOUD, HE TI THROMBIN-MEDIATED MITOGENIC SIGNALING INVOLVES PROTEIN KINASE-C-ALPHA (PKC-ALPHA) IN HUMAN GLOMERULAR MESANGIAL CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Grandaliano, Giuseppe/G-2963-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A58 EP A58 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97400332 ER PT J AU DAHLBERG, CGW QUINN, DA BONVENTRE, JV JOSEPH, PM THOMPSON, BT HALES, CA AF DAHLBERG, CGW QUINN, DA BONVENTRE, JV JOSEPH, PM THOMPSON, BT HALES, CA TI HEPARIN ATTENUATES EGF-STIMULATED INTRACELLULAR ALKALINIZATION OF RAT LUNG FIBROBLASTS VIA ATTENUATION OF NA+/H+ EXCHANGE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A506 EP A506 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97402934 ER PT J AU GONG, JL MCCARTHY, KM TKACHUK, LJ SCHNEEBERGER, EE AF GONG, JL MCCARTHY, KM TKACHUK, LJ SCHNEEBERGER, EE TI PULMONARY INTERSTITIAL MACROPHAGES (IM) AND DENDRITIC CELLS (DC) COOPERATE TO PROCESS PARTICULATE ANTIGEN SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A367 EP A367 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97402122 ER PT J AU HERBERT, V RUDICK, A AF HERBERT, V RUDICK, A TI BILLIONS WILL BE SAVED BY ASSESSING IRON STATUS IN ALL AMERICANS, FOLATE STATUS IN ALL FERTILE FEMALES, AND VITAMIN-B12 STATUS IN ALL AFTER AGE 55 SO FASEB JOURNAL LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET ADM MED CTR,NEW YORK,NY 10468. NR 3 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A412 EP A412 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97402382 ER PT J AU KREISBERG, JI AYO, SH GARONI, J RADNIK, RA AF KREISBERG, JI AYO, SH GARONI, J RADNIK, RA TI THE GLOMERULAR MESANGIUM IN DIABETES-MELLITUS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A454 EP A454 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97402629 ER PT J AU LAVIGNE, L MASON, L FERRANTI, T HAYES, L SCHAUB, R CLINTON, S AF LAVIGNE, L MASON, L FERRANTI, T HAYES, L SCHAUB, R CLINTON, S TI EVALUATION OF AORTIC MACROPHAGE COLONY-STIMULATING FACTOR (M-CSF) AND INTERLEUKIN-1 (IL-1) GENE-EXPRESSION FOLLOWING ENDOTOXIN OR RHM-CSF ADMINISTRATION IN RABBITS SO FASEB JOURNAL LA English DT Meeting Abstract C1 GENET INST,CAMBRIDGE,MA 02140. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A341 EP A341 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97401976 ER PT J AU RUSSELL, W MCKELLAR, C JACKSON, R AF RUSSELL, W MCKELLAR, C JACKSON, R TI MITOCHONDRIAL SUPEROXIDE-DISMUTASE (MNSOD) EXPRESSION IN HYPOXIC HYPOPERFUSED LUNG-TISSUE SO FASEB JOURNAL LA English DT Meeting Abstract C1 BIRMINGHAM VA MED CTR,BIRMINGHAM,AL. UAB,BIRMINGHAM,AL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A219 EP A219 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97401262 ER PT J AU SIMON, BA TSUZAKI, K HALES, CA VENEGAS, JG AF SIMON, BA TSUZAKI, K HALES, CA VENEGAS, JG TI VENTILATION DISTRIBUTION AND REGIONAL IMPEDANCE DURING PARTIAL UNILATERAL BRONCHIAL OBSTRUCTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A10 EP A10 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97400054 ER PT J AU SMITH, RE PHAN, SH ROLLINS, B STRIETER, RM KUNKEL, SL AF SMITH, RE PHAN, SH ROLLINS, B STRIETER, RM KUNKEL, SL TI TIME-DEPENDENT EXPRESSION OF JE IN ASSOCIATION WITH BLEOMYCIN-INDUCED LUNG INJURY SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,DIV PULM & CRIT CARE MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT PATHOL,ANN ARBOR,MI 48109. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A506 EP A506 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97402933 ER PT J AU SYSTROM, DM FISHMAN, RS HROVAT, M KAZEMI, H AF SYSTROM, DM FISHMAN, RS HROVAT, M KAZEMI, H TI AMMONIA BUFFERING, SKELETAL-MUSCLE METABOLISM AND VENTILATION DURING INCREMENTAL EXERCISE - A P-31 MRS STUDY SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A224 EP A224 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97401296 ER PT J AU TOMERA, JF LILFORD, K AF TOMERA, JF LILFORD, K TI CROSS-TALK OF 2ND MESSENGERS DURING THE TRAUMA RESPONSE AFTER BURN INJURY SO FASEB JOURNAL LA English DT Meeting Abstract C1 SHRINERS BURN INST,ANESTHESIA SERV,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A228 EP A228 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97401315 ER PT J AU VANREMMEN, H TAKAHASHI, R RICHARDSON, A AF VANREMMEN, H TAKAHASHI, R RICHARDSON, A TI ALTERATIONS IN THE EXPRESSION OF SPECIFIC GENES IN PRIMARY CULTURES OF HEPATOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A147 EP A147 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97400849 ER PT J AU VENEGAS, JG TREPPO, S ROVIRA, I HALES, CA AF VENEGAS, JG TREPPO, S ROVIRA, I HALES, CA TI PET IMAGING OF LOCAL PULMONARY VENTILATION-PERFUSION RATIOS IN DOGS SO FASEB JOURNAL 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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD FEB 19 PY 1993 VL 7 IS 3 BP A228 EP A228 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KP974 UT WOS:A1993KP97401316 ER PT J AU LIPES, MA ROSENZWEIG, A TAN, KN TANIGAWA, G LADD, D SEIDMAN, JG EISENBARTH, GS AF LIPES, MA ROSENZWEIG, A TAN, KN TANIGAWA, G LADD, D SEIDMAN, JG EISENBARTH, GS TI PROGRESSION TO DIABETES IN NONOBESE DIABETIC (NOD) MICE WITH TRANSGENIC T-CELL RECEPTORS SO SCIENCE LA English DT Article ID POLYMERASE CHAIN-REACTION; VARIABLE REGION GENES; BETA-CHAIN; I-E; CLONAL DELETION; LYMPHOCYTE-T; EXPRESSION; MOLECULES; ANTIBODY; ANTIGEN AB The T cell receptor (TCR) requirements in the pathogenesis of insulin-dependent diabetes were examined with transgenic NOD mice bearing nondisease-related TCR alpha and beta chains. In both TCRbeta and TCRalphabeta transgenic NOD mice the beta chain transgene was expressed by >98% of peripheral T cells. The alpha chain transgene was also highly expressed. Insulitis developed in both sets of transgenic animals with most of the lymphocytes in the lesion expressing the transgenic beta chain and with depletion of the endogenous TCR V(beta) genes. Nonetheless, NOD animals transgenic for TCRbeta and TCRalphabeta developed diabetes similar to controls. Thus, skewing the TCR repertoire did not diminish autoimmune susceptibility in NOD mice. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RP LIPES, MA (reprint author), JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215, USA. NR 36 TC 55 Z9 55 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 19 PY 1993 VL 259 IS 5098 BP 1165 EP 1169 DI 10.1126/science.8267690 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KM917 UT WOS:A1993KM91700040 PM 8267690 ER PT J AU CHOW, YK HIRSCH, MS MERRILL, DP BECHTEL, LJ ERON, JJ KAPLAN, JC DAQUILA, RT AF CHOW, YK HIRSCH, MS MERRILL, DP BECHTEL, LJ ERON, JJ KAPLAN, JC DAQUILA, RT TI USE OF EVOLUTIONARY LIMITATIONS OF HIV-1 MULTIDRUG RESISTANCE TO OPTIMIZE THERAPY SO NATURE LA English DT Article ID REVERSE-TRANSCRIPTASE INHIBITORS; VIRUS; REPLICATION; ZIDOVUDINE; DERIVATIVES; SENSITIVITY; INVITRO; MUTANTS; AZT AB WILD-TYPE reverse transcriptase has evolved for the survival of human immunodeficiency virus type 1 (HIV-1) by natural selection1. In contrast, therapy relying on inhibitors of reverse transcriptase by nucleosides like zidovudine (AZT) or dideoxyinosine (ddI), and by non-nucleosides like pyridinones or nevirapine2-6, may exert different selection pressures on this enzyme. Therefore the acquisition of resistance to reverse transcriptase inhibitors by selection of mutations in the pol gene7-15 may require compromises in enzyme function that affect viral replication. As single mutations are unlikely to confer broad resistance when combinations of reverse transcriptase inhibitors are used, multiple mutations may occur that result in further compromises. Certain drug combinations may prevent the co-existence of adequate reverse transcription function and multi-drug resistance (MDR). Unlike bacterial or eukaryotic drug resistance, retroviral drug resistance is conferred only by mutations in its own genome16 and is limited by genome size. Combining drugs directed against the same essential viral protein may thus prevent HIV-1 MDR, whereas the conventional approach of targeting different HIV-1 proteins for combination therapy may not, because genomes with resistance mutations in different HIV-1 genes might recombine to develop MDR17. Here we show that several mutations in the HIV-1 reverse transcriptase gene that confer resistance to inhibitors of this enzyme can attenuate viral replication. We tested whether combinations of mutations giving rise to single-agent resistance might further compromise or even abolish viral replication, and if multidrug-resistant viruses could be constructed. Certain combinations of mutations conferring resistance to AZT, ddI and pyridinone are incompatible with viral replication. These results indicate that evolutionary limitations exist to restrict development of MDR. Furthermore, a therapeutic strategy exploiting these limitations by using selected multidrug regimens directed against the same target may prevent development of MDR. This approach, which we call convergent combination therapy, eliminated HIV-1 replication and virus breakthrough in vitro, and may be applicable to other viral targets. Moreover, elimination of reverse transcription by convergent combination therapy may also limit MDR. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CHOW, YK (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,GRAY 5,BOSTON,MA 02114, USA. NR 30 TC 148 Z9 150 U1 1 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD FEB 18 PY 1993 VL 361 IS 6413 BP 650 EP 654 DI 10.1038/361650a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KM776 UT WOS:A1993KM77600068 PM 7679778 ER PT J AU JASANOFF, A WEISS, MA AF JASANOFF, A WEISS, MA TI AROMATIC HISTIDINE INTERACTIONS IN THE ZINC FINGER MOTIF - STRUCTURAL INEQUIVALENCE OF PHENYLALANINE AND TYROSINE IN THE HYDROPHOBIC CORE SO BIOCHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR-IIIA; PROTEIN ZFY; DNA RECOGNITION; RESONANCE ASSIGNMENTS; ARCHITECTURAL RULES; SECONDARY STRUCTURE; BINDING DOMAINS; NMR STRUCTURE; HEN LYSOZYME; EVEN FINGER AB The classical Zn finger (Cys-X2,4-Cys-X3-Phe-X5-Leu-X2-His-X3,4-His). The phenycontains an aromatic-histidine interaction (underlined) in its hydrophobic core-whose importance is suggested by the marked destablization of a Phe --> Leu analogue [Mortishire-Smith, R. J., Lee, M. S., Bolinger, L., & Wright, P. E. (1992) FEBS Lett. 1, 11-15]. In some Zn finger sequences the central Phe is occasionally replaced by Tyr, and when present, this substitution is generally conserved among species. To investigate whether Tyr would participate in an analogous aromatic-histidine interaction, we have determined the solution structure in a Phe --> Tyr mutant domain. Its global fold (the betabetaalpha motif) is similar to that of the Phe domain. Although the variant Tyr maintains edge-to-face packing against the proximal histidine, the phenolic ring is displaced toward solvent. Such displacement increases the solvent accessibility of the Tyr p-OH group and reduces steric overlap (and possible electrostatic repulsion) between the Tyr O(zeta) and His pi electrons. The Tyr analogue exhibits reduced dynamic stability (as indicated by more rapid exchange of amide protons in D2O) and may alternate in rapid equilibrium between major and minor conformers. Inequivalent Tyr-His and Phe-His interactions are likely to be general features of Zn finger architecture. Molecular modeling based on the Zif268 cocrystal structure [Pavletich, N. P., & Pabo, C. O. (1991) Science 252, 809-817] suggests that the variant Tyr p-OH group may readily be positioned to contribute a novel hydrogen bond to a DNA phosphate. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 46 TC 23 Z9 24 U1 1 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 16 PY 1993 VL 32 IS 6 BP 1423 EP 1432 DI 10.1021/bi00057a005 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KM703 UT WOS:A1993KM70300005 PM 8431422 ER PT J AU HUA, QX LADBURY, JE WEISS, MA AF HUA, QX LADBURY, JE WEISS, MA TI DYNAMICS OF A MONOMERIC INSULIN ANALOG - TESTING THE MOLTEN-GLOBULE HYPOTHESIS SO BIOCHEMISTRY LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; PANCREATIC TRYPSIN-INHIBITOR; FOLDED APOMYOGLOBIN INTERMEDIATE; DES-PENTAPEPTIDE-INSULIN; PROTON CHEMICAL-SHIFTS; CARBONIC ANHYDRASE-B; ALPHA-LACTALBUMIN; RECEPTOR-BINDING; DISTANCE GEOMETRY; 2D NMR AB The structure of insulin exhibits local and nonlocal differences among crystal forms and so provides an important model for analysis of protein dynamics. A novel combination of order and disorder has recently been inferred from 2D-NMR studies of the monomeric analogue des-pentapeptide(B26-B30) insulin (DPI) under acidic conditions [the molten-globule hypothesis; Hua, Q. X., Kochoyan, M., & Weiss, M. A. (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 2379-2383]. Distance-geometry structures are similar in general to crystal structures but differ by rigid-body displacements of alpha-helices; the hydrophobic core is not well ordered due to insufficient long-range restraints. To test whether such informational uncertainty may represent physical disorder, we have performed complementary studies of the thermal unfolding of DPI and its interaction with 1-anilino-8-naphthalenesulfonate (ANS). Experimental design is based on a predicted analogy between DPI and A-state models of protein-folding intermediates (the ''molten globule''). Unfolding is monitored by five distinct biophysical probes: photochemical dynamic nuclear polarization (photo-CIDNP), differential scanning calorimetry (DSC), circular dichroism (CD), H-1-NMR chemical shifts, and slowly exchanging amide H-1-NMR resonances in D2O solution. The results provide evidence that DPI adopts a compact partially folded state. Because the 2D-NMR spectrum of an engineered insulin monomer under physiological conditions is similar to that of DPI under acidic conditions [Weiss, M. A., Hua, Q. X., Frank, B. H., Lynch, C., & Shoelson, S. E. (1991) Biochemistry 30, 7373-7389], we propose that the functional form of insulin is a molten globule. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. YALE UNIV,DEPT CHEM,NEW HAVEN,CT 06511. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NCRR NIH HHS [1S10 RR04862-01] NR 80 TC 56 Z9 56 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 16 PY 1993 VL 32 IS 6 BP 1433 EP 1442 DI 10.1021/bi00057a006 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KM703 UT WOS:A1993KM70300006 PM 8431423 ER PT J AU ALBERT, M JENIKE, M NIXON, R NOBEL, K AF ALBERT, M JENIKE, M NIXON, R NOBEL, K TI THYROTROPIN RESPONSE TO THYROTROPIN-RELEASING-HORMONE IN PATIENTS WITH DEMENTIA OF THE ALZHEIMER TYPE SO BIOLOGICAL PSYCHIATRY LA English DT Article DE TRH; ALZHEIMERS DISEASE; DEPRESSION ID STIMULATION TEST; DEPRESSION; TRH; DISEASE; DIAGNOSIS AB Eleven patients with senile dementia of the Alzheimer type and 11 age-matched control subjects were given the thyrotropin-releasing hormone (TRH) test. The two groups did not differ with respect to peak thyrotropin (TSH) response or TSH levels at baseline, 20, 30, and 45 min after TRH injection. There were significant differences between the groups on Hamilton Depression Rating Scale scores (p < 0.03), although neither group met clinical criteria for depression. Items that were significantly different pertained to depressed mood, loss of interest, loss of insight, suicidal ideation, and obsessional symptoms. C1 HEBREW REHABIL CTR AGED,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT & NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MCLEAN HOSP,BELMONT,MA 02178. RP ALBERT, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,CNY-9,BOSTON,MA 02114, USA. FU NIA NIH HHS [P01-AG04390] NR 21 TC 8 Z9 8 U1 0 U2 0 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 FEB 15 PY 1993 VL 33 IS 4 BP 267 EP 271 DI 10.1016/0006-3223(93)90293-M PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KU362 UT WOS:A1993KU36200007 PM 8471680 ER PT J AU DAVIES, K TEPAS, EC NATHAN, DG MATHEYPREVOT, B AF DAVIES, K TEPAS, EC NATHAN, DG MATHEYPREVOT, B TI INTERLEUKIN-3 EXPRESSION BY ACTIVATED T-CELLS INVOLVES AN INDUCIBLE, T-CELL-SPECIFIC FACTOR AND AN OCTAMER BINDING-PROTEIN SO BLOOD LA English DT Article ID GENE-EXPRESSION; TRANSCRIPTIONAL REGULATION; LYMPHOCYTES-T; IL-2 GENE; IDENTIFICATION; ELEMENTS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,D1630A,44 BINNEY ST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [5T32CA09172-17]; NIDDK NIH HHS [R01 DK41758] NR 13 TC 22 Z9 22 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1993 VL 81 IS 4 BP 928 EP 934 PG 7 WC Hematology SC Hematology GA KM419 UT WOS:A1993KM41900009 PM 8428000 ER PT J AU WAGATA, T SHIBAGAKI, I IMAMURA, M SHIMADA, Y TOGUCHIDA, J YANDELL, DW IKENAGA, M TOBE, T ISHIZAKI, K AF WAGATA, T SHIBAGAKI, I IMAMURA, M SHIMADA, Y TOGUCHIDA, J YANDELL, DW IKENAGA, M TOBE, T ISHIZAKI, K TI LOSS OF 17P, MUTATION OF THE P53 GENE, AND OVEREXPRESSION OF P53 PROTEIN IN ESOPHAGEAL SQUAMOUS-CELL CARCINOMAS SO CANCER RESEARCH LA English DT Article ID TUMOR-ANTIGEN; LUNG-CANCER; HEPATOCELLULAR-CARCINOMA; POINT MUTATIONS; ALLELE LOSS; SHORT ARM; FREQUENT; CHROMOSOME-17; RETINOBLASTOMA; EXPRESSION AB We analyzed mutations of the p53 gene by single-strand conformation polymorphism analysis of polymerase chain reaction products and direct sequencing through all coding exons and exon-intron junctions in 32 cases with esophageal squamous cell carcinoma. Mutations were detected in 15 of 32 (47%) tumor samples, in which G:C to T:A transversions were rather frequent (33%). Previously, we reported deletion of chromosome 17p where the p53 gene is located in 45% of Japanese esophageal squamous cell carcinoma, and here the relationship between mutation of the p53 gene and loss of 17p was analyzed. Mutations were observed in 12 of 16 patients with loss of 17p, whereas only 2 of 11 without loss were positive for mutations, suggesting that mutations of the p53 gene were closely associated with a 17p deletion. Furthermore, we immunohistochemically analyzed the expression of p53 protein in esophageal squamous cell carcinoma tumor tissues using a monoclonal antibody. Five of 6 tumors with missense mutations of the p53 gene were positively stained, while in tumors with nonsense mutations or without mutations of the p53 gene staining was very weak or negative. These results suggest a good correlation between mutations and abnormal expression of the p53 gene. C1 KYOTO UNIV,FAC MED,CTR RADIAT BIOL,YOSHIDA KONOECHO,SAKYO KU,KYOTO 606,JAPAN. KYOTO UNIV,FAC MED,DEPT SURG 1,SAKYO KU,KYOTO 606,JAPAN. KYOTO UNIV,FAC MED,DEPT ORTHOPAED SURG,SAKYO KU,KYOTO 606,JAPAN. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 40 TC 160 Z9 167 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 FEB 15 PY 1993 VL 53 IS 4 BP 846 EP 850 PG 5 WC Oncology SC Oncology GA KL963 UT WOS:A1993KL96300027 PM 8094033 ER PT J AU AUSTIN, JP URIE, MM CARDENOSA, G MUNZENRIDER, JE AF AUSTIN, JP URIE, MM CARDENOSA, G MUNZENRIDER, JE TI PROBABLE CAUSES OF RECURRENCE IN PATIENTS WITH CHORDOMA AND CHONDROSARCOMA OF THE BASE OF SKULL AND CERVICAL-SPINE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE CHORDOMAS; CHONDROSARCOMAS; RECURRENCES; LOCAL CONTROL; PROTON THERAPY; 3D TREATMENT PLANNING ID RADIATION-THERAPY AB Purpose: 141 patients with chordoma and chondrosarcoma of the base of skull and cervical spine were treated with proton and photon irradiation between 1980 and 1989. The local disease was controlled in 111 of these patients. This study reviews the 26 patients who have had their disease recur, and who have evaluable diagnostic studies to examine for probable causes of recurrence. Methods and Materials: The histologies of the recurrent tumors were 21 non-chondroid chordomas, two chondroid chordomas, and three chondrosarcomas. The prescribed doses ranged from 67 Cobalt-Gray-Equivalent (CGE) to 72 CGE (average of 69 CGE). Doses to small regions of the tumor were deliberately reduced where they abutted certain normal tissues (brain stem, spinal cord, optic chiasm, and optic nerves) in order to keep these structures at acceptance dose levels. The first study, CT or MR scan, on which there was evidence of increase in tumor was carefully evaluated and that volume transferred to the CT scan on which the treatment plan had been developed. The 3D dose distribution in the region of recurrence was carefully analyzed and a judgement made as to the most probable cause of recurrence. Results: Approximately one quarter (6 of 26) of the cases failed in the prescribed dose region. More than half (15 of 26) failed in regions where tumor dose was limited by normal tissue constraints. Approximately 10% of the patients recurred in the surgical pathway and 10% were judged to be marginal misses. Conclusions: Overall, 75% of the patients failed in regions receiving less than the prescribed dose. All tumors which failed in the high dose region had volume greater than 75 cc. Patients with cervical spine disease had a higher rate of recurrence (10 or 26) and larger tumors (average volume of 102 cc) than those with base of skull disease (16 of 115) with an average volume of 63 cc. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 15 TC 88 Z9 89 U1 0 U2 2 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 FEB 15 PY 1993 VL 25 IS 3 BP 439 EP 444 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KP477 UT WOS:A1993KP47700008 PM 8436522 ER PT J AU GALVIN, JM SMITH, AR AF GALVIN, JM SMITH, AR TI IS EFFECTIVE-PENUMBRA A USEFUL CONCEPT FOR MLC SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Letter C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. RP GALVIN, JM (reprint author), NYU MED CTR,DEPT RADIAT ONCOL,566 1ST AVE,ROOM HC107,NEW YORK,NY 10016, USA. NR 5 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD FEB 15 PY 1993 VL 25 IS 3 BP 571 EP 571 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KP477 UT WOS:A1993KP47700028 PM 8436538 ER PT J AU RIEDEL, H PARISSENTI, AM HANSEN, H SU, LH SHIEH, HL AF RIEDEL, H PARISSENTI, AM HANSEN, H SU, LH SHIEH, HL TI STIMULATION OF CALCIUM-UPTAKE IN SACCHAROMYCES-CEREVISIAE BY BOVINE PROTEIN KINASE-C-ALPHA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHORBOL ESTER; CA-2+ INFLUX; YEAST-CELLS; SIGNAL TRANSDUCTION; ENDOTHELIAL-CELLS; MATING PHEROMONE; GENE-EXPRESSION; DOWN-REGULATION; MEMBRANE; ACTIVATION AB Ca2+ plays essential roles as a second messenger often in synergism with the calcium- and phospholipid-dependent phorbol ester, receptor, protein kinase C (PKC), which stimulates Ca2+ influx in various cell types in a potential positive feedback mechanism. To address the compatibility of these mechanisms between lower eukaryotes and mammals, we have stably expressed bovine PKCalpha in the yeast Saccharomyces cerevisiae. We find that phorbol ester binding sites are created which stimulate a specific calcium- and phospholipid-dependent catalytic activity in vitro. Phorbol ester activation in vivo stimulates PKC down-regulation, uptake of extracellular Ca2+, Ca2+ dependence of cell viability, and changes in cell morphology. This may represent activation of a putative PKC-mediated signaling pathway utilized by functional yeast homologs of mammalian PKC isoforms. These are suggested by some protein data; however, their genes have not yet been characterized (Simon, A. J., Milner, Y., Saville, S. P., Dvir, A., Mochly-Rosen, D., and Orr, E. (1991) Proc. R. Soc. Lond. B 243, 165-171). Our findings indicate that bovine PKCalpha is functional in yeast and stimulates calcium uptake in a manner similar to some of its responses in mammalian cells, which suggests compatible aspects of higher and lower eukaryotic signaling pathways and the feasibility of dissecting parts of the action of common signaling mediators in a simple genetic model. C1 BRIGHAM & WOMENS HOSP, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP JOSLIN DIABET CTR, MOLEC BIOL SECT, BOSTON, MA 02215 USA. NR 52 TC 18 Z9 18 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 15 PY 1993 VL 268 IS 5 BP 3456 EP 3462 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KM161 UT WOS:A1993KM16100068 PM 8429022 ER PT J AU ACTON, S RESNICK, D FREEMAN, M EKKEL, Y ASHKENAS, J KRIEGER, M AF ACTON, S RESNICK, D FREEMAN, M EKKEL, Y ASHKENAS, J KRIEGER, M TI THE COLLAGENOUS DOMAINS OF MACROPHAGE SCAVENGER RECEPTORS AND COMPLEMENT COMPONENT-C1Q MEDIATE THEIR SIMILAR, BUT NOT IDENTICAL, BINDING SPECIFICITIES FOR POLYANIONIC LIGANDS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; HAMSTER-CELL MUTANTS; CHOLESTEROL DEPOSITION; OVARY CELLS; PROTEIN; C1Q; MOLECULES; HOMOLOGY; ATHEROSCLEROSIS; ENDOCYTOSIS AB Macrophage scavenger receptors have been implicated in the development of atheroselerosis and other macrophage-associated functions, including host defense. The mechanism by which these receptors bind a wide array of polyanions, such as acetylated low density lipoprotein (Ac-LDL), with high affinity has not yet been elucidated; however, it has been proposed that the positively charged extracellular collagenous domain of scavenger receptors plays a key role in ligand binding. To test this proposal, we generated truncation mutants of the bovine and murine scavenger receptors and studied their expression in transiently transfected COS cells. These mutants contain only 8 (bovine) or 5 (murine) of the 24 Gly-X-Y tripeptide repeats found in the collagenous domains of the full-length receptors. Immunochemical analyses established that the truncation of the bovine scavenger receptor did not interfere significantly with its synthesis, trimerization, post-translational processing, intracellular transport, surface expression, or stability. However, unlike their full-length counterparts, the truncated bovine and murine receptors were unable to bind Ac-LDL. Thus, the collagenous domain was necessary for normal ligand binding. In addition, cotransfection of the expression vector for the truncated bovine scavenger receptor with that for the full-length receptor resulted in dramatically reduced activity of the full-length construct (dominant negative effect). A ligand bead-binding assay was used to show that the isolated collagenous domain from a different protein, complement component C1q, could bind a wide variety of polyanions with a specificity which was similar, but not identical, to that of scavenger receptors. These results suggest that the collagenous domain of the scavenger receptor is both necessary and sufficient to determine the broad binding specificity that characterizes this unusual receptor. Scavenger receptors and C1q, along with the mannose-binding protein, conglutinin, and lung surfactant apoprotein A, help define a set of proteins which all contain short collagenous domains and which all appear to participate in host defense. Their short collagenous domains may contribute significantly to their host-defense functions. C1 MIT,DEPT BIOL,RM E25-236,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL41484, HL45098]; NIAID NIH HHS [AI-27168] NR 45 TC 123 Z9 123 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 15 PY 1993 VL 268 IS 5 BP 3530 EP 3537 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KM161 UT WOS:A1993KM16100079 PM 8429029 ER PT J AU MCCAFFREY, PG PERRINO, BA SODERLING, TR RAO, A AF MCCAFFREY, PG PERRINO, BA SODERLING, TR RAO, A TI NF-ATP, A LYMPHOCYTE-T DNA-BINDING PROTEIN THAT IS A TARGET FOR CALCINEURIN AND IMMUNOSUPPRESSIVE DRUGS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR; CYCLOSPORINE-A; KAPPA-B; ACTIVATION; IDENTIFICATION; REQUIREMENTS; SPECIFICITY; RECEPTOR; CELLS AB The nuclear factor of activated T cells (NF-AT) is essential for transcription of the interleukin-2 gene upon T cell activation. Here we use a technique involving elution and renaturation of proteins from SDS-acrylamide gels to identify a DNA-binding component of NF-AT (NF-AT(p)) that is present in hypotonic extracts of T cells prior to activation and appears in nuclear extracts when T cells are activated. NF-AT(p) is present in resting T cells predominantly in a form migrating with an apparent molecular weight of 110,000-140,000, while NF-AT(p) from nuclear extracts of activated T cells migrates with a lower apparent molecular weight (90,000-125,000). This difference is likely to reflect dephosphorylation of NF-AT(p) since treatment of NF-AT(p) with calf intestinal phosphatase or the calcium- and calmodulin-dependent phosphatase calcineurin in vitro results in a similar decrease in its apparent molecular weight. We show that NF-AT(p) is dephosphorylated in cell lysates by a calcium-dependent process that is blocked by inclusion of EGTA or a specific peptide inhibitor of calcineurin in the cell lysis buffer. Moreover, dephosphorylation of NF-AT(p) in cell extracts is inhibited by prior treatment of T cells with the immunosuppressive drugs cyclosporin A or FK506, which inhibit the phosphatase activity of calcineurin when complexed with their specific binding proteins, cyclophilin and FK506-binding protein. This work identifies NF-AT(p) as a DNA-binding phosphoprotein and a target for the drug/immunophilin/calcineurin complexes thought to mediate the inhibition of interleukin-2 gene induction by cyclosporin A and FK506. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. OREGON HLTH SCI UNIV,VOLLUM INST ADV BIOMED RES,PORTLAND,OR 97201. RP MCCAFFREY, PG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA42471]; NIGMS NIH HHS [GM41292] NR 21 TC 270 Z9 271 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 15 PY 1993 VL 268 IS 5 BP 3747 EP 3752 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KM161 UT WOS:A1993KM16100109 PM 7679116 ER PT J AU HUSSEY, RE CLAYTON, LK DIENER, A MCCONKEY, DJ HOWARD, FD RODEWALD, HR DADAMIO, L DALLENBACH, F STEIN, H SCHMIDT, EV KOYASU, S REINHERZ, EL AF HUSSEY, RE CLAYTON, LK DIENER, A MCCONKEY, DJ HOWARD, FD RODEWALD, HR DADAMIO, L DALLENBACH, F STEIN, H SCHMIDT, EV KOYASU, S REINHERZ, EL TI OVEREXPRESSION OF CD3-ETA DURING THYMIC DEVELOPMENT DOES NOT ALTER THE NEGATIVE SELECTION PROCESS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL-RECEPTOR; ANTIGEN RECEPTOR; MONOCLONAL-ANTIBODY; TRANSGENIC MICE; ZETA-CHAIN; B-CELLS; CD3-EPSILON SUBUNITS; SIGNAL TRANSDUCTION; INVERSE CORRELATION; MOLECULAR-CLONING AB To elucidate the role of CD3eta in thymic development and to determine whether CD3eta is involved in the negative selection process, CD3eta was overexpressed >100 fold in transgenic (tg) mice using a Thy-1 promoter and regulatory elements. CD3eta was readily observed in the majority of cortical thymocytes and in a fraction of medullary thymocytes in tg mice by immunohistochemical staining with an anti-CD3eta-specific mAb. In contrast, endogenous CD3eta levels were too low to detect in normal littermates. Flow cytometric analysis demonstrated an increased level of TCR on thymocytes with intermediate TCR density in tg animals and parallel biochemical studies showed a marked increased in TCR-associated CD3zeta-eta heterodimers and CD3eta-eta homodimers relative to controls. Despite this change in surface TCR phenotype, there was no significant alteration in the total numbers or proportion of CD4+CD8+ double-positive or CD4+CD8- or CD4-CD8+ single-positive thymocytes or peripheral T cells. Percentages of SP Vbeta5, Vbeta6, and Vbeta8 thymocytes in tg animals were unaltered compared to normal littermates when backcrossed either to C57BL/6 (H-2b) or DBA/2 (H-2d) backgrounds. Furthermore, induction of DNA fragmentation with anti-CD3epsilon mAb treatment in vivo was not significantly different for tg and normal littermates. Collectively, these data imply that CD3eta is not a limiting component of the negative selection process. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FREE UNIV BERLIN,KLINIKUM STEGLITZ,INST PATHOL,W-1000 BERLIN 45,GERMANY. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. RP HUSSEY, RE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Koyasu, Shigeo/J-5583-2015 OI Koyasu, Shigeo/0000-0001-9585-3038 FU NIAID NIH HHS [AI19807] NR 55 TC 8 Z9 8 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1993 VL 150 IS 4 BP 1183 EP 1194 PG 12 WC Immunology SC Immunology GA KM706 UT WOS:A1993KM70600004 PM 8094404 ER PT J AU ROCK, KL FLEISCHACKER, C GAMBLE, S AF ROCK, KL FLEISCHACKER, C GAMBLE, S TI PEPTIDE-PRIMING OF CYTOLYTIC T-CELL IMMUNITY INVIVO USING BETA-2-MICROGLOBULIN AS AN ADJUVANT SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CLASS-I MOLECULES; MAJOR HISTOCOMPATIBILITY COMPLEX; TOXIC LYMPHOCYTES-T; FREE SYNTHETIC PEPTIDE; MONOCLONAL-ANTIBODIES; ANTIGEN RECOGNITION; BINDING; INDUCTION; INVITRO; SURFACE AB CTL recognize oligopeptides bound to MHC class I molecules. immunization of animals with antigenic peptides has often failed to stimulate CTL responses. We confirm that immunizations with several peptides, including natural and optimally active antigenic sequences, do not prime cytotoxic immunity in mice. However, immunization with peptides together with human beta2-microglobulin primes Ag-specific CTL. Priming is observed when animals receive injections either i.v. with ex vivo peptide/beta2-microglobulin-pulsed cells or s.c. with an admixture of peptide and beta2-microglobulin. Beta2-microglobulin promotes the priming of CTL immunity if it is added with peptide, but not if it is added after cells are exposed to peptide. Synthetic peptides and mixtures of peptides from enzymatically cleaved Ag are immunogenic. When a tryptic digest of OVA or the synthetic peptide (OVA258-276) are used as immunogens, the CTL that respond recognize the endogenously processed epitope presented by an OVA-transfected target cell. The peptide + beta2-microglobulin-primed CTL are CD4-CD8+ and are class I MHC restricted. Using the immunization protocol with beta2-microglobulin, we have primed CTL responses with peptides from OVA, Sendai virus, and vesicular stomatitis virus. These results may explain previous failures to prime CTL with peptides in vivo and provide a novel approach for developing peptide-based vaccines for viral diseases. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROCK, KL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-31337] NR 43 TC 39 Z9 41 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1993 VL 150 IS 4 BP 1244 EP 1252 PG 9 WC Immunology SC Immunology GA KM706 UT WOS:A1993KM70600010 PM 8381832 ER PT J AU MACLEAN, JA SU, Z GUO, Y SY, MS COLVIN, RB WONG, JT AF MACLEAN, JA SU, Z GUO, Y SY, MS COLVIN, RB WONG, JT TI ANTI-CD3 - ANTI-IL-2 RECEPTOR BISPECIFIC MONOCLONAL-ANTIBODY - TARGETING OF ACTIVATED T-CELLS INVITRO SO JOURNAL OF IMMUNOLOGY LA English DT Article ID KIDNEY-TRANSPLANT RECIPIENTS; TUMOR NECROSIS FACTOR; ALLOGRAFT SURVIVAL; RENAL-ALLOGRAFTS; INFILTRATING LYMPHOCYTES; OKT3; REJECTION; INTERLEUKIN-2; MICE; IMMUNOSUPPRESSION AB T cells are major mediators of graft rejection and many autoimmune diseases. During the Ag recognition process, T cells often become activated. We tested the hypothesis that an anti-CD3:anti-CD25 (CD3,25) bispecific mAb (BSMAB) can effectively and selectively target activated T cells. By flow cytometric analysis, the CD3,25 BSMAB was shown to bind avidly to activated T cells that coexpress CD3 and CD25 (p55 chain of the IL-2R), achieving higher levels than the parent anti-CD3 and anti-CD25 mAb. It bound only weakly to unstimulated T cells. The CD3,25 BSMAB effectively redirected CTL to lyse CD25-bearing PHA-stimulated T lymphoblasts and the IL2-dependent CTLL tumor cell line in chromium release assays. It was highly effective in blocking MLR as shown by inhibition of [H-3]TdR incorporation. However, the CD3,25 BSMAB has a low potential to activate resting T cells, as it induced only minimal [H-3]TdR incorporation even in the presence of exogenous IL-2. In the absence of exogenous IL-2, the CD3,25 BSMAB was unable to induce [H-3]TdR incorporation. In contrast, the parent anti-CD3 mAb induced a high degree of incorporation. In summary, the CD3,25 BSMAB selectively targets activated CD25-expressing T cells and lymphomas although maintaining a low activation potential for unstimulated T cells, potentially advantageous properties that can be exploited for immunotherapy. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,GEN MED SERV,CLIN IMMUNOL & ALLERGY UNIT,BOSTON,MA 02114. RP MACLEAN, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,COX 5,BOSTON,MA 02114, USA. FU NCI NIH HHS [5T32CA09216-12]; NIAID NIH HHS [R29AI27050] NR 35 TC 11 Z9 11 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1993 VL 150 IS 4 BP 1619 EP 1628 PG 10 WC Immunology SC Immunology GA KM706 UT WOS:A1993KM70600048 PM 8432997 ER PT J AU LEIFER, D KRAINC, D YU, YT MCDERMOTT, J BREITBART, RE HENG, J NEVE, RL KOSOFSKY, B NADALGINARD, B LIPTON, SA AF LEIFER, D KRAINC, D YU, YT MCDERMOTT, J BREITBART, RE HENG, J NEVE, RL KOSOFSKY, B NADALGINARD, B LIPTON, SA TI MEF2C, A MADS MEF2-FAMILY TRANSCRIPTION FACTOR EXPRESSED IN A LAMINAR DISTRIBUTION IN CEREBRAL-CORTEX SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MUSCLE-SPECIFIC ENHANCER; CDNA CLONES; GENE; IDENTIFICATION; ELEMENT; LOCALIZATION; PROTEINS; PROMOTER; BRAIN; SRF AB We have cloned cDNA encoding a human transcription factor that belongs to the MEF2 (myocyte-specific enhancer-binding factor 2) subfamily of the MADS (MCM1-agamous-deficiens-serum response factor) gene family. This factor, which we have named MEF2C, binds specifically to the MEF2 element and activates transcription via this element. Specific isoforms of this factor are found exclusively in brain and are robustly expressed by neurons in cerebral cortex. In situ hybridization indicates that the factor is expressed preferentially in certain neuronal layers of cortex and that expression declines during postnatal development. The unusual pattern of expression in brain suggests that this transcription factor may be important in the development of cortical architecture. C1 CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT CARDIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT SYSTEMAT BOT,BOSTON,MA 02114. MCLEAN HOSP,DEPT PSYCHIAT,BELMONT,MA 02178. RP LEIFER, D (reprint author), CHILDRENS HOSP MED CTR,DEPT SYSTEMAT BOT,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY06087]; NICHD NIH HHS [HD00888] NR 25 TC 167 Z9 169 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 FEB 15 PY 1993 VL 90 IS 4 BP 1546 EP 1550 DI 10.1073/pnas.90.4.1546 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KM607 UT WOS:A1993KM60700083 PM 7679508 ER PT J AU FISHER, DE PARENT, LA SHARP, PA AF FISHER, DE PARENT, LA SHARP, PA TI HIGH-AFFINITY DNA-BINDING MYC ANALOGS - RECOGNITION BY AN ALPHA-HELIX SO CELL LA English DT Article ID LEUCINE-ZIPPER; SACCHAROMYCES-CEREVISIAE; DIMERIZATION SPECIFICITY; NEGATIVE REGULATOR; PROTEIN; FOS; JUN; TRANSCRIPTION; COMPLEX; DOMAINS AB Myc and other basic-helix-loop-helix-leucine zipper (b-HLH-ZIP) proteins bind the sequence CACGTG. Exhaustive mutagenesis in the basic domain identified four amino acids critical for DNA binding with spacing suggestive of an alpha-helical face. Surprisingly, two highly conserved amino acids were nonessential for DNA binding. Circular dichroism demonstrated a DNA-induced alpha-helical transition. A series of analogs were constructed with multiple simultaneous alanine substitutions at nonessential positions and a critical lysine for arginine substitution. In this way 35-fold higher specific affinity for CACGTG was obtained as compared with the basic domain of c-Myc. These b-HLH-ZIP proteins appear to bind the same palindromic sequence and may compete for common sites in vivo. Additionally, a C-terminal basic region clamp motif was identified that was also identifiable in crystal structures from several different families of DNA-binding factors. C1 CHILDRENS HOSP MED CTR,DEPT PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. RP FISHER, DE (reprint author), MIT,CTR CANC RES,DEPT BIOL,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [P01-CA42063, P30-CA14051] NR 53 TC 79 Z9 79 U1 1 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD FEB 12 PY 1993 VL 72 IS 3 BP 467 EP 476 DI 10.1016/0092-8674(93)90122-7 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KM162 UT WOS:A1993KM16200015 PM 8431949 ER PT J AU MALKIN, D FRIEND, SH AF MALKIN, D FRIEND, SH TI GERM LINE P53 MUTATIONS IN A FAMILIAL SYNDROME OF BREAST-CANCER, SARCOMAS, AND OTHER NEOPLASMS (SCIENCE, VOL 250, PG 1233, 1990) SO SCIENCE LA English DT Correction, Addition C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,MOLEC GENET LAB,BOSTON,MA 02129. RP MALKIN, D (reprint author), HOSP SICK CHILDREN,DIV HEMATOL ONCOL,555 UNIV AVE,TORONTO M5G 1X8,ONTARIO,CANADA. NR 3 TC 17 Z9 17 U1 3 U2 10 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 12 PY 1993 VL 259 IS 5097 BP 878 EP 878 DI 10.1126/science.8438145 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KL800 UT WOS:A1993KL80000006 PM 8438145 ER PT J AU ROSSAINT, R FALKE, KJ LOPEZ, F SLAMA, K PISON, U ZAPOL, WM AF ROSSAINT, R FALKE, KJ LOPEZ, F SLAMA, K PISON, U ZAPOL, WM TI INHALED NITRIC-OXIDE FOR THE ADULT RESPIRATORY-DISTRESS SYNDROME SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID SELECTIVE PULMONARY VASODILATOR; CARDIAC-OUTPUT; PERFUSION DISTRIBUTIONS; CAPILLARY-PRESSURE; RELAXING FACTOR; BLOOD-FLOW; HYPERTENSION; NITROPRUSSIDE; VENTILATION; SHEEP AB Background. The adult respiratory distress syndrome is characterized by pulmonary hypertension and right-to-left shunting of venous blood. We investigated whether inhaling nitric oxide gas would cause selective vasodilation of ventilated lung regions, thereby reducing pulmonary hypertension and improving gas exchange. Methods. Nine of 10 consecutive patients with severe adult respiratory distress syndrome inhaled nitric oxide in two concentrations for 40 minutes each. Hemodynamic variables, gas exchange, and ventilation-perfusion distributions were measured by means of multiple inert-gas-elimination techniques during nitric oxide inhalation; the results were compared with those obtained during intravenous infusion of prostacyclin. Seven patients were treated with continuous inhalation of nitric oxide in a concentration of 5 to 20 parts per million (ppm) for 3 to 53 days. Results. Inhalation of nitric oxide in a concentration of 18 ppm reduced the mean (+/-SE) pulmonary-artery pressure from 37+/-3 mm Hg to 30+/-2 mm Hg (P = 0.008) and decreased intrapulmonary shunting from 36+/-5 percent to 31+/-5 percent (P = 0.028). The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FiO2), an index of the efficiency of arterial oxygenation, increased during nitric oxide administration from 152+/-15 mm Hg to 199+/-23 mm Hg (P = 0.008), although the mean arterial pressure and cardiac output were unchanged. Infusion of prostacyclin reduced pulmonary-artery pressure but increased intrapulmonary shunting and reduced the PaO2/FiO2 and systemic arterial pressure. Continuous nitric oxide inhalation consistently lowered the pulmonary-artery pressure and augmented the PaO2/FiO2 for 3 to 53 days. Conclusions. Inhalation of nitric oxide by patients with severe adult respiratory distress syndrome reduces the pulmonary-artery pressure and increases arterial oxygenation by improving the matching of ventilation with perfusion, without producing systemic vasodilation. Randomized, blinded trials will be required to determine whether inhaled nitric oxide will improve outcome. C1 FREE UNIV BERLIN,KLINIKUM RUDOLF VIRCHOW WEDDING,ANAESTHESIOL & OPERAT INTENS MED KLIN,W-1000 BERLIN 65,GERMANY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-42397] NR 48 TC 1247 Z9 1274 U1 1 U2 10 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 11 PY 1993 VL 328 IS 6 BP 399 EP 405 DI 10.1056/NEJM199302113280605 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA KL584 UT WOS:A1993KL58400005 PM 8357359 ER PT J AU CHRISTEN, WG MANSON, JE GLYNN, RJ BURING, JE ROSNER, B HENNEKENS, CH SEDDON, JM AF CHRISTEN, WG MANSON, JE GLYNN, RJ BURING, JE ROSNER, B HENNEKENS, CH SEDDON, JM TI CIGARETTE-SMOKING AND RISK OF CATARACTS - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP CHRISTEN, WG (reprint author), BRIGHAM & WOMENS HOSP,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 10 PY 1993 VL 269 IS 6 BP 748 EP 748 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KK544 UT WOS:A1993KK54400025 ER PT J AU KHARBANDA, S NAKAMURA, T KUFE, D AF KHARBANDA, S NAKAMURA, T KUFE, D TI INDUCTION OF THE C-JUN PROTOONCOGENE BY A PROTEIN KINASE-C-DEPENDENT MECHANISM DURING EXPOSURE OF HUMAN EPIDERMAL-KERATINOCYTES TO ETHANOL SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID DNA-BINDING ACTIVITY; LARYNGEAL-CANCER; PHARYNGEAL CANCER; ALCOHOL; CELLS; FOS; ACTIVATION; TOBACCO; GENE; RISK AB The present work demonstrates that ethanol induces expression of the c-jun proto-oncogene in human keratinocytes. Increased c-jun mRNA levels were detectable at 1 hr of exposure to 1% ethanol and at 24 hr remained above that in control keratinocytes. An increase in c-jun expression was also detectable at ethanol concentrations of 0. 1 and 0.5%. Similar findings were obtained for the related jun-B and c-fos early response genes. The results also demonstrate that ethanol exposure is associated with increases in protein kinase C activity in both the cytosol and membrane fractions. This increase was detectable at 5 min and maximal at 30-60 min. The finding that induction of c-jun expression by ethanol was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggested that this effect is mediated by protein kinase C. Furthermore, down-regulation of protein kinase C by prolonged exposure to 12-O-tetradecanoylphorbol-13-acetate was associated with a block in ethanol-induced c-jun expression. We also demonstrated that ethanol exposure is associated with rapid (5-30 min) increases in intracellular levels of diradylglycerol. Taken together, these findings demonstrate that the exposure of keratinocytes to ethanol results in the activation of protein kinase C and c-jun expression. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA19589] NR 36 TC 34 Z9 34 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD FEB 9 PY 1993 VL 45 IS 3 BP 675 EP 681 DI 10.1016/0006-2952(93)90142-J PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KP631 UT WOS:A1993KP63100020 PM 8442767 ER PT J AU ANDERSON, WM DELINCK, DL BENNINGER, L WOOD, JM SMILEY, ST CHEN, LB AF ANDERSON, WM DELINCK, DL BENNINGER, L WOOD, JM SMILEY, ST CHEN, LB TI CYTOTOXIC EFFECT OF THIACARBOCYANINE DYES ON HUMAN COLON-CARCINOMA CELLS AND INHIBITION OF BOVINE HEART MITOCHONDRIAL NADH-UBIQUINONE REDUCTASE-ACTIVITY VIA A ROTENONE-TYPE MECHANISM BY 2 OF THE DYES SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID RHODAMINE-123; DEHYDROGENASE; ACCUMULATION; DEQUALINIUM; INVITRO AB Five lipophilic-cationic thiacarbocyanine compounds differing in the side chains (methyl-S13, ethyl-S23, propyl-S33, butyl-S43, and pentyl-S53) and a related thiadicarbocyanine compound with ethyl side chains (S25) exhibited a selective cytotoxic effect on human colon carcinoma cells compared to green monkey kidney epithelial cells. The inhibitory concentration for 50% inhibition of growth (IC50) for the carcinoma cells ranged from 13 nM for S13 and S23 to 160 nM for S25. The carcinoma cells were 4- to 100-fold more sensitive than the normal cells. Two of the five compounds, S13 and S23, selectively inhibited NADH oxidase activity with bovine heart submitochondrial particles (SMP). There was no discernable inhibitory effect by the other three thiacarbocyanine compounds on electron transport chain activity. The primary site of inhibition within the respiratory chain for S13 and S23 appeared to be the NADH to coenzyme Q portion of the mitochondrial electron transport chain. Artificial electron acceptors for this segment of respiratory chain were used to localize the inhibitory site. Using SMP, both S13 and S23 inhibited reduction of menadione, duroquinone, and coenzyme Q. Using purified complex I (NADH-ubiquinone reductase) (EC 1.6.99.3), S13 slightly inhibited reduction of juglone, duroquinone, and coenzyme Q, whereas S23 had no effect on any of the substrates. When rotenone-saturated SMP were used, the inhibitory effects of S13, but not S23, on the reduction of menadione were abolished, as was the inhibitory effect of S13 on coenzyme Q reduction when rotenone-insensitive complex I was used as the source of the enzyme. These results suggest that (1) S13 and S23 inhibition of NADH-ubiquinone reductase activity is enhanced by the membrane environment of the enzyme, and (2) the inhibition appears to be in part akin to the inhibiting mode of rotenone. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ANDERSON, WM (reprint author), INDIANA UNIV,SCH MED,NW CTR MED EDUC,3400 BROADWAY,GARY,IN 46408, USA. FU NHLBI NIH HHS [HL32829] NR 21 TC 28 Z9 28 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD FEB 9 PY 1993 VL 45 IS 3 BP 691 EP 696 DI 10.1016/0006-2952(93)90144-L PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KP631 UT WOS:A1993KP63100022 PM 8442768 ER PT J AU GERARD, NP LU, B HE, XP EDDY, RL SHOWS, TB GERARD, C AF GERARD, NP LU, B HE, XP EDDY, RL SHOWS, TB GERARD, C TI HUMAN CHEMOTAXIS RECEPTOR GENES CLUSTER AT 19Q13.3-13.4 - CHARACTERIZATION OF THE HUMAN C5A RECEPTOR GENE SO BIOCHEMISTRY LA English DT Article ID PLATELET-ACTIVATING-FACTOR; HUMAN INTERLEUKIN-8 RECEPTOR; FORMYL PEPTIDE RECEPTOR; FUNCTIONAL EXPRESSION; HUMAN-NEUTROPHILS; HL-60 CELLS; CHROMOSOME LOCALIZATION; INSITU HYBRIDIZATION; LEUCYL-PHENYLALANINE; MOLECULAR-CLONING AB The human C5a anaphylatoxin and formyl peptide receptor genes, as well as two genes with high sequence identity to the formyl peptide receptor, FPRH1 and FPRH2, have been mapped to chromosome 19 (Lu et al., 1992). Further analysis reveals that these genes are present in the 19q13.3 band adjacent to the 13.3-13.4 interface. MRNAs for the C5a and formyl peptide receptors, as well as for FPRH1, are expressed in cAMP differentiated U937 cells and human eosinophils, while all four transcripts are expressed in human lung. This observation opens the possibility for coordinate regulation of these genes. In order to initiate the mapping of fine structure at this locus, genomic clones have been analyzed. All four of the genes have a similar structure, with the receptor protein encoded in a single exon. Detailed characterization of the C5a receptor gene reveals a two exon structure, with the 5' untranslated sequence and initiating methionine located in the first exon. An intron of approximately 9 kb separates exon 1 from the receptor-encoding exon 2. The region of genomic DNA flanking the 5' untranslated sequence possesses promoter activity when transfected into the myeloid-derived rat basophilic leukemia RBL-1 cells, but the same region is inactive when transfected into nonmyeloid cells. Deletional analyses indicate that C5a receptor 5' flanking region contains both cell-specific suppressor and promoter regions. C1 CHILDRENS HOSP MED CTR,DEPT PEDIAT,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,THORNDIKE LAB,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT HUMAN GENET,BUFFALO,NY 14263. RP GERARD, NP (reprint author), CHILDRENS HOSP MED CTR,INA SUE PERLMUTTER LAB,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL 36162] NR 47 TC 69 Z9 70 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 9 PY 1993 VL 32 IS 5 BP 1243 EP 1250 DI 10.1021/bi00056a007 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KL458 UT WOS:A1993KL45800007 PM 8383526 ER PT J AU GALLUSSER, A KIRCHHAUSEN, T AF GALLUSSER, A KIRCHHAUSEN, T TI RECONSTITUTION OF A MAMMALIAN AP-2 COMPLEX FROM ITS RECOMBINANT SUBUNITS EXPRESSED IN ESCHERICHIA-COLI SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CBR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 37 EP 37 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600129 ER PT J AU BIDDISON, WE GAMMON, MC HARRER, T WALKER, BD UTZ, U ZWEERINK, HJ AF BIDDISON, WE GAMMON, MC HARRER, T WALKER, BD UTZ, U ZWEERINK, HJ TI PRESENTATION OF ENDOGENOUS PEPTIDES TO MHC CLASS-I RESTRICTED CTL IN TRANSPORT DELETION MUTANT T2 CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MERCK RES LABS,RAHWAY,NJ. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 53 EP 53 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600182 ER PT J AU WANECK, GL BROWN, D ROLLINS, CT FLAVELL, RA FLYER, DC AF WANECK, GL BROWN, D ROLLINS, CT FLAVELL, RA FLYER, DC TI FAILURE OF GPI-ANCHORED DB MOLECULES TO PRESENT MOMULV ANTIGEN TO CTL CORRELATES WITH DIFFERENCES IN INTRACELLULAR TRAFFICKING SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02129. MGH,CTR CANC,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. YALE UNIV,SCH MED,IMMUNOBIOL SECT,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,HHMI,NEW HAVEN,CT 06510. PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,DEPT MICROBIOL & IMMUNOL,HERSHEY,PA 17033. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 63 EP 63 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600222 ER PT J AU WILLIAMS, DB MARGOLESE, L AHLUWALIA, N DEGEN, E WANECK, GL AF WILLIAMS, DB MARGOLESE, L AHLUWALIA, N DEGEN, E WANECK, GL TI CHARACTERIZATION OF THE INTERACTION BETWEEN THE CLASS-I HEAVY-CHAIN AND THE MOLECULAR CHAPERONE, P88 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02129. UNIV TORONTO,DEPT BIOCHEM,TORONTO M5S 1A8,ONTARIO,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 64 EP 64 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600223 ER PT J AU OSTRANDROSENBERG, S BASKAR, S NABAVI, N FREEMAN, G NADLER, L GLIMCHER, L AF OSTRANDROSENBERG, S BASKAR, S NABAVI, N FREEMAN, G NADLER, L GLIMCHER, L TI COSTIMULATION THROUGH MURINE-B7 MOLECULE RESTORES IMMUNOGENICITY OF AUTOLOGOUS TUMOR-CELLS EXPRESSING TRUNCATED MHC CLASS-II MOLECULES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 U MD,DEPT BIOL,BALTIMORE,MD 21228. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 71 EP 71 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600251 ER PT J AU SLUDER, AE RUVKUN, G AF SLUDER, AE RUVKUN, G TI A CAENORHABDITIS-ELEGANS MEMBER OF THE NUCLEAR HORMONE RECEPTOR GENE FAMILY IS EXPRESSED DURING EARLY EMBRYOGENESIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 120 EP 120 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600426 ER PT J AU AUSUBEL, FM GLAZEBROOK, J GREENBERG, J KATAGIRI, F MINDRINOS, M YU, GL AF AUSUBEL, FM GLAZEBROOK, J GREENBERG, J KATAGIRI, F MINDRINOS, M YU, GL TI ANALYSIS OF THE ARABIDOPSIS DEFENSE RESPONSE TO PSEUDOMONAS PATHOGENS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 129 EP 129 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600451 ER PT J AU KOLODNER, R HALL, S JOHNSON, A TISHKOFF, D AF KOLODNER, R HALL, S JOHNSON, A TISHKOFF, D TI NOVEL HOMOLOGOUS PAIRING PROTEINS FROM SACCHAROMYCES-CEREVISIAE AND ESCHERICHIA-COLI SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CELLULAR & MOLEC BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 146 EP 146 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600508 ER PT J AU FISHER, DE SHARP, PA AF FISHER, DE SHARP, PA TI DESIGN OF HIGH-AFFINITY DNA-BINDING MYC ANALOGS - CRITICAL SIDE-CHAIN AND CONFORMATIONAL REQUIREMENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 8 PY 1993 SU 17C BP 236 EP 236 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN466 UT WOS:A1993KN46600806 ER PT J AU WILKISON, WO SPIEGELMAN, BM AF WILKISON, WO SPIEGELMAN, BM TI BIOSYNTHESIS OF THE VASOACTIVE LIPID MONOBUTYRIN - CENTRAL ROLE OF DIACYLGLYCEROL SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HORMONE-SENSITIVE LIPASE; RAT ADIPOSE-TISSUE; PROTEIN KINASE-C; 3T3 ADIPOCYTES; CELLS; ANGIOGENESIS; STIMULATION; SPECIFICITY; METABOLISM; MECHANISM AB Monobutyrin (1-butyrylglycerol) is a simple lipid secreted by adipocytes that stimulates both angiogenesis and vasodilation of microvascular beds. While monobutyrin production is increased during lipolysis, little is known about the biosynthetic pathway of this short chain monoacylglycerol. We show here that diacylglycerol, an intermediate in the lipolytic pathway, can stimulate monobutyrin synthesis from an adipocyte particulate fraction and does so by acting as a substrate. The biosynthetic route involves the acylation of diacylglycerol with butyryl-CoA to form a transient triacylglycerol intermediate. This intermediate is then hydrolyzed by a lipase(s) with specificity for long chain fatty acyl groups to form monobutyrin. Based on this information, a novel pathway for the synthesis of monobutyrin is proposed. Preliminary characterization of these enzymatic activities with respect to their cell-type specificity indicates that the acyltransferase activity is found in several cell types, albeit at lower levels than in adipocytes. The lipase activity appears to be two distinct steps, with both steps being adipocyte differentiation-dependent. These results indicate the likely biochemical basis for the restriction of monobutyrin synthesis to fat cells and also suggests a molecular basis for the close linkage between lipolysis, monobutyrin synthesis, and vasodilation. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP WILKISON, WO (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK 42420, DK08277] NR 35 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 5 PY 1993 VL 268 IS 4 BP 2844 EP 2849 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KK815 UT WOS:A1993KK81500086 PM 8428959 ER PT J AU FRIEND, SH AF FRIEND, SH TI GENETIC MODELS FOR STUDYING CANCER SUSCEPTIBILITY SO SCIENCE LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP FRIEND, SH (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,BOSTON,MA 02129, USA. NR 15 TC 22 Z9 23 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 5 PY 1993 VL 259 IS 5096 BP 774 EP 775 DI 10.1126/science.8430329 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KL110 UT WOS:A1993KL11000020 PM 8430329 ER PT J AU SHINKAI, Y KOYASU, S NAKAYAMA, K MURPHY, KM LOH, DY REINHERZ, EL ALT, FW AF SHINKAI, Y KOYASU, S NAKAYAMA, K MURPHY, KM LOH, DY REINHERZ, EL ALT, FW TI RESTORATION OF T-CELL DEVELOPMENT IN RAG-2 DEFICIENT MICE BY FUNCTIONAL TCR TRANSGENES SO SCIENCE LA English DT Article ID ANTIGEN RECEPTOR; MONOCLONAL-ANTIBODY; SCID MUTATION; V(D)J RECOMBINATION; EXPRESSION; REPAIR; CHAIN; DIFFERENTIATION; THYMOCYTES; BIOLOGY AB Introduction of TCRalpha transgene, TCRbeta transgene, or both into RAG-2-/- mice differentially rescues T cell development. RAG-2-/- mice have small numbers of TCR-CD4-CD8- (double negative, DN) thymocytes that express CD3gammadeltaepsilon and zeta proteins intracellularly. Introduction of a TCRbeta transgene, but not a TCRalpha transgene, into the RAG-2-/- background restored normal numbers of thymocytes. These cells were CD4+CD8+ (double positive, DP) and expressed small amounts of surface TCRbeta chain dimers in association with CD3gammadeltaepsilon but not zeta. RAG-2-/- mice that expressed alpha and beta TCR transgenes developed both DP and single positive thymocytes. Thus, the TCRbeta subunit, possibly in association with a novel CD3 complex, participates in the DN to the DP transition. C1 CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT GENET,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT GENET,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT MOLEC MICROBIOL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. RI Shinkai, Yoichi/N-3909-2014; Koyasu, Shigeo/J-5583-2015 OI Shinkai, Yoichi/0000-0002-6051-2484; Koyasu, Shigeo/0000-0001-9585-3038 FU NIAID NIH HHS [AI19807, AI20047] NR 33 TC 350 Z9 350 U1 1 U2 12 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 5 PY 1993 VL 259 IS 5096 BP 822 EP 825 DI 10.1126/science.8430336 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KL110 UT WOS:A1993KL11000036 PM 8430336 ER PT J AU LEAF, A AF LEAF, A TI PREVENTIVE MEDICINE FOR OUR AILING HEALTH-CARE SYSTEM SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID MYOCARDIAL-INFARCTION; HEART-DISEASE; REHABILITATION; REGRESSION; MORBIDITY; MORTALITY; TRIALS C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP LEAF, A (reprint author), W ROXBURY VA MED CTR,DEPT MED,1400 VFW PKWY,BOSTON,MA 02132, USA. NR 16 TC 30 Z9 30 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 3 PY 1993 VL 269 IS 5 BP 616 EP 618 DI 10.1001/jama.269.5.616 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA KJ444 UT WOS:A1993KJ44400028 PM 8421366 ER PT J AU THOR, AD YANDELL, DW AF THOR, AD YANDELL, DW TI PROGNOSTIC-SIGNIFICANCE OF P53 OVEREXPRESSION IN NODE-NEGATIVE BREAST-CARCINOMA - PRELIMINARY STUDIES SUPPORT CAUTIOUS OPTIMISM SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. RP THOR, AD (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,100 BLOSSOM ST,COX 5,BOSTON,MA 02114, USA. NR 12 TC 37 Z9 37 U1 0 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 FEB 3 PY 1993 VL 85 IS 3 BP 176 EP 177 DI 10.1093/jnci/85.3.176 PG 2 WC Oncology SC Oncology GA KJ687 UT WOS:A1993KJ68700002 PM 8423618 ER PT J AU PATARCA, R FLETCHER, MA CANTOR, H AF PATARCA, R FLETCHER, MA CANTOR, H TI STRUCTURAL FEATURES OF 2 T-CELL-SPECIFIC GENES THAT SUGGEST A POTENTIAL ROLE IN HTLV-I-ASSOCIATED PATHOLOGY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID EXPRESSION AB The Rpt-1 gene product is an intranuclear protein expressed by CD4+ T-cells, which may regulate expression of the interleukin-2 receptor. Structural analysis of Rpt-1 reveals structural motifs that are shared by a group of transcriptional regulatory proteins with oncogenic potential. We suggest that altered expression of Rpt-1 may be associated with HTLV-I-dependent T-cell leukemias. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,IMMUNOPATHOL LAB,BOSTON,MA 02115. RP PATARCA, R (reprint author), UNIV MIAMI,SCH MED,EM PAPPER LAB CLIN IMMUNOL,POB 016960,MIAMI,FL 33101, USA. FU NIAID NIH HHS [AI 13600, AI 12184] NR 13 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1993 VL 9 IS 2 BP 105 EP 107 DI 10.1089/aid.1993.9.105 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA KQ327 UT WOS:A1993KQ32700001 PM 8096144 ER PT J AU BECKER, HC HALE, RL AF BECKER, HC HALE, RL TI REPEATED EPISODES OF ETHANOL WITHDRAWAL POTENTIATE THE SEVERITY OF SUBSEQUENT WITHDRAWAL SEIZURES - AN ANIMAL-MODEL OF ALCOHOL-WITHDRAWAL KINDLING SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE ETHANOL WITHDRAWAL; SEIZURES; KINDLING; MICE; HANDLING-INDUCED CONVULSIONS ID PHYSICAL-DEPENDENCE; MICE; SINGLE; RATS AB Prior experience with ethanol (EtOH) withdrawal may sensitize an individual to subsequent withdrawal episodes. It has been hypothesized that the progressive intensification of the EtOH withdrawal syndrome following repeated episodes of EtOH intoxication and withdrawal may represent the manifestations of a ''kindling'' mechanism. The purpose of this study was to develop an animal model of EtOH withdrawal that is sensitive to the effects of prior withdrawal experience. Adult male C3H mice were chronically exposed to EtOH vapor in inhalation chambers prior to withdrawal testing. A multiple withdrawal (MW) group received 3 cycles of 16 hr EtOH vapor separated by 8-hr periods of abstinence; a single withdrawal (SW) group received a single bout of EtOH exposure (16 hr); a third group (SW-CONT) experienced a single withdrawal episode after receiving the equivalent amount of EtOH intoxication as the MW group (16 x 3 = 48 hr), but in a continuous (uninterrupted) fashion; and a fourth group (C) served as controls, not receiving any EtOH exposure throughout the study. Severity of the withdrawal response was assessed by scoring handling-induced convulsions hourly for the first 10 hr and then at 24 hr postwithdrawal. The results indicated that the severity of EtOH withdrawal seizures was significantly greater in animals that had a prior history of withdrawal episodes (MW group) in comparison to a separate group of animals that were tested following a single withdrawal from the some 16-hr intoxication period (SW group). Moreover, the intensity of withdrawal seizures in MW animals was significantly greater than in animals exposed to an equivalent total amount of intoxication (48 hr), but only withdrawn a single time (SW-CONT group). Differences in the severity of EtOH withdrawal seizures due to differences in prior withdrawal experience do not appear to be related to compromised health of the animals or to differences in the level of intoxication (blood EtOH levels) immediately preceding withdrawal assessment. As such, these results support the ''kindling'' hypothesis of EtOH withdrawal and provide a model with which to study potential mechanisms underlying the phenomenon. C1 MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC 29425. RP BECKER, HC (reprint author), RALPH H JOHNSON VET ADM MED CTR,RES SERV,109 BEE ST,CHARLESTON,SC 29401, USA. NR 31 TC 182 Z9 184 U1 2 U2 6 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD FEB PY 1993 VL 17 IS 1 BP 94 EP 98 DI 10.1111/j.1530-0277.1993.tb00731.x PG 5 WC Substance Abuse SC Substance Abuse GA KP433 UT WOS:A1993KP43300014 PM 8452212 ER PT J AU TRAVIN, MI BOUCHER, CA NEWELL, JB LARAIA, PJ FLORES, AR EAGLE, KA AF TRAVIN, MI BOUCHER, CA NEWELL, JB LARAIA, PJ FLORES, AR EAGLE, KA TI VARIABLES ASSOCIATED WITH A POOR PROGNOSIS IN PATIENTS WITH AN ISCHEMIC TL-201 EXERCISE TEST SO AMERICAN HEART JOURNAL LA English DT Article ID CORONARY-ARTERY DISEASE; MYOCARDIAL-INFARCTION; DIAGNOSTIC-TOOL; BYPASS-SURGERY; CHEST PAIN; TL-201; SCINTIGRAPHY; SEVERITY; AGE AB To determine the exercise workload, ECG, and thallium-201 image parameters that are most closely associated with a poor prognosis from ischemic heart disease, the test results of 268 patients were reviewed. Only patients with unequivocal thallium-201 redistribution were selected. A multivariate analysis was performed to find the variables that were most strongly associated with the outcomes of coronary revascularization, myocardial infarction, and cardiac death during a follow-up period of 25 +/- 19 months. Patients who underwent early elective revascularization had poorer exercise tolerance and more thallium image abnormalities than those with no events. In the remaining patients myocardial infarction was most closely related to the extent and severity of thallium ischemia (p = 0.0086), whereas cardiac death was associated with abnormal thallium lung uptake (p = 0.0082) and an inability to exercise to 9.6 MET (p = 0.0144). Thus unlike myocardial infarction, cardiac death is best predicted by variables that reflect poor left ventricular function rather than those that indicate ischemia. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. SPAULDING REHABIL HOSP,DIV CARDIOL,BOSTON,MA 02114. NR 32 TC 34 Z9 34 U1 0 U2 1 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 FEB PY 1993 VL 125 IS 2 BP 335 EP 344 DI 10.1016/0002-8703(93)90009-X PN 1 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KL170 UT WOS:A1993KL17000009 PM 8427125 ER PT J AU DEC, GW FIFER, MA HERRMANN, HC COCCASPOFFORD, D SEMIGRAN, MJ AF DEC, GW FIFER, MA HERRMANN, HC COCCASPOFFORD, D SEMIGRAN, MJ TI LONG-TERM OUTCOME OF ENOXIMONE THERAPY IN PATIENTS WITH REFRACTORY HEART-FAILURE SO AMERICAN HEART JOURNAL LA English DT Article ID RECENT CLINICAL DEVELOPMENTS; POSITIVE INOTROPIC AGENTS; ORAL MILRINONE; MULTICENTER TRIAL; SURVIVAL; CARDIOMYOPATHY; MECHANISMS; MORTALITY; MDL-17043; PLACEBO AB Few options are available for patients with severe heart failure that is unresponsive to therapy with digoxin, diuretics, and vasodilators. The clinical responses and predictors of survival were studied in 41 consecutive patients with New York Heart Association (NYHA) class IV heart failure during long-term oral enoximone therapy (mean dose 232 +/- 15 mg/day). The mean age was 60 +/- 1 years, and the initial left ventricular ejection fraction was 0.19 +/- 0.01. The cause of heart failure was either coronary artery disease (n = 23) or dilated cardiomyopathy (n = 18). Symptomatic improvement occurred in the majority (83%) of patients; 24% improved two or more NYHA classes. Although the 12-month mortality rate for the entire group was high (54 +/- 8%), a subgroup of patients with dilated cardiomyopathy achieved a sustained benefit with a decrease in symptoms >1 NYHA class, fewer hospitalizations, and a survival rate at 24 months of 60%. Multivariate analysis identified the cause of heart failure, left ventricular ejection fraction, and clinical improvement within 60 days of enoximone therapy as predictors of a favorable long-term outcome. The presence of coronary artery disease was most predictive of early mortality (p < 0.0002), with only 5% of patients surviving >18 months compared to 66% of those with dilated cardiomyopathy. Median survival rates were 132 +/- 31 and 921 +/- 214 days (p < 0.001) for the coronary artery disease and dilated cardiomyopathy populations, respectively. Oral enoximone can provide symptomatic improvement and a palliative option for the majority of patients with refractory heart failure resulting from cardiomyopathy. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DEC, GW (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,CARDIAC UNIT,BOSTON,MA 02114, USA. NR 27 TC 16 Z9 16 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD FEB PY 1993 VL 125 IS 2 BP 423 EP 429 DI 10.1016/0002-8703(93)90021-Z PN 1 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KL170 UT WOS:A1993KL17000021 PM 8427136 ER PT J AU KREMPF, M HOERR, RA PELLETIER, VA MARKS, LM GLEASON, R YOUNG, VR AF KREMPF, M HOERR, RA PELLETIER, VA MARKS, LM GLEASON, R YOUNG, VR TI AN ISOTOPIC STUDY OF THE EFFECT OF DIETARY CARBOHYDRATE ON THE METABOLIC-FATE OF DIETARY LEUCINE AND PHENYLALANINE SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE CARBOHYDRATE; PROTEIN SPARING; LEUCINE; PHENYLALANINE; SPLANCHNIC UPTAKE; FLUX ID AMINO-ACID; YOUNG MEN; SUBSTRATE AVAILABILITY; GLUCOSE-METABOLISM; PROTEIN-SYNTHESIS; INGESTION; INFUSION; KINETICS; INSULIN; LYSINE AB The fate of dietary leucine and phenylalanine was studied in five healthy, young adult men, by using a dual, stable isotope-tracer infusion approach to estimate amino acid fluxes, splanchnic (Sp) uptake, and delivery of absorbed amino acid to the peripheral circulation. Subject received two, 4-h tracer infusions of [1-C-13]leucine and [N-15]phenylalanine infused through a feeding tube placed in the duodenum, and [5,5,5-H-2(3)]leucine, [ring-H-2(5)]phenylalanine, and [6,6-H-2(2)]glucose infused simultaneously by vein. In one experiment subjects received an amino acid mixture (83 mg amino acid . kg-1 . h-1) via the feeding tube and in the other experiment amino acids were supplied with carbohydrate (CHO) (167 mg . kg-1 . h-1). Sp uptake of dietary leucine decreased with added dietary CHO (29% of ingested leucine for amino acids alone vs 20% with CHO; P < 0.05) but was not different for phenylalanine (P > 0.05). Addition of CHO decreased both release of leucine via protein breakdown and leucine oxidation and increased body leucine balance (P < 0.05). C1 MIT, CLIN RES CTR, ROOM E18-613, 50 AMES ST, CAMBRIDGE, MA 02142 USA. MIT, SCH SCI, CAMBRIDGE, MA 02142 USA. MASSACHUSETTS GEN HOSP, SHRINERS BURNS INST, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK 15856] NR 34 TC 34 Z9 34 U1 0 U2 2 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 FEB PY 1993 VL 57 IS 2 BP 161 EP 169 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA KK283 UT WOS:A1993KK28300008 PM 8424384 ER PT J AU PRINCE, MR FRISOLI, JK AF PRINCE, MR FRISOLI, JK TI BETA-CAROTENE ACCUMULATION IN SERUM AND SKIN SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE ATHEROSCLEROSIS; CAROTENOIDS; LASER ANGIOPLASTY; NUTRITION; LIPID; LIPOPROTEIN; PHARMACOKINETICS ID PLASMA-CONCENTRATIONS; ERYTHROPOIETIC PROTOPORPHYRIA; VITAMIN-A; LASER; ABSORPTION; THERAPY; ANGINA; MEN AB The accumulation of beta-carotene in serum an skin was evaluated in human volunteers. A single 51-mg dose of beta-carotene given in the absence of dietary fat resulted in no detectable change in serum beta-carotene. The same dose administered with 200 g fat increased serum beta-carotene 2.5-fold at 40 h. Similarly, administering beta-carotene daily in three divided doses with meals raised the serum beta-carotene concentration three times as high compared with the same total dose administered once a day; both regimens had the same time constant for serum accumulation: 9-10 d. Remittance measurements of skin color demonstrated that the accumulation of beta-carotene in skin was delayed by up to 2 wk compared with serum accumulation. These data indicate that beta-carotene absorption requires dietary fat and is enhanced by administering with meals but there is a long time constant for serum (10 d) and tissue (several weeks) accumulation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LAB,BOSTON,MA 02114. RP PRINCE, MR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL46384, HL44274] NR 31 TC 141 Z9 147 U1 1 U2 11 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 FEB PY 1993 VL 57 IS 2 BP 175 EP 181 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA KK283 UT WOS:A1993KK28300010 PM 8424385 ER PT J AU SOBER, AJ AF SOBER, AJ TI WHAT IS EARLY MELANOMA - RESPONSE SO AMERICAN JOURNAL OF DERMATOPATHOLOGY LA English DT Article RP SOBER, AJ (reprint author), MASSACHUSETTS GEN HOSP,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 0193-1091 J9 AM J DERMATOPATH JI Am. J. Dermatopathol. PD FEB PY 1993 VL 15 IS 1 BP 48 EP 48 PG 1 WC Dermatology SC Dermatology GA KL855 UT WOS:A1993KL85500009 ER PT J AU BERGOFFEN, J TROFATTER, J PERICAKVANCE, MA HAINES, JL CHANCE, PF FISCHBECK, KH AF BERGOFFEN, J TROFATTER, J PERICAKVANCE, MA HAINES, JL CHANCE, PF FISCHBECK, KH TI LINKAGE LOCALIZATION OF X-LINKED CHARCOT-MARIE-TOOTH DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID SENSORY NEUROPATHY; HEREDITARY MOTOR; DOMINANT INHERITANCE; DNA; FAMILY; POLYMORPHISMS; POLYMERASE; PROBES; LOCUS AB Charcot-Marie-Tooth disease (CMT), also known as hereditary motor and sensory neuropathy, is a heterogeneous group of slowly progressive, degenerative disorders of peripheral nerve. X-linked CMT (CMTX) (McKusick 302800), a subdivision of type I, or demyelinating, CMT is an X-linked dominant condition with variable penetrance. Previous linkage analysis using RFLPs demonstrated linkage to markers on the proximal long and short arms of the X chromosome, with the more likely localization on the proximal long arm of the X chromosome. Available variable simple-sequence repeats (VSSRs) broaden the possibilities for linkage analysis. This paper presents new linkage data and recombination analysis derived from work with four VSSR markers -AR, PGKP1, DXS453, and DXYS1X-in addition to analysis using RFLP markers described elsewhere. These studies localize the CMTX gene to the proximal Xq segment between PGKP1 (Xq11.2-12) and DXS72 (Xq21.1), with a combined maximum multipoint lod score of 15.3 at DXS453 (theta = 0). C1 CHILDRENS HOSP,DEPT HUMAN GENET & MOLEC BIOL,PHILADELPHIA,PA 19104. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. UNIV UTAH,MED CTR,DIV MED GENET,SALT LAKE CITY,UT 84112. RP BERGOFFEN, J (reprint author), UNIV PENN,SCH MED,DEPT NEUROL,CLIN RES BLDG,422 CURIE BLVD,ROOM 280,PHILADELPHIA,PA 19104, USA. RI Haines, Jonathan/C-3374-2012 FU NINDS NIH HHS [NS08075, NS26330] NR 31 TC 86 Z9 87 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD FEB PY 1993 VL 52 IS 2 BP 312 EP 318 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA KN275 UT WOS:A1993KN27500009 PM 8430694 ER PT J AU SNYDMAN, DR RUBIN, RH WERNER, BG AF SNYDMAN, DR RUBIN, RH WERNER, BG TI NEW DEVELOPMENTS IN CYTOMEGALOVIRUS PREVENTION AND MANAGEMENT SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE CYTOMEGALOVIRUS; CMV HYPERIMMUNE GLOBULIN ID RENAL-TRANSPLANT RECIPIENTS; IMMUNE GLOBULIN; VIRUS INFECTIONS; ALLOGRAFT RECIPIENTS; CONTROLLED TRIAL; ORAL ACYCLOVIR; DISEASE; BLOOD; GANCICLOVIR; TRANSFUSIONS C1 TUFTS UNIV,SCH MED,BOSTON,MA 02111. HARVARD UNIV,NEW ENGLAND MED CTR HOSP,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MASSACHUSETTS STATE LAB INST,BOSTON,MA. RI Snydman, David/O-3889-2014 OI Snydman, David/0000-0003-0119-3978 NR 47 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 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD FEB PY 1993 VL 21 IS 2 BP 217 EP 228 PG 12 WC Urology & Nephrology SC Urology & Nephrology GA KL622 UT WOS:A1993KL62200016 PM 8381578 ER PT J AU FINE, MJ SINGER, DE HANUSA, BH LAVE, JR KAPOOR, WN AF FINE, MJ SINGER, DE HANUSA, BH LAVE, JR KAPOOR, WN TI VALIDATION OF A PNEUMONIA PROGNOSTIC INDEX USING THE MEDISGROUPS COMPARATIVE HOSPITAL DATABASE SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID COMMUNITY-ACQUIRED PNEUMONIA; ACUTE MYOCARDIAL-INFARCTION; MORTALITY DATA; LENGTH; STAY AB PURPOSE: Our purpose was to validate a previously developed pneumonia-specific prognostic index in a large, multicenter population. PATIENTS AND METHODS. We developed a pneumonia-specific prognostic index in a prospective, multicenter study of 346 patients with clinical and radiographic evidence of pneumonia admitted to 3 Pittsburgh hospitals (the derivation cohort), and validated the index in 14,199 patients with a principal ICD-9-CM diagnosis of pneumonia admitted to 78 hospitals in the 1989 MedisGroups Comparative Hospital Database (the validation cohort). The prognostic index classified patients into rive ordered risk classes based on six predictors of mortality. age greater than 65 years, pleuritic chest pain, a vital sign abnormality, altered mental status, neoplastic and high-risk pneumonia etiology. Each patient in the validation cohort was assigned to a risk class by obtaining values for the index's six predictors in the MedisGroups population. The performance of the prognostic index in the derivation and validation cohorts was assessed by comparing hospital mortality rates within each of the index's five prognostic risk classes. RESULTS: The hospital mortality rate was 13.0% in the derivation cohort, and 11.1% in the validation cohort (p = 026). The agreement in the risk class-specific mortality rates was striking with the exception of class V: in class I mortality was 0% in the derivation cohort versus 1% in the validation cohort; in class II, 0% versus 1.1%; class III, 10.9% versus 8.6%; class IV, 21.8% versus 26.2%; and class V, 73.7% versus 37.7%. There were no statistically significant differences in mortality rates within the first four risk class, which represented the vast majority of patients in the derivation (94%) as well as the validation (98%) cohorts. CONCLUSIONS: These data support the generalizability of a pneumonia-specific prognostic index. This index, which performs exceptionally well in classifying low-risk patients, may help physicians identify patients with community-acquired pneumonia who could safely be managed in the ambulatory setting, or if hospitalized, the patients that could be treated with abbreviated inpatient care. C1 UNIV PITTSBURGH,GRAD SCH PUBL HLTH,PITTSBURGH,PA 15261. MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114. RP FINE, MJ (reprint author), UNIV PITTSBURGH,DEPT MED,DIV GEN MED,167 LOTHROP HALL,190 LOTHROP ST,PITTSBURGH,PA 15261, USA. FU AHRQ HHS [R01 HSO 6468] NR 18 TC 132 Z9 133 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB PY 1993 VL 94 IS 2 BP 153 EP 159 DI 10.1016/0002-9343(93)90177-Q PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA KL407 UT WOS:A1993KL40700007 PM 8430711 ER PT J AU EMANUEL, EJ AF EMANUEL, EJ TI THE CRUZAN DECISION - REPLY SO AMERICAN JOURNAL OF MEDICINE LA English DT Letter RP EMANUEL, EJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB PY 1993 VL 94 IS 2 BP 231 EP 232 DI 10.1016/0002-9343(93)90199-Y PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KL407 UT WOS:A1993KL40700028 ER PT J AU CHOI, MY EHRLICH, HP AF CHOI, MY EHRLICH, HP TI U75412E, A LAZAROID, PREVENTS PROGRESSIVE BURN ISCHEMIA IN A RAT BURN MODEL SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID DEPENDENT LIPID-PEROXIDATION; OXYGEN-FREE-RADICALS; THERMAL-INJURY; REPERFUSION INJURY; TISSUE-INJURY; LUNG INJURY; EDEMA; SKIN; ALLOPURINOL; INHIBITORS AB Thermal energy causes an immediate, irreversible injury at the burn site followed by a delayed, reversible tissue loss in the area surrounding the burn site due to progressive ischemia. We investigated the role of lipid peroxidation in the pathogenesis of progressive ischemia in a rat burn model. The burn model consisted of a row of four 10 x 20 mm burns separated by three unburned 5 x 20 mm skin bridges (interspaces). The interspaces became ischemic and necrotic by 24 hours, producing a single wound with the merger of the burn sites. U75412E, a lipid peroxidation inhibitor, preserved vascular patency, restored blood flow, prevented a rise in tissue conjugated dienes, and maintained tissue viability in the interspaces. Four separate burn wounds healed between three viable strips of hair-bearing interspaces. The treatment was effective, when given systemically during the period between 2 hours before and 1 hour after the burn. U75412E prevented progressive burn ischemia and the expansion of tissue loss. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,WOUND HEALING LAB,BLDG 1400,CAMBRIDGE,MA 02142. FU NIGMS NIH HHS [GM-32705] NR 31 TC 40 Z9 42 U1 0 U2 0 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 FEB PY 1993 VL 142 IS 2 BP 519 EP 528 PG 10 WC Pathology SC Pathology GA KL858 UT WOS:A1993KL85800021 PM 8434647 ER PT J AU FUKAYAMA, S TASHJIAN, AH BRINGHURST, FR AF FUKAYAMA, S TASHJIAN, AH BRINGHURST, FR TI ROLE OF PROTEIN KINASE-A IN THE REGULATION OF CYTOSOLIC FREE CALCIUM IN HUMAN OSTEOBLAST-LIKE SAOS-2 CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE-RESISTANT PHENOTYPE; ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE-DEPENDENT PROTEIN KINASE; CALCIUM-ADENOSINE-TRIPHOSPHATASE ID INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; PARATHYROID-HORMONE; CYCLIC-AMP; ALKALINE-PHOSPHATASE; RESISTANT PHENOTYPE; PITUITARY-CELLS; THAPSIGARGIN; RELEASE; INHIBITION; LINE AB We have used wild-type and adenosine 3',5'-cyclic monophosphate (cAMP)-resistant mutant osteoblast-like SaOS-2 cells to investigate the role of protein kinase A (PKA) in the regulation of cytosolic free Ca2+ concentration ([Ca2+]i). Basal levels of [Ca2+]i were the same in wild-type (127 +/- 6.1 nM) and transfected (117 +/- 6.8 nM) SaOS-2 cells, although Ca-45(2+) efflux was slower in the transfected cells. In wild-type cells, thapsigargin (TG, greater-than-or-equal-to 200 nM), an inhibitor of the Ca2+-ATPase activity of the endoplasmic reticulum, acutely increased [Ca2+], (by up to 2-fold), which then returned promptly to basal [Ca2+]i. In cAMP-resistant cells, TG elicited a significantly greater acute rise in [Ca2+]i, which then decayed to an elevated plateau level. In mutant cells, high concentrations of dibutyryladenosine 3',5'cyclic monophosphate, which overcome the PKA blockade, restored the changes in [Ca2+], to the wild-type pattern. In cAMP-resistant, TG-blocked cells, ionomycin (or alpha-thrombin) induced a further elevation in [Ca2+]i, which then declined rapidly to the original basal level. We conclude that basal PKA activity is involved actively in regulation of [Ca2+]i in SaOS-2 cells by promoting Ca2+ efflux from the cell and, possibly, by inhibiting Ca2+ release from or stimulating net Ca2+ sequestration into the ER. We have also obtained evidence for an alternate Ca2+-triggered Ca2+ reuptake mechanism in SaOS-2 cells that is not dependent on either Ca2+-ATPase or PKA. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT MOLEC CELLULAR TOXICOL,BOSTON,MA 02115. RP FUKAYAMA, S (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NIADDK NIH HHS [AM-11794]; NIDDK NIH HHS [DK-10206] NR 30 TC 8 Z9 8 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 FEB PY 1993 VL 264 IS 2 BP C464 EP C470 PN 1 PG 7 WC Physiology SC Physiology GA KN680 UT WOS:A1993KN68000027 PM 8383434 ER PT J AU RUSSO, JJ SWEADNER, KJ AF RUSSO, JJ SWEADNER, KJ TI NA+-K+-ATPASE SUBUNIT ISOFORM PATTERN MODIFICATION BY MITOGENIC INSULIN CONCENTRATION IN 3T3-L1 PREADIPOCYTES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE DIFFERENTIATION; CYTODIFFERENTIATION; ISOZYME; SODIUM PUMP; GENE EXPRESSION; ISOBUTYLMETHYLXANTHINE; DEXAMETHASONE ID ADIPOCYTE DIFFERENTIATION; ADIPOSE CONVERSION; CATALYTIC SUBUNIT; CELL LINE; (NA+,K+)-ATPASE; IDENTIFICATION; NA,K-ATPASE; SYNTHETASE; CULTURE AB When 3T3 preadipocyte cell lines are induced to differentiate to the adipocyte phenotype, the expression of Na+-K+-ATPase isoforms changes. Some disparities have been noted by investigators who used different hormonal conditions to stimulate adipocyte conversion, however. In the present report we investigated the effect of high concentrations of insulin on the 3T3-L1 cell line, to determine whether it affected Na+-K+-ATPase expression separately from its ability to promote phenotypic conversion. The effect of insulin was compared with that of dexamethasone and 3-isobutyl-1-methylxanthine. Changes in Na+-K+-ATPase subunit expression were seen regardless of the hormonal stimulus. Induction of alpha2-mRNA and reduction of beta1-mRNA were always observed. At the protein level, too, induction of alpha2-protein was noted; alpha1-protein levels were not markedly affected. The change in alpha-isoform protein and mRNA levels did not correspond quantitatively with the fraction of cells that were morphologically converted, suggesting that it is an early event in differentiation. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT BIOCHEM & MOLEC BIOPHYS,NEW YORK,NY 10032. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. FU CSP VA [CU-503968]; NHLBI NIH HHS [HL-36271]; NIGMS NIH HHS [GM-36618] NR 22 TC 24 Z9 24 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1993 VL 264 IS 2 BP C311 EP C316 PN 1 PG 6 WC Physiology SC Physiology GA KN680 UT WOS:A1993KN68000007 PM 7680529 ER PT J AU CINCOTTA, AH MACEACHERN, TA MEIER, AH AF CINCOTTA, AH MACEACHERN, TA MEIER, AH TI BROMOCRIPTINE REDIRECTS METABOLISM AND PREVENTS SEASONAL ONSET OF OBESE HYPERINSULINEMIC STATE IN SYRIAN-HAMSTERS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HYPERINSULINEMIA; NEUROENDOCRINE ACTIVITIES; CIRCADIAN RHYTHMS; PROLACTIN; CORTISOL ID GLUCOSE CLAMP TECHNIQUE; TOTAL-BODY WATER; FREE FATTY-ACID; MESOCRICETUS-AURATUS; INSULIN RESISTANCE; PHOTOPERIODIC CONTROL; CIRCADIAN VARIATION; DOPAMINE-RECEPTORS; ENERGY-METABOLISM; PROLACTIN PERMITS AB Bromocriptine redirects metabolism and prevents seasonal onset of the obese hyperinsulinemic state in Syrian hamsters. Metabolic and hormonal effects of bromocriptine were studied in seasonally obese female Syrian hamsters, Mesocricetus auratus. Daily injections of bromocriptine and vehicle (controls) were made at light onset (10:14-h light-dark cycle) for 10 wk. After 9 wk of treatment blood samples were taken every 4 h during a day for assays of hormones, glucose, triglyceride, and fatty acids, and after 10 wk of treatment, tests were carried out to measure insulin-stimulated glucose disposal during a hyperinsulinemic clamp, lipid mobilization (rate of glycerol appearance), protein turnover (lysine flux and deamination), and body composition (deuterium dilution). Bromocriptine reduced percent body fat by 53% and increased percent lean body mass by 8%. It also decreased triglyceride levels by 52% and plasma free fatty acid concentration during the dark-near light onset by 49% and glycerol appearance by 25%. Protein synthesis and catabolism were increased by 62 and 56%, respectively, and deamination of amino acid was decreased by 53% by bromocriptine. Bromocriptine reduced plasma concentration of insulin throughout the day, especially at light onset, by 78% without change in baseline glucose level and markedly decreased steady state plasma glucose (by 40%) during a continuous infusion of insulin and glucose. It also reduced the nocturnal plasma concentration of prolactin by 90%, cortisol by 70%, and thyroid hormones (thyroxine and triiodothyronine) by 50% and dramatically altered the circadian profiles of these hormones and insulin. Bromocriptine apparently shifts metabolism from that found in obese, hyperinsulinemic hamsters during winter to conditions resembling those of lean euinsulinemic hamsters during other seasons. These marked metabolic changes are thought to result from changes in the phase relations of circadian neuroendocrine oscillations that are believed to regulate seasonal metabolic conditions. C1 LOUISIANA STATE UNIV,DEPT ZOOL & PHYSIOL,BATON ROUGE,LA 70803. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. RP CINCOTTA, AH (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 74 TC 48 Z9 49 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1993 VL 264 IS 2 BP E285 EP E293 PN 1 PG 9 WC Physiology SC Physiology GA KN680 UT WOS:A1993KN68000052 PM 8447396 ER PT J AU GUNNING, M CUERO, C SOLOMON, R SILVA, P AF GUNNING, M CUERO, C SOLOMON, R SILVA, P TI C-TYPE NATRIURETIC PEPTIDE RECEPTORS AND SIGNALING IN RECTAL GLAND OF SQUALUS-ACANTHIAS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE NATRIURETIC PEPTIDES; GUANOSINE 3',5'-CYCLIC MONOPHOSPHATE ACCUMULATION; PARTICULATE GUANYLATE CYCLASE; RECEPTOR-LINKED GUANYLATE CYCLASE; SIGNAL TRANSDUCTION; SHARK ID GUANYLATE-CYCLASE; CYCLIC-GMP; ATRIAL; ACTIVATION; SECRETION; DOGFISH; CELLS; HEART AB Recent evidence suggests that the newly described natriuretic peptide, C-type natriuretic peptide (CNP), may be the circulating form of natriuretic peptide in the shark. In the shark CNP has a major site of action in the rectal gland, which augments chloride secretion in response to stimulation by volume loading or CNP infusion. We therefore examined the shark rectal gland for natriuretic peptide receptors and determined the presence of guanylate cyclase-linked receptors and non-guanylate cyclase-linked receptors for CNP in this tissue. CNP binds with uniform high affinity (dissociation constant of 78 +/- 11 pM) to receptors of high density (receptor density of 61 +/- 0.7 fmol/mg protein) in plasma membranes prepared from the rectal gland. By use of rat atrial natriuretic peptide (rANP) as a competing ligand, two classes of receptors become apparent in this population, both of which have similar affinity for CNP, but different affinities for rANP. The low-molecular-weight natriuretic peptide receptor-specific peptide, des-[Gln116 Ser117, Gly118, Leu119,Gly120]rANP-(102-121), binds to 50% of the receptors in the rectal gland, but fails to bind to the remaining 50% even at micromolar concentrations. Porcine brain natriuretic peptide (pBNP) binds with uniformly diminished affinity to all receptors, whereas the unrelated peptide, porcine vasoactive intestinal peptide, does not bind these receptors. The importance of the integrity of the ring structure of CNP is underlined by the significant loss of affinity when the peptide ring is opened. Guanylate cyclase measurements demonstrate that, whereas CNP is a potent stimulator of enzyme activity (27.79 +/- 3.19 pmol.mg protein-1.min-1, 10(-7) M CNP; 8.56 +/- 0.93 pmol.mg protein-1.min-1, basal), both rANP and pBNP have little or no effect. Modifications to the CNP structure result in diminished cyclase activating potential of the peptide, and the broken ring structure peptide [CNP-(7-21)] has no activity. We conclude that the shark rectal gland expresses two populations of receptors for natriuretic peptides, one of which is linked to guanylate cyclase and the second of which resembles the low-molecular-weight receptor described for ANP. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HARVARD CTR STUDY KIDNEY DIS,BOSTON,MA 02115. RP GUNNING, M (reprint author), HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT MED,DIV RENAL MED,LMOB 9D,185 PILGRIM ST,BOSTON,MA 02215, USA. FU NCRR NIH HHS [RR-05591]; NIDDK NIH HHS [DK-18078] NR 20 TC 21 Z9 21 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1993 VL 264 IS 2 BP F300 EP F305 PN 2 PG 6 WC Physiology SC Physiology GA KN681 UT WOS:A1993KN68100107 PM 8095372 ER PT J AU SAXENHOFER, H FITZGIBBON, WR PAUL, RV AF SAXENHOFER, H FITZGIBBON, WR PAUL, RV TI URODILATIN - BINDING-PROPERTIES AND STIMULATION OF CGMP GENERATION IN RAT-KIDNEY CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ATRIAL NATRIURETIC FACTOR; GLOMERULAR MESANGIUM; INNER MEDULLARY COLLECTING DUCT; RECEPTORS; CELL CULTURE; GUANYLATE CYCLASE ID ATRIAL NATRIURETIC PEPTIDE; PARTICULATE GUANYLATE-CYCLASE; RENAL GLOMERULI; HEART-FAILURE; PORCINE BRAIN; CYCLIC-GMP; RECEPTORS; HORMONE; ACTIVATION; MEMBRANES AB Urodilatin (URO) [ANP-(95-126)] is an analogue of atrial natriuretic peptide (alpha-ANP) [ANP-(99-126)] that was first isolated from human urine. In rat mesangial cells, URO competed with high affinity for non-guanylate cyclase-coupled ANPR-C receptors [concentration at which 50% labeled ligand is displaced (IC50) almost-equal-to 70 pM], but with lesser affinity to the guanylate cyclase-linked ANPR-A receptors (IC50 almost-equal-to 800 pM). alpha-ANP bound to both receptors with similar affinity [dissociation constant (K(d)) almost-equal-to 150 pM]. In papillary collecting duct homogenates, which possess only ANPR-A receptors, the apparent K(d) value averaged 229 pM for alpha-ANP and 2.7 nM for URO. Intravenous URO was at least as potent and effective as alpha-ANP in inducing diuresis and natriuresis in anesthetized rats, but URO was approximately 10-fold less potent in stimulating guanosine 3',5'-cyclic monophosphate generation in mesangial and inner medullary collecting duct cells. We conclude that URO has a lesser affinity than alpha-ANP for guanylate cyclase-coupled ANP receptors in the kidney and that the relative natriuretic potency of URO in vivo cannot be directly attributed to its binding characteristics with ANPR-A receptors. C1 MED UNIV S CAROLINA,DIV NEPHROL,171 ASHLEY AVE,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,DIV NEPHROL,CHARLESTON,SC 29425. NR 36 TC 29 Z9 29 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1993 VL 264 IS 2 BP F267 EP F273 PN 2 PG 7 WC Physiology SC Physiology GA KN681 UT WOS:A1993KN68100102 PM 8095370 ER PT J AU PODOLSKY, DK AF PODOLSKY, DK TI REGULATION OF INTESTINAL EPITHELIAL PROLIFERATION - A FEW ANSWERS, MANY QUESTIONS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Note DE EPITHELIUM; MUCOSA; TRANSFORMING GROWTH FACTOR; INTESTINE; COLON ID EPIDERMAL GROWTH-FACTOR; PANCREATIC SPASMOLYTIC POLYPEPTIDE; STEM-CELL ZONE; FACTOR-ALPHA; MUCOSAL ULCERATION; TRANSGENIC MICE; FACTOR RECEPTOR; ADULT-MOUSE; FACTOR-BETA; RAT AB The epithelium of the gastrointestinal tract mucosa is a highly dynamic and diverse mixture of cell populations requiring exquisite integration of the processes of cellular proliferation, differentiation, and senescence. It is likely that the proliferative compartment of the intestinal epithelium encompasses a hierarchy of totipotent and pluripotent stem cells in a manner similar to that which generates diversity in hematopoietic cell populations. Identification and characterization of the stem cell and progenitor populations in the intestine has been limited by the absence of markers or culture systems to identify these cells. Regulation of the proliferative compartment may be accomplished through the combined integration of key peptide growth factors and constituents of the extracellular matrix. The relative contribution of the epithelial populations themselves and the contributions made by associated cell populations such as pericryptal fibroblasts remain unclear. Recent studies have suggested that the transforming growth factors-alpha and -beta, two structurally unrelated peptide growth factors, might serve to regulate the balanced proliferation and turnover of intestinal epithelial cells. The proproliferative effects of TGF-alpha may be counterbalanced by the proliferation-inhibiting TGF-beta. Recent studies have demonstrated close interregulation of these peptides, which act through autocrine and paracrine mechanisms in model intestinal epithelial cell lines. C1 MASSACHUSETTS GEN HOSP,NEW ENGLAND REG PRIMATE RES CTR STUDY INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. RP PODOLSKY, DK (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,JACKSON 7,50 FRUIT ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [R01DK-41557, P30DK-43351] NR 70 TC 92 Z9 94 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 FEB PY 1993 VL 264 IS 2 BP G179 EP G186 PN 1 PG 8 WC Physiology SC Physiology GA KN680 UT WOS:A1993KN68000056 PM 8447399 ER PT J AU DURANTE, W SCHINI, VB CATOVSKY, S KROLL, MH VANHOUTTE, PM SCHAFER, AI AF DURANTE, W SCHINI, VB CATOVSKY, S KROLL, MH VANHOUTTE, PM SCHAFER, AI TI PLASMIN POTENTIATES INDUCTION OF NITRIC-OXIDE SYNTHESIS BY INTERLEUKIN-1-BETA IN VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CYTOKINE; FIBRINOLYSIS; TISSUE PLASMINOGEN ACTIVATOR ID ACUTE MYOCARDIAL-INFARCTION; L-ARGININE; ENDOTHELIAL-CELLS; GROWTH-FACTOR; PLATELET-AGGREGATION; INHIBITION; ACTIVATOR; NITRATE; SYNTHASE; THROMBOLYSIS AB Experiments were performed to examine the effect of the major fibrinolytic protease, plasmin, on the production of nitric oxide from interleukin-1beta (IL-1beta)-treated cultured human and rat aortic smooth muscle cells. Incubation of vascular smooth muscle cells with IL-1beta resulted in significant accumulation of nitrite and nitrate in the culture media. Plasmin, either added exogenously or generated by the reaction of tissue plasminogen activator with plasminogen, potentiated the IL-1beta-mediated release of nitrite and nitrate from smooth muscle cells in a concentration-dependent manner, without affecting the production of nitrite and nitrate from cells untreated with IL-1beta. This potentiating effect was abolished when plasmin was incubated with the protease inhibitor, alpha2-antiplasmin. The perfusates from columns containing IL-1beta-treated smooth muscle cells relaxed detector blood vessels without endothelium, and the addition of IL-1beta-treated smooth muscle cells to suspensions of indomethacin-treated platelets inhibited their aggregation. Untreated smooth muscle cells or cells treated with plasmin alone did not have such effects. However, the simultaneous treatment of smooth muscle cells with IL-1beta and plasmin markedly enhanced both the relaxing activities of the perfusates and the inhibition of platelet aggregation. Treatment of smooth muscle cells with N(G)-nitro-L-arginine inhibited the cytokine-mediated effects as well as the potentiating effect of plasmin. These results demonstrate that plasmin can enhance the production of nitric oxide by IL-1beta-treated vascular smooth muscle cells. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. BAYLOR COLL MED,CTR EXPTL THERAPEUT,HOUSTON,TX 77030. RP DURANTE, W (reprint author), HOUSTON VET AFFAIRS MED CTR,MED SERV,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. RI Vanhoutte, Paul/B-4533-2009 FU NHLBI NIH HHS [HL46356, HL-31183, HL-36045] NR 36 TC 50 Z9 50 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 FEB PY 1993 VL 264 IS 2 BP H617 EP H624 PN 2 PG 8 WC Physiology SC Physiology GA KN681 UT WOS:A1993KN68100048 PM 8447474 ER PT J AU SCHINI, VB CATOVSKY, S DURANTE, W SCOTTBURDEN, T SCHAFER, AI VANHOUTTE, PM AF SCHINI, VB CATOVSKY, S DURANTE, W SCOTTBURDEN, T SCHAFER, AI VANHOUTTE, PM TI THROMBIN INHIBITS INDUCTION OF NITRIC-OXIDE SYNTHASE IN VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INTERLEUKIN-1; PLATELET AGGREGATION; RAT AORTA; NITRITE; HIRUDIN ID TRANSFORMING GROWTH FACTOR-BETA-1; CULTURED ENDOTHELIAL-CELLS; FACTOR-LIKE PROTEIN; GUANOSINE-MONOPHOSPHATE; GUANYLATE-CYCLASE; ARTERIAL INJURY; PLATELET; RELEASE; RESPONSIVENESS; PROLIFERATION AB Experiments were designed to examine whether thrombin affects the production of nitric oxide-like factor(s) evoked by interleukin-1beta (IL-1beta) in cultured smooth muscle cells from the rat aorta. IL-1beta stimulated the release of nitrite (a stable oxidation product of nitric oxide) from cultured smooth muscle cells. Thrombin inhibited in a concentration-dependent manner the release of nitrite caused by IL-1beta. The inhibition was prevented by hirudin (a thrombin inhibitor) and required the presence of thrombin before or during the induction period. Under bioassay conditions, the perfusates from columns containing IL-1beta-treated smooth muscle cells relaxed detector rat aortic rings without endothelium. The addition of IL-1beta-treated smooth muscle cells to suspensions of indomethacin-treated platelets inhibited their aggregation. Control untreated smooth muscle cells or cells treated with thrombin alone did not have such effects. The treatment of smooth muscle cells with IL-1beta in combination with thrombin blunted both the relaxing activities of the perfusates under bioassay conditions and the inhibition of platelet aggregation. These observations indicate that thrombin inhibits the production of nitric oxide-like factor(s) evoked by the inducible nitric oxide synthase in cultured smooth muscle cells from rat aorta. C1 BAYLOR COLL MED,CTR EXPTL THERAPEUT,809 E,1 BAYLOR PLAZA,HOUSTON,TX 77030. HOUSTON VET AFFAIRS MED CTR,MED SERV,HOUSTON,TX 77030. FU NHLBI NIH HHS [HL-46356, HL-31183, HL-36045] NR 35 TC 33 Z9 33 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 FEB PY 1993 VL 264 IS 2 BP H611 EP H616 PN 2 PG 6 WC Physiology SC Physiology GA KN681 UT WOS:A1993KN68100047 PM 7680540 ER PT J AU HAMILTON, JD COURVILLE, TJ RICHMAN, B HANSON, P SWANSON, C STAFFORD, J AF HAMILTON, JD COURVILLE, TJ RICHMAN, B HANSON, P SWANSON, C STAFFORD, J TI QUALITY ASSESSMENT AND IMPROVEMENT IN GROUP-PSYCHOTHERAPY SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article AB Objective: The authors sought a practical means of monitoring and evaluating group psychotherapy, using existing clinical resources, for purposes of quality improvement and education on a large general hospital psychiatric service. Method: Monitoring indicators were developed which addressed 1) the integration of group psychotherapy into treatment planning and 2) the competence and technique of group psychotherapists. The second indicator was assessed by skilled observers using a newly constructed Group Psychotherapy Rating Scale in direct observation of group psychotherapy sessions. The rating scale was examined for interrater reliability and, as a measure of construct validity, for its ability to distinguish the performance of professional staff therapists from that of trainees. Results: The indicators provided useful monitors of the use and quality of group psychotherapy. The rating scale bad satisfactory interrater reliability and construct validity. The immediate constructive educational critique given by the observers of the therapy groups was highly valued by group therapists. Conclusions: The monitoring and evaluation program proved to be a practical, positive, and inexpensive means of assuring and improving the quality of group psychotherapy in a clinical setting. C1 BAYLOR COLL MED,DEPT PSYCHIAT & BEHAV SCI,HOUSTON,TX 77030. RP HAMILTON, JD (reprint author), HOUSTON VA MED CTR,PSYCHIAT SERV 116A,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 10 TC 4 Z9 4 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD FEB PY 1993 VL 150 IS 2 BP 316 EP 320 PG 5 WC Psychiatry SC Psychiatry GA KJ624 UT WOS:A1993KJ62400020 PM 8422084 ER PT J AU RIGOTTI, NA STOTO, MA BIERER, MF ROSEN, A SCHELLING, T AF RIGOTTI, NA STOTO, MA BIERER, MF ROSEN, A SCHELLING, T TI RETAIL STORES COMPLIANCE WITH A CITY NO-SMOKING LAW SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article AB Objectives. Laws restricting smoking in public places and work-places can protect the public only if they are obeyed. We sought to assess compliance with a Cambridge, Mass, no-smoking ordinance. Methods. We prospectively observed 174 retail stores 1 month before and 3, 11, and 24 months after the law took effect. At 24 months, we interviewed one employee per store. Results. Full compliance with the law was low; at 24 months, only 4% of stores displayed the mandated sign and were free of smokers and smoke. Fewer than half the stores posted any no-smoking sign. Sign prevalence increased over 2 years (22% to 41%, P < .001), but the frequency of smoke or smokers (13% and 10%, respectively, at baseline) did not change. According to employees interviewed at 24 months, 38% of stores illegally permitted customers or employees to smoke. These stores had more smoke and fewer signs than did stores prohibiting-smoking. Compliance was poor in liquor and convenience stores. Employees who had been told how to handle customers' smoking were more likely to enforce the law. Conclusions. Compliance with a no-smoking law is not guaranteed. For retail stores, compliance may improve if stores adopt no-smoking policies, post signs, and teach employees to enforce the law. C1 HARVARD UNIV,JOHN F KENNEDY SCH GOVT,INST STUDY SMOKING BEHAV & POLICY,CAMBRIDGE,MA 02138. BOSTON UNIV,MED CTR,HLTH CARE RES UNIT,BOSTON,MA 02215. UNIV MARYLAND,COLL PK,MD 20742. RP RIGOTTI, NA (reprint author), MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114, USA. NR 12 TC 13 Z9 13 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD FEB PY 1993 VL 83 IS 2 BP 227 EP 232 DI 10.2105/AJPH.83.2.227 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KW273 UT WOS:A1993KW27300012 PM 8427328 ER PT J AU BROWN, JH BERMAN, JJ BLICKMAN, JG CHEW, FS AF BROWN, JH BERMAN, JJ BLICKMAN, JG CHEW, FS TI PRIMARY ILEOCECAL TUBERCULOSIS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID ABDOMINAL TUBERCULOSIS; CT C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 4 TC 7 Z9 7 U1 0 U2 4 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 FEB PY 1993 VL 160 IS 2 BP 278 EP 278 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK577 UT WOS:A1993KK57700013 PM 8424334 ER PT J AU DISLER, DG KATTAPURAM, SV CHEW, FS ROSENTHAL, DI PATEL, D AF DISLER, DG KATTAPURAM, SV CHEW, FS ROSENTHAL, DI PATEL, D TI MENISCAL TEARS OF THE KNEE - PRELIMINARY COMPARISON OF 3-DIMENSIONAL MR RECONSTRUCTION WITH 2-DIMENSIONAL MR IMAGING AND ARTHROSCOPY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID ARTHROGRAPHY; INJURIES AB OBJECTIVE. A pilot study was performed to evaluate the usefulness of three-dimensional (3D) MR reconstructions in detecting meniscal tears. MATERIALS AND METHODS. Reconstructions of 24 knee menisci were made by using data from standard two-dimensional (2D) MR images. The results were compared with findings on 2D MR images and at arthroscopy. RESULTS. All 17 arthroscopically proved meniscal tears were shown on the 3D reconstructions. Seven tears in five patients were shown on 3D reconstruction but not on 2D MR images, even on retrospective examination. Three of the seven were radial tears and four were horizontal tears. The seven missed tears were all located in the posterior horns. CONCLUSION. Three-dimensional reconstructions are accurate for determining meniscal abnormalities and may be better than 2D imaging for evaluating the posterior horns of the menisci. Three-dimensional reconstructions may be indicated when 2D MR imaging shows no abnormality in patients in whom clinical findings strongly suggest a meniscal tear. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPED,BOSTON,MA 02114. NR 19 TC 15 Z9 15 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 FEB PY 1993 VL 160 IS 2 BP 343 EP 345 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK577 UT WOS:A1993KK57700027 PM 8424347 ER PT J AU LEV, MH BLICKMAN, JG AF LEV, MH BLICKMAN, JG TI EXTRAGONADAL YOLK-SAC TUMOR - SONOGRAPHIC AND CT FINDINGS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note ID GERM-CELL TUMORS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,DIV PEDIAT IMAGING,34 FRUIT ST,BOSTON,MA 02114. NR 8 TC 13 Z9 14 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 FEB PY 1993 VL 160 IS 2 BP 370 EP 371 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK577 UT WOS:A1993KK57700034 PM 8424353 ER PT J AU CHEW, FS AF CHEW, FS TI MANUSCRIPT PEER-REVIEW - GENERAL CONCEPTS AND THE AJR PROCESS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material ID QUALITY C1 HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP, 32 FRUIT ST, BOSTON, MA 02114 USA. OI Chew, Felix/0000-0003-2711-2013 NR 24 TC 5 Z9 5 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA SN 0361-803X EI 1546-3141 J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD FEB PY 1993 VL 160 IS 2 BP 409 EP 411 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK577 UT WOS:A1993KK57700044 PM 8424363 ER PT J AU YOUNG, RH AF YOUNG, RH TI UNUSUAL AND NEW ASPECTS OF OVARIAN GERM-CELL TUMORS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY 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 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 FEB PY 1993 VL 17 IS 2 BP 200 EP 201 DI 10.1097/00000478-199302000-00014 PG 2 WC Pathology; Surgery SC Pathology; Surgery GA KJ461 UT WOS:A1993KJ46100014 ER PT J AU SZABO, MD CROSBY, G HURFORD, WE STRAUSS, HW AF SZABO, MD CROSBY, G HURFORD, WE STRAUSS, HW TI MYOCARDIAL PERFUSION FOLLOWING ACUTE SUBARACHNOID HEMORRHAGE IN PATIENTS WITH AN ABNORMAL ELECTROCARDIOGRAM SO ANESTHESIA AND ANALGESIA LA English DT Article ID NERVOUS-SYSTEM; SCINTIGRAPHY; DAMAGE AB To test the hypothesis that acute subarachnoid hemorrhage is associated with abnormal myocardial perfusion, we assessed myocardial blood flow with thallium scintigraphy in 19 patients with a confirmed subarachnoid hemorrhage and an abnormal electrocardiogram. A thallium scan was performed at the bedside of each patient 3 +/- 2 days (mean +/- SD) after subarachnoid hemorrhage and subsequently was analyzed both qualitatively and quantitatively. Patients averaged 58 +/- 13 yr of age and 68% had one or more cardiac risk factors. The neurologic condition of patients on the day of the scan was Il (median; range I-V) on the standard 5-point scale of Botterell. Abnormalities on a standard 12-lead electrocardiogram obtained on the same day as the scan consisted of repolarization changes in most patients; 10 had T wave inversions and 8 had nonspecific ST segment changes. Thirty-two percent (n = 6) of patients had an abnormal thallium scan. There were, however, no features of the clinical history, electrocardiogram pattern, or neurologic condition that were associated with a positive scan. For instance, 2 of 4 patients with diffuse deeply inverted T waves had a normal thallium scan, whereas the scan was abnormal in 2 of 8 patients with minor nonspecific electrocardiographic abnormalities. The thallium scan was also positive in neurologically intact (grade 1) as well as severely injured (grade V) patients. Thus, abnormal myocardial perfusion and possibly myocardial ischemia occur frequently following subarachnoid hemorrhage, but no specific electrocardiographic characteristic identifies patients with a perfusion abnormality. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. RP SZABO, MD (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,FRUIT ST,BOSTON,MA 02114, USA. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 30 TC 26 Z9 26 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 BP 253 EP 258 PG 6 WC Anesthesiology SC Anesthesiology GA KY037 UT WOS:A1993KY03700009 PM 8424500 ER PT J AU CASTELLI, I DROP, LJ ALFILLE, PH SCHOUTEN, R WELCH, C DAGOSTINO, R ZASLAVSKY, A AF CASTELLI, I DROP, LJ ALFILLE, PH SCHOUTEN, R WELCH, C DAGOSTINO, R ZASLAVSKY, A TI ST SEGMENTS AND HYPERTENSION DURING ECT SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 SU S BP S38 EP S38 PG 1 WC Anesthesiology SC Anesthesiology GA KY039 UT WOS:A1993KY03900038 ER PT J AU DENMAN, W GOUDSOUZIAN, N AF DENMAN, W GOUDSOUZIAN, N TI NEUROMUSCULAR EFFECTS OF MIVACURIUM FOLLOWING VECURONIUM IN ADULTS SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114. NR 3 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 SU S BP S75 EP S75 PG 1 WC Anesthesiology SC Anesthesiology GA KY039 UT WOS:A1993KY03900075 ER PT J AU GOUDSOUZIAN, N DENMAN, W AF GOUDSOUZIAN, N DENMAN, W TI NEUROMUSCULAR EFFECTS OF MIVACURIUM FOLLOWING ATRACURIUM IN CHILDREN SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. 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 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 SU S BP S124 EP S124 PG 1 WC Anesthesiology SC Anesthesiology GA KY039 UT WOS:A1993KY03900123 ER PT J AU HESSELVIK, JF ANGLE, P DAMBRA, MN AF HESSELVIK, JF ANGLE, P DAMBRA, MN TI VECURONIUM BY LOW-DOSE INFUSION IN NORMOTHERMIC AND HYPOTHERMIC CORONARY-BYPASS SURGERY SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,CARDIAC ANESTHESIA GRP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 SU S BP S141 EP S141 PG 1 WC Anesthesiology SC Anesthesiology GA KY039 UT WOS:A1993KY03900140 ER PT J AU MARTYN, JAJ WANG, C ITANI, M AF MARTYN, JAJ WANG, C ITANI, M TI ALPHA-ACID GLYCOPROTEIN BUT NOT ALBUMIN CAN REVERSE THE NEUROMUSCULAR EFFECTS OF D-TUBOCURARINE IN MICE SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 1 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 SU S BP S245 EP S245 PG 1 WC Anesthesiology SC Anesthesiology GA KY039 UT WOS:A1993KY03900243 ER PT J AU PANZA, WS BEHRINGER, EC AF PANZA, WS BEHRINGER, EC TI INTUBATION IN THE POSTANESTHESIA CARE UNIT SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. 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 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 SU S BP S319 EP S319 PG 1 WC Anesthesiology SC Anesthesiology GA KY039 UT WOS:A1993KY03900317 ER PT J AU ROTTER, SJ HUSAIN, M ALLYN, JW TORCHIANA, DF PHILBIN, DM AF ROTTER, SJ HUSAIN, M ALLYN, JW TORCHIANA, DF PHILBIN, DM TI THE EFFECT OF NORMOTHERMIC PERFUSION WITH A MEMBRANE-OXYGENATOR ON PLASMA OPIOID CONCENTRATIONS SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT CARDIAC ANESTHESIA,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1993 VL 76 IS 2 SU S BP S360 EP S360 PG 1 WC Anesthesiology SC Anesthesiology GA KY039 UT WOS:A1993KY03900358 ER PT J AU ABELSON, MB GEORGE, MA GAROFALO, C AF ABELSON, MB GEORGE, MA GAROFALO, C TI DIFFERENTIAL-DIAGNOSIS OF OCULAR ALLERGIC DISORDERS SO ANNALS OF ALLERGY LA English DT Review ID GIANT PAPILLARY CONJUNCTIVITIS; MAJOR BASIC-PROTEIN; LATE-PHASE REACTION; VERNAL CONJUNCTIVITIS; HUMAN TEARS; MAST-CELLS; CROMOLYN SODIUM; TRYPTASE LEVELS; SKIN REACTION; ANAPHYLAXIS C1 EYE RES INST,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 85 TC 43 Z9 46 U1 0 U2 0 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 SN 0003-4738 J9 ANN ALLERGY JI Ann. Allergy PD FEB PY 1993 VL 70 IS 2 BP 95 EP 109 PG 15 WC Allergy SC Allergy GA KM627 UT WOS:A1993KM62700001 PM 8430929 ER PT J AU TODRES, ID AF TODRES, ID TI PEDIATRIC AIRWAY CONTROL AND VENTILATION SO ANNALS OF EMERGENCY MEDICINE LA English DT Article DE AIRWAY; FOREIGN BODY; VENTILATION AB Emphasis on a clear airway is a primary requisite for effective CPR. Airway control in the trauma victim needs special consideration of the possibility of associated cervical vertebrae and spinal cord injury; thus, modification of the patient positioning for transport is essential. Emphasis on visualization of chest movement is the most important factor in assessing adequacy of ventilation. Experience in the use of bag-valve-mask devices requires appropriate instruction and on-going practice. Small bag volume devices limit the ability to provide adequate tidal volumes and prolong inspiratory times. Tracheal intubation provides optimal airway management. In-field use of this procedure will depend upon the skill and experience of the operator. Validation of correctness of tracheal tube placement is critical; seeing the tube pass the glottic opening on laryngoscopy, bilateral and equal chest movement, auscultation of breath sounds in the chest. Methods to measure end-tidal CO2 as a valuable check for tube position is a useful adjunct but must not be relied upon. Foreign body management continues to be controversial and remains unchanged for the present; ie, the infant < 1 year of age the recommendations are back blows followed by chest thrusts. Above 1 year of age, abdominal thrusts (Heimlich maneuver) is recommended. RP TODRES, ID (reprint author), MASSACHUSETTS GEN HOSP,NEONATAL UNIT,ELLISON 317,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 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 0196-0644 J9 ANN EMERG MED JI Ann. Emerg. Med. PD FEB PY 1993 VL 22 IS 2 BP 440 EP 444 PN 2 PG 5 WC Emergency Medicine SC Emergency Medicine GA KM729 UT WOS:A1993KM72900023 PM 8434844 ER PT J AU LIPTON, SA AF LIPTON, SA TI HUMAN-IMMUNODEFICIENCY-VIRUS INFECTED MACROPHAGES, GP120, AND N-METHYL-D-ASPARTATE RECEPTOR-MEDIATED NEUROTOXICITY SO ANNALS OF NEUROLOGY LA English DT Letter ID COAT PROTEIN; HIV-1 C1 BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP LIPTON, SA (reprint author), CHILDRENS HOSP MED CTR,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI,BOSTON,MA 02115, USA. NR 9 TC 55 Z9 56 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD FEB PY 1993 VL 33 IS 2 BP 227 EP 228 DI 10.1002/ana.410330218 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA KX547 UT WOS:A1993KX54700017 PM 8434889 ER PT J AU RAUCH, SD XU, WZ NADOL, JB AF RAUCH, SD XU, WZ NADOL, JB TI HIGH JUGULAR BULB - IMPLICATIONS FOR POSTERIOR-FOSSA NEUROTOLOGIC AND CRANIAL BASE SURGERY SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE CRANIAL BASE SURGERY; INTERNAL AUDITORY CANAL; JUGULAR BULB; POSTERIOR FOSSA; NEUROTOLOGIC SURGERY; TEMPORAL BONE ANATOMY ID OTOLOGIC SURGERY; BONE AB The suboccipital-retrosigmoid approach to the internal auditory canal and cerebellopontine angle is being used with increasing frequency for neurotologic surgery, including vestibular nerve section and resection of acoustic neuroma. It offers wide exposure of the cerebellopontine angle and the cranial nerve VII-VIII complex as it courses from the brain stem to the temporal bone. Exposure of the internal auditory canal can be achieved by removing its posterior bony wall. Safe utilization of this approach requires familiarity with the variable position of structures within the petrous bone, including the lateral venous sinus and jugular bulb. We report here a case in which bleeding resulted from injury to a high jugular bulb during surgical exposure of the internal auditory canal via the suboccipital route and discuss the regional anatomy of the jugular bulb based on study of 378 consecutive temporal bone specimens from the collection of the Massachusetts Eye and Ear Infirmary. High jugular bulb was defined as encroachment of the dome of the bulb within 2 mm of the floor of the internal auditory canal. Forty-six percent of scoreable specimens met this criterion. However, when donors less than 6 years of age were excluded, a high jugular bulb was identified in 63% of specimens. Relevance to neurotologic surgery of the posterior fossa is presented. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. RP RAUCH, SD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. NR 19 TC 31 Z9 35 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD FEB PY 1993 VL 102 IS 2 BP 100 EP 107 PG 8 WC Otorhinolaryngology SC Otorhinolaryngology GA KL623 UT WOS:A1993KL62300004 PM 8427492 ER PT J AU LEVINE, RA BUSABA, N BROWN, MC AF LEVINE, RA BUSABA, N BROWN, MC TI LASER-DOPPLER MEASUREMENTS AND ELECTROCOCHLEOGRAPHY DURING ISCHEMIA OF THE GUINEA-PIG COCHLEA - IMPLICATIONS FOR HEARING PRESERVATION IN ACOUSTIC NEUROMA SURGERY SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE ACOUSTIC NEUROMA; BLOOD FLOW VELOCITY; COCHLEA; DOPPLER VELOCIMETRY; ELECTROCOCHLEOGRAPHY; LASER VELOCIMETRY ID AUDITORY EVOKED-POTENTIALS; TISSUE BLOOD-FLOW; SPECTROSCOPY; FLOWMETER; ANGLE; REMOVAL AB Interruption of cochlear blood flow has been implicated as one of the causes of the sensorineural hearing loss that may occur during acoustic neuroma surgery. With the guinea pig as an animal model for cerebellopontine angle surgery, laser-Doppler measurements were used to estimate the cochlear blood flow changes caused by compression of the eighth nerve complex. With compression, the laser-Doppler measurements decreased abruptly; somewhat later, the electrocochleographic potentials declined. When compression was released, laser-Doppler measurements usually returned immediately, followed later by return of the electrical potentials. Some of these potentials, including the compound action potential of the auditory nerve, often became transiently larger than their precompression values. Interposing bone between the laser-Doppler probe and the otic capsule, so that the total bone thickness approximated the thickness of the human otic capsule, decreased the laser-Doppler measurement, but changes caused by compression were still apparent. Thus, although the human otic capsule is much thicker than the guinea pig capsule, it may still be possible to make laser-Doppler estimates of human cochlear blood flow. Laser-Doppler monitoring during acoustic neuroma surgery may be beneficial, because it could give earlier warning of ischemia than is currently available from electrocochleographic monitoring, thereby enabling earlier corrective action. Electrocochleography complements laser-Doppler measurements by indicating the physiologic state of the cochlea. C1 HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,BOSTON,MA 02114. RP LEVINE, RA (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC01089, DC00119] NR 34 TC 32 Z9 36 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD FEB PY 1993 VL 102 IS 2 BP 127 EP 136 PG 10 WC Otorhinolaryngology SC Otorhinolaryngology GA KL623 UT WOS:A1993KL62300010 PM 8427498 ER PT J AU WILLETT, CG LEWANDROWSKI, K WARSHAW, AL EFIRD, J COMPTON, CC AF WILLETT, CG LEWANDROWSKI, K WARSHAW, AL EFIRD, J COMPTON, CC TI RESECTION MARGINS IN CARCINOMA OF THE HEAD OF THE PANCREAS - IMPLICATIONS FOR RADIATION-THERAPY SO ANNALS OF SURGERY LA English DT Article ID CURATIVE RESECTION; CANCER AB A retrospective review of the pathology and clinical course of 72 patients undergoing resection of carcinoma of the head of the pancreas was undertaken to identify the frequency of tumor involvement at standard surgical transection margins (stomach, duodenum, pancreas, and bile duct) as well as the peripancreatic soft tissue margin and the potential clinical significance of these findings. Of 72 patients undergoing resection, 37 patients (51%) were found to have tumor extension to the surgical margins. The most commonly involved margin was peripancreatic soft tissue (27 patients) followed by pancreatic transection line (14 patients) and bile duct transection line (4 patients). For 37 patients with tumor present at a resection margin, there were no survivors beyond 41 months. No difference in survival or local control was seen between 14 patients receiving postoperative radiation therapy and 5-fluorouracil (5-FU) compared with 23 patients not receiving additional treatment. In contrast, the 5-year actuarial survival and local control of 35 patients undergoing resection without tumor invasion to a resection margin was 22% and 43%, respectively. The 5-year survival and local control of 16 patients receiving adjuvant radiation therapy and 5-FU was 29% and 42%, respectively, whereas these figures were 18% and 31% for 19 patients not receiving adjuvant therapy (p > 0.10). Because residual local tumor after resection is common, preoperative radiation therapy may be beneficial in this disease. It should minimize the risk of dissemination during operative manipulation and facilitate a curative resection by promoting tumor regression. Because local failure rates approach 60% after resection and adjuvant therapy even in cases having clear resection margins, intraoperative radiation therapy to the tumor bed at the time of resection also might be considered. Protocols evaluating the feasibility and efficacy of preoperative radiation therapy and resection with intraoperative radiation therapy for patients with pancreatic cancer are underway, C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN BLDG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 12 TC 295 Z9 298 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD FEB PY 1993 VL 217 IS 2 BP 144 EP 148 DI 10.1097/00000658-199302000-00008 PG 5 WC Surgery SC Surgery GA KN628 UT WOS:A1993KN62800008 PM 8094952 ER PT J AU SUEN, HC MATHISEN, DJ GRILLO, HC LEBLANC, J MCLOUD, TC MONCURE, AC HILGENBERG, AD AF SUEN, HC MATHISEN, DJ GRILLO, HC LEBLANC, J MCLOUD, TC MONCURE, AC HILGENBERG, AD TI SURGICAL-MANAGEMENT AND RADIOLOGICAL CHARACTERISTICS OF BRONCHOGENIC CYSTS SO ANNALS OF THORACIC SURGERY LA English DT Article ID SUPERIOR VENA-CAVA; FOREGUT CYSTS; LUNG; COMPRESSION; MEDIASTINUM AB Forty-two patients with bronchogenic cysts were treated over a 30-year period (1962 to 1991). The location was mediastinal in 37 and intrapulmonary in 5. Cysts were symptomatic in 21 patients (50%) and complications occurred in 11 (26%). The complications included infection in 5 patients, hemorrhage into the cyst in 2 patients, dysphagia due to esophageal compression in 2, adenocarcinoma arising from a bronchogenic cyst in an 8 1/2-year-old girl, and an esophagobronchopleurocutaneous fistula as a result of previous incomplete resection in 1 patient. Magnetic resonance imaging has been found to provide specific diagnostic information about bronchogenic cysts. All but 2 patients were treated with complete excision. One patient was managed by observation and another had drainage of the cyst by mediastinoscopy. Complications of treatment occurred in only 2 patients. One had a minor wound infection and the other had Clostridium difficile enterocolitis. Only 4 patients were lost to follow-up. No late complication or recurrence developed in those patients having complete excision. We recommend complete excision in most instances to confirm the diagnosis, relieve symptoms, and prevent complications. C1 MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NR 24 TC 98 Z9 106 U1 0 U2 3 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 FEB PY 1993 VL 55 IS 2 BP 476 EP 481 PG 6 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA KK914 UT WOS:A1993KK91400029 PM 8431062 ER PT J AU MUEHRCKE, DD TORCHIANA, DF AF MUEHRCKE, DD TORCHIANA, DF TI WARM HEART-SURGERY IN PATIENTS WITH COLD AUTOIMMUNE DISORDERS SO ANNALS OF THORACIC SURGERY LA English DT Article ID HYPOTHERMIA; MANAGEMENT AB Continuous warm antegrade delivery of cardioplegia while maintaining systemic normothermia is a new method of performing coronary artery bypass grafting. It can be used to avoid the detrimental effects of hypothermia in patients with cold autoimmune disease. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG CARDIOVASC UNIT,BOSTON,MA 02114. NR 5 TC 3 Z9 3 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 FEB PY 1993 VL 55 IS 2 BP 532 EP 533 PG 2 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA KK914 UT WOS:A1993KK91400044 PM 8431076 ER PT J AU ELIOPOULOS, GM KLIMM, K ELIOPOULOS, CT FERRARO, MJ MOELLERING, RC AF ELIOPOULOS, GM KLIMM, K ELIOPOULOS, CT FERRARO, MJ MOELLERING, RC TI INVITRO ACTIVITY OF CP-99,219, A NEW FLUOROQUINOLONE, AGAINST CLINICAL ISOLATES OF GRAM-POSITIVE BACTERIA SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID BETA-LACTAMASE; RESISTANCE; FAECALIS AB The in vitro activity of the fluoroquinolone CP-99,219 against gram-positive bacteria was compared with those of five other antimicrobial agents. Against ciprofloxacin-susceptible staphylococci and against streptococci, MICs were less-than-or-equal-to 0.12 and less-than-or-equal-to 0.5 mug/ml, respectively. CP-99,219 was also more active than ciprofloxacin against ciprofloxacin-resistant staphylococci, most enterococci, Leuconostoc spp., and lactobacilli. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RP ELIOPOULOS, GM (reprint author), NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215, USA. NR 9 TC 128 Z9 128 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 FEB PY 1993 VL 37 IS 2 BP 366 EP 370 PG 5 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA KK750 UT WOS:A1993KK75000043 PM 8452372 ER PT J AU PICKERING, JW PRAHL, SA VANWIERINGEN, N BEEK, JF STERENBORG, HJCM VANGEMERT, MJC AF PICKERING, JW PRAHL, SA VANWIERINGEN, N BEEK, JF STERENBORG, HJCM VANGEMERT, MJC TI DOUBLE-INTEGRATING-SPHERE SYSTEM FOR MEASURING THE OPTICAL-PROPERTIES OF TISSUE SO APPLIED OPTICS LA English DT Article DE OPTICAL PROPERTIES; ABSORPTION COEFFICIENT; SCATTERING COEFFICIENT; ANISOTROPY FACTOR; INTEGRATING SPHERE; ADDING-DOUBLING; TISSUE OPTICS ID SCATTERING PHASE FUNCTIONS; MAMMALIAN-TISSUES; LIGHT-SCATTERING; ABSORPTION; COEFFICIENTS; REFLECTANCE AB A system is described and evaluated for the simultaneous measurement of the intrinsic optical properties of tissue: the scattering coefficient, the absorption coefficient, and the anisotropy factor. This system synthesizes the theory of two integrating spheres and an intervening scattering sample with the inverse adding-doubling algorithm, which employs the adding-doubling solution of the radiative transfer equation to determine the optical properties from the measurement of the light flux within each sphere and of the unscattered transmission. The optical properties may be determined simultaneously, which allows for measurements to be made while the sample undergoes heating, chemical change, or some other external stimulus. An experimental validation of the system with tissue phantoms resulted in the determination of the optical properties with a < 5% deviation when the optical density was between 1 and 10 and the albedo was between 0.4 and 0.95. C1 MASSACHUSETTS GEN HOSP, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. RP PICKERING, JW (reprint author), UNIV AMSTERDAM, ACAD MED CTR, CTR LASER, MEIBERGDREEF 9, 1105 AZ AMSTERDAM, NETHERLANDS. RI Sterenborg, Henricus/H-9401-2013; OI Sterenborg, Henricus/0000-0002-6007-2992; Pickering, John William/0000-0001-9475-0344 NR 27 TC 272 Z9 282 U1 4 U2 39 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 0003-6935 J9 APPL OPTICS JI Appl. Optics PD FEB 1 PY 1993 VL 32 IS 4 BP 399 EP 410 PG 12 WC Optics SC Optics GA KJ631 UT WOS:A1993KJ63100006 PM 20802704 ER PT J AU DOMANKEVITZ, Y LEE, MS NISHIOKA, NS AF DOMANKEVITZ, Y LEE, MS NISHIOKA, NS TI EFFECTS OF IRRADIANCE AND SPOT SIZE ON PULSED HOLMIUM LASER ABLATION OF TISSUE SO APPLIED OPTICS LA English DT Article ID RADIATION AB Threshold radiant exposures for pulsed holmium laser ablation of tissue were measured with a high-speed framing camera. The effects of laser irradiance and beam size on ablation threshold were investigated. Threshold radiant exposure decreased with increasing laser irradiance over the range of 10(5)-10(7) W/cm2. Over the range of spot sizes examined (243-970 mum) an increase in the laser beam diameter reduced the laser irradiance required for ablation. At larger spot sizes the ablation event was occasionally initiated from multiple sites. These results suggest that the rate of energy deposition and laser-beam geometry affect the events preceding the onset of ablation and should be considered when pulsed laser ablation of tissue is modeled or quantified. C1 HARVARD UNIV, SCH MED, DEPT MED, MED SERV, GASTROINTESTINAL UNIT, BOSTON, MA 02115 USA. RP DOMANKEVITZ, Y (reprint author), MASSACHUSETTS GEN HOSP, WELLMANN LABS PHOTOMED, BOSTON, MA 02114 USA. NR 9 TC 6 Z9 6 U1 0 U2 0 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 0003-6935 J9 APPL OPTICS JI Appl. Optics PD FEB 1 PY 1993 VL 32 IS 4 BP 569 EP 573 PG 5 WC Optics SC Optics GA KJ631 UT WOS:A1993KJ63100028 PM 20802726 ER PT J AU KENET, RO KANG, S KENET, BJ FITZPATRICK, TB SOBER, AJ BARNHILL, RL AF KENET, RO KANG, S KENET, BJ FITZPATRICK, TB SOBER, AJ BARNHILL, RL TI CLINICAL-DIAGNOSIS OF PIGMENTED LESIONS USING DIGITAL EPILUMINESCENCE MICROSCOPY - GRADING PROTOCOL AND ATLAS SO ARCHIVES OF DERMATOLOGY LA English DT Article ID SURFACE MICROSCOPY; SKIN-LESIONS; MALIGNANT-MELANOMA AB Background and Design.-Epiluminescence microscopy (ELM) is a clinical technique that permits in vivo visual inspection of pigmented anatomic structures of the epidermis, dermoepidermal junction, and papillary dermis. A protocol is proposed for systematic visual inspection of pigmented lesions. Seventy pigmented lesions were imaged with a digital ELM camera system. Images were visually inspected for eight ''global'' ELM features, 23 ''local'' ELM features, and 18 network features. An atlas of the most clinically significant ELM features is presented with pilot estimates of their sensitivity and specificity for detecting melanoma. Results.-Preliminary data suggest that ELM features that may be most specific for melanoma include multicomponent pattern, nodular pattern, pseudopods, radial streaming, blue-gray areas, whitish veil (milky way), and sharp network margins. Epiluminescence microscopic features that may be most sensitive for melanoma include pigment dots, peripheral erythema, peripheral dark network patches, marked mean network irregularity, network line thickness variability, radial streaming, blue-gray areas, and whitish veil (milky way). Epiluminescence microscopic features that may be most sensitive for severe melanocyte atypia include pigment dots, peripheral erythema, hypopigmented network patches, peripheral dark network patches, marked mean network irregularity, and focal absence of network. In addition, features that may have a very high specificity for benign lesions include saccular pattern (suggests hemangioma), globular pattern (suggests a compound or dermal nevus), and multiple comedolike openings (suggests seborrheic keratosis). Conclusions.-Features most sensitive for severe atypia and melanoma could form the basis for a screening test for considering biopsy. Features most specific for melanoma then could be applied to further triage management of pigmented lesions that meet initial screening criteria. In addition, features with very high specificity for benign lesions may help develop ELM criteria to avoid unnecessary surgery. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. CORNELL UNIV,MED CTR,COLL MED,DEPT MED,NEW YORK,NY 10021. CORNELL UNIV,MED CTR,NEW YORK HOSP,DEPT MED,DIV DERMATOL,NEW YORK,NY 10021. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,DIV DERMATOPATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 23 TC 209 Z9 210 U1 0 U2 6 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD FEB PY 1993 VL 129 IS 2 BP 157 EP 174 DI 10.1001/archderm.129.2.157 PG 18 WC Dermatology SC Dermatology GA KL861 UT WOS:A1993KL86100003 PM 8434973 ER PT J AU VALSANIA, P WARRAM, JH RAND, LI KROLEWSKI, AS AF VALSANIA, P WARRAM, JH RAND, LI KROLEWSKI, AS TI DIFFERENT DETERMINANTS OF NEOVASCULARIZATION ON THE OPTIC DISK AND ON THE RETINA IN PATIENTS WITH SEVERE NONPROLIFERATIVE DIABETIC-RETINOPATHY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID MEMORIAL LECTURE; RISK; PREVALENCE; DIAGNOSIS; AGE AB Almost all patients with type I and many with type II diabetes develop proliferative retinopathy. This entity consists of two components: new blood vessels on the optic disc (NVD), which frequently lead to visual loss, and new blood vessels elsewhere on the retina (NVE), which do not pose such a serious threat to vision. This study examined determinants of neovascularization specifically on the optic disc in eyes with severe nonproliferative retinopathy. The study eyes were under surveillance as the untreated control eyes of participants in the Diabetic Retinopathy Study. During the 5-year follow-up period, NVE developed in almost all of the eyes, whereas the cumulative incidence of NVD in these same eyes was 64% and varied according to several factors. The risk of NVD in a study eye was increased if the contralateral treated eye had NVD rather than NVE or severe nonproliferative retinopathy (odds ratio [OR], 6.1; P<.0001). It was also increased if the study eye had, at the baseline examination, soft exudates and intraretinal microvascular abnormalities (OR, 5.7; P=.002) or soft exudates alone (OR, 4.0; P=.04). Nephropathy and poor glycemic control were each associated with a two-fold increase in risk but neither was statistically significant. Eyes of individuals over 40 years of age were protected from the development of NVD (OR, 0.5; P<.05). The findings of this study support the hypothesis that, in patients with diabetes, the development of NVD is determined by different factors than the development of NVE. C1 JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET SECT,1 JOSLIN PL,BOSTON,MA 02215. S RAFFAELE HOSP,EPIDEMIOL,MILAN,ITALY. JOSLIN DIABET CTR,DIV RES,EYE RES SECT,BOSTON,MA 02215. NR 24 TC 14 Z9 15 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 FEB PY 1993 VL 111 IS 2 BP 202 EP 206 PG 5 WC Ophthalmology SC Ophthalmology GA KM276 UT WOS:A1993KM27600019 PM 7679270 ER PT J AU PAVILACK, MA FOSTER, CS KOWAL, VO DUTT, JE ALBERT, DM AF PAVILACK, MA FOSTER, CS KOWAL, VO DUTT, JE ALBERT, DM TI PERIPSEUDOPHAKIC MEMBRANE - PATHOLOGICAL FEATURES SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID INTRAOCULAR LENSES; DISTINCT COLLAGENS AB A 70-year-old woman underwent anterior segment reconstruction with repeated penetrating keratoplasty for visual rehabilitation. On removal of the failed keratoplasty button, the posterior chamber intraocular lens was found to be en-cased in a dense fibrous membrane that almost totally obliterated the anterior and posterior chambers of the eye. Anterior segment reconstruction included excision of the fibrous membrane, removal of the intraocular lens, iridoplasty, gonioplasty, anterior vitrectomy, and repeated penetrating keratoplasty. Recognition of fibrous tissue that extended through each of the four positioning holes of the optic of the lens implant and its transection was essential in avoiding complications during removal of the intraocular lens. Histopathologic and ultrastructural examination of the excised membrane revealed areas of metaplastic lens epithelium and fibrous scar tissue. This study, using immunofluorescence, is the first, to our knowledge, to characterize the specific collagenous components of a peripseudophakic membrane. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,UVEITIS & IMMUNOL SERV,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,PATHOL SERV,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,CORNEA SERV,BOSTON,MA 02114. NR 16 TC 4 Z9 4 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 FEB PY 1993 VL 111 IS 2 BP 240 EP 244 PG 5 WC Ophthalmology SC Ophthalmology GA KM276 UT WOS:A1993KM27600027 PM 8431163 ER PT J AU MARGOLIS, HC ZHANG, YP GEWIRTZ, A VANHOUTE, J MORENO, EC AF MARGOLIS, HC ZHANG, YP GEWIRTZ, A VANHOUTE, J MORENO, EC TI CARIOGENIC POTENTIAL OF POOLED PLAQUE FLUID FROM EXPOSED ROOT SURFACES IN HUMANS SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE PLAQUE FLUID; ROOT CARIES; CARIES ID CARIES-SUSCEPTIBLE INDIVIDUALS; AMINO-ACID PROFILES; HUMAN DENTAL PLAQUE; ENAMEL; PH; SOLUBILITY; PELLICLE; LESIONS; INVITRO; CALCIUM AB The composition of pooled plaque fluid from exposed root surfaces of five population samples was determined before and at selected times (3, 7 and 15 min) after a 5 and 10% sucrose rinse. Subjects were 45-65 yr old, had exposed, sound root surfaces, and were grouped according to root caries status [caries-free (CF), no root caries history; caries-positive (CP), recorded root caries experience]. Samples were obtained only from the sound surfaces of the CF and CP subjects after overnight fasting. Plaque samples from each subgroup were pooled under mineral oil and maintained on ice. Plaque fluid was then isolated by centrifugation and analysed for organic acids and inorganic ions (ion chromatography), and pH (microelectrodes). From these data, the degree of saturation [DS(TM)] in plaque fluid with respect to tooth mineral (TM) was calculated. Before exposure to sucrose, plaque fluids from the CF and the CP subgroups had similar ionic compositions. These fluids were also found to be supersaturated with respect to tooth mineral. After exposure to sucrose, a rapid decrease in plaque fluid pH was observed, which corresponded primarily to lactic acid production. For all times examined, mean pH and DS(TM) values were lower and lactic acid concentrations were higher in the CP than the CF samples. Lower values of DS(TM) suggest that plaque fluid from CP subjects had a measurably greater cariogenic potential. Calcium concentrations also increased significantly and to comparable levels in all plaque fluid samples after sucrose exposure, despite lower acid production in CF samples. These results appear to be associated with the further finding that whole plaque from the CF subgroups contained significantly more calcium than that from the CP subjects. Thus the presence and availability of mineral ions such as calcium within plaque may play an important part in controlling enamel demineralization. In general, the chemical composition of plaque fluid from root surfaces before and after sucrose exposure was similar to that previously found for samples from coronal surfaces. Taking these results into consideration, along with the fact that dentine mineral is more soluble than enamel mineral, it can be concluded that the driving force in plaque fluid for the demineralization of exposed root tissue is greater than that for enamel demineralization. RP MARGOLIS, HC (reprint author), FORSYTH DENT CTR,140 THE FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07493, DE-03187, DE-07009] NR 26 TC 13 Z9 18 U1 0 U2 1 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 FEB PY 1993 VL 38 IS 2 BP 131 EP 138 DI 10.1016/0003-9969(93)90197-T PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KV294 UT WOS:A1993KV29400005 PM 8476342 ER PT J AU POLLACK, MH HAMMERNESS, P AF POLLACK, MH HAMMERNESS, P TI ADJUNCTIVE YOHIMBINE FOR TREATMENT IN REFRACTORY DEPRESSION SO BIOLOGICAL PSYCHIATRY LA English DT Note ID RECEPTOR; ANTIDEPRESSANT; DESIPRAMINE; BUPROPION RP POLLACK, MH (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,15 PARKMAN ST,ACC 815,BOSTON,MA 02114, USA. NR 9 TC 17 Z9 17 U1 0 U2 0 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 FEB 1 PY 1993 VL 33 IS 3 BP 220 EP 221 DI 10.1016/0006-3223(93)90145-4 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KR263 UT WOS:A1993KR26300014 PM 8448273 ER PT J AU DALTON, LA MILLER, KW AF DALTON, LA MILLER, KW TI PHASE-BEHAVIOR OF DIELAIDOYLPHOSPHATIDYLCHOLINE BILAYERS IN THE PRESENCE OF ETHANOL STUDIED BY EPR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1993 VL 64 IS 2 BP A74 EP A74 PN 2 PG 1 WC Biophysics SC Biophysics GA KP517 UT WOS:A1993KP51700414 ER PT J AU MOHRAZ, M ARYSTARKHOVA, E SWEADNER, KJ AF MOHRAZ, M ARYSTARKHOVA, E SWEADNER, KJ TI MEMBRANE TOPOLOGY OF THE ALPHA SUBUNIT OF NA,K-ATPASE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NYU,SCH MED,NEW YORK,NY 10016. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1993 VL 64 IS 2 BP A331 EP A331 PN 2 PG 1 WC Biophysics SC Biophysics GA KP517 UT WOS:A1993KP51701902 ER PT J AU PRAT, AG BERTORELLO, AM AUSIELLO, DA CANTIELLO, HF AF PRAT, AG BERTORELLO, AM AUSIELLO, DA CANTIELLO, HF TI ACTIN-FILAMENTS MEDIATE PROTEIN-KINASE A (PKA) ACTIVATION OF EPITHELIAL NA+ CHANNELS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1993 VL 64 IS 2 BP A81 EP A81 PN 2 PG 1 WC Biophysics SC Biophysics GA KP517 UT WOS:A1993KP51700459 ER PT J AU RAINES, DE MILLER, KW AF RAINES, DE MILLER, KW TI SPIN-LABEL STUDIES INTO THE EFFECTS OF ETHANOL ON LIPID-PROTEIN INTERACTIONS IN RECONSTITUTED ACETYLCHOLINE-RECEPTOR VESICLES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1993 VL 64 IS 2 BP A287 EP A287 PN 2 PG 1 WC Biophysics SC Biophysics GA KP517 UT WOS:A1993KP51701642 ER PT J AU JUBINSKY, PT NATHAN, DG WILSON, DJ SIEFF, CA AF JUBINSKY, PT NATHAN, DG WILSON, DJ SIEFF, CA TI A LOW-AFFINITY HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR MURINE ERYTHROPOIETIN HYBRID RECEPTOR FUNCTIONS IN MURINE CELL-LINES SO BLOOD LA English DT Note ID GM-CSF; HEMATOPOIETIC-CELLS; SIGNAL TRANSDUCTION; EXPRESSION CLONING; MOLECULAR-CLONING; BETA-CHAIN; GROWTH; DIFFERENTIATION; SPECIFICITY; SUBUNIT C1 CHILDRENS HOSP MED CTR,DIV PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. MEHARRY MED COLL,SCH GRAD STUDIES,DIV BIOMED SCI,NASHVILLE,TN 37208. RP JUBINSKY, PT (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DANA 1628,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM 13452] NR 23 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 0006-4971 J9 BLOOD JI Blood PD FEB 1 PY 1993 VL 81 IS 3 BP 587 EP 591 PG 5 WC Hematology SC Hematology GA KK811 UT WOS:A1993KK81100003 PM 8427955 ER PT J AU KATAYAMA, N CLARK, SC OGAWA, M AF KATAYAMA, N CLARK, SC OGAWA, M TI GROWTH-FACTOR REQUIREMENT FOR SURVIVAL IN CELL-CYCLE DORMANCY OF PRIMITIVE MURINE LYMPHOHEMATOPOIETIC PROGENITORS SO BLOOD LA English DT Article ID HEMATOPOIETIC STEM-CELLS; COLONY-STIMULATING FACTOR; C-KIT; INTERLEUKIN-3-DEPENDENT PROLIFERATION; CULTURE; DIFFERENTIATION; IDENTIFICATION; LIGAND; 5-FLUOROURACIL; ENHANCEMENT C1 VET AFFAIRS MED CTR,RALPH H JOHNSON DEPT,109 BEE ST,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. GENET INST,CAMBRIDGE,MA. FU NIDDK NIH HHS [DK32294] NR 24 TC 77 Z9 77 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 1 PY 1993 VL 81 IS 3 BP 610 EP 616 PG 7 WC Hematology SC Hematology GA KK811 UT WOS:A1993KK81100007 PM 7678992 ER PT J AU ECKARDT, JR ROODMAN, GD BOLDT, DH CLARK, GM ALVAREZ, R PAGE, C GASKILL, H LEMAISTRE, CF AF ECKARDT, JR ROODMAN, GD BOLDT, DH CLARK, GM ALVAREZ, R PAGE, C GASKILL, H LEMAISTRE, CF TI COMPARISON OF ENGRAFTMENT AND ACUTE GVHD IN PATIENTS UNDERGOING CRYOPRESERVED OR FRESH ALLOGENEIC BMT SO BONE MARROW TRANSPLANTATION LA English DT Article ID BLOOD MONONUCLEAR-CELLS; DIMETHYL-SULFOXIDE; BONE-MARROW; LYMPHOCYTE-T; MONOCLONAL-ANTIBODIES; SURFACE-MARKERS; TRANSPLANTATION; DIFFERENTIATION; LEUKEMIA; RECOVERY AB Coordination of marrow donation for allogeneic BMT is a common logistical problem. The use of cryopreserved donor marrow would facilitate scheduling and avoid potential problems due to donor employment, injury, infection or death. We analysed results of 10 matched related BMTs performed with cryopreserved donor marrow and compared them with 33 matched related BMTs using fresh bone marrow over a 4 year period. No difference in time to engraftment of granulocytes and platelets or transfusion requirements were demonstrated for the two groups. However, there was less GVHD in patients who received cryopreserved donor marrow (chi2, p = 0.03; Fisher's exact test (two-sided) p = 0.067) despite comparable risk factors. The reason for this difference is unclear. Our results indicate that the use, of cryopreserved bone marrow for allogeneic BMT patients is at least equivalent to the use of fresh bone marrow. A prospective randomized trial is needed to determine if a true difference exists in the incidence or severity of acute GVHD and to determine if recurrence rate is different between the two groups. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP ECKARDT, JR (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT ONCOL 111J,7400 MERTON MINTOR,SAN ANTONIO,TX 78284, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 39 TC 19 Z9 19 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 FEB PY 1993 VL 11 IS 2 BP 125 EP 131 PG 7 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA KK597 UT WOS:A1993KK59700007 PM 8435661 ER PT J AU SHORTEN, GD ALI, HH GOUDSOUZIAN, NG AF SHORTEN, GD ALI, HH GOUDSOUZIAN, NG TI NEOSTIGMINE AND EDROPHONIUM ANTAGONISM OF MODERATE NEUROMUSCULAR BLOCK INDUCED BY PANCURONIUM OR TUBOCURARINE SO BRITISH JOURNAL OF ANAESTHESIA LA English DT Article DE ANTAGONISTS; NEUROMUSCULAR RELAXANTS; EDROPHONIUM; NEOSTIGMINE; NEUROMUSCULAR RELAXANTS; PANCURONIUM; TUBOCURARINE ID ATRACURIUM; VECURONIUM; REVERSAL AB Edrophonium and neostigmine are anticholin-esterase drugs used commonly to antagonize competitive neuromuscular block. Although it has a faster onset of action than neostigmine, edrophonium is unreliable when used to antagonize deep neuromuscular block. We have compared the antagonist characteristics of these two drugs when used to antagonize a moderate degree of pancuronium- or tubocurarine-induced neuromuscular block. Forty ASA I or II patients undergoing surgical procedures were allocated randomly to receive either pancuronium 70 mug kg-1 or tubocurarine 0.5 mg kg-1 and to receive either edrophonium 0.5 mg kg-1 or neostigmine 0.05 mg kg-1. Antagonism was attempted when the first response to train-of-four (TOF) stimulation recovered spontaneously to 25% of the control height. Neuromuscular function was monitored using the evoked integrated electromyogram of the first dorsal interosseous muscle of the hand. Adequate recovery was defined as the achievement of a TOF ratio of 0.70 or greater. Only seven of 20 patients who received edrophonium demonstrated adequate recovery 30 min after antagonism. Under the conditions described in this study, edrophonium 0.5 mg kg-1 was less effective as an antagonist than neostigmine 0.05 mg kg-1. C1 MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. NR 13 TC 2 Z9 2 U1 0 U2 0 PU PROF SCI PUBL PI LONDON PA TAVISTOCK HOUSE EAST, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-0912 J9 BRIT J ANAESTH JI Br. J. Anaesth. PD FEB PY 1993 VL 70 IS 2 BP 160 EP 162 DI 10.1093/bja/70.2.160 PG 3 WC Anesthesiology SC Anesthesiology GA KK586 UT WOS:A1993KK58600010 PM 8435259 ER PT J AU HUANG, ZH BYUN, B MATSUBARA, T MOSKOWITZ, MA AF HUANG, ZH BYUN, B MATSUBARA, T MOSKOWITZ, MA TI TIME-DEPENDENT BLOCKADE OF NEUROGENIC PLASMA EXTRAVASATION IN DURA-MATER BY 5-HT1B/D AGONISTS AND ENDOPEPTIDASE 24.11 SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE CP-93,129; SUMATRIPTAN; ENDOPEPTIDASE 24.11; 5-HT1B RECEPTORS; 5-HT1D RECEPTORS; MIGRAINE; DURA MATER; NEUROGENIC INFLAMMATION ID FERRET TRACHEA; INDUCED CONTRACTION; BLOOD-VESSELS; RAT; BRAIN; STIMULATION; INHIBITION; SECRETION; RECEPTOR; RELEASE AB 1 The delayed effects of stimulating the trigeminal ganglion unilaterally in rats and guinea-pigs were assessed by measuring the leakage of radiolabelled albumin from blood into the dura mater at intervals for up to 120 min after a 5 min stimulation period (5 Hz, 0.6 mA, 5 ms). 2 [I-125]-albumin (50 muCi kg-1) was injected i.v. as a tracer 0, 20, 50, 80 or 110 min after stimulation and the animals were killed 10 min later. Extravasation of plasma protein developed for up to 90 min poststimulation. 3 To examine the mechanism underlying delayed plasma protein extravasation, CP-93,129 (5-HT1B receptor agonist, 460 nmol kg-1), sumatriptan (5-HT1B/D receptor agonist, 24 nmol kg-1), or neutral endopeptidase 24.11 (1 nmol kg-1) were administered 45 or 75 min after trigeminal stimulation and 5 min before radiolabelled albumin. The extravasation response was reduced at 45 min. CP-23,129 also blocked extravasation when injected 25 min after capsaicin administration (1 mumol kg-1). 4 If the tracer was injected 5 min prior to electrical trigeminal stimulation, endopeptidase 24.11 (1 nmol kg-1) given 10 min before stimulation blocked the leakage (as reported previously for CP-93,129 or sumatriptan). All three compounds blocked the leakage when administered 30 min (but not 60 min) poststimulation in this paradigm. 5 The data support the previously made contention that neuropeptide release from sensory fibres mediates the plasma extravasation response following trigeminal ganglion stimulation, and that release and plasma leakage continue many minutes beyond the stimulation period. Hence, drugs that inhibit neuropeptide release (CP-93,129, sumatriptan), or enhance breakdown of neuropeptide mediators (endopeptidase 24.11) block the delayed extravasation response. Extravasation developing later than 45 min poststimulation was not neurogenically mediated. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG & NEUROL SERV,STROKE RES LAB,BOSTON,MA 02114. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS 21558] NR 21 TC 30 Z9 30 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD FEB PY 1993 VL 108 IS 2 BP 331 EP 335 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KJ829 UT WOS:A1993KJ82900011 PM 8383561 ER PT J AU ZIETMAN, AL SHIPLEY, WU WILLETT, CG AF ZIETMAN, AL SHIPLEY, WU WILLETT, CG TI RESIDUAL DISEASE AFTER RADICAL SURGERY OR RADIATION-THERAPY FOR PROSTATE-CANCER - CLINICAL-SIGNIFICANCE AND THERAPEUTIC IMPLICATIONS SO CANCER LA English DT Article; Proceedings Paper CT 1ST NATIONAL CONF ON PROSTATE CANCER CY FEB 13-15, 1992 CL SAN FRANCISCO, CA SP AMER CANC SOC, AMER ACAD FAMILY PHYSICIANS, AMER COLL RADIOL, AMER COLL SURGEONS, COMMISS CANC, AMER UROL ASSOC, NATL ASSOC ONCOL SOCIAL WORKERS, NATL ASSOC SOCIAL WORKERS, ONCOL NURSING SOC, SOC SURG ONCOL DE PROSTATE CARCINOMA; RADIATION THERAPY; RADICAL PROSTATECTOMY; RESIDUAL DISEASE ID EXTERNAL BEAM RADIATION; POSITIVE SURGICAL MARGINS; STAGE-C ADENOCARCINOMA; POSTOPERATIVE RADIOTHERAPY; METASTATIC DISSEMINATION; ADJUVANT RADIOTHERAPY; ANTIGEN LEVELS; LOCAL-CONTROL; FOLLOW-UP; CARCINOMA AB Radical treatment for prostate cancer aims at complete eradication of tumor. This review of published data makes clear that the goal is less frequently achieved than commonly presumed. Following radical prostatectomy extracapsular disease, carrying a significant risk of local recurrence, is found from 12-68% of the time depending on the clinical tumor stage. Local regrowth is associated with a poorer prognosis. A substantial proportion of patients whose prostate glands are rebiopsied more than 18 months after radiation therapy also have residual tumor. This again predicts for clinical relapse. The likelihood of a positive rebiopsy is dependent on original tumor size and current prostate specific antigen (PSA) levels. Strategies for managing residual disease are critically discussed. RP ZIETMAN, AL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 70 TC 78 Z9 78 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1993 VL 71 IS 3 SU S BP 959 EP 969 DI 10.1002/1097-0142(19930201)71:3+<959::AID-CNCR2820711411>3.0.CO;2-L PG 11 WC Oncology SC Oncology GA KM674 UT WOS:A1993KM67400010 PM 7679046 ER PT J AU HEGEN, M CAMERINI, D FLEISCHER, B AF HEGEN, M CAMERINI, D FLEISCHER, B TI FUNCTION OF DIPEPTIDYL PEPTIDASE-IV (CD26, TP103) IN TRANSFECTED HUMAN T-CELLS SO CELLULAR IMMUNOLOGY LA English DT Article ID HUMAN LYMPHOCYTE-T; HUMAN CD4; ACTIVATION ANTIGEN; MOLECULAR-CLONING; EXPRESSION; RECEPTOR; COMPLEX; INTERLEUKIN-2; GLYCOPROTEIN; ANTIBODIES C1 UNIV MAINZ,DEPT MED 1,LANGENBECKSTR 1,W-6500 MAINZ,GERMANY. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 41 TC 34 Z9 34 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 FEB PY 1993 VL 146 IS 2 BP 249 EP 260 DI 10.1006/cimm.1993.1024 PG 12 WC Cell Biology; Immunology SC Cell Biology; Immunology GA KY237 UT WOS:A1993KY23700003 PM 7909722 ER PT J AU LEVINE, SM ANZUETO, A GIBBONS, WJ CALHOON, JH JENKINSON, SG TRINKLE, JK BRYAN, CL AF LEVINE, SM ANZUETO, A GIBBONS, WJ CALHOON, JH JENKINSON, SG TRINKLE, JK BRYAN, CL TI GRAFT POSITION AND PULMONARY-FUNCTION AFTER SINGLE LUNG TRANSPLANTATION FOR OBSTRUCTIVE LUNG-DISEASE SO CHEST LA English DT Article ID EMPHYSEMA AB Single lung transplantation (SLT) has become a therapeutic option for the treatment of end-stage obstructive lung disease. Between January 1989 and June 1990, there were 14 patients with end-stage obstructive lung disease who underwent SLT. Eleven of these patients were surviving at 1 year following transplantation. Three of the patients had received left-sided SLT, and eight had received right-sided SLT. In the patients receiving left-sided SLT, the native right lung radiographically appeared to compress the left lung graft. In the patients receiving right-sided SLT, the native left lung did not appear to compress the right lung graft. We hypothesized that right SLT may provide a functional advantage over left SLT for patients with obstructive lung disease. We compared pulmonary function test results before and after transplantation (approximately 3 and 12 months) and compared quantitative ventilation-perfusion lung scan results between the patients with left SLT and those with right SLT. Additionally, we compared graded-exercise test results at 3 and 12 months after transplant between the two groups. Our data revealed no statistical difference in pulmonary function test results or graded-exercise test results between the two groups, although patients undergoing right SLT showed greater increases in FEV1 and forced vital capacity than those undergoing left SLT. Quantitative ventilation and perfusion were greater to the graft in patients receiving right-sided SLT than in patients receiving left-sided SLT, most likely due to the larger size of the right lung. We conclude that there is no functional difference between patients undergoing left or right SLT for end-stage obstructive lung disease. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. RP LEVINE, SM (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT 111E,SAN ANTONIO,TX 78284, USA. NR 9 TC 16 Z9 16 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 FEB PY 1993 VL 103 IS 2 BP 444 EP 448 DI 10.1378/chest.103.2.444 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA KL712 UT WOS:A1993KL71200027 PM 8432134 ER PT J AU ROBERTS, JD LANG, P BIGATELLO, LM VLAHAKES, GJ ZAPOL, WM AF ROBERTS, JD LANG, P BIGATELLO, LM VLAHAKES, GJ ZAPOL, WM TI INHALED NITRIC-OXIDE IN CONGENITAL HEART-DISEASE SO CIRCULATION LA English DT Article DE HYPERTENSION, PULMONARY ARTERY; CONGENITAL HEART DISEASE; ENDOTHELIUM-DERIVED RELAXING FACTOR; NITRIC OXIDE ID SELECTIVE PULMONARY VASODILATOR; ENDOTHELIAL-CELLS; CHILDREN; VASOCONSTRICTION; ACETYLCHOLINE; NITROPRUSSIDE; RELAXATION; HEMOGLOBIN; SURGERY; OXYGEN AB Background. Congenital heart lesions may be complicated by pulmonary arterial smooth muscle hyperplasia, hypertrophy, and hypertension. We assessed whether inhaling low levels of nitric oxide (NO), an endothelium-derived relaxing factor, would produce selective pulmonary vasodilation in pediatric patients with congenital heart disease and pulmonary hypertension. We also compared the pulmonary vasodilator potencies of inhaled NO and oxygen in these patients. Methods and Results. In 10 sequentially presenting, spontaneously breathing patients, we determined whether inhaling 20-80 ppm by volume of NO at inspired oxygen concentrations (FIO2) of 0.21-0.3 and 0.9 would reduce the pulmonary vascular resistance index (Rp). We then compared breathing oxygen with inhaling NO. Inhaling 80 ppm NO at FIO2 0.21-0.3 reduced mean pulmonary artery pressure from 48+/-19 to 40+/-14 mm Hg and Rp from 658+/-421 to 491+/-417 dyne . sec . cm-5 . m-2 (mean+/-SD, both p<0.05). Increasing the FIO2 to 0.9 without adding NO did not reduce mean pulmonary artery pressure but reduced Rp and increased the ratio of pulmonary to systemic blood flow (Q(p)/Q(s)), primarily by increasing Q(p) (p<0.05). Breathing 80 ppm NO at FIO2 0.9 reduced mean pulmonary artery pressure and Rp to the lowest levels and increased Q(p) and Q(p)/Q(s) (all p<0.05). While breathing at FIO2 0.9, inhalation of 40 ppm NO reduced Rp (p<0.05); the maximum reduction of Rp occurred while breathing 80 ppm NO. Inhaling 80 ppm NO at FIO2 0.21-0.9 did not alter mean aortic pressure or systemic vascular resistance. Methemoglobin levels were unchanged by breathing up to 80 ppm NO for 30 minutes. Conclusions. Inhaled NO is a potent and selective pulmonary vasodilator in pediatric patients with congenital heart disease complicated by pulmonary artery hypertension. Inhaling low levels of NO may provide an important and safe means for evaluating the pulmonary vasodilatory capacity of patients with congenital heart disease without producing systemic vasodilation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. RP ROBERTS, JD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-42397] NR 34 TC 298 Z9 305 U1 2 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1993 VL 87 IS 2 BP 447 EP 453 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KL647 UT WOS:A1993KL64700017 PM 8425292 ER PT J AU ROBERTS, JD CHEN, TY KAWAI, N WAIN, J DUPUY, P SHIMOUCHI, A BLOCH, K POLANER, D ZAPOL, WM AF ROBERTS, JD CHEN, TY KAWAI, N WAIN, J DUPUY, P SHIMOUCHI, A BLOCH, K POLANER, D ZAPOL, WM TI INHALED NITRIC-OXIDE REVERSES PULMONARY VASOCONSTRICTION IN THE HYPOXIC AND ACIDOTIC NEWBORN LAMB SO CIRCULATION RESEARCH LA English DT Article DE ENDOTHELIUM-DERIVED RELAXING FACTOR; NITRIC OXIDE; PULMONARY CIRCULATION; NEWBORN LAMBS; CGMP ID ENDOTHELIUM-DEPENDENT RELAXATION; RELAXING FACTOR; GUANYLATE-CYCLASE; CYCLIC-GMP; L-ARGININE; ACETYLCHOLINE; HEMOPROTEINS; ACTIVATION; HEMOGLOBIN; ARTERIES AB We determined whether inhaling low levels of nitric oxide (NO) gas could selectively reverse hypoxic pulmonary vasoconstriction in the near-term newborn lamb and whether vasodilation would be attenuated by respiratory acidosis. To examine the mechanism of air and NO-induced pulmonary vasodilation soon after birth, we measured plasma and lung cGMP levels in the newly ventilated fetal lamb. Breathing at FIO2 0.10 nearly doubled the pulmonary vascular resistance index in newborn lambs and decreased pulmonary blood flow primarily by reducing left-to-right blood How through the ductus arteriosus. Inhaling 20 ppm NO at FIO2 0.10 completely reversed hypoxic pulmonary vasoconstriction within minutes. Maximum pulmonary vasodilation occurred during inhalation of greater-than-or-equal-to 80 ppm NO. Breathing 8% CO2 at FIO2 0.10 elevated the pulmonary vascular resistance index to a level similar to breathing at FIO2 0.10 without added CO2. Respiratory acidosis did not attenuate pulmonary vasodilation by inhaled NO. In none of our studies did inhaling NO produce systemic hypotension or elevate methemoglobin levels. Four minutes after initiating ventilation with air in the fetal lamb lung, cGMP concentration nearly doubled without changing preductal plasma cGMP concentration. Ventilation with 80 ppm NO at FIO2 0.21 increased both lung and preductal plasma cGMP concentration threefold. Our data suggest that inhaled NO gas is a rapid and potent selective vasodilator of the newborn pulmonary circulation with an elevated vascular tone due to hypoxia and respiratory acidosis that acts by increasing lung cGMP concentration. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. RP ROBERTS, JD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. OI Polaner, David/0000-0001-8716-6289 FU NHLBI NIH HHS [HL-42397] NR 48 TC 151 Z9 154 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD FEB PY 1993 VL 72 IS 2 BP 246 EP 254 PG 9 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA KG813 UT WOS:A1993KG81300002 PM 8380356 ER PT J AU TOMERA, JF KUKULKA, SP LILFORD, K AF TOMERA, JF KUKULKA, SP LILFORD, K TI CROSS-TALK OF 2ND MESSENGERS DURING THE SYSTEMIC TRAUMA RESPONSE FOLLOWING BURN INJURY - HOW, WHEN, AND WHERE SO CIRCULATORY SHOCK LA English DT Article DE ADENOSINE 3'/5'-CYCLIC MONOPHOSPHATE; CALCIUM; GASTROCNEMIUS MUSCLE; MOUSE; POLYINOSITOLS; SIGNAL TRANSDUCTION SYSTEM ID GASTROCNEMIUS-MUSCLE; PHOSPHOLIPASE-C; CYCLIC-AMP; PHOSPHORYLATION; TUBOCURARINE; ACTIVATION; RECEPTORS; ENDOTOXIN; PATHWAYS; PROTEINS AB The systemic effects of trauma from large body surface area (% BSA) burns were evaluated in terms of second messenger levels involving polyinositol phosphates as they related to adenosine 3':5'-cyclic monophosphate (cAMP), myoplasmic Ca2+, and active tension. Gastrocnemius muscles were harvested after muscle twitch at postburn day 21. Levels of polyinositols were measured by incorporation of myo-[2-H-3]-inositol, with separation of the phosphates by anion-exchange chromatography. Analysis of variance was used for statistical evaluation. Multivariate relationships between the: 1) independent polyinositol forms (H-3-inositol, I1P, and I1,4, P2) and dependent I1,4,5, P3 existed for control (R2 = 0.71) and 20% BSA burn (R2 = 0.67) groups; 2) the independent polyinositol forms (I1 P, I1,4,P2, and I1,4,5,P3) and dependent cAMP for control (R2 = 0.73), 20% BSA (R2 = 0.99), and 50% BSA (R2 = 0.99) groups; 3) independent polyinositol forms (I1 P, I1,4,P2, and I1,4,5,P3) and dependent Ca-45(2+) for the control (R2 = 0.99), 20% BSA (R2 = 0.44), and 50% BSA (R2 = 0.82) groups; and 4) independent polyinositol forms (I1 P, I1,4,P2, and I1,4,5,P3) and dependent active tension for 20% BSA (R2 = 0.97) and 50% BSA (R2 = 0.64) burn groups. Numerous interrelationships existed with each of the multivariate tests. These analyses confirm that several independent polyinositols contribute to changes in the second messengers of I1,4,5,P3, cAMP, and Ca2+ in skeletal muscle as a result of the systemic trauma of burn injury. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIOL,BOSTON,MA 02115. RP TOMERA, JF (reprint author), HARVARD UNIV,SCH MED,SHRINERS BURNS INST,ANESTHESIA SERV,CLIN PHARMACOL LAB,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 31 TC 17 Z9 17 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0092-6213 J9 CIRC SHOCK JI Circ. Shock PD FEB PY 1993 VL 39 IS 2 BP 128 EP 138 PG 11 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KK475 UT WOS:A1993KK47500007 PM 8387897 ER PT J AU DOTTA, F TIBERTI, C PREVITI, M ANASTASI, E ANDREANI, D LENTI, L PONTIERI, GM GIANANI, R APPEL, MC EISENBARTH, GS DIMARIO, U AF DOTTA, F TIBERTI, C PREVITI, M ANASTASI, E ANDREANI, D LENTI, L PONTIERI, GM GIANANI, R APPEL, MC EISENBARTH, GS DIMARIO, U TI RAT PANCREATIC GANGLIOSIDE EXPRESSION - DIFFERENCES BETWEEN A MODEL OF AUTOIMMUNE ISLET B-CELL DESTRUCTION AND A NORMAL STRAIN SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; I DIABETES-MELLITUS; ANTIBODIES; ASSAY; LIVER; MOUSE C1 UNIV ROME LA SAPIENZA,DEPT EXPTL MED GEN PATHOL 1,I-00185 ROME,ITALY. UNIV MASSACHUSETTS,SCH MED,DEPT PATHOL,WORCESTER,MA 01605. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,IMMUNOL SECT,BOSTON,MA 02115. UNIV RC,DEPT CLIN & EXPTL MED,CATANZARO,ITALY. UNIV MESSINA,DEPT INTERNAL MED,I-98100 MESSINA,ITALY. RP DOTTA, F (reprint author), UNIV ROME LA SAPIENZA,MED ENDOCRINOL CLIN 2,I-00185 ROME,ITALY. RI Dotta, Francesco/H-3788-2012; OI Dotta, Francesco/0000-0003-4947-7478 FU NIDDK NIH HHS [DK 41090, R01 DK 366 41-08] NR 28 TC 15 Z9 15 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 FEB PY 1993 VL 66 IS 2 BP 143 EP 149 DI 10.1006/clin.1993.1018 PG 7 WC Immunology; Pathology SC Immunology; Pathology GA KJ524 UT WOS:A1993KJ52400007 PM 8453786 ER PT J AU LARAR, GN JANICEK, MJ KAPLAN, WD AF LARAR, GN JANICEK, MJ KAPLAN, WD TI GA-67 SCINTIGRAPHY AFTER BONE-MARROW HARVEST - SIGNIFICANCE OF SACROILIAC ASYMMETRY IN THE LYMPHOMA PATIENT SO CLINICAL NUCLEAR MEDICINE LA English DT Article ID NON-HODGKIN LYMPHOMA; SKELETAL; DISEASE AB The importance of recognizing asymmetric Ga-67 citrate uptake in the sacroiliac region after bone marrow harvest and transplant is discussed in a case of non-Hodgkin's lymphoma. The patient underwent chemotherapy, irradiation, and autologous bone marrow transplant for stage IV disease. Ga-67 scintigraphy revealed sacroiliac asymmetry suggesting medial iliac reparative changes after bone marrow harvest. Iliac bone marrow biopsy showed no evidence of infection or of recurrent tumor. Subsequent follow-up imaging and open biopsy demonstrated lymphomatous invasion of adjacent soft tissue where initial findings were thought to represent benign, postharvest changes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RADIOL,DIV NUCL MED,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT PROGRAM NUCL MED,BOSTON,MA 02115. NR 11 TC 4 Z9 4 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-9762 J9 CLIN NUCL MED JI Clin. Nucl. Med. PD FEB PY 1993 VL 18 IS 2 BP 126 EP 129 DI 10.1097/00003072-199302000-00008 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KL748 UT WOS:A1993KL74800008 PM 8432056 ER PT J AU SMITH, C YOHN, J MORELLI, J DORMISH, J KANE, M ZAMORA, M AF SMITH, C YOHN, J MORELLI, J DORMISH, J KANE, M ZAMORA, M TI IDENTIFICATION OF PUTATIVE ENDOTHELIN-1 RECEPTORS IN CULTURED HUMAN-MALIGNANT MELANOMA-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV COLORADO,SCH MED,DEPT DERMATOL,DENVER,CO 80202. UNIV COLORADO,SCH MED,DEPT MED,DENVER,CO 80202. DENVER VAMC,DENVER,CO. UC,CTR CANC,DENVER,CO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1993 VL 41 IS 1 BP A31 EP A31 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KH410 UT WOS:A1993KH41000161 ER PT J AU SMITH, C YOHN, J MORELLI, J DORMISH, J KANE, M ZAMORA, M AF SMITH, C YOHN, J MORELLI, J DORMISH, J KANE, M ZAMORA, M TI EVIDENCE FOR AN ENDOTHELIN-1 AUTOCRINE SYSTEM IN NORMAL HUMAN KERATINOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV COLORADO,SCH MED,DEPT DERMATOL,DENVER,CO 80202. UNIV COLORADO,SCH MED,DEPT MED,DENVER,CO 80202. DENVER VAMC,DENVER,CO. UC,CTR CANC,DENVER,CO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1993 VL 41 IS 1 BP A4 EP A4 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KH410 UT WOS:A1993KH41000017 ER PT J AU SU, A COMER, J COLLINS, J AF SU, A COMER, J COLLINS, J TI CYTOSOLIC CALCIUM IN COLONIC-CARCINOMA CELL-DIFFERENTIATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97201. NR 2 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1993 VL 41 IS 1 BP A107 EP A107 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KH410 UT WOS:A1993KH41000588 ER PT J AU SUMNER, AE CHIN, MM ABRAHM, JL BERRY, GT ALLEN, RH STABLER, SP AF SUMNER, AE CHIN, MM ABRAHM, JL BERRY, GT ALLEN, RH STABLER, SP TI PREVALENCE OF VITAMIN-B12 DEFICIENCY IN PATIENTS WITH A HISTORY OF GASTRIC-SURGERY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV PENN,PHILADELPHIA COLL PHARM,SCH MED,PHILADELPHIA,PA 19104. UNIV PENN,PHILADELPHIA VA MED CTR,PHILADELPHIA,PA 19104. UNIV PENN,MED COLL PENN,PHILADELPHIA,PA 19104. UNIV COLORADO,DENVER,CO 80202. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1993 VL 41 IS 1 BP A20 EP A20 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KH410 UT WOS:A1993KH41000106 ER PT J AU SILVA, P EPSTEIN, FH AF SILVA, P EPSTEIN, FH TI SECRETION OF NITRATE BY RECTAL GLAND OF SQUALUS-ACANTHIAS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-PHYSIOLOGY LA English DT Article ID ASCITES TUMOR-CELLS; CHLORIDE TRANSPORT; ESCHERICHIA-COLI; SODIUM; COTRANSPORT; IONS AB 1. Rectal glands secrete nitrate at 30% of their capacity to secrete chloride. 2. Nitrate secretion is directly related to its concentration at constant chloride concentrations. 3. Chloride has a biphasic effect on nitrate secretion. 4. Hill coefficients at chloride < 100 mM are equal to 1, while at 100 mM indicate inhibition of nitrate by chloride. 6. Lineweaver-Burk plots at chloride < 100 indicate a single site, while at 100 mM indicate inhibition of nitrate by chloride. 7. Bumetanide inhibits nitrate secretion. 8. The data suggest that nitrate interacts with one of the two chloride sites of the chloride transporter. C1 MT DESERT ISL BIOL LAB,SALSBURY COVE,ME 04672. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,JOSLIN DIABET CTR,HARVARD CTR STUDY KIDNEY DIS,BOSTON,MA 02215. FU NHLBI NIH HHS [NIHHL35998]; NICHD NIH HHS [NI-HDK18078]; NIEHS NIH HHS [1-P30-ES03828] NR 19 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 0300-9629 J9 COMP BIOCHEM PHYS A JI Comp. Biochem. Physiol. A-Physiol. PD FEB PY 1993 VL 104 IS 2 BP 255 EP 259 DI 10.1016/0300-9629(93)90313-S PG 5 WC Biochemistry & Molecular Biology; Physiology; Zoology SC Biochemistry & Molecular Biology; Physiology; Zoology GA KL976 UT WOS:A1993KL97600012 PM 8095877 ER PT J AU HE, WW GUSTAFSON, ML HIROBE, S DONAHOE, PK AF HE, WW GUSTAFSON, ML HIROBE, S DONAHOE, PK TI DEVELOPMENTAL EXPRESSION OF 4 NOVEL SERINE THREONINE KINASE RECEPTORS HOMOLOGOUS TO THE ACTIVIN TRANSFORMING GROWTH-FACTOR-BETA TYPE-II RECEPTOR FAMILY SO DEVELOPMENTAL DYNAMICS LA English DT Article DE SERINE THREONINE KINASE RECEPTORS; UROGENITAL RIDGE; GONAD; ACTIVIN; TGF-BETA; MULLERIAN INHIBITING SUBSTANCE ID MULLERIAN INHIBITING SUBSTANCE; OVARIAN FOLLICULAR-FLUID; PROTEIN-KINASE; TGF-BETA; CONSERVED FEATURES; OOCYTE MEIOSIS; CLONING; GENE; REGRESSION; SEQUENCE AB Serine/threonine kinase transmembrane proteins are a new family of growth factor signal transducers that includes several isoforms of the activin type II receptor and the type II receptor for transforming growth factor-beta. In an effort to clone the receptor for Mullerian inhibiting substance, a member of the transforming growth factor-beta superfamily, oligonucleotide primers designed from conserved regions of these receptors' kinase domains were used for PCR amplification of fetal rat urogenital ridge cDNA. We isolated four novel receptors in this manner (designated R1-R4), each of which has structural features of the previously cloned kinases, including a small extracellular ligand-binding domain, a single hydrophobic transmembrane domain, and an intracellular serine/threonine kinase domain. In addition, each has characteristic kinase subdomains and conserved serine/threonine kinase sequences found in this family. Northern analysis revealed mRNA expression of R1-R4 in several tissues, including fetal urogenital ridge, testis, and ovary, as well as brain and lung. In situ hybridization further localized R1 to mesenchyme of the 14.5 to 15-day fetal rat Mullerian duct and to oocytes of preantral and antral follicles, sites that are consistent with the predicted localization of Mullerian inhibiting substance receptor. In addition, R2 localized specifically to seminiferous tubules of the postnatal testis. These newest members of the activin and transforming growth factor-beta type II receptor family should help define the molecular mechanisms by which this ligand superfamily affects cell growth and differentiation via membrane phosphorylation. (C) 1993 Wiley-Liss, Inc. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. RP MASSACHUSETTS GEN HOSP, PEDIAT SURG RES LAB, WARREN 10, BOSTON, MA 02114 USA. NR 44 TC 149 Z9 157 U1 1 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1058-8388 EI 1097-0177 J9 DEV DYNAM JI Dev. Dyn. PD FEB PY 1993 VL 196 IS 2 BP 133 EP 142 PG 10 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA LL239 UT WOS:A1993LL23900006 PM 8395914 ER PT J AU SPIRO, MJ CROWLEY, TJ AF SPIRO, MJ CROWLEY, TJ TI INCREASED RAT MYOCARDIAL TYPE-VI COLLAGEN IN DIABETES-MELLITUS AND HYPERTENSION SO DIABETOLOGIA LA English DT Article DE DIABETES-MELLITUS; HYPERTENSION; DIABETIC CARDIOMYOPATHY; TYPE-VI COLLAGEN; TYPE-IV COLLAGEN; TYPE-I COLLAGEN; LAMININ; MYOSIN ID GLOMERULAR BASEMENT-MEMBRANE; BASAL LAMINAR THICKNESS; CONNECTIVE-TISSUE; INSULIN-TREATMENT; CARDIOMYOPATHY; HEART; PROTEINS; MUSCLE; PROTEOGLYCAN; CARDIOPATHY AB Diabetic cardiomyopathy, a condition characterized by the accumulation of carbohydrate-containing material surrounding the myocardial small blood vessels, has been studied in alloxan-diabetic normotensive and hypertensive rats. Immunochemical techniques were used to monitor several extracellular matrix constituents present in extracts of cardiac tissue, namely types I, IV and VI collagen, laminin and fibronectin, as well as myosin. These studies have indicated that after induction of diabetes, type VI collagen but none of the other matrix components studied, was significantly increased (from 2.29 +/- 0.04 mg/g in normal to 2.85 +/- 0.18 mg/g in diabetic ventricles, p < 0.01). Hypertension, whether induced by the clipping of one renal artery or genetically determined (spontaneously hypertensive rats), resulted in a similar elevation in type VI collagen (2.71 +/- 0.12 mg/g, p < 0.005.compared to normal rats). In the presence of diabetes plus hypertension the effect was not additive, the type VI collagen level being 2.93 +/- 0.15 (p < 0.001 compared to normal rats). Basement membrane collagen (type IV) in the myocardium appeared to be unaffected by diabetes or hypertension and the myosin contents of the hearts of the four experimental groups were similar. Quantitative determinations indicate that compared to type IV collagen, laminin or fibronectin, type VI collagen represents the major periodic acid-Schiff-reactive extracellular constituent of the rat ventricle. Its preferential increase in the heart in diabetes may provide insight into the molecular mechanisms of the diabetic microvascular disease. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SPIRO, MJ (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NHLBI NIH HHS [HL31315] NR 38 TC 42 Z9 43 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD FEB PY 1993 VL 36 IS 2 BP 93 EP 98 DI 10.1007/BF00400687 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KH647 UT WOS:A1993KH64700001 PM 8458534 ER PT J AU SHOELSON, SE SIVARAJA, M WILLIAMS, KP HU, P SCHLESSINGER, J WEISS, MA AF SHOELSON, SE SIVARAJA, M WILLIAMS, KP HU, P SCHLESSINGER, J WEISS, MA TI SPECIFIC PHOSPHOPEPTIDE BINDING REGULATES A CONFORMATIONAL CHANGE IN THE PI 3-KINASE SH2 DOMAIN ASSOCIATED WITH ENZYME ACTIVATION SO EMBO JOURNAL LA English DT Article DE GROWTH FACTOR RECEPTOR; INSULIN RECEPTOR; ONCOGENE; SIGNAL TRANSDUCTION; TYROSINE KINASE ID RECEPTOR TYROSINE KINASES; SIGNAL TRANSDUCTION; PHOSPHATIDYLINOSITOL KINASE; PHOSPHOLIPASE-C; PDGF RECEPTOR; MIDDLE-T; PROTEIN; PHOSPHORYLATION; PURIFICATION; PI3-KINASE AB SH2 (src-homology 2) domains define a newly recognized binding motif that mediates the physical association of target phosphotyrosyl proteins with downstream effector enzymes. An example of such phosphoprotein-effector coupling is provided by the association of phosphatidylinositol 3-kinase (PI 3-kinase) with specific phosphorylation sites within the PDGF receptor, the c-Src/polyoma virus middle T antigen complex and the insulin receptor substrate IRS-1. Notably, phosphoprotein association with the SH2 domains of p85 also stimulates an increase in catalytic activity of the PI 3-kinase p110 subunit, which can be mimicked by phosphopeptides corresponding to targeted phosphoprotein phosphorylation sites. To investigate how phosphoprotein binding to the p85 SH2 domain stimulates p110 catalytic activation, we have examined the differential effects of phosphotyrosine and PDGF receptor-, IRS-1- and c-Src-derived phosphopeptides on the conformation of an isolated SH2 domain of PI 3-kinase. Although phosphotyrosine and both activating and non-activating phosphopeptides bind to the SH2 domain, activating phosphopeptides bind with higher affinity and induce a qualitatively distinct conformational change as monitored by CD and NMR spectroscopy. Amide proton exchange and protease protection assays further show that high affinity, specific phosphopeptide binding induces non-local dynamic SH2 domain stabilization. Based on these findings we propose that specific phosphoprotein binding to the p85 subunit induces a change in SH2 domain structure which is transmitted to the p110 subunit and regulates enzymatic activity by an allosteric mechanism. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NYU MED CTR,DEPT PHARMACOL,NEW YORK,NY 10016. RP SHOELSON, SE (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115, USA. OI Hu, Patrick/0000-0002-5611-8062 FU NCRR NIH HHS [1 S10 RR04862]; NIDDK NIH HHS [DK08366, DK40949] NR 46 TC 152 Z9 154 U1 0 U2 5 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD FEB PY 1993 VL 12 IS 2 BP 795 EP 802 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KL717 UT WOS:A1993KL71700046 PM 8382612 ER PT J AU GWOSDOW, AR SPENCER, JA OCONNELL, NA ABOUSAMRA, AB AF GWOSDOW, AR SPENCER, JA OCONNELL, NA ABOUSAMRA, AB TI INTERLEUKIN-1 ACTIVATES PROTEIN-KINASE A AND STIMULATES ADRENOCORTICOTROPIC HORMONE-RELEASE FROM ATT-20 CELLS SO ENDOCRINOLOGY LA English DT Article ID ANTERIOR-PITUITARY-CELLS; RECOMBINANT HUMAN INTERLEUKIN-1-ALPHA; SIGNAL TRANSDUCTION; BETA-ENDORPHIN; LINE ATT-20; ACTH RELEASE; CYCLIC-AMP; MECHANISMS; PHOSPHORYLATION; SECRETION AB Studies from this and other laboratories have shown that interleukin-1 (IL-1) stimulates ACTH secretion directly from AtT-20 cells. The present studies were conducted to determine the signal transduction mechanisms activated by IL-1 to stimulate ACTH release. IL-1 significantly (P < 0.05) elevated ACTH release after incubation periods of 4, 8, and 24 h. IL-1-induced ACTH release was not additive to that of CRF, cholera toxin, 8-bromo-cAMP, or forskolin. In contrast, IL-1 and the phorbol ester phorbol 12-myristate 13-acetate together produced a greater increase (P < 0.05) in ACTH release than either agent alone. IL-1 did not stimulate cAMP accumulation at any time period between 5 min and 24 h and did not affect cAMP accumulation induced by CRF, cholera toxin, or forskolin. The lack of additivity between IL-1 and CRF, cholera toxin, 8-bromo-cAMP, and forskolin suggests that IL-1 stimulates ACTH release by a pathway that shares some common step(s) with CRF. Because IL-1 did not affect cAMP accumulation, the effect of IL-1 on protein kinase A (PKA) was investigated. IL-1 began to increase (P < 0.05) PKA activity at 15 min and remained elevated for 2 h before returning to control levels. IL-1 stimulation of PKA and the lack of additivity between IL-1 and CRF, forskolin, and cholera toxin indicate that PKA is the intracellular mediator used by IL-1 to stimulate ACTH release in AtT-20 cells. C1 SHRINERS BURN INST,BOSTON,MA 02114. RP GWOSDOW, AR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BULFINCH 3,FRUIT ST,BOSTON,MA 02114, USA. OI Abou-Samra, Abdul/0000-0001-8735-1142 FU NIDDK NIH HHS [1 R29 DK41419-01A1] NR 27 TC 33 Z9 33 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 FEB PY 1993 VL 132 IS 2 BP 710 EP 714 DI 10.1210/en.132.2.710 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KJ819 UT WOS:A1993KJ81900035 PM 8381071 ER PT J AU MEYER, TE WAEBER, G LIN, J BECKMANN, W HABENER, JF AF MEYER, TE WAEBER, G LIN, J BECKMANN, W HABENER, JF TI THE PROMOTER OF THE GENE ENCODING 3',5'-CYCLIC ADENOSINE-MONOPHOSPHATE (CAMP) RESPONSE ELEMENT BINDING-PROTEIN CONTAINS CAMP RESPONSE ELEMENTS - EVIDENCE FOR POSITIVE AUTOREGULATION OF GENE-TRANSCRIPTION SO ENDOCRINOLOGY LA English DT Article ID CYCLIC-AMP; AUTO-REGULATION; LEUCINE ZIPPER; RNA-POLYMERASE; RECEPTOR GENE; DNA ELEMENTS; FACTOR CREB; ADENOSINE-3',5'-MONOPHOSPHATE; EXPRESSION; ACTIVATION AB The transcriptional transactivational activities of the phosphoprotein cAMP-response element-binding protein (CREB) are activated by the cAMP-dependent protein kinase A signaling pathway. Dimers of CREB bind to the palindromic DNA element 5'-TGACGTCA-3' (or similar motifs) called cAMP-responsive enhancers (CREs) found in the control regions of many genes, and activate transcription in response to phosphorylation of CREB by protein kinase A. Earlier we reported on the cyclical expression of the CREB gene in the Sertoli cells of the rat testis that occurred concomitant with the FSH-induced rise in cellular cAMP levels and suggested that transcription of the CREB gene may be autoregulated by cAMP-dependent transcriptional proteins. We now report the structure of the 5'-flanking sequence of the human CREB gene containing promoter activity. The promoter has a high content of guanosines and cytosines and lacks canonical TATA and CCAAT boxes typically found in the promoters of genes in eukaryotes. Notably, the promoter contains three CREs and transcriptional activities of a promoter-luciferase reporter plasmid transfected to placental JEG-3 cells are increased 3- to 5-fold over basal activities in response to either cAMP or 12-o-tetradecanoyl phorbol-14-acetate, and give 6- to 7-fold responses when both agents are added. The CREs bind recombinant CREB and endogenous CREB or CREB-like proteins contained in placental JEG-3 cells and also confer cAMP-inducible transcriptional activation to a heterologous minimal promoter. Our studies suggest that the expression of the CREB gene is positively autoregulated in trans. C1 MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,50 BLOSSOM ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-25532, DK-30457] NR 51 TC 98 Z9 100 U1 0 U2 3 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD FEB PY 1993 VL 132 IS 2 BP 770 EP 780 DI 10.1210/en.132.2.770 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KJ819 UT WOS:A1993KJ81900043 PM 8381074 ER PT J AU ABOUSAMRA, AB JUPPNER, H KHALIFA, A KARGA, H KONG, XF SCHIFFERALBERTS, D XIE, LY SEGRE, GV AF ABOUSAMRA, AB JUPPNER, H KHALIFA, A KARGA, H KONG, XF SCHIFFERALBERTS, D XIE, LY SEGRE, GV TI PARATHYROID-HORMONE (PTH) STIMULATES ADRENOCORTICOTROPIN RELEASE IN ATT-20 CELLS STABLY EXPRESSING A COMMON RECEPTOR FOR PTH AND PTH-RELATED PEPTIDE SO ENDOCRINOLOGY LA English DT Article ID 3',5'-MONOPHOSPHATE-DEPENDENT PROTEIN-KINASE; ADENYLATE-CYCLASE; ATT20 CELLS; CYCLIC-AMP; COMPARTMENTALIZATION; CALCIUM; ACTIVATION; MECHANISMS; MEMBRANE; STORES AB Complementary DNA encoding a rat bone PTH/PTHrP receptor was stably expressed in the murine corticotroph cell line, AtT-20. Several clones, expressing variable numbers of PTH/PTHrP receptors, were developed. In contrast to the relatively low binding affinity (apparent K(d) = 15 nm) observed in COS-7 cells transiently expressing the PTH/PTHrP receptor, all AtT-20 stable transfectants bound [Nle8,18,Tyr34]bPTH(1-34)NH2 (NlePTH) with an affinity that was indistinguishable from that observed in ROS 17/2.8 cells expressing native PTH/PTHrP receptors. Additionally, NlePTH dramatically increased cAMP accumulation and ACTH release in AtT-20 cells expressing the PTH/PTHrP receptor with an ED50 of 0.6 +/- 0.3 and 0.3 +/- 0.1 nm, respectively. The high binding affinity and the high efficacy of NlePTH in stimulating cAMP accumulation and ACTH release indicate that the PTH/PTHrP receptor is efficiently coupled to the intracellular signalling system responsible for stimulation of ACTH release in AtT-20 cells. No additivity of cAMP accumulation or of ACTH release was observed when these cells were treated with maximally active concentrations of both NlePTH and CRF. This suggests that the receptors for both of these hormones share the same intracellular effectors, and that intracellular signaling in AtT-20 cells is not compartmentalized. Additionally, the ability of NlePTH to stimulate ACTH release in AtT-20 cells, a function that is normally performed by CRF, demonstrates promiscuity between activated receptors and distal biological functions. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP ABOUSAMRA, AB (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114, USA. OI Abou-Samra, Abdul/0000-0001-8735-1142 NR 28 TC 6 Z9 6 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD FEB PY 1993 VL 132 IS 2 BP 801 EP 805 DI 10.1210/en.132.2.801 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KJ819 UT WOS:A1993KJ81900047 PM 7678801 ER PT J AU KELSEY, PJ WARSHAW, AL AF KELSEY, PJ WARSHAW, AL TI EUS - AN ADDED TEST OR A REPLACEMENT FOR SEVERAL SO ENDOSCOPY LA English DT Editorial Material ID ENDOSCOPIC ULTRASONOGRAPHY; PANCREATIC-CANCER; DIAGNOSIS; RESECTABILITY C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,15 PARKMAN ST,SUITE 336,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 12 TC 4 Z9 4 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0013-726X J9 ENDOSCOPY JI Endoscopy PD FEB PY 1993 VL 25 IS 2 BP 179 EP 181 DI 10.1055/s-2007-1010280 PG 3 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA KX966 UT WOS:A1993KX96600008 PM 8491137 ER PT J AU LYNCH, RD TKACHUK, LJ JI, XR RABITO, CA SCHNEEBERGER, EE AF LYNCH, RD TKACHUK, LJ JI, XR RABITO, CA SCHNEEBERGER, EE TI DEPLETING CELL CHOLESTEROL ALTERS CALCIUM-INDUCED ASSEMBLY OF TIGHT JUNCTIONS BY MONOLAYERS OF MDCK CELLS SO EUROPEAN JOURNAL OF CELL BIOLOGY LA English DT Article DE TIGHT JUNCTION ASSEMBLY; MEMBRANE CHOLESTEROL ID ZONULA-OCCLUDENS; EPITHELIAL-CELLS; PROTEINS; MEMBRANES; ISOPRENYLATION AB A role for lipids in the formation of tight junctions (TJ) has been proposed. Attempts to relate changes in whole cell phospholipid composition to the formation of TJs, however, have yielded equivocal results. The object in the present study was to relate changes in TJ of MDCK cells more specifically to alterations in plasma membrane lipids. Cholesterol, which resides primarily in the plasma membrane, was reduced by 25% after incubation of cell monolayers for 24 h in a low Ca2+ medium supplemented with (1-2 muM) Lovastatin, an inhibitor of hydroxymethylglutarylcoenzyme A (HMG-CoA) reductase. This was associated with a halving of the time required for Ca2+ to induce TJ formation as monitored by transepithelial electrical resistance (TER). [H-3]Mannitol flux, and morphometric measurements made on freeze fracture replicas confirm that the effects on TER reflect changes in the characteristics of the paracellular pathway. Peak and steady state values of TER were also elevated over control values. The changes in cholesterol content and the time course for TJ assembly were apparent at levels of Lovastatin which do not affect prenylation of proteins, and were prevented if 5 mm mevalonate was present along with Lovastatin. Paradoxically, despite a decrease of approximately 1/3 in the Ca concentration required to yield maximum rates of TJ assembly, Ca-45(2+) uptake was actually reduced after cholesterol depletion. The data suggest that cholesterol may modulate the properties of membrane proteins and/or phospholipids which interact with Ca2+, possibly on the exoplasmic leaflet, during TJ assembly. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,COX BLDG 5,BOSTON,MA 02114. UNIV MASSACHUSETTS,DEPT BIOL SCI,LOWELL,MA. MASSACHUSETTS GEN HOSP,DEPT NUCL MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL25822] NR 45 TC 18 Z9 18 U1 0 U2 0 PU WISSENSCHAFTLICHE VERLAG MBH PI STUTTGART PA BIRKENWALDSTRASSE 44, POSTFACH 10 10 61, 70009 STUTTGART, GERMANY SN 0171-9335 J9 EUR J CELL BIOL JI Eur. J. Cell Biol. PD FEB PY 1993 VL 60 IS 1 BP 21 EP 30 PG 10 WC Cell Biology SC Cell Biology GA KP777 UT WOS:A1993KP77700003 PM 8462597 ER PT J AU MALANOSKI, GJ ELIOPOULOS, GM FERRARO, MJ MOELLERING, RC AF MALANOSKI, GJ ELIOPOULOS, GM FERRARO, MJ MOELLERING, RC TI EFFECT OF PH VARIATION ON THE SUSCEPTIBILITY OF HELICOBACTER-PYLORI TO 3 MACROLIDE ANTIMICROBIAL AGENTS AND TEMAFLOXACIN SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Note ID ERADICATE CAMPYLOBACTER-PYLORI; STOMACH; ERYTHROMYCIN; ANTIBIOTICS; FAILURE AB The in vitro susceptibility of 27 dinical isolates of Helicobacter pylori to erythromycin, clarithromycin, azithromycin and temafloxacin under various pH conditions was evaluated. Clarithromycin (MIC90 0.03 mug/ml) was found to be significantly more active than either erythromycin (MIC90 0.125 mug/ml) or azithromycin (MIC90 0.25 mug/ml) at a neutral pH. Lowering the pH to 5.75 resulted in a loss in efficacy from 8- to 32-fold for all three macrolides studied. The MIC90 of clarithromycin (0.5 mug/ml) remained lower than those of azithromycin (2 mug/ml) and erythromycin (4 mug/ml). No synergism or antagonism was observed with combinations of clarithromycin and temafloxacin at either the neutral or lower pH values. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MALANOSKI, GJ (reprint author), NEW ENGLAND DEACONESS HOSP,DEPT MED,DIV INFECT DIS,185 PILGRIM RD,BOSTON,MA 02215, USA. NR 13 TC 52 Z9 53 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 FEB PY 1993 VL 12 IS 2 BP 131 EP 133 DI 10.1007/BF01967591 PG 3 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA KU491 UT WOS:A1993KU49100013 PM 8388791 ER PT J AU BRAMSON, RT SHERMAN, JM BLICKMAN, JG AF BRAMSON, RT SHERMAN, JM BLICKMAN, JG TI PEDIATRIC BRONCHOGRAPHY PERFORMED THROUGH THE FLEXIBLE BRONCHOSCOPE SO EUROPEAN JOURNAL OF RADIOLOGY LA English DT Article DE BRONCHOGRAPHY, PEDIATRIC; BRONCHOSCOPE AB Ten children, ranging in age from 2 months to 16 years, were evaluated by bronchograms performed during bronchoscopy. Nine of the ten children had significant pathology demonstrated by the bronchogram that elucidated findings unclear from other imaging procedures at the time of bronchoscopy. Despite the generally negative opinions about the utility of bronchograms in children, information obtained by bronchography can be quite useful. Bronchography during bronchoscopy proved to be quick, simple, and safe. RP BRAMSON, RT (reprint author), MASSACHUSETTS GEN HOSP,DIV PEDIAT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 16 Z9 15 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0720-048X J9 EUR J RADIOL JI Eur. J. Radiol. PD FEB PY 1993 VL 16 IS 2 BP 158 EP 161 DI 10.1016/0720-048X(93)90016-G PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KU499 UT WOS:A1993KU49900016 PM 8462583 ER PT J AU LIANG, TJ JEFFERS, L REDDY, RK SILVA, MO CHEINQUER, H FINDOR, A DEMEDINA, M YARBOUGH, PO REYES, GR SCHIFF, ER AF LIANG, TJ JEFFERS, L REDDY, RK SILVA, MO CHEINQUER, H FINDOR, A DEMEDINA, M YARBOUGH, PO REYES, GR SCHIFF, ER TI FULMINANT OR SUBFULMINANT NON-A, NON-B VIRAL-HEPATITIS - THE ROLE OF HEPATITIS-C AND HEPATITIS-E VIRUSES SO GASTROENTEROLOGY LA English DT Article ID INFECTION; SERUM; RNA; GENOME; LIVER; ASSAY; CDNA; IDENTIFICATION; FAILURE; REGIONS C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV MIAMI,SCH MED,CTR LIVER DIS,MIAMI,FL 33152. VET ADM MED CTR,MIAMI,FL 33125. GENELABS INC,REDWOOD CITY,CA. RP LIANG, TJ (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,GASTROINTESTINAL UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-54524]; NIDDK NIH HHS [DK-01952] NR 38 TC 120 Z9 120 U1 0 U2 4 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 FEB PY 1993 VL 104 IS 2 BP 556 EP 562 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KM861 UT WOS:A1993KM86100028 PM 8381099 ER PT J AU LEFKOWITCH, JH SCHIFF, ER DAVIS, GL PERRILLO, RP LINDSAY, K BODENHEIMER, HC BALART, LA ORTEGO, TJ PAYNE, J DIENSTAG, JL GIBAS, A JACOBSON, IM TAMBURRO, CH CAREY, W OBRIEN, C SAMPLINER, R VANTHIEL, DH FEIT, D ALBRECHT, J MESCHIEVITZ, C SANGHVI, B VAUGHAN, RD AF LEFKOWITCH, JH SCHIFF, ER DAVIS, GL PERRILLO, RP LINDSAY, K BODENHEIMER, HC BALART, LA ORTEGO, TJ PAYNE, J DIENSTAG, JL GIBAS, A JACOBSON, IM TAMBURRO, CH CAREY, W OBRIEN, C SAMPLINER, R VANTHIEL, DH FEIT, D ALBRECHT, J MESCHIEVITZ, C SANGHVI, B VAUGHAN, RD TI PATHOLOGICAL DIAGNOSIS OF CHRONIC HEPATITIS-C - A MULTICENTER COMPARATIVE-STUDY WITH CHRONIC HEPATITIS-B SO GASTROENTEROLOGY LA English DT Article ID LIVER-CELL DYSPLASIA; SPORADIC NON-A; HEPATOCELLULAR-CARCINOMA; POSTTRANSFUSION HEPATITIS; ALCOHOLIC PATIENTS; VIRUS-ANTIBODIES; CONTROLLED TRIAL; INFECTION; TRANSFUSION; FEATURES C1 UNIV MIAMI,MIAMI,FL 33152. UNIV FLORIDA,GAINESVILLE,FL 32611. ST LOUIS VET AFFAIRS MED CTR,ST LOUIS,MO. WASHINGTON UNIV,ST LOUIS,MO 63130. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. MT SINAI MED CTR,NEW YORK,NY 10029. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121. DIGEST DIS ASSOCIATES,HINSDALE,IL. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CORNELL UNIV,MED CTR,NEW YORK HOSP,NEW YORK,NY 10021. UNIV LOUISVILLE,LOUISVILLE,KY 40292. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. HOSP UNIV PENN,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,TUCSON,AZ. UNIV PITTSBURGH,PITTSBURGH,PA 15260. HACKENSACK MED CTR,HACKENSACK,NJ. UNIV ARIZONA,TUCSON,AZ 85721. SCHERING PLOUGH CORP,KENILWORTH,NJ. CONNAUGHT LABS,SWIFTWATER,PA. NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY 10032. RP LEFKOWITCH, JH (reprint author), COLUMBIA UNIV COLL PHYS & SURG,DEPT PATHOL,630 W 168TH ST,NEW YORK,NY 10032, USA. FU NCRR NIH HHS [M01RR01066-11, 5M01RR00082, RR-00865] NR 42 TC 324 Z9 333 U1 2 U2 3 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 FEB PY 1993 VL 104 IS 2 BP 595 EP 603 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KM861 UT WOS:A1993KM86100034 PM 8425703 ER PT J AU SANDERSON, IR WALKER, WA AF SANDERSON, IR WALKER, WA TI UPTAKE AND TRANSPORT OF MACROMOLECULES BY THE INTESTINE - POSSIBLE ROLE IN CLINICAL DISORDERS (AN UPDATE) SO GASTROENTEROLOGY LA English DT Review ID EPIDERMAL GROWTH-FACTOR; INFLAMMATORY BOWEL-DISEASE; RAT SMALL-INTESTINE; GASTROINTESTINAL MUCOSAL BARRIER; RECEPTOR-MEDIATED TRANSPORT; ILEAL EPITHELIAL-CELLS; CATHEPSIN-D ACTIVITIES; MOUSE SMALL-INTESTINE; CELIAC-DISEASE; SUCKLING RAT C1 MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,MUCOSAL IMMUNOL LAB,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. FU NICHD NIH HHS [R01-HD12437]; NIDDK NIH HHS [R01-DK37521, P01-DK33506] NR 199 TC 229 Z9 233 U1 2 U2 10 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 FEB PY 1993 VL 104 IS 2 BP 622 EP 639 PG 18 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KM861 UT WOS:A1993KM86100038 PM 8425707 ER PT J AU GRIMES, R REDDY, SV LEACH, RJ SCARCEZ, T ROODMAN, GD SAKAGUCHI, AY LALLEY, PA WINDLE, JJ AF GRIMES, R REDDY, SV LEACH, RJ SCARCEZ, T ROODMAN, GD SAKAGUCHI, AY LALLEY, PA WINDLE, JJ TI ASSIGNMENT OF THE MOUSE TARTRATE-RESISTANT ACID-PHOSPHATASE GENE (ACP5) TO CHROMOSOME-9 SO GENOMICS LA English DT Note ID MUS-MUSCULUS; EXPRESSION C1 CANC THERAPY & RES CTR,8122 DATAPOINT DR,SAN ANTONIO,TX 78229. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. WAYNE STATE UNIV,SCH MED,DETROIT,MI 48201. OI Windle, Jolene/0000-0001-6690-385X FU NIAMS NIH HHS [AR41336] NR 8 TC 17 Z9 17 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD FEB PY 1993 VL 15 IS 2 BP 421 EP 422 DI 10.1006/geno.1993.1079 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KP145 UT WOS:A1993KP14500026 PM 8449511 ER PT J AU PETTY, EM ARNOLD, A MARX, SJ BALE, AE AF PETTY, EM ARNOLD, A MARX, SJ BALE, AE TI A PULSED-FIELD GEL-ELECTROPHORESIS (PFGE) MAP OF 12 LOCI ON CHROMOSOME-11Q11-Q13 SO GENOMICS LA English DT Note ID SMALL REGION; LONG ARM; ONCOGENE; LOCALIZATION; BCL-1; GENE C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NIDDKD,METAB DIS BRANCH,BETHESDA,MD 20892. RP PETTY, EM (reprint author), YALE UNIV,SCH MED,DEPT FORENS MED,NEW HAVEN,CT 06510, USA. FU NCI NIH HHS [CA55909, CA50497-04]; NIGMS NIH HHS [GM07439] NR 15 TC 8 Z9 8 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD FEB PY 1993 VL 15 IS 2 BP 423 EP 425 DI 10.1006/geno.1993.1080 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KP145 UT WOS:A1993KP14500027 PM 8449512 ER PT J AU FREEMAN, DM HENDRIX, DK SHAH, D FAN, LF WEISS, TF AF FREEMAN, DM HENDRIX, DK SHAH, D FAN, LF WEISS, TF TI EFFECT OF LYMPH COMPOSITION ON AN INVITRO PREPARATION OF THE ALLIGATOR LIZARD COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; INVITRO PREPARATION; LYMPH COMPOSITION; HAIR CELLS ID OUTER HAIR-CELLS; INNER-EAR; INDUCED MOTILITY; GUINEA-PIG; TECTORIAL MEMBRANE; MENIERES-DISEASE; DEPOLARIZATION; TRANSDUCTION; TRANSMISSION; MECHANISM AB The effects of different artificial lymphs on the cochlear duct of the alligator lizard were studied in an in vitro preparation. The duct was dissected and cemented to the glass floor of a chamber that had been filled with an artificial lymph. The vestibular membrane was removed and latex beads (1-5 mum in diameter) were allowed to settle on the endolymphatic surface of the duct. During perfusion with an artificial lymph solution, the positions of beads were measured and video images of the duct were obtained. Artificial lymphs were isosmotic and included artificial endolymph (AE), artificial perilymph (AP), Leibovitz's L-15 culture medium, an AE solution whose calcium concentration was the same as that of AP, and AE and AP solutions in which gluconate was substituted for chloride ions. Results obtained in AE were consistently different from those in other lymphs. The displacements of beads, the projected area of the papilla, the occurrence of blebs, and direct observation of cells in the duct all indicated that the tissue swelled in AE (with or without 2 mmol/l Ca) but showed no consistent shrinking or swelling in any of the other artificial lymphs. Thus for the solutions we used, the presence of both potassium and chloride was required to elicit the swelling response to isosmotic artificial lymphs. There were some regional differences in the swelling response: the swelling of the endolymphatic surface of the tissue in a direction orthogonal to the basilar membrane surface was smaller on the free-standing region of the basilar papilla than either on the tectorial membrane or on the hyaline epithelial cells. The preparation was osmotically stable in AP and in both AE and AP solutions in which gluconate was substituted for chloride ions. After exposure to these solutions for as much as 300 min, the preparation showed no gross signs of deterioration visible with the light microscope, and continued to exhibit a highly specific osmotic response to the composition of the bathing medium. C1 MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114. RP FREEMAN, DM (reprint author), MIT,DEPT ELECT ENGN & COMP SCI,ROOM 36-865,77 MASSACHUSETTS AVE,CAMBRIDGE,MA 02139, USA. NR 38 TC 11 Z9 11 U1 1 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 FEB PY 1993 VL 65 IS 1-2 BP 83 EP 98 DI 10.1016/0378-5955(93)90204-E PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300007 PM 8458762 ER PT J AU STONE, RM MAYER, RJ AF STONE, RM MAYER, RJ TI TREATMENT OF THE NEWLY DIAGNOSED ADULT WITH DENOVO ACUTE MYELOID-LEUKEMIA SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; BONE-MARROW TRANSPLANTATION; ACUTE MYELOGENOUS LEUKEMIA; HIGH-DOSE CYTARABINE; COLONY-STIMULATING FACTOR; ACUTE MYELOCYTIC-LEUKEMIA; ACUTE NONLYMPHOBLASTIC LEUKEMIA; CYTOSINE-ARABINOSIDE THERAPY; ACUTE MYELOBLASTIC-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STONE, RM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115, USA. NR 87 TC 55 Z9 57 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 FEB PY 1993 VL 7 IS 1 BP 47 EP 64 PG 18 WC Oncology; Hematology SC Oncology; Hematology GA KL332 UT WOS:A1993KL33200003 PM 8449864 ER PT J AU STONE, RM MAYER, RJ AF STONE, RM MAYER, RJ TI THE APPROACH TO THE ELDERLY PATIENT WITH ACUTE MYELOID-LEUKEMIA SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID DOSE CYTOSINE-ARABINOSIDE; ACUTE NONLYMPHOCYTIC LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; ACUTE MYELOBLASTIC-LEUKEMIA; COLONY-STIMULATING FACTOR; ACUTE GRANULOCYTIC LEUKEMIA; REFRACTORY ACUTE-LEUKEMIA; ACUTE MYELOCYTIC-LEUKEMIA; NON-LYMPHOCYTIC LEUKEMIA; COOPERATIVE GROUP GIMEMA C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STONE, RM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115, USA. NR 65 TC 25 Z9 25 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 FEB PY 1993 VL 7 IS 1 BP 65 EP 79 PG 15 WC Oncology; Hematology SC Oncology; Hematology GA KL332 UT WOS:A1993KL33200004 PM 7680642 ER PT J AU TAKAHASHI, T LASKER, JM ROSMAN, AS LIEBER, CS AF TAKAHASHI, T LASKER, JM ROSMAN, AS LIEBER, CS TI INDUCTION OF CYTOCHROME P-4502E1 IN THE HUMAN LIVER BY ETHANOL IS CAUSED BY A CORRESPONDING INCREASE IN ENCODING MESSENGER-RNA SO HEPATOLOGY LA English DT Article ID N-NITROSODIMETHYLAMINE DEMETHYLASE; RAT-LIVER; INDUCIBLE CYTOCHROME-P-450; INSITU HYBRIDIZATION; GENE; ACID; DNA; EXPRESSION; SEQUENCES; P450IIE1 AB The propensity of centrilobular liver damage to develop in alcohol abusers after exposure to various hepatotoxins, including ethanol itself, has been linked to the induction by ethanol of P-4502E1, a microsomal P-450 enzyme that bioactivates these agents to reactive metabolites. Whereas long-term ethanol consumption elicits a marked increase in hepatic P-4502E1 content, the molecular mechanism by which ethanol produces this effect is the subject of controversy in animals, and it has not been elucidated in human beings. Possible mechanisms include increased enzyme synthesis stemming from elevated 2E1 messenger RNA levels, enhanced translation of preexisting messenger RNA or stabilization of P-4502E1 protein. To determine which, if any, of these mechanisms underlies P-4502E1 induction in human beings, we examined the effects of ethanol intake on the hepatic intralobular distribution of P-4502E1 messenger RNA and the corresponding protein. Liver sections derived from needle biopsy specimens were obtained from five recently drinking alcoholics (last drink no more than 36 hr before) and eight control subjects (five abstaining alcoholics [last drink 96 hr or more before] and three nondrinkers). In situ hybridization of these liver sections with a hu an P-4502E1 complementary DNA probe was used to localize P-4502E1 messenger RNA transcripts. Quantitative image analysis of hybridized sections from control subjects revealed that P-4502E1 transcript content in perivenular (zone 3) hepatocytes was significantly higher (p < 0.05) than in midzonal (zone 2) and periportal (zone 1) cells (18.3 +/- 1, 9.5 +/- 2 and 3.1 +/- 2 arbitrary density units, respectively, mean +/- S.E.M.). In recent drinkers, acinar regions containing P-4502E1 transcripts were elevated 2.9-fold compared with those in controls (32.8% +/- 7% vs. 11.2% +/- 2%; p < 0.01), with this messenger RNA increase occurring mainly in perivenular cells (29.6 +/- 3 vs. 18.3 +/- 1 units; p < 0.01). P-4502E1 protein distribution, assessed by the immunohistochemical staining of liver sections with P-4502E1 antibodies, was found to be analogous to that of the messenger RNA in control subjects (the level in perivenular cells was greater than that in midzonal cells, which was greater than that in periportal cells), whereas recent drinkers exhibited marked elevations in enzyme content in both perivenular and midzonal hepatocytes. Moreover, cellular levels of P-4502E1 protein and messenger RNA were significantly correlated (r(s) = 0.79; p < 0.001) in all patients. Our results indicate that the induction by ethanol of P-4502E1 protein in human liver tissue is associated with, and appears to stem from, a corresponding increase of P-4502E1 messenger RNA. This ethanol-mediated enhancement of P-4502E1 enzyme levels mediated through the encoding messenger RNA, a process occurring primarily in perivenular hepatocytes, may explain why these cells are preferentially damaged after exposure to P-4502E1-activated hepatotoxins. C1 BRONX VET AFFAIRS MED CTR,ALCOHOL RES CTR,130 W KINGSBRIDGE RD,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,BRONX,NY 10468. MT SINAI MED SCH,NEW YORK,NY 10468. FU NIAAA NIH HHS [AA-03508, AA-05934, AA-07842] NR 47 TC 193 Z9 199 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 FEB PY 1993 VL 17 IS 2 BP 236 EP 245 DI 10.1016/0270-9139(93)90083-Y PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KM171 UT WOS:A1993KM17100012 PM 8428720 ER PT J AU BACHWICH, D DIENSTAG, J AF BACHWICH, D DIENSTAG, J TI APLASTIC-ANEMIA AND HEPATITIS-C - MOLECULAR-BIOLOGY EXONERATES ANOTHER SUSPECT SO HEPATOLOGY LA English DT Article ID NON-B-HEPATITIS; NON-A-HEPATITIS; VIRAL-HEPATITIS; VIRUS; SEQUENCES AB Objective.-To test the hypothesis that the rare, often fatal, syndrome of hepatitis-associated aplasia is associated with hepatitis C virus infection. Design. - Case series. Setting.-Tertiary referral centers in the United States, Japan, Italy, and Germany. Patients.-Twenty-eight patients with onset of aplastic anemia within 90 days after seeking medical attention for jaundice, or having serum transaminase levels 150% or more of normal (hepatitis-associated aplasia patients) and three patients who developed aplastic anemia following liver transplantation for non-A, non-B, hepatitis. Outcome Measures.-Presence of hepatitis C in serum, bone marrow, and liver samples, detected by the polymerase chain reaction; antibody testing, and percentage of activated peripheral cytotoxic T lymphocytes determined by immunophenotyping. Results.-Hepatitis ribonucleic acid was present in the serum samples of 10 (36%) patients with hepatitis-associated aplasia. However, hepatitic C virus viremia was associated with transfusions received after the onset of aplasia: seven (58%) of 12 patients with hepatitis-associated aplasia who had received 21 or more units of blood products at the time of serum sampling were viremic, compared with only three (19%) of 16 patients with hepatitis-associated aplasia who had received 20 or less units of blood products (P < .05). Hepatitis C virus was not found in blood and bone marrow samples of three National Institutes of Health case patients tested at the time of diagnosis. None of three livers from non-A, non-B hepatitis patients who developed aplastic anemia after liver transplantation contained hepatitis C virus ribonucleic acid. Activated CD8+ T lymphocytes were elevated three- to 20-fold early in the course of hepatitis-associated aplasia. Conclusions. - Our results implicate a novel, non-A, non-B, and non-C agent in both hepatitis-associated aplasia and fulminant hepatitis. RP BACHWICH, D (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 12 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD FEB PY 1993 VL 17 IS 2 BP 340 EP 342 DI 10.1016/0270-9139(93)90097-7 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KM171 UT WOS:A1993KM17100026 PM 8381384 ER PT J AU SEDERER, LI SUMMERGRAD, P AF SEDERER, LI SUMMERGRAD, P TI ECONOMIC GRAND ROUNDS - CRITERIA FOR HOSPITAL ADMISSION SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID PSYCHIATRIC-HOSPITALIZATION C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SEDERER, LI (reprint author), MCLEAN HOSP,CLIN SERV,115 MILL ST,BELMONT,MA 02178, USA. NR 20 TC 10 Z9 10 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD FEB PY 1993 VL 44 IS 2 BP 116 EP 118 PG 3 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA KK103 UT WOS:A1993KK10300006 PM 8432494 ER PT J AU MIRZA, NM RELIAS, V YUNIS, EJ PACHAS, WN DASGUPTA, JD AF MIRZA, NM RELIAS, V YUNIS, EJ PACHAS, WN DASGUPTA, JD TI DEFECTIVE SIGNAL TRANSDUCTION VIA T-CELL RECEPTOR-CD3 STRUCTURE IN T-CELLS FROM RHEUMATOID-ARTHRITIS PATIENTS SO HUMAN IMMUNOLOGY LA English DT Article ID SYNOVIAL-FLUID LYMPHOCYTES; CYTOPLASMIC FREE CALCIUM; PROTEIN-KINASE-C; CLASS-I ANTIGENS; TYROSINE PHOSPHORYLATION; MONOCLONAL-ANTIBODIES; PHORBOL-ESTER; HLA-DR; ACTIVATION; EXPRESSION AB T cells from patients with active RA are known to produce low levels of IL-2 and proliferate poorly in response to various mitogenic stimuli. The present work shows that cross-linking of CD3 antigen on patients' T-cell surface induces two- to threefold lower Ca2+ response than in T cells from age-matched controls. Immunofluorescence studies indicate that the attenuated signal may be due to the suppressed expression of CD3 and/or CD45 molecules on patients' T cells. In the majority of the patients, the level of CD45 expression is reduced by 60%-70% as compared with that in the control T cells. Therefore, the poor mitogenic response of patient cells is apparently due to a defect in early stages of signal transduction through the T-cell receptor (TCR-CD3). C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,44 BINNEY ST,BOSTON,MA 02115. SPAULDING REHABIL HOSP,BOSTON,MA 02114. NR 57 TC 25 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD FEB PY 1993 VL 36 IS 2 BP 91 EP 98 DI 10.1016/0198-8859(93)90111-D PG 8 WC Immunology SC Immunology GA KW824 UT WOS:A1993KW82400004 PM 8463125 ER PT J AU FIENBERG, R MARK, EJ GOODMAN, M MCCLUSKEY, RT NILES, JL AF FIENBERG, R MARK, EJ GOODMAN, M MCCLUSKEY, RT NILES, JL TI CORRELATION OF ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES WITH THE EXTRARENAL HISTOPATHOLOGY OF WEGENERS (PATHERGIC) GRANULOMATOSIS AND RELATED FORMS OF VASCULITIS SO HUMAN PATHOLOGY LA English DT Article DE ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES; WEGENERS GRANULOMATOSIS; POLYARTERITIS-NODOSA; PULMONARY CAPILLARITIS; CHURG-STRAUSS SYNDROME; PATHERGIC ID MYELOID LYSOSOMAL-ENZYMES; CHURG-STRAUSS-SYNDROME; SYSTEMIC VASCULITIS; NEUTROPHIL-CYTOPLASM; ANTICYTOPLASMIC AUTOANTIBODIES; CRESCENTIC GLOMERULONEPHRITIS; MICROSCOPIC POLYARTERITIS; PULMONARY HEMORRHAGE; DIAGNOSIS; BIOPSY C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,COX 5,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. FU NIDDK NIH HHS [5 RO1 DK42722] NR 51 TC 68 Z9 68 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD FEB PY 1993 VL 24 IS 2 BP 160 EP 168 DI 10.1016/0046-8177(93)90295-R PG 9 WC Pathology SC Pathology GA KP034 UT WOS:A1993KP03400008 PM 8381764 ER PT J AU CANTOR, H CRUMP, AL RAMAN, VK LIU, H MARKOWITZ, JS GRUSBY, MJ GLIMCHER, LH AF CANTOR, H CRUMP, AL RAMAN, VK LIU, H MARKOWITZ, JS GRUSBY, MJ GLIMCHER, LH TI IMMUNOREGULATORY EFFECTS OF SUPERANTIGENS - INTERACTIONS OF STAPHYLOCOCCAL ENTEROTOXINS WITH HOST MHC AND NON-MHC PRODUCTS SO IMMUNOLOGICAL REVIEWS LA English DT Review ID CLASS-II MOLECULES; ACQUIRED IMMUNODEFICIENCY SYNDROME; T-CELLS; MONOCLONAL-ANTIBODIES; VIRUS-INFECTION; IMMUNE-RESPONSE; INTEGRIN VLA-4; RECEPTOR; ANTIGENS; COMPLEX C1 HARVARD UNIV,SCH MED,DEPT PATHOL,IMMUNOPATHOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. RP CANTOR, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI13600, AI31541, AI12184] NR 68 TC 24 Z9 24 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0105-2896 J9 IMMUNOL REV JI Immunol. Rev. PD FEB PY 1993 VL 131 BP 27 EP 42 DI 10.1111/j.1600-065X.1993.tb01528.x PG 16 WC Immunology SC Immunology GA KV852 UT WOS:A1993KV85200002 PM 8486393 ER PT J AU BOVERI, JF PARRY, RL RUFFIN, WK GUSTAFSON, ML LEE, KW HE, WW DONAHOE, PK AF BOVERI, JF PARRY, RL RUFFIN, WK GUSTAFSON, ML LEE, KW HE, WW DONAHOE, PK TI TRANSFECTION OF THE MULLERIAN INHIBITING SUBSTANCE GENE INHIBITS LOCAL AND METASTATIC TUMOR-GROWTH SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE MULLERIAN INHIBITING SUBSTANCE; GENE TRANSFECTION; TUMOR INHIBITION; METASTASES ID OVARIAN FOLLICULAR-FLUID; HUMAN CANCER-CELLS; FACTOR-BETA; COLONY GROWTH; NUDE-MICE; RB GENE; PURIFICATION; EXPRESSION; MELANOMA; PROTEIN AB Mullerian Inhibiting Substance (MIS), a gonadal growth factor important in sexual differentiation, has antiproliferative activity against several human carcinoma cell lines. In this study, we examine the effect of MIS-transfection on the growth characteristics of Chinese hamster ovary (CHO) and human ocular melanoma (OM431) cells, compared to wild-type lines and a CHO line transfected with a noncleavable, inactive MIS mutant. MIS-transfection inhibited proliferation of CHO cells in double-layer agarose, tumor spheroid, and murine subrenal capsule assays, as well as growth of CHO and OM431 cells in pulmonary metastasis studies. These results anticipate further study of targeted gene therapy of certain human tumors with MIS gene constructs. C1 MASSACHUSETTS GEN HOSP,DIV GYNECOL ONCOL & SURG ONCOL,PEDIAT SURG SERV,BOSTON,MA 02114. VINCENT MEM HOSP,PEDIAT SURG SERV,PEDIAT SURG RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NR 52 TC 7 Z9 7 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 FEB PY 1993 VL 2 IS 2 BP 135 EP 143 PG 9 WC Oncology SC Oncology GA KJ433 UT WOS:A1993KJ43300002 PM 21573527 ER PT J AU TEICHER, BA HOLDEN, SA ARA, G LIU, JTC ROBINSON, MF FLODGREN, P DUPUIS, N NORTHEY, D AF TEICHER, BA HOLDEN, SA ARA, G LIU, JTC ROBINSON, MF FLODGREN, P DUPUIS, N NORTHEY, D TI CYCLOOXYGENASE INHIBITORS - INVITRO AND INVIVO EFFECTS ON ANTITUMOR ALKYLATING-AGENTS IN THE EMT-6 MURINE MAMMARY-CARCINOMA SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE CYCLOOXYGENASE INHIBITORS; ALKYLATING AGENTS; MAMMARY CARCINOMA ID LEWIS LUNG-CARCINOMA; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; L5178Y LYMPHOBLASTS INVITRO; GLUTATHIONE S-TRANSFERASES; THROMBOXANE SYNTHESIS; COLON CARCINOGENESIS; TUMOR-CELLS; PROSTAGLANDIN; INDOMETHACIN; SULINDAC AB The nonsteroidal antiinflammatory drugs that inhibit cyclooxygenase block the formation of prostanoids in vivo. These agents may be useful as modulators of cytotoxic anticancer therapies. EMT-6 mouse mammary carcinoma cells growing in culture were exposed for 1 h or 24 h to eleven different nonsteroidal antiinflammatory agents or acetaminophen. None of these drugs was very cytotoxic. A concentration of 50muM of the nonsteroidal antiinflammatory drugs or acetaminophen was chosen for modulator combination studies with the antitumor alkylating agents CDDP, L-PAM, BCNU and 4-HC in cell culture. Several of the modulators protected the EMT-6 cells from the cytotoxicity of the antitumor alkylating agents; however, diflunisal, sulindac, indomethacin, acetaminophen and in some cases ibuprofen and tolmetin were positive modulators of the antitumor alkylating agents under the cell culture conditions tested. EMT-6 tumor cell survival studies and bone marrow CFU-GM survival studies were carried out with seven of the modulators and various doses of cyclophosphamide. Tolmetin, ibuprofen, sulindac, piroxicam and diflunisal in combination with cyclophosphamide produced increased tumor cell killing compared with cyclophosphamide alone without marked changes in toxicity to the bone marrow derived CFU-GM. In EMT-6 tumor growth delay experiments, none of the six modulators tested affected the growth of the tumors; however, tolmetin, ibuprofen, diflunisal and sulindac increased the tumor growth delay obtained with standard dose-schedules of cyclophosphamide or CDDP. When minocycline, a collagenase inhibitor, was added to treatment regimens including diflunisal or sulindac and either cyclophosphamide, CDDP or L-PAM further increases in tumor growth delay were obtained especially when L-PAM was the cytotoxic therapeutic agent. The number of lung metastases and the percentage lung metastases with diameters >3 mm were reduced by treatment with the modulator combinations alone and further reduced with the addition of the antitumor alkylating agents. These results indicate that agents which inhibit signaling pathways among tumor cells and between tumor cells and normal cells can be useful additions to cytotoxic therapies. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 54 TC 12 Z9 12 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 FEB PY 1993 VL 2 IS 2 BP 145 EP 153 PG 9 WC Oncology SC Oncology GA KJ433 UT WOS:A1993KJ43300003 PM 21573528 ER PT J AU MACARTHUR, CJ GLIKLICH, R MCGILL, TJI PEREZATAYDE, A AF MACARTHUR, CJ GLIKLICH, R MCGILL, TJI PEREZATAYDE, A TI SINUS COMPLICATIONS IN MUCOPOLYSACCHARIDOSIS I H/S (HURLER-SCHEIE SYNDROME) SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY LA English DT Article DE HURLER-SCHEIE SYNDROME; MUCOPOLYSACCARIDOSES; NASAL POLYPOSIS; ANTRAL-CHOANAL POLYP; ENDOSCOPIC SINUS SURGERY AB Hurler-Scheie syndrome is a genetic compound of two mucopolysaccharidoses, the Hurler and Scheie syndromes. The genetic error of metabolism caused by this syndrome produces intermediary systemic effects in the affected individuals. Lacking the enzyme alpha-L-iduronidase, glycosaminoglycans are deposited in the tissues, causing multiple systemic effects and creating many problems for the otolaryngologist. Although early bone marrow transplantation is currently being performed to prevent or reverse many of the systemic manifestations of this disorder, there remains a large population of children past the age at which bone marrow transplantation can be effective. Sinus complications have not previously been reported in the mucopolysaccharidoses and may be more frequently recognized as these patients' longevity increases. We present a patient with Hurler-Scheie syndrome who developed severe nasal polyposis requiring sinus endoscopic removal. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP MACARTHUR, CJ (reprint author), UNIV CALIF IRVINE,DEPT OTOLARYNGOL,101 CITY DR,ORANGE,CA 92668, USA. NR 8 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-5876 J9 INT J PEDIATR OTORHI JI Int. J. Pediatr. Otorhinolaryngol. PD FEB PY 1993 VL 26 IS 1 BP 79 EP 87 DI 10.1016/0165-5876(93)90199-D PG 9 WC Otorhinolaryngology; Pediatrics SC Otorhinolaryngology; Pediatrics GA KN983 UT WOS:A1993KN98300009 PM 8444549 ER PT J AU DAHLBERG, WK LITTLE, JB FLETCHER, JA SUIT, HD OKUNIEFF, P AF DAHLBERG, WK LITTLE, JB FLETCHER, JA SUIT, HD OKUNIEFF, P TI RADIOSENSITIVITY INVITRO OF HUMAN SOFT-TISSUE SARCOMA CELL-LINES AND SKIN FIBROBLASTS DERIVED FROM THE SAME PATIENTS SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY LA English DT Article ID RADIATION-THERAPY; SURVIVAL CURVES; HUMAN-TUMORS; RADIOTHERAPY; CANCER; HEAD; NECK; RADIORESPONSIVENESS AB Skin fibroblast cell strains and tumour cell lines were established from 12 patients with various types of soft tissue neoplasms, and radiation survival curve parameters were measured in vitro. Soft tissue sarcoma cells were consistently more sensitive to X-irradiation than fibroblasts isolated from the same patient, and were also more sensitive as a group than cell lines derived from 34 other human tumours. There was a general correlation in radiosensitivity between fibroblasts and tumour cells derived from the same patient, indicating that some component of tumour cell sensitivity may relate to genetic factors in the host. Such genetic factors, however, do not explain all of the heterogeneity in tumour cell response. The response of soft tissue sarcoma in vivo may be dependent on complex radiomodifying factors other than inherent radiation sensitivity, thus making it difficult to predict clinical outcome by use of assays which use survival of irradiated tumour cell lines in vitro as an endpoint. C1 HARVARD UNIV,SCH PUBL HLTH,RADIOBIOL LAB,665 HUNTINGTON AVE,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. FU NCI NIH HHS [CA48096, CA13311, CA47542] NR 25 TC 45 Z9 45 U1 0 U2 2 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0955-3002 J9 INT J RADIAT BIOL JI Int. J. Radiat. Biol. PD FEB PY 1993 VL 63 IS 2 BP 191 EP 198 DI 10.1080/09553009314550251 PG 8 WC Biology; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA KL919 UT WOS:A1993KL91900007 PM 8094415 ER PT J AU ETHIER, CR COLOMA, FM DEKATER, AW ALLINGHAM, RR AF ETHIER, CR COLOMA, FM DEKATER, AW ALLINGHAM, RR TI RETROPERFUSION STUDIES OF THE AQUEOUS OUTFLOW SYSTEM .1. EVALUATION OF TECHNIQUE USING N-ETHYL MALEIMIDE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE AQUEOUS OUTFLOW PATHWAY; ANGULAR AQUEOUS PLEXUS; BOVINE EYE; MORPHOLOGY; SCHLEMM CANAL; WASHOUT ID TRABECULAR MESHWORK; INTRAOCULAR-PRESSURE; CYNOMOLGUS MONKEY; CYTOCHALASIN-B; HUMOR OUTFLOW; RESISTANCE; FACILITY; SCHLEMM; ROUTES; EYES AB Purpose. The goal of this study was to develop a new technique to deliver drugs or other agents to the lumen of the angular aqueous plexus/Schlemm's canal (AAP/SC) while bypassing the trabecular meshwork, thereby gaining insight into AAP/SC inner wall function. Methods. The anterior chamber is held at a small negative pressure and fluid is allowed to flow retrograde from the limbal vessels, through the collector channels, and into the AAP/SC (''retroperfusion''). Facility measurements are combined with histologic and tracer studies in bovine eyes. Results. (1) Retroperfusion with a saline solution does not alter facility or change outflow pathway morphology; (2) fluid is able to move retrograde from the scleral surface and enter the lumen of the AAP; and (3) retroperfusion with N-ethyl maleimide causes a dose-dependent increase in washout rate and concomitant inner wall breaks. Conclusions. It is hypothesized that the observed increase in washout is due to leakage of extracellular materials through breaks in the inner wall. C1 UNIV TORONTO,INST BIOMED ENGN,TORONTO M5S 1A4,ONTARIO,CANADA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. RP ETHIER, CR (reprint author), UNIV TORONTO,DEPT MECH ENGN,5 KINGS COLL RD,TORONTO M5S 1A4,ONTARIO,CANADA. NR 19 TC 2 Z9 2 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 FEB PY 1993 VL 34 IS 2 BP 385 EP 394 PG 10 WC Ophthalmology SC Ophthalmology GA KP018 UT WOS:A1993KP01800015 PM 8440593 ER PT J AU FAZELY, F SHARMA, PL FRATAZZI, C GREENE, MF WYAND, MS MEMON, MA PENNINCK, D RUPRECHT, RM AF FAZELY, F SHARMA, PL FRATAZZI, C GREENE, MF WYAND, MS MEMON, MA PENNINCK, D RUPRECHT, RM TI SIMIAN IMMUNODEFICIENCY VIRUS-INFECTION VIA AMNIOTIC-FLUID - A MODEL TO STUDY FETAL IMMUNOPATHOGENESIS AND PROPHYLAXIS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE ANIMAL MODEL; PEDIATRIC AIDS; ULTRASOUND-GUIDED INOCULATION OF AMNIOTIC FLUID; PLACENTAL INFECTION ID CYTOTOXIC LYMPHOCYTES-T; RHESUS-MONKEYS; HIV-1 INFECTION; AIDS VIRUS; TRANSMISSION; MACAQUES; RETROVIRUS; SEQUENCE; FETUS; CELLS AB The rising prevalence of infection with the human immunodeficiency cy virus type 1 (HIV-1) in young women will increase the number of infected children worldwide. Because HIV-1 seems to be transmitted mostly intrapartum, fetal infection probably occurs mainly via skin or mucous membrane exposure. A model for this route of fetal infection has been established in primates. After injecting the simian immunodeficiency virus (SIV) into amniotic fluid during late gestation, six of seven rhesus monkeys were born infected. All infected neonates were viable and showed signs of disease, such as low birth weights, lymphadenopathy, and rashes. Cytotoxic T-cell responses to SIV were absent in neonates, but present in mothers. The high fetal infection rate allows studies of lentiviral immunopathogenesis during ontogeny and the development of strategies to prevent maternal HIV-1 transmission. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. TSI MASON LABS,WORCESTER,MA. TUFTS UNIV,SCH VET MED,DEPT MED,N GRAFTON,MA. TUFTS UNIV,SCH VET MED,DEPT SURG,N GRAFTON,MA. FU NCIRD CDC HHS [IP30 28691-01]; NIAID NIH HHS [R01-AI-32330] NR 39 TC 40 Z9 40 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD FEB PY 1993 VL 6 IS 2 BP 107 EP 114 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KK252 UT WOS:A1993KK25200001 PM 8433276 ER PT J AU YAO, XJ GARZON, S BOISVERT, F HASELTINE, WA COHEN, EA AF YAO, XJ GARZON, S BOISVERT, F HASELTINE, WA COHEN, EA TI THE EFFECT OF VPU ON HIV-1-INDUCED SYNCYTIA FORMATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1; CYTOPATHIC EFFECTS; VPU; SYNCYTIA ID IMMUNODEFICIENCY-VIRUS TYPE-1; HTLV-III/LAV ENVELOPE; HIV-1; GENE; REPLICATION; PROTEIN; IDENTIFICATION; GLYCOPROTEIN; RNAS; NEF AB To investigate the role of vpu in the cytopathicity of human immunodeficiency type 1 (HIV-1), the MT4 CD4+ T-cell line was infected with viruses that were isogenic except for their ability to produce the vpu protein. The experiments described here demonstrate that expression of vpu reduces HIV-1 cytopathic effects by decreasing the rate of syncytia formation. By reducing the concentration of gp 120 at the cell surface, vpu limits cell killing by syncytia formation. C1 UNIV MONTREAL,FAC MED,DEPT MICROBIOL & IMMUNOL,RETROVIROL HUMAINE LAB,MONTREAL H3C 3J7,QUEBEC,CANADA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. FU NCI NIH HHS [P30 CA06516]; PHS HHS [A124845, P30 A128691] NR 21 TC 46 Z9 46 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD FEB PY 1993 VL 6 IS 2 BP 135 EP 141 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KK252 UT WOS:A1993KK25200005 PM 8094456 ER PT J AU PLATT, R ZUCKER, JR ZALEZNIK, DF HOPKINS, CC DELLINGER, EP KARCHMER, AW BRYAN, CS BURKE, JF WIKLER, MA MARINO, SK HOLBROOK, KF TOSTESON, TD AF PLATT, R ZUCKER, JR ZALEZNIK, DF HOPKINS, CC DELLINGER, EP KARCHMER, AW BRYAN, CS BURKE, JF WIKLER, MA MARINO, SK HOLBROOK, KF TOSTESON, TD TI PERIOPERATIVE ANTIBIOTIC-PROPHYLAXIS AND WOUND-INFECTION FOLLOWING BREAST SURGERY SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article; Proceedings Paper CT MEETING ON PROPHYLAXIS AT THE MARGINS CY MAY 09-10, 1992 CL BISHOPSTROWE, ENGLAND ID META-ANALYSIS; SCIENTIFIC DISCIPLINE; CLINICAL-TRIALS C1 NEW ENGLAND DEACONESS HOSP,INFECT CONTROL UNIT,BOSTON,MA 02215. BETH ISRAEL HOSP,INFECT CONTROL UNIT,BOSTON,MA 02215. SMITHKLINE BEECHAM LABS,DIV ANTIINFECT,PHILADELPHIA,PA. BRIGHAM & WOMENS HOSP,INFECT CONTROL UNIT,BOSTON,MA 02115. CHANNING LABS,INFECT CONTROL UNIT,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INFECT CONTROL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. UNIV WASHINGTON,DEPT SURG,SEATTLE,WA 98195. UNIV WASHINGTON,HARBORVIEW MED CTR,SEATTLE,WA 98104. UNIV S CAROLINA,COLUMBIA,SC 29208. RP PLATT, R (reprint author), CHANNING LABS,DEPT MED,180 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 11 TC 51 Z9 52 U1 0 U2 1 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD FEB PY 1993 VL 31 SU B BP 43 EP 48 PG 6 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA KQ824 UT WOS:A1993KQ82400006 PM 8449845 ER PT J AU TORRES, A KACMAREK, RM KIMBALL, WR QVIST, J STANEK, K WHYTE, R ZAPOL, WM AF TORRES, A KACMAREK, RM KIMBALL, WR QVIST, J STANEK, K WHYTE, R ZAPOL, WM TI REGIONAL DIAPHRAGMATIC LENGTH AND EMG ACTIVITY DURING INSPIRATORY PRESSURE SUPPORT AND CPAP IN AWAKE SHEEP SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE QUIET BREATHING; ESOPHAGEAL PRESSURE; TRANSDIAPHRAGMATIC PRESSURE; GASTRIC PRESSURE; CRURAL; COSTAL ID MECHANICAL VENTILATION; RESPONSES; MUSCLES AB We examined diaphragmatic mechanics in awake sheep during quiet breathing (QB) and the randomized application of 5, 10, and 15 cmH2O continuous positive airway pressure (CPAP), inspiratory pressure support (IPS), and equal combinations of IPS and CPAP (IPS/CPAP). We measured esophageal, gastric, and transphragmatic (Pdi) pressures and regional length, shortening, and electromyogram (EMG) activity of both costal and crural diaphragmatic segments. Segmental resting length normalized to QB decreased during 15 cmH2O CPAP (costal, 19.2 +/- 3.3%; crural, 7.5 +/- 2.1%; P < 0.05) and during 15/15 cmH2O IPS/CPAP (costal 25.3 +/- 4.8%, crural 9.9 +/- 2.6%; P < 0.05). Only during 15 cmH2O IPS did costal shortening fraction increase (67% QB; P < 0.05). Compared with QB, during 15 cmH2O CPAP, end-tidal CO2 increased 6 Torr, regional EMG activity increased threefold, and Pdi increased 58%. During 15 cmH2O IPS these values decreased 3 Torr, threefold, and 44%, respectively, but during IPS/CPAP they remained unchanged. Expiratory gastric pressure (Exp-Pga) reached 4.3 +/- 0.4 cmH2O at 15 cmH2O CPAP, but during IPS/CPAP Exp-Pga was less (maximum of 1.7 +/- 0.4 CmH2O) than at comparable CPAP (P < 0.05), despite the shorter diaphragmatic length. We conclude that 1) IPS alters the actions of the diaphragm during CPAP, 2) Exp-Pga is poorly coupled to diaphragmatic end-expiratory length, and 3) both IPS and the release of Exp-Pga assist active diaphragmatic shortening. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RESP CARE,BOSTON,MA 02114. RP TORRES, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-23591] NR 19 TC 11 Z9 11 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD FEB PY 1993 VL 74 IS 2 BP 695 EP 703 PG 9 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA KN704 UT WOS:A1993KN70400027 PM 8458784 ER PT J AU THOMPSON, BT STEIGMAN, DM SPENCE, CL JANSSENS, SP HALES, CA AF THOMPSON, BT STEIGMAN, DM SPENCE, CL JANSSENS, SP HALES, CA TI CHRONIC HYPOXIC PULMONARY-HYPERTENSION IN THE GUINEA-PIG - EFFECT OF 3 LEVELS OF HYPOXIA SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE PULMONARY VASCULAR RESISTANCE; COR PULMONALE; RIGHT VENTRICULAR HYPERTROPHY; POLYCYTHEMIA; HYPOXIC VASOCONSTRICTION ID HIGH-ALTITUDE; CIRCULATION; ARTERIES; DISEASE; GROWTH; CATTLE; RATS AB Chronic hypoxia [inspiratory Po2 (PI(O2)) = 76 Torr for 10 days] produces pulmonary hypertension and vascular remodeling in the guinea pig. Increasing the duration of hypoxia from 10 to 21 days does not increase further pulmonary arterial pressure or medial thickening. To see if increasing severity of hypoxia affects the magnitude of pulmonary hypertension and remodeling, we exposed three groups of male Hartley guinea pigs to three levels of normobaric hypoxia for 10 days: PI(O2) = 90 (n = 6), 78 (n = 6), and 65 Torr (n = 5). Pulmonary arterial pressure increased from 14 +/- 1 (+/- SE, n = 7) in room air to 23 +/- 3 mmHg when PI(O2) = 90 Torr (P < 0.05). Pulmonary arterial pressure was slightly higher when PI(O2) - 78 or 65 Torr (25 +/- 1 and 26 +/- 1 mmHg, respectively) but did not reach statistical significance vs. PI(O2) = 90 Torr. Total pulmonary vascular resistance increased from 0.049 +/- 0.004 in room air to between 0.084 +/- 0.006 and 0.101 +/- 0.003 mmHg . min . kg . ml-1 (P < 0.05) in the three hypoxic groups; again there was no difference in total pulmonary vascular resistance among hypoxic groups. Medial thickness of alveolar duct and terminal bronchiole arteries increased with hypoxia, but there was no significant difference among the hypoxic groups. The percentage of intra-acinar vessels with thick walls (a measure of muscular extension) increased when PI(O2) = 78 Torr and nearly doubled when PI(O2) = 65 Torr in comparison to control. We conclude that increasing the severity of hypoxia in the guinea pig does not result in greater pulmonary hypertension or medial thickening but does increase the degree of vascular extension. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP THOMPSON, BT (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,PULM CRIT CARE UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-07354, HL-39150] NR 19 TC 12 Z9 12 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD FEB PY 1993 VL 74 IS 2 BP 916 EP 921 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA KN704 UT WOS:A1993KN70400060 PM 8458815 ER PT J AU LITWIN, CM CALDERWOOD, SB AF LITWIN, CM CALDERWOOD, SB TI CLONING AND GENETIC-ANALYSIS OF THE VIBRIO-VULNIFICUS-FUR GENE AND CONSTRUCTION OF A FUR MUTANT BY INVIVO MARKER EXCHANGE SO JOURNAL OF BACTERIOLOGY LA English DT Article ID CYTOTOXIN-HEMOLYSIN GENE; IRON UPTAKE SYSTEM; ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; REGULATORY GENE; CONSTITUTIVE EXPRESSION; SALMONELLA-TYPHIMURIUM; ELASTOLYTIC PROTEASE; SUICIDE VECTOR; VIRULENCE AB Vibrio vulnificus infections have been associated with iron overload and preexisting liver disease. Iron may play a major role in the pathogenesis of V. vulnificus infections. Many virulence genes, as well as genes involved in the transport of iron by bacteria, are regulated by iron, with increased expression under low-iron conditions. In Escherichia coli and Vibrio cholerae, transcriptional regulation by iron depends on the fur gene. We utilized Southern hybridization under low- and high-stringency conditions with both E. coli and V. cholerae fur gene probes to demonstrate that there are fur-homologous sequences in the DNAs of V. vulnificus, Vibrio fischeri, and Aeromonas sp. but not in the DNAs of the other bacterial species tested. We developed a restriction map and cloned the fur-homologous sequence from V. vulnificus. The hybridizing clone of V. vulnificus chromosomal DNA complemented a V. cholerae fur mutant. DNA sequence analysis confirmed the presence of a 149-amino-acid open reading frame that was 77% homologous to E. coli Fur and 93% homologous to V. cholerae Fur. Primer extension localized a single promoter for the V. vulnificus fur gene. Northern (RNA) blot analysis and beta-galactosidase assays of an operon fusion to lacZ suggested that there was not significant regulation of transcription of V. vulnificus fur by iron or the E. coli Fur protein. We used marker exchange to construct a V. vulnificus fur deletion mutant and confirmed its phenotype by observing overexpression of iron-regulated outer membrane proteins on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The fur deletion mutant of V. vulnificus will be helpful in future studies of the role of iron in V. vulnificus pathogenesis. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. RP LITWIN, CM (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. OI Litwin, Christine/0000-0002-4311-7714 FU NIAID NIH HHS [AI27329]; NIGMS NIH HHS [N01-GM-7-2110] NR 65 TC 68 Z9 70 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD FEB PY 1993 VL 175 IS 3 BP 706 EP 715 PG 10 WC Microbiology SC Microbiology GA KJ722 UT WOS:A1993KJ72200019 PM 7678593 ER PT J AU HALL, SD KANE, MF KOLODNER, RD AF HALL, SD KANE, MF KOLODNER, RD TI IDENTIFICATION AND CHARACTERIZATION OF THE ESCHERICHIA-COLI RECT PROTEIN, A PROTEIN ENCODED BY THE RECE REGION THAT PROMOTES RENATURATION OF HOMOLOGOUS SINGLE-STRANDED-DNA (J BACTERIOL, VOL 175, PG 278, 1993) SO JOURNAL OF BACTERIOLOGY LA English DT Correction, Addition C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. RP HALL, SD (reprint author), HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. NR 1 TC 2 Z9 2 U1 3 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD FEB PY 1993 VL 175 IS 4 BP 1211 EP 1211 PG 1 WC Microbiology SC Microbiology GA KL849 UT WOS:A1993KL84900041 ER PT J AU TRIPPEL, SB WROBLEWSKI, J MAKOWER, AM WHELAN, MC SCHOENFELD, D DOCTROW, SR AF TRIPPEL, SB WROBLEWSKI, J MAKOWER, AM WHELAN, MC SCHOENFELD, D DOCTROW, SR TI REGULATION OF GROWTH-PLATE CHONDROCYTES BY INSULIN-LIKE GROWTH-FACTOR I AND BASIC FIBROBLAST GROWTH-FACTOR SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID RABBIT ARTICULAR CHONDROCYTES; SULFATED PROTEOGLYCAN SYNTHESIS; SOMATOMEDIN-C; DNA-SYNTHESIS; RAT CALVARIA; IGF-I; CELL-PROLIFERATION; MONOLAYER-CULTURE; HORMONE; CARTILAGE AB A study was performed in order to investigate the possible functional roles of insulin-like growth-factor I (IGF-I) and basic fibroblast growth factor (bFGF) in the regulation of mitotic and metabolic activity of growth-plate chondrocytes. Chondrocytes from the distal radial growth plates of calves and the costal physeal cartilage of rats were exposed to these factors, individually and in combination, in primary monolayer culture, to assess their effects. The data showed that bFGF had both a greater potency and a greater efficacy as a mitogen for bovine growth-plate chondrocytes than did IGF-I. The maximum incorporation of H-3-thymidine by bFGF was 8.3 times that in serum-free (control) cultures; the maximum stimulation of incorporation by IGF-I was 2.5 times that in the control medium. In contrast, IGF-I stimulated a maximum incorporation of S-35-sulfate into glycosaminoglycans that was 2.6 times that in the IGF-I se rum-free control cultures, while bFGF had no effect or was mildly inhibitory. When used together, these two factors acted synergistically. Incorporation of H-3-thymidine was more than two times greater than the sum of the effects of the growth factors when used alone and 20.5 times greater than that of the growth factor-free control cultures. Physeal chondrocytes from six-day-old rats were mitotically more responsive to bFGF than to IGF-I, but they were more responsive to IGF-I when they had been derived from twenty-eight-day-old rats. Interaction between bFGF and factors in the serum enhanced the mitotic activity of the rat chondrocytes, but bFGF did not interact with IGF-I under the same experimental conditions. In the presence of bFGF, there was a reduction in the stimulation by IGF-I of incorporation of S-35-sulfate and a decrease in the percentage of chondrocytes containing alkaline phosphatase. These growth factors also influenced cellular morphology in culture. In the presence of IGF-I or serum, the rat chondrocytes manifested the polygonal morphology typical of chondrocytes in culture, while bFGF promoted a more elongated spindle shape. Removal of bFGF and replacement by IGF-I restored the polygonal morphology, indicating that this transition is reversible. CLINICAL RELEVANCE: These results suggest that both IGF-I and bFGF participate in the regulation of skeletal growth and that they differ with regard to the specific cellular functions that they regulate. IGF-I stimulates both cellular mitotic activity and synthesis of extracellular matrix. Although bFGF appeared to be a more efficacious and more potent mitogen than IGF-I, it failed to stimulate the differentiated chondrocyte functions that were tested. These data are consistent with a general anabolic role for IGF-I in the growth plate and with the support of an immature, proliferative cellular phenotype for bFGF. The data also suggest that IGF-I and bFGF interact to regulate skeletal growth and development. Such interactions offer a more versatile means of regulation of growth than would be afforded by the two factors acting independently. Additional studies are needed to elucidate the mechanisms underlying these relationships and their application in vivo. C1 ALKERMES,CAMBRIDGE,MA 02139. KAROLINSKA INST,INST MED NOBEL,S-10401 STOCKHOLM 60,SWEDEN. RP TRIPPEL, SB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [AR31068] NR 54 TC 108 Z9 117 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD FEB PY 1993 VL 75A IS 2 BP 177 EP 189 PG 13 WC Orthopedics; Surgery SC Orthopedics; Surgery GA KM708 UT WOS:A1993KM70800004 PM 8423178 ER PT J AU PIERSON, JL HARRIS, WH AF PIERSON, JL HARRIS, WH TI EXTENSIVE OSTEOLYSIS BEHIND AN ACETABULAR COMPONENT THAT WAS WELL FIXED WITH CEMENT - A CASE-REPORT SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Note ID TOTAL HIP-ARTHROPLASTY; AGGRESSIVE GRANULOMATOUS LESIONS; LOCALIZED BONE-RESORPTION; TOTAL JOINT REPLACEMENT; STRESS DISTRIBUTIONS; FEMORAL COMPONENTS; POLYETHYLENE; LYSIS; WEAR; REGION C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT ORTHOPAED SURG, HIP & IMPLANT UNIT, BOSTON, MA 02114 USA. RP MASSACHUSETTS GEN HOSP, ORTHOPAED BIOMECH LAB, BOSTON, MA 02114 USA. NR 38 TC 25 Z9 25 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02492 USA SN 0021-9355 EI 1535-1386 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD FEB PY 1993 VL 75A IS 2 BP 268 EP 271 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA KM708 UT WOS:A1993KM70800015 PM 8423188 ER PT J AU COLGAN, SP PARKOS, CA DELP, C ARNAOUT, MA MADARA, JL AF COLGAN, SP PARKOS, CA DELP, C ARNAOUT, MA MADARA, JL TI NEUTROPHIL MIGRATION ACROSS CULTURED INTESTINAL EPITHELIAL MONOLAYERS IS MODULATED BY EPITHELIAL EXPOSURE TO IFN-GAMMA IN A HIGHLY POLARIZED FASHION SO JOURNAL OF CELL BIOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; INTERCELLULAR-ADHESION MOLECULE-1; INFLAMMATORY BOWEL-DISEASE; INTERFERON-GAMMA; ENDOTHELIAL-CELLS; IMMUNE INTERFERON; BARRIER FUNCTION; LEUKOCYTE TRANSMIGRATION; OCCLUDING JUNCTIONS; MONOCLONAL-ANTIBODY AB Neutrophil, or polymorphonuclear leukocyte (PMN), migration across intestinal epithelial barriers, such as occurs in many disease states, appears to result in modifications of epithelial barrier and ion transport functions (Nash, S., J. Stafford, and J. L. Madara. 1987. J. Clin. Invest. 80:1104-1113; Madara, J. L., C. A. Parkos, S. P. Colgan, R. J. MacLeod, S. Nash, J. B. Matthews, C. Delp, and W. I. Lencer. 1992. J. Clin. Invest. 89:1938-1944). Here we investigate the effects of epithelial exposure to IFN-gamma on PMN migration across cultured monolayers of the human intestinal epithelial cell line T84. Transepithelial migration of PMN was initially assessed in the apical-to-basolateral direction, since previous studies indicate general qualitative similarities between PMN migration in the apical-to-basolateral and in the basolateral-to-apical directions. In the apical-to-basolateral direction, epithelial exposure to IFN-gamma markedly upregulated transepithelial migration of PMN in a dose- and time-dependent fashion as measured by both electrical and myeloperoxidase assays. This IFN-gamma-elicited effect on transmigration was specifically due to a. IFN-gamma effect on epithelial cells and was not secondary to IFN-gamma effects on epithelial tight junction permeability. Moreover, this IFN-gamma effect was dependent on epithelial protein synthesis, and involved a pathway in which CD11b/18, but not ICAM-1 or CDlla/18, appeared to play a crucial role in PMN-epithelial adhesion. IFN-gamma also substantially modified PMN transepithelial migration in the natural, basolateral-to-apical direction. The IFN-gamma effect on naturally directed transmigration was also specifically due to an IFN-gamma effect on epithelial cells, showed comparable time and dose dependency to that of oppositely directed migration, was CD11b/18 dependent, and required epithelial protein synthesis. Additionally, however, important qualitative differences existed in how IFN-gamma affected transmigration in the two directions. In contrast to apical-to-basolateral directed migration, IFN-gamma markedly downregulated transepithelial migration of PMN in the natural direction. This downregulation of PMN migration in the natural direction, however, was not due to failure of PMN to move across filters and into monolayers. Indeed, IFN-gamma exposure to epithelia increased the number of PMN which had moved into the basolateral space of the epithelium in naturally directed transmigration. These results represent the first detailed report of influences on PMN transepithelial migration by a cytokine, define conditions under which a qualitative difference in PMN transepithelial migration exists, and suggest that migration of PMN across epithelia in the natural direction may involve multiple steps which can be differentially regulated by cytokines. Specifically, it appears that in naturally directed migration, IFN-gamma may enhance the retention time of the recruited PMN in the paracellular space below tight junctions, and does so, at least in part, by downregulating a PMN-epithelial interactive event required for subsequent transjunctional migration. We speculate that such retention of PMN at this specific anatomic location, the site wherein the transition from the external environment to the internal milieu occurs, may serve an important role in mucosal defense. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02138. HARVARD UNIV,SCH MED,HARVARD DIGEST DIS CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP COLGAN, SP (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115, USA. RI Parkos, Charles/B-3896-2009; Colgan, Sean/B-4573-2009 FU NIAID NIH HHS [AI21964]; NIDDK NIH HHS [DK33506, DK35932] NR 48 TC 141 Z9 141 U1 0 U2 1 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 FEB PY 1993 VL 120 IS 3 BP 785 EP 798 DI 10.1083/jcb.120.3.785 PG 14 WC Cell Biology SC Cell Biology GA KJ440 UT WOS:A1993KJ44000022 PM 8093887 ER PT J AU DIAMOND, MS GARCIAAGUILAR, J BICKFORD, JK CORBI, AL SPRINGER, TA AF DIAMOND, MS GARCIAAGUILAR, J BICKFORD, JK CORBI, AL SPRINGER, TA TI THE I-DOMAIN IS A MAJOR RECOGNITION SITE ON THE LEUKOCYTE INTEGRIN MAC-1 (CD11B/CD18) FOR 4 DISTINCT ADHESION LIGANDS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID COMPLEMENT RECEPTOR TYPE-3; ARG-GLY-ASP; HUMAN VONWILLEBRAND-FACTOR; P150,95 GLYCOPROTEIN FAMILY; BOVINE PLASMA FIBRONECTIN; MOLECULE-1 ALPHA-SUBUNIT; AMINO-ACID SEQUENCE; CELL-SURFACE; MONOCLONAL-ANTIBODIES; BETA-SUBUNIT AB Despite the identification and characterization of several distinct ligands for the leukocyte integrin (CD11/CD18) family of adhesion receptors, little is known about the structural regions on these molecules that mediate ligand recognition. In this report, we use alpha subunit chimeras of Mac-1 (CD11b/CD18) and p150,95 (CD11c/CD18), and an extended panel of newly generated and previously characterized mAbs specific to the alpha chain of Mac-1 to map the binding sites for four distinct ligands for Mac-1: iC3b, fibrinogen, ICAM-1, and the as-yet uncharacterized counter-receptor responsible for neutrophil homotypic adhesion. Epitopes of mAbs that blocked ligand binding were mapped with the chimeras and used to localize the ligand recognition sites because the data obtained from functional assays with the Mac-1/p150,95 chimeras were not easily interpreted. Results show that the I domain on the alpha chain of Mac-1 is an important recognition site for all four ligands, and that the NH2-terminal and perhaps divalent cation binding regions but not the COOH-terminal segment may contribute. The recognition sites in the I domain appear overlapping but not identical as individual Mac-1-ligand interactions are distinguished by the discrete patterns of inhibitory mAbs. Additionally, we find that the alpha subunit NH2-terminal region and divalent cation binding region, despite being separated by over 200 amino acids of the I domain, appear structurally apposed because three mAbs require the presence of both of these regions for antigenic reactivity, and chimeras that contain the NH2 terminus of p150,95 require the divalent cation binding region of p150,95 to associate firmly with the beta subunit. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. RP DIAMOND, MS (reprint author), HARVARD UNIV,SCH MED,COMM CELL & DEV BIOL,BOSTON,MA 02115, USA. RI Corbi, Angel/B-7194-2011 OI Corbi, Angel/0000-0003-1980-5733 FU NCI NIH HHS [CA31799]; NIGMS NIH HHS [T32 GM007753, T32GM07753-11] NR 98 TC 449 Z9 457 U1 0 U2 2 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 FEB PY 1993 VL 120 IS 4 BP 1031 EP 1043 DI 10.1083/jcb.120.4.1031 PG 13 WC Cell Biology SC Cell Biology GA KL802 UT WOS:A1993KL80200018 PM 7679388 ER PT J AU WEAVER, DR STEHLE, JH STOPA, EG REPPERT, SM AF WEAVER, DR STEHLE, JH STOPA, EG REPPERT, SM TI MELATONIN RECEPTORS IN HUMAN HYPOTHALAMUS AND PITUITARY - IMPLICATIONS FOR CIRCADIAN AND REPRODUCTIVE RESPONSES TO MELATONIN SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID NOCTURNAL SERUM MELATONIN; PARS-TUBERALIS; PLASMA MELATONIN; RHESUS-MONKEYS; JET-LAG; BRAIN; RHYTHM; AUTORADIOGRAPHY; INHIBITION; SECRETION AB Two major physiological roles for the pineal hormone melatonin (MEL) have been identified in vertebrates: the hormone influences circadian rhythmicity and regulates seasonal responses to changes in day length. These effects of MEL are thought to be due to interaction with specific, high affinity MEL receptors in the suprachiasmatic nucleus (SCN) and hypophysial pars tuberalis (PT), respectively. Using the ligand 2-[I-125]iodo-MEL ([I-125[MEL), we examined putative MEL receptors in these regions in human and monkey tissue specimens by in vitro autoradiography. Specific, high affinity [I-125]MEL-binding sites (K(d), 53.3 +/- 13.0 pM) were consistently observed in the human SCN. In contrast, specific [I-125]MEL binding was detectable in the PT of only one of the eight human specimens examined. Specific [I-125]MEL binding was also detected in the pars distalis of several subjects, but with an inconsistent distribution. In rhesus monkey tissue, MEL receptors were readily detected in the SCN and, as in all other seasonally breeding species examined to date, in the PT. The relative absence of MEL receptors from the human PT suggests that neuroendocrine responses to MEL in humans may occur by fundamentally different mechanisms than those that underlie the photoperiodic regulation of reproduction in seasonally breeding species. C1 HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, PROGRAM NEUROSCI, BOSTON, MA 02115 USA. SUNY HLTH SCI CTR, COLL MED, DEPT PATHOL, SYRACUSE, NY 13210 USA. HARVARD UNIV, MCLEAN HOSP, CTR BRAIN TISSUE RESOURCE, BELMONT, MA 02178 USA. RP WEAVER, DR (reprint author), MASSACHUSETTS GEN HOSP, DEV CHRONOBIOL LAB, CHILDRENS SERV, JACKSON 1226, BOSTON, MA 02114 USA. FU NIA NIH HHS [AG-09301]; NIDDK NIH HHS [DK-42125]; NIMH NIH HHS [MH/NS-31862] NR 52 TC 155 Z9 159 U1 0 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD FEB PY 1993 VL 76 IS 2 BP 295 EP 301 DI 10.1210/jc.76.2.295 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KM445 UT WOS:A1993KM44500008 PM 8381796 ER PT J AU BONADONNA, RC SACCOMANI, MP COBELLI, C DEFRONZO, RA AF BONADONNA, RC SACCOMANI, MP COBELLI, C DEFRONZO, RA TI EFFECT OF INSULIN ON SYSTEM-A AMINO-ACID-TRANSPORT IN HUMAN SKELETAL-MUSCLE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE LIMB BALANCE; 2-METHYLAMINOISOBUTYRIC ACID; 1ST-PASS KINETICS; PROTEIN TURNOVER ID DEPENDENT DIABETIC-PATIENTS; BODY PROTEIN-SYNTHESIS; LEUCINE METABOLISM; RAT HEMICORPUS; HUMAN FOREARM; INVIVO; HYPERINSULINEMIA; INFUSION; TURNOVER; CELLS AB Transmembrane transport of neutral amino acids in skeletal muscle is mediated by at least four different systems (system A, ASC, L, and N(m)), and may be an important target for insulin's effects on amino acid and protein metabolism. We have measured net amino acid exchanges and fractional rates of inward (k(in), min-1) and outward (k(out), min-1) transmembrane transport of 2-methylaminoisobutyric acid (MeAIB, a nonmetabolizable amino acid analogue, specific for system A amino acid transport) in forearm deep tissues (skeletal muscle), by combining the forearm perfusion technique and a novel dual tracer ([1-H-3]-D-mannitol and 2-[1-C-14]-methylaminoisobutyric acid) approach for measuring in vivo the activity of system A amino acid transport. Seven healthy lean subjects were studied. After a baseline period, insulin was infused into the brachial artery to achieve local physiologic hyperinsulinemia (76+/-8 muU/ml vs 6.4+/-1.6 muU/ml in the basal period, P < 0.01) without affecting systemic hormone and substrate concentrations. Insulin switched forearm amino acid exchange from a net output (-2,630+/-1,100 amol / min per kg of forearm tissue) to a net uptake (1,610+/-600 nmol/min per kg, P < 0.01 vs baseline). Phenylalanine and tyrosine balances simultaneously shifted from a net output (-146+/-47 and -173+/-34 nmol/min per kg, respectively) to a zero balance (16.3+/-51 for phenylalanine and 15.5+/-14.3 nmol/min per kg for tyrosine, P < 0.01 vs baseline for both), showing that protein synthesis and breakdown were in equilibrium during hyperinsulinemia. Net negative balances of alanine, methionine, glycine, threonine and asparagine (typical substrates for system A amino acid transport) also were decreased by insulin, whereas serine (another substrate for system A transport) shifted from a zero balance to net uptake. Insulin increased kin of MeAIB from a basal value of 11.8 . 10(-2)+/-1.7 . 10(-2) . min-1 to 13.7 . 10(-2)+/-2.2 . 10(-2). min-1 (P < 0.02 vs the postabsorptive value), whereas k(out) was unchanged. We conclude that physiologic hyperinsulinemia stimulates the activity of system A amino acid transport in human skeletal muscle, and that this effect may play a role in determining the overall concomitant response of muscle amino acid/protein metabolism to insulin. C1 UNIV PISA,CNR,INST CLIN PHYSIOL,METAB UNIT,I-56100 PISA,ITALY. UNIV PADUA,DEPT ELECTR & INFORMAT,I-35131 PADUA,ITALY. UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK24092] NR 55 TC 46 Z9 47 U1 0 U2 2 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 FEB PY 1993 VL 91 IS 2 BP 514 EP 521 DI 10.1172/JCI116230 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KM222 UT WOS:A1993KM22200023 PM 8432860 ER PT J AU SPERLING, RI BENINCASO, AI KNOELL, CT LARKIN, JK AUSTEN, KF ROBINSON, DR AF SPERLING, RI BENINCASO, AI KNOELL, CT LARKIN, JK AUSTEN, KF ROBINSON, DR TI DIETARY OMEGA-3 POLYUNSATURATED FATTY-ACIDS INHIBIT PHOSPHOINOSITIDE FORMATION AND CHEMOTAXIS IN NEUTROPHILS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE FISH OIL; INOSITOL PHOSPHATES; MONOCYTES; PLATELET-ACTIVATING FACTOR; PHOSPHOLIPIDS ID PERFORMANCE LIQUID-CHROMATOGRAPHY; STIMULATED HUMAN-NEUTROPHILS; FISH-OIL; EICOSAPENTAENOIC ACID; RHEUMATOID-ARTHRITIS; INOSITOL 1,4,5-TRISPHOSPHATE; PHOSPHOLIPASE-D; GENERATION; METABOLISM; SUPPLEMENTATION AB Earlier studies demonstrated that dietary omega-3 polyunsaturated fatty acid (PUFA) supplementation attenuates the chemotactic response of neutrophils and the generation of leukotriene (LT) B4 by neutrophils stimulated with calcium ionophore; however, the mechanisms and relationship of these effects were not examined. Neutrophils and monocytes from eight healthy individuals were examined before and after 3 and 10 wk of dietary supplementation with 20 g SuperEPA daily, which provides 9.4 g eicosapentaenoic acid (EPA) and 5 g docosahexaenoic acid. The maximal neutrophil chemotactic response to LTB4, assessed in Boyden microchambers, decreased by 69% after 3 wk and by 93% after 10 wk from prediet values. The formation of [H-3]inositol tris-phosphate (IP3) by [H-3]inositol-labeled neutrophils stimulated by LTB4 decreased by 71% after 3 wk (0.033+/-0.013% [H-3] release, mean+/-SEM) and by 90% after 10 wk (0.011+/-0.011%) from prediet values (0.114+/-0.030%) as quantitated by beta-scintillation counting after resolution on HPLC. LTB4-stimulated neutrophil chemotaxis and IP3 formation correlated significantly (P < 0.0001); each response correlated closely and negatively with the EPA content of the neutrophil phosphatidylinositol (PI) pool (P = 0.0003 and P = 0.0005, respectively). Neither the affinities and densities of the high and low affinity LTB4 receptors on neutrophils nor LTB4-mediated diglyceride formation changed appreciably during the study. Similar results were observed in neutrophils activated with platelet-activating factor (PAF). The summed formation of LTB4 plus LTB5 was selectively inhibited in calcium ionophore-stimulated neutrophils and was also inhibited in zymosan-stimulated neutrophils. The inhibition of the summed formation of LTB4 plus LTB5 in calcium ionophore-stimulated neutrophils and in zymosan-stimulated neutrophils did not correlate significantly with the EPA content of the PI pool. The data indicate that dietary omega-3 PUFA supplementation inhibits the autoamplification of the neutrophil inflammatory response by decreasing LTB4 formation through the inactivation of the LTA epoxide hydrolase and independently by inhibiting LTB4- (and PAF) stimulated chemotaxis by attenuating the formation of IP3 by the PI-selective phospholipase C. This is the initial demonstration that dietary omega-3 PUFA supplementation can suppress signal transduction at the level of the PI-specific phospholipase C in humans. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114. RP SPERLING, RI (reprint author), BRIGHAM & WOMENS HOSP,DEPT RHEUMATOL & IMMUNOL,250 LONGWOOD AVE,ROOM 618,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-28465, AI-22531]; NIAMS NIH HHS [AR-35907] NR 42 TC 227 Z9 231 U1 0 U2 7 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 FEB PY 1993 VL 91 IS 2 BP 651 EP 660 DI 10.1172/JCI116245 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KM222 UT WOS:A1993KM22200038 PM 8381824 ER PT J AU CASSILETH, PA ANDERSEN, J LAZARUS, HM COLVIN, OM BENNETT, JM STADTMAUER, EA KAIZER, H WEINER, RS EDELSTEIN, M OKEN, MM AF CASSILETH, PA ANDERSEN, J LAZARUS, HM COLVIN, OM BENNETT, JM STADTMAUER, EA KAIZER, H WEINER, RS EDELSTEIN, M OKEN, MM TI AUTOLOGOUS BONE-MARROW TRANSPLANT IN ACUTE MYELOID-LEUKEMIA IN 1ST REMISSION SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; CHEMOTHERAPY; SURVIVAL; THERAPY; ADULTS C1 HOSP UNIV PENN,PHILADELPHIA,PA 19104. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. JOHNS HOPKINS UNIV,CTR ONCOL,BALTIMORE,MD 21218. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. UNIV FLORIDA,GAINESVILLE,FL 32611. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. VIRGINIA PIPER CANC INST,MINNEAPOLIS,MN. FU NCI NIH HHS [CA 23318, CA 21115, CA 15488] NR 19 TC 96 Z9 97 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 FEB PY 1993 VL 11 IS 2 BP 314 EP 319 PG 6 WC Oncology SC Oncology GA KK441 UT WOS:A1993KK44100016 PM 8426209 ER PT J AU GOFF, DC BALDESSARINI, RJ AF GOFF, DC BALDESSARINI, RJ TI DRUG-INTERACTIONS WITH ANTIPSYCHOTIC AGENTS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Review ID NEUROLEPTIC MALIGNANT SYNDROME; CHRONIC-SCHIZOPHRENIC PATIENTS; PLASMA HALOPERIDOL LEVELS; CARBAMAZEPINE-INDUCED REDUCTION; ANTI-PARKINSONIAN MEDICATION; DOUBLE-BLIND TRIAL; RADIORECEPTOR ASSAY; REDUCED HALOPERIDOL; CLINICAL-RESPONSE; FLUPHENAZINE DECANOATE C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHIAT RES LABS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHOT DISORDERS PROGRAM,BELMONT,MA. FU NIMH NIH HHS [MH-31154, MH-47370, MH-19053] NR 214 TC 52 Z9 53 U1 2 U2 3 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 FEB PY 1993 VL 13 IS 1 BP 57 EP 67 PG 11 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA KG631 UT WOS:A1993KG63100008 PM 8098051 ER PT J AU SANSONE, C VANHOUTE, J JOSHIPURA, K KENT, R MARGOLIS, HC AF SANSONE, C VANHOUTE, J JOSHIPURA, K KENT, R MARGOLIS, HC TI THE ASSOCIATION OF MUTANS STREPTOCOCCI AND NON-MUTANS STREPTOCOCCI CAPABLE OF ACIDOGENESIS AT A LOW PH WITH DENTAL-CARIES ON ENAMEL AND ROOT SURFACES SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID PLAQUE-FORMING ABILITY; GNOTOBIOTIC-RATS; SELECTIVE MEDIUM; INVIVO; CARIOGENICITY; SALIVA; MITIS AB Coronal dental plaque from each of 12 caries-positive subjects (Group I) was pooled from ''white spot'' tooth surface areas and, separately, from sound surface areas; sound surface areas in each of 18 caries-free subjects (Group II) were sampled similarly. Two samples, one consisting of material from a root-surface lesion and another of plaque from a sound root-surface area, were obtained from each of another 10 subjects (Group III). The samples from Groups I and II were evaluated for: (1) pH-lowering potential in vitro with dispersed plaque suspensions, excess glucose supply, and a 60-minute test; (2) the levels of mutans streptococci (MS) and lactobacilli; and (3) the distribution of the predominant non-mutans streptococci (non-MS) according to their final pH in glucose broth; only microbial analysis was done for the Group III samples. The levels of the MS were generally positively associated with caries. A weaker positive association was found for the levels of those non-MS capable of acidogenesis at low pH (final pH < 4.4). The latter generally far outnumbered the MS in all types of samples. The levels of lactobacilli were nearly always very low. The pH-lowering potential (final pH and pH drop rate) was higher for plaque from ''white spot'' areas than for plaque from sound surface areas (Group I). The samples from caries-free subjects (Group II), however, exhibited a pH-lowering potential which was not significantly different from that of both types of samples from the caries-active subjects (Group I). Collectively, the findings suggest that the role of non-MS capable of acidogenesis at low pH in caries development merits further study. C1 FORSYTH DENT CTR,DEPT CLIN TRIALS & HUMAN EXPERIMENTAT,BOSTON,MA 02115. FORSYTH DENT CTR,DEPT PHYS CHEM,BOSTON,MA 02115. RP SANSONE, C (reprint author), FORSYTH DENT CTR,DEPT ORAL MICROBIOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009, DE-07493] NR 23 TC 96 Z9 99 U1 2 U2 2 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD FEB PY 1993 VL 72 IS 2 BP 508 EP 516 DI 10.1177/00220345930720020701 PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KK857 UT WOS:A1993KK85700007 PM 8423248 ER PT J AU KAUFMAN, AJ KIENE, KL MOY, RL AF KAUFMAN, AJ KIENE, KL MOY, RL TI ROLE OF TISSUE UNDERMINING IN THE TRAPDOOR EFFECT OF TRANSPOSITION FLAPS SO JOURNAL OF DERMATOLOGIC SURGERY AND ONCOLOGY LA English DT Article AB BACKGROUND. The trapdoor or pincushioning effect is a frequent complication of transposition flaps. Several explanations have been proposed for its occurrence, including lymphatic or venous obstruction, scar hypertrophy, excessive subcutaneous fat or flap tissue, and scar contracture. OBJECTIVE. To study the effects of tissue undermining and scar contracture using a guinea pig animal model. METHODS. Circular wounds on the dorsal surface of guinea pigs were repaired with transposition flaps. Half of the recipient beds were undermined widely and half were not undermined. Animals were observed for evidence of the trapdoor phenomenon. RESULTS. Only animals in the group without undermining demonstrated evidence of the trapdoor effect. CONCLUSION. Tissue undermining may prevent the development of the trapdoor effect in transposition flaps. C1 UNIV CALIF LOS ANGELES, SCH MED,W LOS ANGELES VET ADM MED CTR, WADSWORTH DIV,DIV DERMATOL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, JONSSON COMPREHENS CANC CTR, LOS ANGELES, CA USA. NR 13 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0148-0812 J9 J DERMATOL SURG ONC PD FEB PY 1993 VL 19 IS 2 BP 128 EP 132 PG 5 WC Oncology; Dermatology; Surgery SC Oncology; Dermatology; Surgery GA KL831 UT WOS:A1993KL83100004 PM 8429138 ER PT J AU AHMED, AR MOHIMEN, A YUNIS, EJ MIRZA, NM KUMAR, V BEUTNER, EH ALPER, CA AF AHMED, AR MOHIMEN, A YUNIS, EJ MIRZA, NM KUMAR, V BEUTNER, EH ALPER, CA TI LINKAGE OF PEMPHIGUS-VULGARIS ANTIBODY TO THE MAJOR HISTOCOMPATIBILITY COMPLEX IN HEALTHY RELATIVES OF PATIENTS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID INHERITED STRUCTURAL POLYMORPHISM; CLASS-II; JEWISH PATIENTS; HLA; DISEASE; HAPLOTYPES AB Pemphigus vulgaris (PV) is an autoimmune disease caused by high concentrations of antibody to an epidermal cadherin. The disease is associated with two kinds of HLA-DR4, DQ8 haplotypes dominantly distributed among Jewish patients, and these plus DR6, DQ5 haplotypes in non-Jewish patients. Low levels of the PV antibody were found in 48% of a total of 120 asymptomatic parents, children, and siblings of 31 patients, thus exhibiting dominant inheritance. The inheritance of these low levels of antibody in asymptomatic relatives was linked to the major histocompatibility complex with a highly significant logarithm of the odds score of 9.07, almost always to a DR4 or DR6 haplotype of the patient. Disease appears to occur in susceptible individuals with low levels of antibody when a second factor, either environmental or genetic, induces high levels, sufficient to produce blisters. C1 HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. AMER RED CROSS BLOOD SERV,NE REG,DEDHAM,MA 02026. HARVARD UNIV,SCH MED,BOSTON,MA 02115. SUNY BUFFALO,BUFFALO,NY 14223. RP AHMED, AR (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-29583]; NICHD NIH HHS [HD-17461]; NIDDK NIH HHS [DK-26844] NR 25 TC 67 Z9 69 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 FEB 1 PY 1993 VL 177 IS 2 BP 419 EP 424 DI 10.1084/jem.177.2.419 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KJ441 UT WOS:A1993KJ44100018 PM 8426112 ER PT J AU THOMAS, L ETOH, T STAMENKOVIC, I MIHM, MC BYERS, HR AF THOMAS, L ETOH, T STAMENKOVIC, I MIHM, MC BYERS, HR TI MIGRATION OF HUMAN-MELANOMA CELLS ON HYALURONATE IS RELATED TO CD44 EXPRESSION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID ADHESION MOLECULES; SURFACE GLYCOPROTEIN; METASTATIC MELANOMA; MALIGNANT-MELANOMA; TUMOR PROGRESSION; LAMININ; RECEPTOR; BINDING; MEMBRANE; LYMPHOMA AB Phenotypic and functional aspects of melanoma-hyaluronate interactions were investigated by studying the expression of CD44, cell migration, and transmembrane penetration of human melanoma cell lines on hyaluronate-coated substrates. Expression of CD44 was tested by flow cytometry on seven human melanoma cell lines. Strong reactivity with anti-CD44 monoclonal antibody was observed in four of seven of the cell lines. Migration studies of CD44(+) cell lines on hyaluronic acid- and chondroitin-6-sulfate-coated substrates, using time-lapse video-microscopy, showed a dramatic dose-dependent increase in migration rate on hyaluronate but not on chondroitin-6-sulfate. Moreover, CD44(-) cell lines showed no modification in migration rate on either substrate. Addition of soluble hyaluronate produced a dose-dependent inhibition of acceleration of CD44(+) cells on hyaluronate-coated substrates, whereas addition of chondroitin-6-sulfate had no effect. Migration inhibition experiments with soluble CD44 (CD44 receptor globulin) also showed specific blocking of the migration of CD44(+) cells on hyaluronate. Haptotactic invasion was increased in CD44(+) cell lines through hyaluronate-coated polycarbonate membranes, whereas no change was detected on chondroitin-6-sulfate-coated membranes. CD44(-) cell lines showed no response to either type of coating. In the melanoma cell lines tested, the expression of CD44 correlated with in vitro migration and invasiveness on hyaluronate substrates. Taken together, our data are consistent with the suggestion that CD44 may play a role in stimulating in vivo aggressiveness of tumors through hyaluronate-rich stroma. C1 MASSACHUSETTS GEN HOSP, MGH E, BLDG 149, 13TH ST, BOSTON, MA 02128 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DIV DERMATOPATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA-45587, CA-55735] NR 46 TC 84 Z9 86 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD FEB PY 1993 VL 100 IS 2 BP 115 EP 120 DI 10.1111/1523-1747.ep12462776 PG 6 WC Dermatology SC Dermatology GA KM220 UT WOS:A1993KM22000004 PM 8429233 ER PT J AU KOCHEVAR, IE MORAN, M LYON, N FLOTTE, T SIEBERT, E GANGE, RW AF KOCHEVAR, IE MORAN, M LYON, N FLOTTE, T SIEBERT, E GANGE, RW TI EFFECTS OF SYSTEMIC INDOMETHACIN, MECLIZINE, AND BW755C ON CHRONIC ULTRAVIOLET-B-INDUCED EFFECTS IN HAIRLESS MOUSE SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID CONNECTIVE-TISSUE ALTERATIONS; TUMOR NECROSIS FACTOR; DERMAL FIBROBLASTS; VISIBLE CHANGES; COLLAGEN; IRRADIATION; FIBRONECTIN; ELASTIN; DAMAGE; INVIVO AB Chronic exposure of hairless mice to ultraviolet B (UVB) radiation is associated with inflammation as well as an altered macromolecular composition of the dermis. This study was designed to determine whether or not various systemic anti-inflammatory agents inhibit chronic UVB-induced changes in the macromolecular content of the dermis and, if so, whether each agent had the same or different effects. The agents and doses were chosen for their ability to inhibit the changes induced by a single exposure to UVB radiation (increased vasopermeability, neutrophil accumulation, and skin-fold thickness). Indomethacin, a cyclooxygenase inhibitor, and meclizine, an H-1 histamine receptor antagonist, were administered from slow-release pellets. BW755C, a combined cyclooxygenase and lipoxygenase inhibitor, was administered intraperitoneally 30 min prior to UVB exposure. Animals were exposed to UVB three times per week for 20 - 26 weeks or were unirradiated. The elastin, glycosaminoglycan and collagen content of the skin were determined by measuring the desmosine, uronic acid, and hydroxyproline levels, respectively. The amount of each macromolecule per area of skin increased after chronic UVB exposure. The increase in desmosine was inhibited by indomethacin; the increase in hydroxyproline was inhibited by meclizine and BW755C. None of the agents inhibited the uronic acid increase. These results suggest that chronic inflammation contributes to the dermal changes seen in chronically UVB-exposed skin and that different inflammatory mediators are involved in the increases observed in elastin, glycosaminoglycans, and collagen. RP KOCHEVAR, IE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,37 FRUIT ST,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [5 T32 AR07098-16] NR 26 TC 24 Z9 24 U1 2 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD FEB PY 1993 VL 100 IS 2 BP 186 EP 193 DI 10.1111/1523-1747.ep12462804 PG 8 WC Dermatology SC Dermatology GA KM220 UT WOS:A1993KM22000017 PM 8429241 ER PT J AU GATTONICELLI, S CALORINI, L BYERS, HR ETOH, T WANG, ZG FERRONE, S AF GATTONICELLI, S CALORINI, L BYERS, HR ETOH, T WANG, ZG FERRONE, S TI ABNORMALITIES IN HLA CLASS-I ANTIGEN EXPRESSION BY MELANOMA-CELLS - STRUCTURAL CHARACTERIZATION AND FUNCTIONAL IMPLICATIONS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID NATURAL-KILLER CELLS; HUMAN SOLID TUMORS; MEDIATED LYSIS; IMMUNODEFICIENT MICE; PARTIAL SUPPRESSION; GENE-EXPRESSION; B2M GENE; T-CELLS; C-MYC; SUSCEPTIBILITY C1 NEW YORK MED COLL,DEPT MICROBIOL & IMMUNOL,VALHALLA,NY 10595. NEW ENGLAND MED CTR,DEPT RADIAT ONCOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. FU NCI NIH HHS [CA39559] NR 37 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD FEB PY 1993 VL 100 IS 2 SU S BP S226 EP S230 PG 5 WC Dermatology SC Dermatology GA KN117 UT WOS:A1993KN11700018 PM 8433012 ER PT J AU MONTGOMERY, WW AF MONTGOMERY, WW TI MONTGOMERY SAFE T-TUBE PLUG SO JOURNAL OF LARYNGOLOGY AND OTOLOGY LA English DT Letter RP MONTGOMERY, WW (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU HEADLEY BROTHERS LTD PI ASHFORD PA INVICTA PRESS, ASHFORD, KENT, ENGLAND TN24 8HH SN 0022-2151 J9 J LARYNGOL OTOL JI J. Laryngol. Otol. PD FEB PY 1993 VL 107 IS 2 BP 171 EP 171 PG 1 WC Otorhinolaryngology SC Otorhinolaryngology GA KW963 UT WOS:A1993KW96300022 ER PT J AU MARGOSSIAN, SS WHITE, HD LEFFORD, J HOLT, JC MALHOTRA, A STAFFORD, WF SLAYTER, HS AF MARGOSSIAN, SS WHITE, HD LEFFORD, J HOLT, JC MALHOTRA, A STAFFORD, WF SLAYTER, HS TI FUNCTIONAL-EFFECTS OF LC1-REASSOCIATION WITH CARDIAC PAPAIN MG.S1 SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Article ID RABBIT SKELETAL-MUSCLE; ESSENTIAL LIGHT CHAIN; AMINO-ACID-SEQUENCE; MYOSIN SUBFRAGMENT-1; HEAVY-CHAINS; TROPONIN-TROPOMYOSIN; BIOCHEMICAL KINETICS; ELECTRON-MICROSCOPY; MONOCLONAL-ANTIBODY; ATP HYDROLYSIS AB The effect of LC1 on cardiac myosin structure and activity was investigated using as a model S1 prepared by papain digestion in the presence of Mg2+. The resulting S1 contained LC2 but a part of the N-terminal region of LC1 was cleaved. Sequencing the N-terminal part of the band migrating below LC1 on SDS gels revealed it to consist of alternating alanyl and prolyl residues thus establishing LC1 as the origin of this band. However, Western blots did not reveal any LC1 while radioimmunoassays indicated it to be present at the 5% level suggesting the anti-LC1 antibody used in these experiments did not recognize the C-terminal portion of LC1 still attached to Mg - S1. Mixing a 10-15 M excess of isolated light chains with Mg . S1 in the presence of 10 mm ATP, 12 mM MgCl2, 4.7 M NH4Cl allowed LC1 to recombine with LC1-deficient Mg . S1. Equilibrium ultracentrifugation analysis revealed a highly heterogeneous LC1-deficient S1 which upon recombination with intact LC1 became monodisperse as indicated by the superimposition of molecular weight averages all across the centrifuge cell. LC1-deficient Mg - S1 had a V(m) of 0.4 s-1, K(a) of 30 mum and a K(bind) of 28 mum. In the presence of intact LC1, Vm rose to 0.8 s-1 while K(a) and K(bind) were reduced to 7.5 and 12 muM, respectively. The fourfold decrease in K(a) strongly indicated an increased affinity for actin by Mg . S1 in the presence of uncleaved LC1. Also, Ca2+-regulation of dog heart myofibrils was suppressed when Ca2+-activated MgATPase assays, as a function of Ca2+, were performed in the presence of anti-LC1 antibodies. These observations suggest the presence of intact, uncleaved LC1 in S1 is required for the stability of S1 heavy chains and proper Ca2+-regulation. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. MONTEFIORE MED CTR,BRONX,NY 10467. EASTERN VIRGINIA MED SCH,DEPT BIOCHEM,NORFOLK,VA 23501. RORER BIOTECHNOL,KING OF PRUSSIA,PA 19406. BOSTON BIOMED RES INST,DEPT MUSCLE RES,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP MARGOSSIAN, SS (reprint author), YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT BIOCHEM & ORTHOPAED RES,BRONX,NY 10461, USA. FU NHLBI NIH HHS [HL41776, HL26569, HL 33014] NR 64 TC 15 Z9 15 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD FEB PY 1993 VL 14 IS 1 BP 3 EP 14 DI 10.1007/BF00132175 PG 12 WC Cell Biology SC Cell Biology GA KQ510 UT WOS:A1993KQ51000001 PM 8478426 ER PT J AU TAKAHASHI, T NOWAKOWSKI, RS CAVINESS, VS AF TAKAHASHI, T NOWAKOWSKI, RS CAVINESS, VS TI CELL-CYCLE PARAMETERS AND PATTERNS OF NUCLEAR-MOVEMENT IN THE NEOCORTICAL PROLIFERATIVE ZONE OF THE FETAL MOUSE SO JOURNAL OF NEUROSCIENCE LA English DT Article DE NEUROGENESIS; NEOCORTICAL HISTOGENESIS; CELL CYCLE; PROLIFERATION; BROMODEOXYURIDINE; VENTRICULAR ZONE; SUBVENTRICULAR ZONE; MOUSE ID RADIAL GLIAL-CELLS; CENTRAL NERVOUS-SYSTEM; CEREBRAL-CORTEX; RHESUS-MONKEY; MIGRATION; ORIGIN; GOLGI; TIME; DIFFERENTIATION; TELENCEPHALON AB Cytogenesis is the critical determinant of the total number of neurons that contribute to the formation of the cerebral cortex and the rate st which the cells are produced. Two distinct cell populations constitute the proliferative population, a pseudostratified ventricular epithelium (PVE) lying within the ventricular zone (VZ) at the margin of the ventricle, and a secondary proliferative population that is intermixed with the PVE within the VZ but also is distributed through the overlying subventricular and intermediate zones of the cerebral wall. The present analysis, based upon cumulative S-phase labeling of the proliferative cells with 5-bromo-2'deoxyuridine, is principally concerned with the PVE of the gestational-day-14 (E14) murine cerebral wall. It has immediate but also more far reaching general objectives. The most immediate objective, essential to the design and interpretation of later experiments, is to provide estimates of critical parameters of cytogenesis for the PVE. The growth fraction is virtually 100%. The lengths of the overall cell cycle, S-, G2+M-, and G1-phases are 15.1 hr, 3.8 hr, 2 hr, and 9.3 hr, respectively. The PVE is homogeneous with respect to cell cycle length. For methodological considerations, these estimates are more accurate than estimates of the same parameters obtained in earlier analyses based upon S-phase labeling with tritiated thymidine. It is particularly with respect to a shorter length of S-phase determined here that the present values are different from those obtained with thymidine. At a more innovative level, the temporal and spatial resolution of nuclear movement made possible by the methods developed here will allow, in a way not previously attempted, a fine-grained tracking of nuclear movement as cells execute the successive stages of the cell cycle or exit the cycle subsequent to mitosis. Such observations are pertinent to our understanding of the regulatory mechanisms of neocortical histogenesis and the cell biological mechanisms that govern the proliferative cycle of the ventricular epithelium itself. It is known that the velocity of nuclear movement in the PVE is maximum in G2 (fourfold increase from S-phase) and minimum in M and early G1. It has been determined here that after the initiation of G1 there is a substantial differential in the time that postmitotic cells spend before they start their ascent toward the outer margin of the PVE; that is, some nuclei leave the ventricular surface shortly after mitosis (within 1.5 hr) while the more sluggish group of cells stays in the vicinity of the ventricular surface for up to 6 hr. Once postmitotic nuclei begin their ascent from the ventricular surface, they accelerate progressively through the outer half of the PVE. The analysis also shows that the cells are entering and leaving S-phase at equal rates, evidence in confirmation of the hypothesis that proliferation in the developing mouse cerebral wall at E14 is asynchronous. C1 UMDNJ,ROBERT WOOD JOHNSON MED SCH,DEPT NEUROSCI & CELL BIOL,PISCATAWAY,NJ 08854. RP TAKAHASHI, T (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,25 FRUIT ST,BOSTON,MA 02114, USA. RI Nowakowski, Richard/C-3217-2016; OI Nowakowski, Richard/0000-0002-5006-3670 FU NINDS NIH HHS [NS12005, NS28061] NR 61 TC 249 Z9 252 U1 0 U2 2 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD FEB PY 1993 VL 13 IS 2 BP 820 EP 833 PG 14 WC Neurosciences SC Neurosciences & Neurology GA KL123 UT WOS:A1993KL12300035 PM 8426239 ER PT J AU FRIM, DM SHORT, MP ROSENBERG, WS SIMPSON, J BREAKEFIELD, XO ISACSON, O AF FRIM, DM SHORT, MP ROSENBERG, WS SIMPSON, J BREAKEFIELD, XO ISACSON, O TI LOCAL PROTECTIVE EFFECTS OF NERVE GROWTH FACTOR-SECRETING FIBROBLASTS AGAINST EXCITOTOXIC LESIONS IN THE RAT STRIATUM SO JOURNAL OF NEUROSURGERY LA English DT Article DE NERVE GROWTH FACTOR; GENE TRANSFER; FIBROBLAST GRAFT; EXCITOTOXICITY; STRIATUM; RAT ID GENETICALLY MODIFIED CELLS; EXCITATORY AMINO-ACIDS; CHOLINERGIC NEURONS; QUINOLINIC ACID; GENE-TRANSFER; BRAIN INJURY; TRANSPLANTATION; DISEASES; NEUROTOXICITY; IMPLANTATION AB Neurotrophic factors, such as nerve growth factor (NGF), in addition to their role in neuronal development, have protective effects on neuronal survival. Intracerebral implantation of cells genetically altered to secrete high levels of NGF is also found to promote neuronal survival in experimental lesioning models of the brain. The range of activity for such biological delivery systems has not yet been well described either spatially or temporally. Therefore, the authors chose to study the local and distant protective effects of an NGF-secreting rat fibroblast cell line implanted in an excitotoxic lesion model of Huntington's disease. They found that preimplantion of NGF-secreting fibroblasts placed within the corpus callosum reduced the maximum cross-sectional area of a subsequent excitotoxic lesion in the ipsilateral striatum by 80% when compared to the effects of a non-NGF-secreting fibroblast graft, and by 83% when compared to excitotoxic lesions in ungrafted animals (p < 0.003). However, NGF-secreting cells placed in the contralateral corpus callosum failed to affect striatal lesion size significantly when compared to contralateral or ipsilateral non-NGF-secreting cell implants. Of note, fibroblasts were clearly visible within the graft site at 7 and 18 days after implantation; however, few cells within the grafts stained positively for NGF peptide or for the messenger ribonucleic acid (mRNA) encoding the transfected NGF gene-construct at either time point. These results show that biological delivery systems for NGF appear to have a profound but local effect on neuronal excitotoxicity, which will necessitate careful neurosurgical placement for maximum effect. Furthermore, the ability of this genetically altered cell line to synthesize NGF mRNA and peptide appears to decrease spontaneously in vivo, a characteristic that will need to be addressed before this method of biological delivery can be utilized as a treatment for chronic degenerative diseases. C1 MCLEAN HOSP, NEUROREGENERAT LAB, MRC-119, 115 MILL, BELMONT, MA 02178 USA. MASSACHUSETTS GEN HOSP, CTR NEUROSCI, NEUROSURG SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROL SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, PROGRAM NEUROSURG, BOSTON, MA 02115 USA. FU NINDS NIH HHS [NS 24279, NS 29178, NS 30064] NR 41 TC 87 Z9 95 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI ROLLING MEADOWS PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA SN 0022-3085 EI 1933-0693 J9 J NEUROSURG JI J. Neurosurg. PD FEB PY 1993 VL 78 IS 2 BP 267 EP 273 DI 10.3171/jns.1993.78.2.0267 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA KJ328 UT WOS:A1993KJ32800015 PM 8421209 ER PT J AU RABITO, CA MOORE, RH BOUGAS, C DRAGOTAKES, SC AF RABITO, CA MOORE, RH BOUGAS, C DRAGOTAKES, SC TI NONINVASIVE, REAL-TIME MONITORING OF RENAL-FUNCTION - THE AMBULATORY RENAL MONITOR SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID GLOMERULAR-FILTRATION-RATE; CADMIUM TELLURIDE DETECTOR; TRACER CLEARANCE TECHNIQUE; TECHNETIUM-99M DTPA; PLASMA-CLEARANCE; QUALITY-CONTROL; CDTE DETECTOR; TC-99M-DTPA; IOTHALAMATE; CREATININE AB The objective of this study was to develop a method for the noninvasive, continuous and real-time monitoring of renal function. A radiation detector attached to a miniature data logger was used to monitor the clearance of the glomerular filtration agent Tc-99m-diethylenetriaminepentaacetic acid from the extracellular space. The rate constant (k) for this clearance showed an excellent correlation with simultaneous glomerular filtration rate (GFR) measurements performed with a standard I-125-iothalamate clearance technique in 50 patients. Moreover, the reproducibility of the k measurement for an individual or a population was superior to the GFR measurement performed with the standard clearance technique. The procedure was also used to monitor the renal function in patients at risk for acute renal failure during angiography or in the intensive care unit under noninvasive and near real-time conditions. The results show that the technique detects rapid changes in renal function with a resolution time of 5 min in patients with normal renal function and 15 min in patients with severely impaired renal function. Since the method is noninvasive, precise and provides a near real-time measurement of GFR, its use may lead to an improvement in the management of patients in situations in which a rapid measurement is the major concern. RP RABITO, CA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114, USA. NR 33 TC 38 Z9 38 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD FEB PY 1993 VL 34 IS 2 BP 199 EP 207 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK926 UT WOS:A1993KK92600010 PM 8429337 ER PT J AU SORENSEN, G LANDO, H PECHACEK, TF AF SORENSEN, G LANDO, H PECHACEK, TF TI PROMOTING SMOKING CESSATION AT THE WORKPLACE - RESULTS OF A RANDOMIZED CONTROLLED INTERVENTION STUDY SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID HEART-DISEASE; PREVENTION; EDUCATION AB This paper presents results from a preliminary short-term work-site intervention study aimed al smoking cessation. The 3-month intervention included consultation for employers on the adoption of a nonsmoking policy, training for nonsmokers to provide assistance to smokers attempting to quit, and cessation classes for smokers. Eight work sites from Bloomington, Minnesota were recruited to the study and randomly assigned to an intervention or comparison condition after a baseline survey of all employees. To assess the effect of the intervention, smokers were surveyed 1 and 6 months after the intervention was completed. At the 1-month follow-up, the overall quit rate in the intervention group was 12% compared to 5% in the control group (P < .05). At the 6-month follow-up, 12% of smokers in the intervention group reported quitting, compared to 9% in the control group (P <.05). Co-worker support for quitting was higher in the intervention group compared to the comparison group. Cessation was highest overall among smokers whose co-workers-frequently asked them not to smoke and among those who worked with a high proportion of nonsmokers. These results indicate that a short-term, multifaceted smoking cessation program implemented in work sites can affect smoking cessation rates as well as the work-site norms about smoking. C1 SUNY BUFFALO,SCH MED & BIOL SCI,DEPT SOCIAL & PREVENT MED,BUFFALO,NY 14260. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. RP SORENSEN, G (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [2T32 HL07328, 5R01 HL25523] NR 20 TC 34 Z9 34 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1076-2752 J9 J OCCUP ENVIRON MED JI J. Occup. Environ. Med. PD FEB PY 1993 VL 35 IS 2 BP 121 EP 126 DI 10.1097/00043764-199302000-00011 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KL603 UT WOS:A1993KL60300007 PM 8433182 ER PT J AU SCHREIBER, RA KLEINMAN, RE AF SCHREIBER, RA KLEINMAN, RE TI GENETICS, IMMUNOLOGY, AND BILIARY ATRESIA - AN OPENING OR A DIVERSION SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION LA English DT Editorial Material ID REOVIRUS TYPE-3 INFECTION; HISTOCOMPATIBILITY COMPLEX; TWINS C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA 02114 USA. RP SCHREIBER, RA (reprint author), MCGILL UNIV, MONTREAL CHILDRENS HOSP,RES INST, DIV GASTROENTEROL & NUTR,ROOM D-594, 2300 TUPPER ST, MONTREAL H3H 1P3, QUEBEC, CANADA. NR 30 TC 55 Z9 59 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0277-2116 EI 1536-4801 J9 J PEDIATR GASTR NUTR JI J. Pediatr. Gastroenterol. Nutr. PD FEB PY 1993 VL 16 IS 2 BP 111 EP 113 DI 10.1097/00005176-199302000-00001 PG 3 WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics GA KL601 UT WOS:A1993KL60100001 PM 8450373 ER PT J AU SAENZ, NC SCHNITZER, JJ ERAKLIS, AE HENDREN, WH GRIER, HE MACKLIS, RM SHAMBERGER, RC AF SAENZ, NC SCHNITZER, JJ ERAKLIS, AE HENDREN, WH GRIER, HE MACKLIS, RM SHAMBERGER, RC TI POSTERIOR MEDIASTINAL MASSES SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article DE MEDIASTINAL MASS, POSTERIOR; NEUROBLASTOMA; GANGLIONEUROBLASTOMA; GANGLIONEUROMA ID NEURO-BLASTOMA; PROGNOSTIC FACTORS; CHILDREN; TUMORS; GANGLIONEUROBLASTOMA; NEUROBLASTOMAS; AMPLIFICATION C1 CHILDRENS HOSP MED CTR,DEPT SURG,FEGAN 3,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIAT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 20 TC 26 Z9 27 U1 1 U2 3 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 FEB PY 1993 VL 28 IS 2 BP 172 EP 176 DI 10.1016/S0022-3468(05)80268-4 PG 5 WC Pediatrics; Surgery SC Pediatrics; Surgery GA KM707 UT WOS:A1993KM70700014 PM 8437074 ER PT J AU SIBER, GR WERNER, BG HALSEY, NA REID, R ALMEIDOHILL, J GARRETT, SC THOMPSON, C SANTOSHAM, M AF SIBER, GR WERNER, BG HALSEY, NA REID, R ALMEIDOHILL, J GARRETT, SC THOMPSON, C SANTOSHAM, M TI INTERFERENCE OF IMMUNE GLOBULIN WITH MEASLES AND RUBELLA IMMUNIZATION SO JOURNAL OF PEDIATRICS LA English DT Article ID ANTIBODY-RESPONSE; VACCINE; CHILDREN; INFANTS; INFECTIONS; AGE AB Passively acquired antibody may interfere with the active antibody response to live viral vaccines such as measles and rubella. To evaluate the duration of this inhibitory effect, we measured the measles and rubella antibody responses of Apache children immunized with measles, mumps, and rubella vaccine at varying intervals after administration of an immune globulin termed bacterial polysaccharide immune globulin (BPIG). This specific immune globulin contained measles and rubella antibody titers similar to those in standard intramuscularly and intravenously administered immune globulins. Antibody responses to measles vaccine were inhibited for up to 5 months after a BPIG dose of 80 mg IgG per kilogram of body weight, but responses to rubella vaccine were inhibited for only 2 months. Most children who had a decreased measles antibody response to primary measles, mumps, and rubella immunization given 11/2 to 4 months after BPIG administration responded to a booster immunization given 6 months after their lost BPIG dose. We conclude that high doses of immune globulin (>10 mg/kg) may inhibit the antibody response to measles for more than 3 months. We propose that the interval between administration of immune globulin and measles and rubella immunization be adjusted on the basis of the dose of immune globulin. C1 MASSACHUSETTS STATE LAB INST, MASSACHUSETTS PUBL HLTH BIOL LABS, BOSTON, MA USA. MASSACHUSETTS STATE LAB INST, VIROL LABS, BOSTON, MA USA. JOHNS HOPKINS UNIV, SCH MED, DEPT INT HLTH, CTR AMER INDIANA & ALASKAN NAT HLTH, BALTIMORE, MD 21205 USA. US PHS, INDIAN HOSP, WHITERIVER, AZ USA. RP SIBER, GR (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, INST INFECT DIS, 44 BINNEY ST, BOSTON, MA 02115 USA. FU NIAID NIH HHS [AI 20738, AI 24996, AI 18125] NR 30 TC 40 Z9 45 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 FEB PY 1993 VL 122 IS 2 BP 204 EP 211 DI 10.1016/S0022-3476(06)80114-9 PG 8 WC Pediatrics SC Pediatrics GA KL328 UT WOS:A1993KL32800005 PM 8429432 ER PT J AU LORR, M STRACK, S AF LORR, M STRACK, S TI SOME NEO-PI 5-FACTOR PERSONALITY PROFILES SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article ID CLUSTER-ANALYSIS; MODEL; TESTS AB The aim of this study was to identify any clusters of score profiles to be found in a college sample of 236 subjects administered the five-factor NEO [Neuroticism, Extroversion, Openness] Personality Inventory (Costa & McCrae, 1985). Application of Ward's agglomerative hierarchical procedure to the score profiles disclosed six clusters that were replicated in a K-means partitioning process. The six clusters were then compared by a one-way analysis of variance (ANOVA) with respect to their mean five higher order scores on the Interpersonal Style Inventory (Lorr, 1986). The highly significant F tests provided confirmation of the characteristics of the cluster profiles isolated. C1 US DEPT VET AFFAIRS,OUTPATIENT CLIN,LOS ANGELES,CA. RP LORR, M (reprint author), CATHOLIC UNIV AMER,INST LIFE CYCLE,WASHINGTON,DC 20064, USA. NR 29 TC 7 Z9 7 U1 0 U2 1 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0022-3891 J9 J PERS ASSESS JI J. Pers. Assess. PD FEB PY 1993 VL 60 IS 1 BP 91 EP 99 DI 10.1207/s15327752jpa6001_6 PG 9 WC Psychology, Clinical; Psychology, Social SC Psychology GA KK615 UT WOS:A1993KK61500006 PM 16370836 ER PT J AU BUCKNER, CK FISHLEDER, RI CONKLIN, R WILL, JA DORAN, O GRAZIANO, FM AF BUCKNER, CK FISHLEDER, RI CONKLIN, R WILL, JA DORAN, O GRAZIANO, FM TI PHARMACOLOGICAL MODULATION OF THE INFLUENCE OF THE EPITHELIUM ON IMMUNOLOGICAL-INDUCED AND NONIMMUNOLOGIC-INDUCED HISTAMINE-RELEASE AND CONTRACTION IN GUINEA-PIG SUPERFUSED TRACHEAL STRIPS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID MEDIATOR RELEASE; SMOOTH-MUSCLE; ANTAGONISTS; REMOVAL; POTENT; CELLS AB The influence of the epithelium on contractions and histamine release evoked by ovalbumin and d-tubocurarine has been examined in guinea pig superfused tracheal strips under several experimental conditions. Without drug pretreatment, removal of the epithelium resulted in larger (P < .05) total histamine released by ovalbumin, 10(-4) to 10(-1) mg/ml, and by d-tubocurarine, 3 x 10(-3) M. In the presence of indomethacin, 5 x 10(-6) M, epithelium removal resulted in elevated histamine release only at smaller ovalbumin concentrations, 10(-4) and 10(-3) mg/ml. Indomethacin did not change the influence of the epithelium on histamine release by d-tubocurarine. Indomethacin treatment abolished the influence of the epithelium on ovalbumin-induced tracheal contraction. With indomethacin, larger (P < .05) histamine release was seen with ovalbumin, 10(-1) and 1 mg/ml, when the epithelium was intact. The larger histamine release in response to ovalbumin, 10(-1) mg/ml, in the presence of the epithelium was unaltered by pyrilamine. 10(-6) M, cimetidine, 10(-4) M, and thioperamide, 10(-6) M. to block histamine H-1, H-2 and H-3 receptors, respectively. Therefore, histamine released by ovalbumin does not stimulate histamine release through an action on these receptors when the epithelium is intact. In the presence, but not in the absence, of the epithelium, A64077, 10(-5) M, and ICI198615, 10(-8) and 10(-6) M, inhibitors of 5-lipoxygenase and LTD4/E4 receptors, respectively, inhibited histamine release by ovalbumin, 10(-1) mg/ml. Histamine release by ovalbumin, 10(-4) mg/ml, and d-tubocurarine, 3 x 10(-3) M, studied with or without epithelium was not altered by A64077 or ICI198615. It is concluded that increased histamine release after epithelium removal and challenge by smaller (10(-3) mg/ml) ovalbumin concentrations results, partially, from effects of a released cyclo-oxygenase product(s). Elevated histamine release seen in the presence of the epithelium at larger (10(-1) mg/ml) ovalbumin concentrations results, at least in part, through an action of released peptidoleukotrienes. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53706. RP BUCKNER, CK (reprint author), ICI AMER INC,ICI PHARMACEUT GRP,WILMINGTON,DE 19899, USA. FU NHLBI NIH HHS [HL33237, HL28585] NR 20 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD FEB PY 1993 VL 264 IS 2 BP 717 EP 725 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KM432 UT WOS:A1993KM43200028 PM 7679735 ER PT J AU SCHUMACHER, HR VANLINTHOUDT, D MANNO, CS CUCKLER, JM ATHREYA, BH AF SCHUMACHER, HR VANLINTHOUDT, D MANNO, CS CUCKLER, JM ATHREYA, BH TI DIFFUSE CHONDROLYTIC ARTHRITIS IN SICKLE-CELL DISEASE SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE SICKLE CELL DISEASE; CHONDROLYSIS; SYNOVIUM; ELECTRON MICROSCOPY; PHAGOCYTIC CELLS ID ACTIVATION; CHONDROCYTES; COLLAGENASE; ANEMIA; BONE AB A young black man with sickle cell disease with recurrent painful vasoocclusive crises developed at 16 years of age a rapid disabling polyarticular chondrolysis leading to a bilateral hip arthroplasty in 1 year. Light microscopy showed erosion and chondrocyte loss with deep clones in the cartilage and congested vessels with extravasation of red blood cells and mononuclear cells in the synovium. Electron microscopy of the synovium disclosed partially occluded blood vessels and phagocytic cells containing red blood cell debris and crystalline hemoglobin-like material. These observations suggest a role for the phagocytic cells in the joint destruction. C1 CHILDRENS SEASHORE HOUSE PHILADELPHIA,CTR PEDIAT RHEUMATOL,PHILADELPHIA,PA. CHILDRENS HOSP PHILADELPHIA,DIV HEMATOL,PHILADELPHIA,PA. UNIV PENN,SCH MED,DEPT MED,DEPT ORTHOPAED SURG,PHILADELPHIA,PA 19104. RP SCHUMACHER, HR (reprint author), VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA 19104, USA. NR 27 TC 10 Z9 10 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD FEB PY 1993 VL 20 IS 2 BP 385 EP 389 PG 5 WC Rheumatology SC Rheumatology GA KM696 UT WOS:A1993KM69600034 PM 8474082 ER PT J AU ARAGAM, JR MAIN, J GUERRERO, JL VLAHAKES, GJ SOUTHERN, JF ADAMS, MS WEYMAN, AE LEVINE, RA AF ARAGAM, JR MAIN, J GUERRERO, JL VLAHAKES, GJ SOUTHERN, JF ADAMS, MS WEYMAN, AE LEVINE, RA TI DOPPLER COLOR FLOW MAPPING OF EPICARDIAL CORONARY-ARTERIES - INITIAL OBSERVATIONS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY; ATHEROSCLEROTIC LESIONS; BLOOD-FLOW; VALIDATION; VELOCITY; VISUALIZATION; ULTRASOUND; CATHETER; STENOSES; PATTERNS AB Objectives. We addressed the hypothesis that blood flow could be imaged by Doppler color flow mapping of the coronary arteries and characteristic patterns described in normal and diseased vessels. Background. Echocardiographic imaging of the epicardial coronary arteries has been suggested as a useful adjunct to their intraoperative evaluation. Addition of Doppler color flow mapping could potentially enhance this evaluation by displaying the flow disturbance produced by anatomic lesions whose physiologic significance may otherwise be uncertain. In experimental models, such displays could also potentially provide insights into the pathophysiology of coronary blood flow and stenosis. Methods. Epicardial coronary arteries were examined with a high resolution 7-MHz linear phased-array transducer both in vivo and in vitro. 1) The coronary arteries were studied in the beating hearts of 10 open chest dogs in which experimental stenoses were also created; the maximal extent of the arterial tree in which flow could be seen in the most ideal setting was also examined in four additional excised perfused canine hearts. 2) Six excised human coronary arteries were perfused in a pulsatile manner to determine whether abnormal flow patterns could be prospectively identified and subsequently correlated with pathologic evidence of stenosis. Results. All normal coronary artery segments studied showed homogeneous flow without evidence of flow disturbance. In the excised heart, flow could be visualized to the distal extent of the epicardial vessels; in the open chest model, visualization of the proximal 5 to 6 cm was comparable, although surrounding structures limited access to the terminal portions of the vessels. The stenotic lesions created in the canine hearts (n = 9) showed recognizable alterations in the flow pattern: localized aliasing, proximal blood flow acceleration, distal flow disturbance and recirculatory flow. In the excised human arteries, these features identified 12 lesions, all of which corresponded to areas of greater-than-or-equal-to 50% lumen narrowing by pathologic examination. Conclusion. Blood flow in the epicardial coronary arteries can be imaged by Doppler color flow mapping and characteristic flow patterns described in normal and diseased vessels. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,NONINVAS CARDIAC LAB,BOSTON,MA 02114. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 FU NHLBI NIH HHS [HL 38176] NR 39 TC 11 Z9 11 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 FEB PY 1993 VL 21 IS 2 BP 478 EP 487 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KL126 UT WOS:A1993KL12600029 PM 8426014 ER PT J AU LAM, JYT CHESEBRO, JH BADIMON, L FUSTER, V AF LAM, JYT CHESEBRO, JH BADIMON, L FUSTER, V TI EXOGENOUS PROSTACYCLIN DECREASES VASOCONSTRICTION BUT NOT PLATELET THROMBUS DEPOSITION AFTER ARTERIAL INJURY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID LUMINAL CORONARY ANGIOPLASTY; VASCULAR ENDOTHELIUM; SHEAR RATE; WALL; VASOSPASM; SEROTONIN; MODEL; THROMBOXANE-A2; DIPYRIDAMOLE; RESTENOSIS AB Objectives. The aim of this study was to examine the in vivo effects of increasing doses of prostacyclin (PGI2) on arterial vasoconstriction, platelet deposition and their interrelation after balloon injury of porcine carotid arteries. Background. Extensive platelet deposition and localized vasoconstriction occur acutely after arterial injury in vivo. The platelet deposition and vasoconstriction are directly correlated, and previous studies suggest that platelets may mediate the vasoconstrictive response. However, it is unclear whether vasoconstriction contributes to platelet deposition. Methods. Seven pigs received an intravenous infusion of PGI2 at 10 ng/kg per min (PGI2 10), 8 pigs at 50 ng/kg per min (PGI2 50) and 4 pigs at 500 ng/kg per min (PGI2 500); 24 pigs with saline infusion served as a control group. Results. Vasoconstriction immediately proximal and distal to the balloon-dilated carotid arterial segment where selective endothelial injury occurred was directly related to indium-111-labeled platelet deposition within the dilated segment in both control pigs and PGI2-treated pigs. However, this relation was such that for any given level of platelet deposition relative to control, PGI2 decreased vasoconstriction in a dose-related manner. None of the treatments (PGI2 10, 50 or 500) decreased quantitative In-111-labeled platelet deposition or the proportion of deeply injured arteries with mural thrombus (91%, 70% or 75%, respectively, p = NS) compared with values in control pigs (81%). Thus, vasoconstriction was directly related to platelet deposition in control and PGI2-treated animals, but vasodilation alone did not decrease platelet deposition. Conclusions. Intravenous infusion of PGI2 significantly decreases vasoconstriction but not platelet deposition or mural thrombosis after arterial injury by balloon dilation. It is therefore unlikely that vasoconstriction mediates platelet deposition in this model. At hemodynamically tolerated doses, PGI2 infusion probably will not prevent the thrombotic complications associated with angioplasty. C1 MAYO CLIN & MAYO FDN,DIV CARDIOVASC DIS & INTERNAL MED,ROCHESTER,MN 55905. MASSACHUSETTS GEN HOSP,DIV CARDIOL,BOSTON,MA 02114. RES COUNCIL CANADA,OTTAWA,ON,CANADA. RI BADIMON, LINA/O-4711-2014; Fuster, Valentin/H-4319-2015 OI BADIMON, LINA/0000-0002-9162-2459; Fuster, Valentin/0000-0002-9043-9986 NR 33 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 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD FEB PY 1993 VL 21 IS 2 BP 488 EP 492 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KL126 UT WOS:A1993KL12600030 PM 8426015 ER PT J AU HUTTER, AM AF HUTTER, AM TI INNOVATIONS THAT WORK, MEMBERS WHO CARE - ACC CHAPTERS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material RP HUTTER, AM (reprint author), MASSACHUSETTS GEN HOSP,ACC BLDG,SUITE 467,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD FEB PY 1993 VL 21 IS 2 BP 550 EP 552 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KL126 UT WOS:A1993KL12600040 ER PT J AU ERSHLER, WB AF ERSHLER, WB TI INTERLEUKIN-6 - A CYTOKINE FOR GERONTOLOGISTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID LYMPHOID-CELL NEOPLASMS; II BSF-2/IL-6 GENE; MULTIPLE-MYELOMA; GROWTH-FACTOR; CASTLEMANS DISEASE; SIGNAL TRANSDUCER; PRECURSOR PROTEIN; EXPRESSION; MICE; IL-6 AB Interleukin-6 (IL-6) is a mulfifunctional cytokine that presumably plays its major role as a mediator of several of the acute phase inflammatory responses. These include inflammatory cell and lymphocyte activation and hepatocellular stimulation of acute phase protein synthesis. IL-6 expression is normally low, and serum levels are usually non-detectable in the absence of inflammation. However, with advancing age, serum levels become detectable, and it is proposed that this reflects an age-associated loss in the normal regulation of gene expression for this molecule. The cause of this is most likely multi-factorial, but there is evidence that it relates to an age-associated loss of T cell immunoregulatory functions as well as menopausal loss of estrogen. In any event, the 'inappropriate' presence of IL-6 results in many changes typical of chronic inflammation. There is also speculation that IL-6 may contribute to the pathogenesis of several diseases of late-life including lymphoma, osteoporosis, and Alzheimer's disease. In this review the biology of this important cytokine is presented and its relevance to gerontology is highlighted. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI 53705. UNIV WISCONSIN,DEPT CHEM,GERIATR SECT,MADISON,WI 53706. FU NIA NIH HHS [AG 007831, AG 00451] NR 60 TC 270 Z9 279 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD FEB PY 1993 VL 41 IS 2 BP 176 EP 181 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA KL148 UT WOS:A1993KL14800015 PM 8426042 ER PT J AU SHILATIFARD, A MERKLE, RK HELLAND, DE WELLES, JL HASELTINE, WA CUMMINGS, RD AF SHILATIFARD, A MERKLE, RK HELLAND, DE WELLES, JL HASELTINE, WA CUMMINGS, RD TI COMPLEX-TYPE N-LINKED OLIGOSACCHARIDES OF GP120 FROM HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 CONTAIN SULFATED N-ACETYLGLUCOSAMINE SO JOURNAL OF VIROLOGY LA English DT Article ID PITUITARY GLYCOPROTEIN HORMONES; HAMSTER OVARY CELLS; HIV AGENT INVITRO; DEXTRAN SULFATE; ENVELOPE GLYCOPROTEIN; DICTYOSTELIUM-DISCOIDEUM; MAMMALIAN-CELLS; SIALYLATED OLIGOSACCHARIDES; ENDOPROTEOLYTIC CLEAVAGE; STRUCTURAL DETERMINANTS AB The major envelope glycoproteins gp120 and gp41 of human immunodeficiency virus type 1, the causative agent for human AIDS, contain numerous N-linked oligosaccharides. We report here our discovery that N-acetylglucosamine residues within the complex-type N-linked oligosaccharides of both gp120 and its precursor, gp160, are sulfated. When human Molt-3 cells persistently infected with human T-cell leukemia virus III(B) were metabolically radiolabeled with (SO4)-S-35, gp160, gp120, and to some extent gp41 were radiolabeled. The (SO4)-S-35-labeled oligosaccharides were quantitatively released by N-glycanase treatment and were bound by immobilized Ricinus communis agglutinin I, a lectin that binds to terminal beta-galactosyl residues. The kinetics of release of sulfate upon acid hydrolysis from (SO4)-S-35-labeled gp120 indicate that sulfation occurs in a primary sulfate ester linkage. Methylation analysis of total glycopeptides from Molt-3 cells metabolically radiolabeled with [H-3]glucosamine demonstrates that sulfation occurs at the C-6 position of N-acetylglucosamine. Fragmentation of the gp120-derived (SO4)-S-35-labeled glycopeptides by treatment with hydrazine and nitrous acid and subsequent reduction generated galactosyl-anhydromannitol-6-(SO4)-S-35, which is the expected reaction product from GlcNAc-6-sulfate within a sulfated lactosamine moiety. Charge analysis of the [H-3]galactose- and [H-3]glucosamine-labeled glycopeptides from gp120 and gp160 indicates that approximately 14% of the complex-type N-linked oligosaccharides are sulfated. C1 UNIV OKLAHOMA,HLTH SCI CTR,DEPT BIOCHEM & MOLEC BIOL,POB 26901,941 SL YOUNG BLVD,OKLAHOMA CITY,OK 73104. UNIV GEORGIA,DEPT BIOCHEM,ATHENS,GA 30602. UNIV GEORGIA,COMPLEX CARBOHYDRATE RES CTR,ATHENS,GA 30602. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. FU NCI NIH HHS [P30 CA06516]; NIAID NIH HHS [AI 27135, U01 AI24845] NR 60 TC 40 Z9 40 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 FEB PY 1993 VL 67 IS 2 BP 943 EP 952 PG 10 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000036 PM 8419650 ER PT J AU SHERRARD, DJ HERCZ, G PEI, Y MALONEY, NA GREENWOOD, C MANUEL, A SAIPHOO, C FENTON, SS SEGRE, GV AF SHERRARD, DJ HERCZ, G PEI, Y MALONEY, NA GREENWOOD, C MANUEL, A SAIPHOO, C FENTON, SS SEGRE, GV TI THE SPECTRUM OF BONE-DISEASE IN END-STAGE RENAL-FAILURE - AN EVOLVING DISORDER SO KIDNEY INTERNATIONAL LA English DT Article ID HISTOLOGICAL QUANTITATION; DIALYSIS POPULATION; ALUMINUM DEPOSITION; HIGH PREVALENCE; ILIAC BONE; OSTEODYSTROPHY; HISTOMORPHOMETRY; HYPERCALCEMIA; DEFEROXAMINE; CALCITRIOL AB We have assessed the bone histology in 259 chronic dialysis patients, all of whom were in the same dialysis program. All patients had bone biopsies with quantitative histomorphometry, intact parathyroid hormone (PTH) measurements, basal and deferoxamine stimulated serum aluminum levels. Results demonstrate the increased incidence of the recently described aplastic bone lesion, particularly in patients treated with peritoneal dialysis (PD). Aluminum-related bone disease is much less common than previously described, perhaps in relation to the declining-use of aluminum as a phosphate binder. A different pattern of bone lesions is seen in PD as compared with hemodialysis (HD), with low turnover disorders comprising 66% of the lesions seen in PD and high turnover lesions accounting for 62% of the bone histologic findings in HD. The difference in these patterns may relate to alterations in PTH levels, as mean PTH levels in HD patients were 2-1/2 times the levels found in PD patients (P < 0.0005), while older age, higher prevalence of diabetes and a shorter duration of dialysis may also have contributed to the findings in the PD patients. We suggest that PD, perhaps by maintaining calcium at higher levels, may more effectively suppress the parathyroid gland. C1 UNIV WASHINGTON, SEATTLE, WA 98195 USA. UNIV TORONTO, DEPT MED, TORONTO M5S 1A1, ONTARIO, CANADA. MT SINAI HOSP, SAMUEL LUNENFELD RES INST, CLIN EPIDEMIOL UNIT, TORONTO M5G 1X5, ONTARIO, CANADA. MASSACHUSETTS GEN HOSP, ENDOCRINE UNIT, BOSTON, MA 02114 USA. RP VET ADM MED CTR, DEPT MED, SEATTLE, WA USA. NR 36 TC 565 Z9 583 U1 1 U2 5 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 EI 1523-1755 J9 KIDNEY INT JI Kidney Int. PD FEB PY 1993 VL 43 IS 2 BP 436 EP 442 DI 10.1038/ki.1993.64 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA KH907 UT WOS:A1993KH90700021 PM 8441240 ER PT J AU INGELFINGER, JR AF INGELFINGER, JR TI RENOVASCULAR DISEASE IN CHILDREN SO KIDNEY INTERNATIONAL LA English DT Review ID RENAL-ARTERY STENOSIS; TRANS-LUMINAL ANGIOPLASTY; DIGITAL SUBTRACTION ANGIOGRAPHY; SPONTANEOUSLY HYPERTENSIVE RAT; TERM FOLLOW-UP; NEUROFIBROMATOSIS TYPE-1; FIBROMUSCULAR DYSPLASIA; WILLIAMS SYNDROME; CALCIFIED ELASTOPATHY; OCCLUSIVE DISEASE RP INGELFINGER, JR (reprint author), MASSACHUSETTS GEN HOSP, PEDIAT NEPHROL UNIT, BOSTON, MA 02114 USA. FU NHLBI NIH HHS [HL 40210] NR 164 TC 20 Z9 21 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD FEB PY 1993 VL 43 IS 2 BP 493 EP 505 DI 10.1038/ki.1993.72 PG 13 WC Urology & Nephrology SC Urology & Nephrology GA KH907 UT WOS:A1993KH90700029 PM 8441247 ER PT J AU COBURN, JW AF COBURN, JW TI MINERAL METABOLISM AND RENAL BONE-DISEASE - EFFECTS OF CAPD VERSUS HEMODIALYSIS SO KIDNEY INTERNATIONAL LA English DT Article ID AMBULATORY PERITONEAL-DIALYSIS; CALCIUM MASS-TRANSFER; SERUM ALUMINUM LEVELS; PARATHYROID-HORMONE; VITAMIN-D; SECONDARY HYPERPARATHYROIDISM; PHOSPHATE BINDER; INTRAPERITONEAL DEFEROXAMINE; IONIZED CALCIUM; PLASMA ALUMINUM C1 W LOS ANGELES VET AFFAIRS MED CTR, WADSWORTH DIV, RES SERV, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA USA. RP COBURN, JW (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, WADSWORTH DIV, MED SERV, WILSHIRE & SAWTELLE BLVD, LOS ANGELES, CA 90073 USA. NR 101 TC 25 Z9 25 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 EI 1523-1755 J9 KIDNEY INT JI Kidney Int. PD FEB PY 1993 VL 43 SU 40 BP S92 EP S100 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA KJ410 UT WOS:A1993KJ41000013 PM 8445845 ER PT J AU NISHIKAWA, K ANDRES, G BHAN, AK MCCLUSKEY, RT COLLINS, AB STOW, JL STAMENKOVIC, I AF NISHIKAWA, K ANDRES, G BHAN, AK MCCLUSKEY, RT COLLINS, AB STOW, JL STAMENKOVIC, I TI HYALURONATE IS A COMPONENT OF CRESCENTS IN RAT AUTOIMMUNE GLOMERULONEPHRITIS SO LABORATORY INVESTIGATION LA English DT Article DE CD44; HYALURONIC ACID-BINDING PROTEIN ID RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS; BASEMENT-MEMBRANE DISEASE; T-CELL ACTIVATION; GLOMERULAR CRESCENTS; GOODPASTURE ANTIGEN; HOMING RECEPTOR; MESSENGER-RNA; GROWTH-FACTOR; CD44; NEPHRITIS AB BACKGROUND: Crescent formation is a major feature of rapidly progressive glomerulonephritis and is generally associated with a poor prognosis. Crescents are formed by accumulation of monocyte/macrophages and plasma proteins in Bowman's space, by proliferation of parietal epithelial cells and fibroblasts, and by deposition of the extracellular matrix. Interactions of components of the extracellular matrix with surface receptors of inflammatory cells may be important in crescent formation. One such receptor is the glycoprotein, CD44, whose main ligand is hyaluronate. We performed the present study to determine if hyaluronate is a component of crescents in a model of autoimmune anti-glomerular basement membrane nephritis in rats. EXPERIMENTAL DESIGN: Wistar-Kyoto rats were immunized with bovine glomerular basement membrane, that resulted in severe crescentic glomerulonephritis. Sections of renal tissue were studied with two probes to detect hyaluronate: (a) a soluble CD44-human immunoglobulin fusion protein; and (b) a hyaluronic acid-binding protein. Both probes were revealed by immunofluorescence techniques. The specificity of the reactions was established by selective enzymatic digestions. RESULTS: Marked accumulation of hyaluronate was demonstrated in developing and sclerosing crescents, in association with local infiltration of T lymphocytes and monocyte/macrophages, cells known to express CD44. Lesser amounts of hyaluronate were found in periglomerular infiltrates. CONCLUSIONS: Hyaluronate is an abundant extracellular component of crescents, and may play a critical role in their formation, by its effects on migration and activation of CD44+ lymphocytes, monocyte/macrophages, fibroblasts and epithelial cells. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. OI Stow, Jennifer/0000-0002-5409-9101 FU NCI NIH HHS [CA 55735]; NIDDK NIH HHS [DK-36807]; NIGMS NIH HHS [GM 43257] NR 53 TC 42 Z9 42 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD FEB PY 1993 VL 68 IS 2 BP 146 EP 153 PG 8 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KP470 UT WOS:A1993KP47000003 PM 7680079 ER PT J AU VINK, J THOMAS, L ETOH, T BRUIJN, JA MIHM, MC GATTONICELLI, S BYERS, HR AF VINK, J THOMAS, L ETOH, T BRUIJN, JA MIHM, MC GATTONICELLI, S BYERS, HR TI ROLE OF BETA-1 INTEGRINS IN ORGAN SPECIFIC ADHESION OF MELANOMA-CELLS INVITRO SO LABORATORY INVESTIGATION LA English DT Article DE CELL ADHESION; CRYOSTAT SECTION ID HIGH-ENDOTHELIAL VENULES; ARG-GLY-ASP; EXTRACELLULAR-MATRIX; MALIGNANT-MELANOMA; B-16 MELANOMA; TUMOR-CELLS; FIBRONECTIN RECEPTOR; CANCER METASTASIS; LYMPH-NODES; EXPRESSION AB BACKGROUND: Recent data suggest that the extracellular matrix of organs and heterogeneous integrin expression of tumor cells may influence metastasis distribution. EXPERIMENTAL DESIGN: Three human melanoma cell lines were characterized for integrin expression, in vitro binding to cryostat sections of different organs, and ability to generate experimental metastases in triple immunodeficient mice. RESULTS: The three cell lines exhibited heterogeneous expression of integrins, binding to cryostat sections, and organ colonization. A primary melanoma cell line (PM-WK) did not give rise to experimental metastases, showed scant or mild attachment to only a few organ tissue sections, and showed absent or minimal expression of alpha-integrin subunits tested (VLA 1-6) and alphavbeta3. In contrast, two lymph node derived lines exhibited distinct patterns of organ colonization: MM-RU colonized only the lungs and expressed predominantly alpha2beta1 and alphavbeta3 integrin, whereas MM-AN colonized lung and extrapulmonary sites including pancreas and subcutaneous brown fat and expressed predominantly alpha2beta1 and alpha6beta1 integrin. In vitro, MM-RU exhibited marked attachment to lung, brown fat, kidney, and adrenal with no binding to liver, pancreas, brain, or muscle tissue sections, whereas MM-AN had a similar binding profile but with additional attachment to liver and pancreas. Function blocking anti-beta1 monoclonal antibody inhibited the attachment of MM-RU and MM-AN cells to these tissues (p < 0.001), whereas function blocking anti-alpha5 and an unrelated monoclonal antibody (HLA class 1) did not. Function blocking anti-alpha2 monoclonal antibody inhibited MM-RU cell adhesion (p < 0.001) but not MM-AN adhesion. However, the function blocking monoclonal antibody alpha6beta1 significantly inhibited the binding of MM-AN to these tissues. CONCLUSIONS: These data suggest that alpha2beta1 and alpha6beta1 mediate differential melanoma cell attachment to organ tissue sections in vitro and that differences in integrin expression of these melanoma cells may be involved in differential organ colonization in vivo. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. LEIDEN UNIV,DEPT PATHOL & DERMATOL,2300 RA LEIDEN,NETHERLANDS. NEW ENGLAND MED CTR,DEPT RADIAT ONCOL,BOSTON,MA 02111. NR 50 TC 51 Z9 51 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD FEB PY 1993 VL 68 IS 2 BP 192 EP 203 PG 12 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KP470 UT WOS:A1993KP47000008 PM 7680081 ER PT J AU WILLIAMS, ME SWERDLOW, SH ROSENBERG, CL ARNOLD, A AF WILLIAMS, ME SWERDLOW, SH ROSENBERG, CL ARNOLD, A TI CHROMOSOME-11 TRANSLOCATION BREAKPOINTS AT THE PRAD1/CYCLIN D1 GENE LOCUS IN CENTROCYTIC LYMPHOMA SO LEUKEMIA LA English DT Article ID INTERMEDIATE LYMPHOCYTIC LYMPHOMA; B-CELL LYMPHOMAS; CANDIDATE ONCOGENE; MOLECULAR-CLONING; BCL-1 LOCUS; T(11-14); ABNORMALITIES; REARRANGEMENT; T(11-14)(Q13-Q32); NEOPLASMS AB Centrocytic lymphoma is a CD5-positive B-cell neoplasm. Rearrangements at the chromosome 11q13 bcl-1 breakpoint loci are present in the majority of these lymphomas, as a result of reciprocal translocation with the 14q32 immunoglobulin heavy chain joining genes. Recently, a gene lying approximately 110 kb telomeric of the bcl-1 major translocation cluster breakpoint locus, designated PRAD1, was proposed as a candidate bcl-1 oncogene. Accumulated evidence now indicates that this gene is the postulated bcl-1 oncogens. It encodes a protein with homology to cyclin family proteins designated cyclin D1 (CCND1). In order to determine whether 11q13 translocation breakpoints were present near the PRAD1 coding region in addition to the previously defined bcl-1 sites, we analyzed 27 centrocytic lymphomas by Southern blot using genomic and cDNA probes flanking the first exon of PRAD1. Five samples showed rearrangement at PRAD1 sites. In four of these, the breakpoints could be mapped from approximately one to 25 kb upstream of the first PRAD1 exon; each showed comigration of rearranged PRAD1 and immunoglobulin heavy-chain joining gene bands consistent with the t(11;14)(q13;q32). The fifth case was rearranged with PRAD1 probes only on BamHI-digested DNA, indicating either a point mutation or a polymorphism at this site. This sample also had rearrangement on multiple enzyme digests with the bcl-1 p94PS probe. None of 80 non-centrocytic B-cell neoplasms showed PRAD1 rearrangement. Thus, rearrangement at both bcl-1 and PRAD1 loci is strongly associated with centrocytic lymphoma, and provides a useful molecular marker for classifying this subtype of lymphoma. Furthermore, translocation-induced aberrant expression of the PRAD1 cyclin may lead to deregulated cell cycle control and play an important role in the pathogenesis of centrocytic lymphoma. C1 UNIV PITTSBURGH,DEPT PATHOL & LAB MED,PITTSBURGH,PA 15260. UNIV VIRGINIA,MED CTR,SCH MED,DEPT PATHOL,CHARLOTTESVILLE,VA 22901. UNIV VIRGINIA,MED CTR,SCH MED,DEPT INTERNAL MED,CHARLOTTESVILLE,VA 22901. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. FU NCI NIH HHS [CA 46723, CA 55909]; NIDDK NIH HHS [DK 11794] NR 31 TC 121 Z9 123 U1 1 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD FEB PY 1993 VL 7 IS 2 BP 241 EP 245 PG 5 WC Oncology; Hematology SC Oncology; Hematology GA KN159 UT WOS:A1993KN15900017 PM 8426477 ER PT J AU TURNER, R JEZZARD, P WEN, H KWONG, KK LEBIHAN, D ZEFFIRO, T BALABAN, RS AF TURNER, R JEZZARD, P WEN, H KWONG, KK LEBIHAN, D ZEFFIRO, T BALABAN, RS TI FUNCTIONAL MAPPING OF THE HUMAN VISUAL-CORTEX AT 4 AND 1.5 TESLA USING DEOXYGENATION CONTRAST EPI SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note ID BLOOD; FIELDS; IMAGE; BRAIN; TIME AB The effects of photic stimulation on the visual cortex of human brain were studied by means of gradient-echo echo-planar imaging (EPI). Whole-body 4 and 1.5 T MRI systems, equipped with a small z axis head gradient coil, were used. Variations of image intensity of up to 28% at 4 T, and up to 7% at 1.5 T, were observed in primary visual cortex, corresponding to an increase of blood oxygenation in regions of increased neural activity. The larger effects at 4 T are due to the increased importance of the susceptibility difference between deoxygenated and oxygenated blood at high fields, C1 MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02114. NIH,DEPT DIAGNOST RADIOL,CTR CLIN,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. RP TURNER, R (reprint author), NHLBI,CARDIAC ENERGET LAB,BLDG 10,ROOM B10161,BETHESDA,MD 20892, USA. RI Turner, Robert/C-1820-2008; Balaban, Robert/A-7459-2009; Wen, Han/G-3081-2010; OI Balaban, Robert/0000-0003-4086-0948; Wen, Han/0000-0001-6844-2997; Jezzard, Peter/0000-0001-7912-2251 NR 14 TC 360 Z9 363 U1 0 U2 6 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 FEB PY 1993 VL 29 IS 2 BP 277 EP 279 DI 10.1002/mrm.1910290221 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KM064 UT WOS:A1993KM06400020 PM 8429797 ER PT J AU SIMON, JA AF SIMON, JA TI ASCORBIC-ACID AND CHOLESTEROL GALLSTONES SO MEDICAL HYPOTHESES LA English DT Article ID BILIARY LIPID-COMPOSITION; VITAMIN-C STATUS; ORAL-CONTRACEPTIVES; GUINEA-PIGS; BILE-ACIDS; METABOLISM; PLASMA; WOMEN; HEALTHY; DEFICIENCY AB Decreased activity of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in the catabolism of cholesterol to bile acids, is known to result in increased biliary cholesterol concentration and supersaturation of bile. Supersaturation of bile by cholesterol is a necessary condition for cholesterol gallstone formation. In guinea pigs, the hepatic concentration of ascorbic acid affects the catabolism of cholesterol: hypovitaminosis C reduces cholesterol 7 alpha-hydroxylase activity. Cholesterol gallstones are frequently found in ascorbic acid-deficient guinea pigs. Risk factors for cholesterol gallstones in humans include obesity, aging, estrogen treatment, pregnancy and diabetes. Plasma ascorbic acid levels are reduced in these groups. Vegetarian diets, which typically have high ascorbic acid contents, protect against gallstones. Since ascorbic acid effects the rate-limiting step in the catabolism of cholesterol in the guinea pig and many human risk groups for cholesterol gallstones are associated with reduced ascorbic acid levels, ascorbic acid may play a contributory role in human gallbladder disease. RP SIMON, JA (reprint author), SAN FRANCISCO VA MED CTR,GEN INTERNAL MED SECT 111A1,4150 CLEMENT ST,SAN FRANCISCO,CA 94121, USA. NR 40 TC 22 Z9 23 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 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD FEB PY 1993 VL 40 IS 2 BP 81 EP 84 DI 10.1016/0306-9877(93)90132-A PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KN337 UT WOS:A1993KN33700001 PM 8455479 ER PT J AU POORTMANS, JR JEANLOZ, RW AF POORTMANS, JR JEANLOZ, RW TI URINARY-EXCRETION OF IMMUNOGLOBULINS AND THEIR SUBUNITS IN HUMAN-SUBJECTS BEFORE AND AFTER EXERCISE SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Article AB Immunoglobulins and their subunits in urines collected before and after exercise from healthy human subjects were studied. Quantitative analysis showed that only gammaA- and gammaG-immunoglobulins were excreted as whole molecules in normal urine, at a concentration of 0.35 and 1.70 mug/min., respectively. Exercise enhanced the excretion of both types of molecules. In some cases, gammaD-immunoglobulins were found in ''exercise urine.'' Gel filtration on Sephadex G-150 showed that only gammaG-subunits were present in normal and in ''exercise urine.'' The distribution of gammaG-subunits was not affected by exercise. The authors consider the importance of the present data in relation to renal physiology. C1 MASSACHUSETTS GEN HOSP,CARBOHYDRATE RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. RP POORTMANS, JR (reprint author), UNIV LIBRE BRUXELLES,EFFORT LAB,BRUSSELS 5,BELGIUM. FU NIADDK NIH HHS [AM-3504] NR 37 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD FEB PY 1993 VL 25 IS 2 BP 171 EP 178 PG 8 WC Sport Sciences SC Sport Sciences GA KM063 UT WOS:A1993KM06300001 PM 8450718 ER PT J AU SHOWERS, MO DEMARTINO, JC SAITO, Y DANDREA, AD AF SHOWERS, MO DEMARTINO, JC SAITO, Y DANDREA, AD TI FUSION OF THE ERYTHROPOIETIN RECEPTOR AND THE FRIEND SPLEEN FOCUS-FORMING VIRUS GP55 GLYCOPROTEIN TRANSFORMS A FACTOR-DEPENDENT HEMATOPOIETIC-CELL LINE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; ENV-GENE; MEMBRANE GLYCOPROTEIN; ENVELOPE GLYCOPROTEIN; PRODUCT GP55; CLONING; EXPRESSION; ACTIVATION; GROWTH; ERYTHROLEUKEMIA AB The Friend spleen focus-forming virus (SFFV) gp55 glycoprotein binds to the erythropoietin receptor (EPO-R), causing constitutive receptor signaling and the first stage of Friend erythroleukemia. We have used three independent strategies to further define this transforming molecular interaction. First, using a retroviral selection strategy, we have isolated the cDNAs encoding three fusion polypeptides containing regions of both EPO-R and gp55. These fusion proteins, like full-length gp55, transformed the Ba/F3 factor-dependent hematopoietic cell line and localized the transforming activity of gp55 to its transmembrane domain. Second, we have isolated a mutant of gp55 (F-gp55-M1) which binds, but fails to activate, EPO-R. We have compared the transforming activity of this gp55 mutant with the EPO-R-gp55 fusion proteins and with other variants of gp55, including wild-type polycythemia Friend gp55 and Rauscher gp55. All of the fusion polypeptides and mutant gp55 polypeptides were expressed at comparable levels, and all coimmunoprecipitated with wild-type EPO-R, but only the Friend gp55 and the EPO-R-gp55 fusion proteins constitutively activated wild-type EPO-R. Third, we have examined the specificity of the EPO-R-gp55 interaction by comparing the differential activation of murine and human EPO-R by gp55. Wild-type gp55 had a highly specific interaction with murine EPO-R; gp55 bound, but did not activate, human EPO-R. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. RP SHOWERS, MO (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [R0I-DK43889-01A1] NR 44 TC 31 Z9 31 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 FEB PY 1993 VL 13 IS 2 BP 739 EP 748 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300002 PM 8423798 ER PT J AU GALLO, GJ PRENTICE, H KINGSTON, RE AF GALLO, GJ PRENTICE, H KINGSTON, RE TI HEAT-SHOCK FACTOR IS REQUIRED FOR GROWTH AT NORMAL TEMPERATURES IN THE FISSION YEAST SCHIZOSACCHAROMYCES-POMBE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PROTEIN-BINDING SITES; HUMAN HSP70 PROMOTER; DNA-BINDING; TRANSCRIPTION FACTOR; SACCHAROMYCES-CEREVISIAE; MOLECULAR-CLONING; HELA-CELLS; GENE; ELEMENT; EXPRESSION AB Schizosaccharomyces pombe is becoming an increasingly useful organism for the study of cellular processes, since in certain respects, such as the cell cycle and splicing, it is similar to metazoans. Previous biochemical studies have shown that the DNA binding ability of S. pombe heat shock factor (HSF) is fully induced only under stressed conditions, in a manner similar to that of Drosophila melanogaster and humans but differing from the constitutive binding by HSF in the budding yeasts. We report the isolation of the cDNA and gene for the HSF from S. pombe. S. pombe HSF has a domain structure that is more closely related to the structure of human and D. melanogaster HSFs than to the structure of the budding yeast HSFs, further arguing that regulation of HSF in S. pombe is likely to reflect regulation in metazoans. Surprisingly, the S. pombe HSF gene is required for growth at normal temperatures. We show that the S. pombe HSF gene can be replaced by the D. melanogaster HSF gene and that strains containing either of these genes behave similarly to transiently heat-shocked strains with respect to viability and the level of heat-induced transcripts from heat shock promoters. Strains containing the D. melanogaster HSF gene, however, have lower growth rates and show altered morphology at normal growth temperatures. These data demonstrate the functional conservation of domains of HSF that are required for response to heat shock. They further suggest a general role for HSF in growth of eukaryotic cells under normal (nonstressed) growth conditions. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. FU NIGMS NIH HHS [GM12865, GM43901] NR 48 TC 72 Z9 75 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1993 VL 13 IS 2 BP 749 EP 761 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300003 PM 8423799 ER PT J AU LEES, EM HARLOW, E AF LEES, EM HARLOW, E TI SEQUENCES WITHIN THE CONSERVED CYCLIN BOX OF HUMAN CYCLIN-A ARE SUFFICIENT FOR BINDING TO AND ACTIVATION OF CDC2 KINASE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MATURATION-PROMOTING FACTOR; P34CDC2 PROTEIN-KINASE; CELL-CYCLE; SACCHAROMYCES-CEREVISIAE; M-PHASE; G1-SPECIFIC CYCLINS; MEIOTIC MATURATION; G1 PHASE; PHOSPHORYLATION; YEAST AB Cyclins are pivotal in the coordinate regulation of the cell cycle. By physical association, they are able to activate at least one of the cyclin-dependent kinases, cdc2. How this association between the catalytic moiety and cyclins leads to subsequent activation of the kinase remains unclear. In this report, we describe experiments to investigate this event at a physical level. Our approach was to map the regions required on the cyclin A molecule for interaction with cdc2. We have mapped the contact regions to two small noncontiguous stretches of amino acids, residues 189 to 241 and 275 to 320, both located within the conserved cyclin box domain of the protein. We have further shown that this region not only represents a contact site for cdc2 but apparently represents an intact functional domain with respect to cdc2 activation. This region alone is sufficient to stimulate maturation when injected into immature Xenopus laevis oocytes. This observation implies that events leading to the activation of cdc2 kinase can be mediated through small regions of the cyclin molecule that are located in the cyclin box. These regions contain some of the most highly conserved residues found between all the cyclin members so far identified. This suggests that the cyclin family members may have conserved a similar mechanism to bind and activate cyclin-dependent kinases. RP LEES, EM (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA55339] NR 57 TC 126 Z9 127 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1993 VL 13 IS 2 BP 1194 EP 1201 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300050 PM 8423786 ER PT J AU BHANDARI, B ABBOUD, HE AF BHANDARI, B ABBOUD, HE TI PLATELET DERIVED GROWTH FACTOR-A CHAIN GENE-EXPRESSION IN CULTURED MESANGIAL CELLS - REGULATION BY PHORBOL ESTER AT THE LEVEL OF MESSENGER-RNA ABUNDANCE, TRANSCRIPTION AND MESSENGER-RNA STABILITY SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE CYTOKINE; GROWTH FACTOR; (KIDNEY, HUMAN) ID C-SIS GENE; MICROVASCULAR ENDOTHELIAL-CELLS; GLUTAMINE-SYNTHETASE GENE; HUMAN GLIOBLASTOMA CELLS; SMOOTH-MUSCLE CELLS; B-CHAIN; CYCLIC-AMP; 3T3-L1 ADIPOCYTES; PDGF RECEPTOR; STEROID-HORMONES AB In human renal mesangial cells, platelet derived growth factor (PDGF)-A chain is subject to regulation by protein kinase C (PKC) activator, phorbol ester (phorbol 12-myristate 13-acetate, PMA). Treatment of mesangial cells with PMA increases PDGF-A chain mRNA abundance as analyzed by Northern blot hybridization. In contrast to the effect of PMA, the inactive analog phorbol had no effect on PDGF-A chain mRNA levels, while the PKC inhibitor H7 markedly reduced the PMA-induced increment in PDGF-A chain mRNA. To determine the mechanism by which PMA increases the abundance of this gene, transcription rate was measured by nuclear transcript elongation assay. Treatment of mesangial cells with PMA resulted in a 2-fold increase in PDGF-A chain gene transcription. In addition, we analyzed the effects of PMA on PDGF-A chain mRNA half-life as measured directly by pulse-chase method. PDGF-A chain mRNA has a half-life of about 100 min. The PDGF-A chain mRNA half-life was reduced by 30% (t1/2 = 74 min) when mesangial cells were incubated with PMA. Our results demonstrate that in human renal mesangial cells, the regulation of PDGF-A chain gene expression by PMA is primarily at the level of transcription. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP BHANDARI, B (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK33665, DK43988] NR 49 TC 8 Z9 8 U1 0 U2 0 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 FEB PY 1993 VL 91 IS 1-2 BP 185 EP 191 DI 10.1016/0303-7207(93)90271-K PG 7 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA KL635 UT WOS:A1993KL63500025 PM 8472849 ER PT J AU YAKEL, JL WARREN, RA REPPERT, SM NORTH, RA AF YAKEL, JL WARREN, RA REPPERT, SM NORTH, RA TI FUNCTIONAL EXPRESSION OF ADENOSINE A2B RECEPTOR IN XENOPUS OOCYTES SO MOLECULAR PHARMACOLOGY LA English DT Article ID BRAIN POTASSIUM CHANNEL; RBL-2H3 CELLS; CYCLIC-AMP; RAT-BRAIN; AFFINITY; CURRENTS; BINDING AB RNA was transcribed in vitro from a cDNA clone (RFL9) that encodes the rat adenosine A2b receptor. Xenopus oocytes that had been injected with this RNA several days earlier responded to adenosine (10 mum to 1 mm) with an inward current (45-750 nA) that peaked rapidly and then declined to a lower level; uninjected oocytes showed no effect of adenosine. The current reversed to outward at -25 mV and was blocked by intracellular injection of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid. The action of adenosine (100 mum) was mimicked by 5'-N-ethylcarboxamidoadenosine (10 mum), but not by ATP, N6-cyclohexyladenosine (10 or 100 mum), N6-cyclopentyladenosine (10 mum), 1-deaza-2-chlorocyclopentyladenosine (50 mum), or CGS21680 (1 or 10 mum). It was substantially blocked by 8-cyclopentyl-1,3-dipropylxanthine (1 mum) and by 3,7-dimethyl-1-propargylxanthine (10 mum). The results indicate that activation of adenosine A2b receptors increases a calcium-dependent chloride conductance in Xenopus oocytes, presumably by stimulating phospholipase C. C1 OREGON HLTH SCI UNIV,VOLLUM INST,PORTLAND,OR 97210. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,BOSTON,MA 02114. FU NIDA NIH HHS [DA03160]; NIDDK NIH HHS [DK42125] NR 32 TC 51 Z9 51 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD FEB PY 1993 VL 43 IS 2 BP 277 EP 280 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KN002 UT WOS:A1993KN00200020 PM 8429829 ER PT J AU CALVANIO, R LEVINE, D PETRONE, P AF CALVANIO, R LEVINE, D PETRONE, P TI ELEMENTS OF COGNITIVE REHABILITATION AFTER RIGHT-HEMISPHERE STROKE SO NEUROLOGIC CLINICS LA English DT Review ID RANDOMIZED CONTROLLED TRIAL; RIGHT CEREBRAL INFARCTION; ACQUIRED BRAIN-DAMAGE; LEFT VISUAL NEGLECT; UNILATERAL NEGLECT; SPATIAL NEGLECT; BEHAVIORAL ABNORMALITIES; THALAMIC NEGLECT; ATTENTION; THERAPY C1 SPAULDING REHABIL HOSP,DEPT OCCUPAT THERAPY,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NYU,SCH MED,DEPT NEUROL,NEW YORK,NY 10003. TISCH HOSP,DEPT NEUROL,NEW YORK,NY. RP CALVANIO, R (reprint author), SPAULDING REHABIL HOSP,DEPT NEUROPSYCHOL,125 NASHUA ST,BOSTON,MA 02114, USA. NR 117 TC 19 Z9 19 U1 1 U2 6 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD FEB PY 1993 VL 11 IS 1 BP 25 EP 57 PG 33 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA KM626 UT WOS:A1993KM62600004 PM 8441373 ER PT J AU KEMPER, TL BAUMAN, ML AF KEMPER, TL BAUMAN, ML TI THE CONTRIBUTION OF NEUROPATHOLOGIC STUDIES TO THE UNDERSTANDING OF AUTISM SO NEUROLOGIC CLINICS LA English DT Article ID CELL COUNTS; MEMORY; HIPPOCAMPUS; ETIOLOGY C1 MASSACHUSETTS GEN HOSP,CHILDRENS NEUROL SERV,BOSTON,MA 02114. RP KEMPER, TL (reprint author), BOSTON CITY HOSP,DEPT NEUROL,MED 9,818 HARRISON AVE,BOSTON,MA 02118, USA. NR 30 TC 200 Z9 203 U1 1 U2 11 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD FEB PY 1993 VL 11 IS 1 BP 175 EP 187 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA KM626 UT WOS:A1993KM62600011 PM 8441369 ER PT J AU LO, EH AF LO, EH TI A HEMODYNAMIC ANALYSIS OF INTRACRANIAL ARTERIOVENOUS-MALFORMATIONS SO NEUROLOGICAL RESEARCH LA English DT Article DE ARTERIOVENOUS MALFORMATION; CEREBRAL BLOOD FLOW; HEMORRHAGE; VASCULAR STEAL; BIOMATHEMATICAL MODEL ID CEREBRAL HEMODYNAMICS; BLOOD-FLOW; SYSTEM; STEAL; EMBOLIZATION; DENSITY; MODEL; AVMS AB Abnormal haemodynamics of intracranial arteriovenous malformations (AVMs) may account for a large spectrum of pathophysiology, including vascular steal, haemorrhage, chronic hypoperfusion, and low-grade ischaemia in adjacent brain tissue. The high blood flow rates present in AVMs may also influence treatment complications including, 'perfusion pressure breakthrough' phenomena. In this paper, a biomathematical analysis of haemodynamic alterations in intracranial arteriovenous malformations is presented, based on fluid dynamic formulations of flow rates, cerebral perfusion pressure, intra-AVM pressure gradients, and haemodynamic resistances. The model demonstrates that (1) vascular steal is inversely proportional to the haemodynamic resistance of the AVM, (2) haemorrhage probability is related to the distribution of cerebral perfusion pressure across large thin-walled shunts, (3) normal reperfusion pressure after A VM obliteration is dependent on the ratio of resistance of surrounding vasculature versus any residual AVM, and (4) hyperemic complications post-treatment are likely to occur in high-flow AVMs that demonstrate steal. These results, in general, agree with current clinical impressions. Although the difficulty of obtaining accurate clinical measurements of some of these model parameters precludes a complete empirical testing of the model the biomathematical analysis should provide a useful theoretical framework for understanding the complex haemodynamic perturbations that may influence the pathophysiology and treatment approach for intracranial AVMs. RP LO, EH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR IMAGING & PHARMACEUT RES,MGH E 149,BOSTON,MA 02129, USA. NR 34 TC 19 Z9 23 U1 0 U2 0 PU FOREFRONT PUBL GROUP PI LONDON PA MONOMARK HOUSE 27 OLD GLOUCESTER STREET, LONDON, ENGLAND WC1N 3XX SN 0161-6412 J9 NEUROL RES JI Neurol. Res. PD FEB PY 1993 VL 15 IS 1 BP 51 EP 55 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA KW239 UT WOS:A1993KW23900009 PM 8098854 ER PT J AU LEVINE, DN LEE, JM FISHER, CM AF LEVINE, DN LEE, JM FISHER, CM TI THE VISUAL VARIANT OF ALZHEIMERS-DISEASE - A CLINICOPATHOLOGICAL CASE-STUDY SO NEUROLOGY LA English DT Article ID POSTERIOR CORTICAL ATROPHY; SPATIAL VISION; PROSOPAGNOSIA; DISTURBANCES; DISORDERS; AGRAPHIA; BEHAVIOR; AGNOSIA; DEFECT AB A 59-year-old man developed problems with reading and driving. When first examined, he had great difficulty locating and identifying items by sight. Visual acuity was normal, but contrast sensitivity for low spatial frequencies was severely impaired. The peripheral visual fields were moderately constricted with depressed flicker fusion frequencies, more on the right. Color identification was preserved. The difficulties in identifying and locating objects by sight were aggravated by increasing the complexity and multiplicity of the items in the field of vision and by changing the ambient illumination. Intellect and memory were relatively intact, except for difficulty with calculations. Over a 12-year course the visual defects steadily worsened, and eventually memory and language skills failed. Social manners, perseverance, and affect remained normal. Postmortem examination showed cortical atrophy, predominantly posterior, with abundant neurofibrillary tangles and senile plaques. The density of the tangles was correlated with the severity of the atrophy, being highest in the occipitoparietal areas and lowest in the frontal lobes. Alzheimer's disease can preferentially affect the posterior cerebral hemispheres and cause a dementia presenting with, and dominated by, visual disturbances. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 31 TC 199 Z9 201 U1 0 U2 8 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD FEB PY 1993 VL 43 IS 2 BP 305 EP 313 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA KM768 UT WOS:A1993KM76800010 PM 8437694 ER PT J AU HARDIMAN, O SKLAR, RM BROWN, RH AF HARDIMAN, O SKLAR, RM BROWN, RH TI METHYLPREDNISOLONE SELECTIVELY AFFECTS DYSTROPHIN EXPRESSION IN HUMAN MUSCLE CULTURES SO NEUROLOGY LA English DT Article ID DUCHENNE MUSCULAR-DYSTROPHY; GENE-EXPRESSION; SKELETAL-MUSCLE; CELL LINE; MYOGENESIS; FUSION AB Glucocorticoid therapy slows the progression of Duchenne muscular dystrophy. In muscle cultures, the addition of the glucocorticoid methylprednisolone increases myogenesis in most normal mixed and clonal cultures. Conversely, in some normal clonal and most dystrophic cultures, methylprednisolone inhibits fusion. However, in fusion-arrested normal and Becker muscular dystrophy cultures, dystrophin is expressed independently of fusion and of myosin heavy chain expression, and in some cases, expression is apparently enhanced by methylprednisolone. We suggest that dystrophin is a muscle-specific protein that does not require fusion for expression, and the methylprednisolone-induced enhancement of dystrophin expression may account for some of the clinical benefits of glucocorticoids in vivo. C1 MASSACHUSETTS GEN HOSP,DAY LAB NEUROMUSCULAR RES,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. FU PHS HHS [R01 00787-05] NR 21 TC 14 Z9 16 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 FEB PY 1993 VL 43 IS 2 BP 342 EP 345 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA KM768 UT WOS:A1993KM76800016 PM 8437700 ER PT J AU MCCUE, MP SANDROCK, AW LEE, JM HARRIS, NL HEDLEYWHYTE, ET AF MCCUE, MP SANDROCK, AW LEE, JM HARRIS, NL HEDLEYWHYTE, ET TI PRIMARY T-CELL LYMPHOMA OF THE BRAIN-STEM SO NEUROLOGY LA English DT Article ID CENTRAL-NERVOUS-SYSTEM; PRIMARY CEREBRAL LYMPHOMA; MALIGNANT-LYMPHOMAS; DIAGNOSIS; CNS AB Most primary CNS lymphomas are non-Hodgkin's lymphomas of B-cell lineage. We report a case of a small lymphocytic-type T-cell lymphoma localized primarily to the brainstem and compare the characteristics of primary CNS T-cell lymphomas with those of primary CNS B-cell lymphomas. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT LAB,WARREN 3,14 FRUIT ST,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DIV HLTH SCI & TECHNOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 24 TC 29 Z9 29 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 FEB PY 1993 VL 43 IS 2 BP 377 EP 381 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA KM768 UT WOS:A1993KM76800024 PM 8437706 ER PT J AU CANNON, SC STRITTMATTER, SM AF CANNON, SC STRITTMATTER, SM TI FUNCTIONAL EXPRESSION OF SODIUM-CHANNEL MUTATIONS IDENTIFIED IN FAMILIES WITH PERIODIC PARALYSIS SO NEURON LA English DT Article ID ADYNAMIA EPISODICA HEREDITARIA; ALPHA-SUBUNIT; MESSENGER-RNA; MUSCLE; INACTIVATION; GENE; MEMBRANE; CELLS; MODES; RAT AB Two mutations in the sodium channel alpha subunit that have been implicated as the cause of periodic paralysis were studied by functional expression in a mammalian cell line. Both mutations disrupted inactivation without affecting the time course of the onset of the sodium current or the single-channel conductance. This is the same functional defect that was observed in myotubes cultured from affected patients and proves that these mutations are not benign polymorphisms. Unlike the currents in the myotubes, however, there was no consistent potassium dependence for the noninactivating component. These mutations also define new regions of the sodium channel alpha subunit that are involved in the process of inactivation. C1 MASSACHUSETTS GEN HOSP E,DEPT NEUROL,BOSTON,MA 02129. RP CANNON, SC (reprint author), MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,DEPT NEUROL,BOSTON,MA 02114, USA. OI Strittmatter, Stephen/0000-0001-8188-3092 NR 31 TC 179 Z9 179 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD FEB PY 1993 VL 10 IS 2 BP 317 EP 326 DI 10.1016/0896-6273(93)90321-H PG 10 WC Neurosciences SC Neurosciences & Neurology GA KP685 UT WOS:A1993KP68500018 PM 8382500 ER PT J AU SATHI, S STIEG, PE AF SATHI, S STIEG, PE TI ACQUIRED CHIARI-I MALFORMATION AFTER MULTIPLE LUMBAR PUNCTURES - CASE-REPORT SO NEUROSURGERY LA English DT Article DE CHIARI-I MALFORMATION; DIFFERENTIAL ABSORPTION; SUBDURAL HYGROMA; TRAUMATIC LUMBAR PUNCTURE ID SYRINGOMYELIA; ANOMALIES AB THE AUTHORS PRESENT the history of a patient with a Chiari I malformation ''acquired'' after multiple traumatic lumbar punctures. The genesis of tonsillar descent is believed to be related to persistent leakage of cerebrospinal fluid secondary to the multiple traumatic lumbar punctures. The topic of acquired Chiari I malformations and complications of lumbar puncture is reviewed. C1 BRIGHAM & WOMENS HOSP,CHILDRENS HOSP,DANA FARBER CANCER INST,NEUROSURG SERV,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 26 TC 59 Z9 60 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD FEB PY 1993 VL 32 IS 2 BP 306 EP 309 PG 4 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA KL520 UT WOS:A1993KL52000023 PM 8437671 ER PT J AU KIZUKA, H ELMALEH, DR AF KIZUKA, H ELMALEH, DR TI SELECTIVE MONOMETHYLATION OF THE PRIMARY AMINE FUNCTION USING [C-11] CH3I AND THE N-TRIFLUOROACETYL DERIVATIVE - PREPARATION OF N-[C-11-METHYL]CHLORPHENTERMINE SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Note AB A simple, rapid and efficient method for the preparation of a potential brain blood-flow agent, N-[C-11-methyl]chlorphentermine ([[C-11]NMCP), is described. Optimization of the radiochemical yield of [C-11]NMCP was accomplished by a Gabriel-like reaction which permits the transformation of a primary amine to a secondary amine through a sequence of acylation, deprotonation, monomethylation and saponification. This method precludes the formation of polymethylated by-products which can reduce radiochemical yields, particularly with low specific activity (CO2)-C-11. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV RADIOL SCI & TECHNOL,BOSTON,MA 02114. FU NINDS NIH HHS [NS 20998-03] NR 4 TC 8 Z9 8 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD FEB PY 1993 VL 20 IS 2 BP 239 EP 242 DI 10.1016/0969-8051(93)90121-A PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KL023 UT WOS:A1993KL02300018 PM 8448579 ER PT J AU PUISIEUX, A PONCHEL, F OZTURK, M AF PUISIEUX, A PONCHEL, F OZTURK, M TI P53 AS A GROWTH SUPPRESSOR GENE IN HBV-RELATED HEPATOCELLULAR-CARCINOMA CELLS SO ONCOGENE LA English DT Note ID ANTIGEN; MUTATION; PROTEIN; ALLELES; LIVER AB Mutations of the p53 detected in human hepatocellular carcinomas suggest that its inactivation is a critical step in hepatocellular carcinogenesis. In order to test whether the expression of p53 is compatible with the transformed phenotype of hepatoma cells, we transfected Hep 3B cell line with p53 expression vectors. This cell line, which contains integrated hepatitis B virus sequences, is a good model to study whether the wild-type p53 can function as a tumour suppressor gene in virus-related hepatocellular carcinoma. Wild-type and mutant p53 (Ala143)-expression vectors containing a neo(R) gene were used. The number of antibiotic-resistant colonies was six times lower after transfection with wild-type p53 vector as compared to the mutant vector. As measured by a specific radioimmunoassay, six of eight (75%) colonies randomly selected after mutant p53 transfections expressed the transfected mutant p53 protein. In contrast, out of eight colonies from wild-type p53-transfections, none expressed detectable p53 protein. The absence of p53 protein was due to the selective deletion of transfected wild-type p53 cDNA sequences. These studies demonstrate that the growth of hepatocellular carcinoma cells is not compatible with the expression of wild-type p53. Therefore, p53 should be considered as a tumour suppressor gene in hepatocytes. C1 CTR LEON BERARD,ONCOL MOLEC LAB,F-69373 LYON,FRANCE. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. RI ozturk, mehmet/G-3330-2014 FU NCI NIH HHS [CA-49832, CA-54567] NR 21 TC 38 Z9 38 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1993 VL 8 IS 2 BP 487 EP 490 PG 4 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN006 UT WOS:A1993KN00600028 PM 8381223 ER PT J AU ROSENBERG, CL MOTOKURA, T KRONENBERG, HM ARNOLD, A AF ROSENBERG, CL MOTOKURA, T KRONENBERG, HM ARNOLD, A TI CODING SEQUENCE OF THE OVEREXPRESSED TRANSCRIPT OF THE PUTATIVE ONCOGENE PRAD1/CYCLIN D1 IN 2 PRIMARY HUMAN TUMORS SO ONCOGENE LA English DT Note ID CANDIDATE ONCOGENE; CHROMOSOME 11Q13; SQUAMOUS-CELL; AMPLIFICATION; BCL-1; GENE; CARCINOMAS; EXPRESSION; CYCLINS; LOCUS AB PRAD1 (cyclin Dl) is a recently identified member of the family of cyclin genes, believed to play roles in regulating transitions through the cell cycle. The PRAD1 gene, located at 11q13, has been implicated in the pathogenesis of a variety of tumors, including parathyroid adenomas, t(11;14) bearing B-lymphoid tumors (particularly centrocytic lymphomas) where it is highly likely to be the BCL1 oncogene, and possibly in breast carcinomas and squamous cell cancers of the head and neck as well. PRAD1's tumorigenic influence appears to be effected through overexpression of its normal-sized transcript, but it has not been established whether the transcript's coding sequence is normal or contains oncogenic mutations. We have sequenced the coding region of the overexpressed PRAD1 transcript from two primary tumors with clonal PRAD1 region rearrangements: a benign parathyroid adenoma and a malignant centrocytic lymphoma. Each sequence is identical to the normal PRAD1 cDNA sequence, and presumably encodes normal PRAD1 protein. Thus, PRAD1 likely functions as a direct-acting oncogene whose rearrangement in tumors leads to overexpression or deregulated expression of its normal protein product. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,WELLMAN 503,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA55909]; NIDDK NIH HHS [DK11794] NR 20 TC 60 Z9 60 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1993 VL 8 IS 2 BP 519 EP 521 PG 3 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN006 UT WOS:A1993KN00600034 PM 8426754 ER PT J AU SMITH, DJ ANDERSON, JM KING, WF VANHOUTE, J TAUBMAN, MA AF SMITH, DJ ANDERSON, JM KING, WF VANHOUTE, J TAUBMAN, MA TI ORAL STREPTOCOCCAL COLONIZATION OF INFANTS SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE STREPTOCOCCUS-MITIS; STREPTOCOCCUS-SALIVARIUS; STREPTOCOCCUS-ORALIS; STREPTOCOCCUS-SANGUIS; STREPTOCOCCUS-ANGINOSUS; INFANT ID VIRIDANS STREPTOCOCCI; MILLERI GUTHOF; MUTANS; CAVITY AB The objective of this study was to determine the prevalence and proportions of different streptococcal species among the streptococcal flora during infancy. A total of 60 oral samples were collected by oral swabbing of the buccal mucosa and alveolar ridges of 18 infants before tooth eruption and from buccal and lingual surfaces of teeth after tooth eruption. A total of 549 isolates on mitis salivarius agar were speciated, principally by recently revised biochemical criteria of Kilian et al. Streptococcus mitis biovar 1 predominated, both in prevalence (89%) and proportion of oral streptococci recovered in each sample (median = 87% of streptococcal flora). Streptococcus salivarius was also prevalent (94%) but generally represented a small percentage of the total streptococcal flora (median = 3%). Streptococcus oralis and Streptococcus anginosus strains were detected in approximately one third of predentate and dentate infants in the first year of life. Streptococcus sanguis strains were not detected before tooth eruption, but could be detected in 7/14 of the infants with teeth. Thus, S. mitis constitutes the major component of the initially colonizing streptococcal microbiota of the young infant. C1 FORSYTH DENT CTR, DEPT MICROBIOL, BOSTON, MA 02115 USA. RP FORSYTH DENT CTR, DEPT IMMUNOL, 140 FENWAY, BOSTON, MA 02115 USA. FU NIDCR NIH HHS [DE-06153] NR 20 TC 46 Z9 56 U1 0 U2 1 PU WILEY PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD FEB PY 1993 VL 8 IS 1 BP 1 EP 4 DI 10.1111/j.1399-302X.1993.tb00535.x PG 4 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA KM990 UT WOS:A1993KM99000001 PM 8510978 ER PT J AU WANG, CY STASHENKO, P AF WANG, CY STASHENKO, P TI THE ROLE OF INTERLEUKIN-1-ALPHA IN THE PATHOGENESIS OF PERIAPICAL BONE DESTRUCTION IN A RAT MODEL SYSTEM SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE PERIAPICAL LESION; BONE RESORPTION; INTERLEUKIN-1-ALPHA; BACTERIAL INFECTION ID TUMOR NECROSIS FACTOR; PERIODONTAL-DISEASE; BACTERIAL-INFECTION; ACTIVATING FACTOR; PARATHYROID-HORMONE; INFLAMMATORY CELLS; RESORBING ACTIVITY; MONONUCLEAR-CELLS; MESSENGER-RNA; RESORPTION AB To identify the mediators that stimulate periapical bone resorption following infection, a rat model system was used in which active (rapid) and chronic (slow) phases of bone destruction can be distinguished. Extracts of inflammatory tissues from active lesions contained high levels of bone-resorbing activity, which was destroyed by proteinase K and heat (70-degrees-C), but was unaffected by polymyxin B, indicating the presence of protein mediator(s) rather than lipopolysaccharide. Fast-performance liquid chromatography gel filtration of extracts of active lesions demonstrated that most activity was associated with macromolecules of MW 30-60 kDa and 15-20 kDa, consistent with bone resorptive cytokines, including interleukin 1 (IL-1) and tumor necrosis factor (TNF). Inhibition with cytokine-specific antisera demonstrated that resorbing activity in active lesions was significantly neutralized by anti-IL-1alpha, whereas anti-IL-1beta, anti-TNFalpha and anti-TNFbeta had only slight effect. A lower amount of resorbing activity was present in extracts of chronic lesions, which was also neutralized only by anti-IL1alpha. Inflammatory tissue explants produced more IL-1alpha than IL-1beta in vitro, confirming findings with extracts, and high levels of IL-1alpha were present in active lesions by radioimmunoassay. These data indicate that bone resorption stimulated by bacterial infection is primarily mediated by IL-1alpha in this model. The similarity of cytokines in active and chronic lesions suggests that quantitative rather than qualitative differences in these mediators may account for lesion progression. C1 FORSYTH DENT CTR,DEPT IMMUNOL,140 FENWAY,BOSTON,MA 02115. FU NIDCR NIH HHS [DE 09018] NR 52 TC 79 Z9 84 U1 0 U2 2 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD FEB PY 1993 VL 8 IS 1 BP 50 EP 56 DI 10.1111/j.1399-302X.1993.tb00543.x PG 7 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA KM990 UT WOS:A1993KM99000009 PM 8510985 ER PT J AU WILLIAMS, CS JUPITER, JB AF WILLIAMS, CS JUPITER, JB TI DIAGNOSIS AND TREATMENT OF PROBLEMS OF THE ULNOCARPAL JOINT SO ORTHOPADE LA German DT Article DE ULNOCARPAL JOINT; FOREARM ROTATION; DISTAL RADIOULNAR ARTICULATION; TRIANGULAR FIBROCARTILAGE COMPLEX; ULNAR IMPACTION SYNDROME AB The ulnocarpal joint plays a critical role in hand and wrist function. It serves as part of forearm rotation as well as part of the carpal kinematics. The joint is comprised of the distal radio-ulnar articulation, triangular fibrocartilage complex, lunate, triquetrum, hamate, and pisiform, and the intra and extracapsular ligamentous and soft tissue constraints. Traumatic disruptions as well as chronic inflammatory conditions are commonplace. In addition to standard radiographs, athrography, CT scanning, and MRI studies prove useful. Wrist arthroscopy is becoming of increasing importance in this region of the wrist. Ulnar impaction syndrome may occur associated with malunion of distal radius fracture, ulna positive variance, or chronic TFCC tears. Osteotomy of the distal radius or ulnar shortening osteotomy should be considered. Instability of the distal ulna can be treated with tenodesis procedures, hemiresection arthroplasty, matched ulna resection or the Sauve-Kapandji procedure. RP WILLIAMS, CS (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0085-4530 J9 ORTHOPADE JI Orthopade PD FEB PY 1993 VL 22 IS 1 BP 36 EP 45 PG 10 WC Orthopedics SC Orthopedics GA KP257 UT WOS:A1993KP25700007 PM 8451048 ER PT J AU SHANNON, DC HUNT, CE AF SHANNON, DC HUNT, CE TI SIDS AND SLEEPING POSITION - REPLY SO PEDIATRICS LA English DT Letter ID INFANT-DEATH-SYNDROME; COT DEATH C1 MED COLL OHIO,DEPT PEDIAT,TOLEDO,OH 43699. RP SHANNON, DC (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PULM UNIT,BOSTON,MA 02114, USA. NR 10 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 FEB PY 1993 VL 91 IS 2 BP 511 EP 512 PG 2 WC Pediatrics SC Pediatrics GA KK578 UT WOS:A1993KK57800049 ER PT J AU LILGE, L HAW, T WILSON, BC AF LILGE, L HAW, T WILSON, BC TI MINIATURE ISOTROPIC OPTICAL FIBER PROBES FOR QUANTITATIVE LIGHT DOSIMETRY IN TISSUE SO PHYSICS IN MEDICINE AND BIOLOGY LA English DT Article ID PHOTODYNAMIC THERAPY; REFRACTIVE-INDEX; SCATTERING; DIFFUSION AB A small detector to measure light fluence rates in turbid media and biological tissue, based on an optical fibre with a fluorescent dye-doped tip, is presented. The measured optical power of the fluorescent light transmitted through the fibre is directly proportional to the local fluence rate of the treatment or excitation light at the tip. The detector has been built as small as 170 mum outer diameter, while retaining good mechanical properties for insertion into soft tissue. The detector response is linear with fluence rate over a wide range and isotropic for all angles less than 160-degrees from the forward direction. Hence, the detector can measure accurately the fluence rate in turbid media and biological tissue. This fluorescent tip design has no fundamental restrictions in size and shows comparable isotropy but is less sensitive than, fluence rate detectors based on optical fibres with light-scattering tips. C1 HAMILTON REG CANC CTR,HAMILTON,ON,CANADA. MCMASTER UNIV,HAMILTON L8S 4L8,ONTARIO,CANADA. RP LILGE, L (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LAB PHOTOMED,BOSTON,MA 02114, USA. RI Lilge, lothar/J-6434-2013 NR 25 TC 29 Z9 30 U1 1 U2 4 PU IOP PUBLISHING LTD PI BRISTOL PA TECHNO HOUSE, REDCLIFFE WAY, BRISTOL, ENGLAND BS1 6NX SN 0031-9155 J9 PHYS MED BIOL JI Phys. Med. Biol. PD FEB PY 1993 VL 38 IS 2 BP 215 EP 230 DI 10.1088/0031-9155/38/2/001 PG 16 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA KM278 UT WOS:A1993KM27800001 PM 8437996 ER PT J AU MELAN, MA DONG, XN ENDARA, ME DAVIS, KR AUSUBEL, FM PETERMAN, TK AF MELAN, MA DONG, XN ENDARA, ME DAVIS, KR AUSUBEL, FM PETERMAN, TK TI AN ARABIDOPSIS-THALIANA LIPOXYGENASE GENE CAN BE INDUCED BY PATHOGENS, ABSCISIC-ACID, AND METHYL JASMONATE SO PLANT PHYSIOLOGY LA English DT Article ID STORAGE PROTEIN GENES; HYPERSENSITIVE REACTION; LIPID-PEROXIDATION; SEED LIPOXYGENASE; TOBACCO; LEAVES; IDENTIFICATION; INVOLVEMENT; INHIBITORS; EXPRESSION AB We isolated and characterized a 2.8-kb, full-length, Arabidopsis thaliana cDNA clone encoding a lipoxygenase. DNA sequence analysis showed that the deduced amino acid sequence of the Arabidopsis protein is 72 to 78% similar to that of legume seed lipoxygenases. DNA blot analysis indicated that Arabidopsis contains a single gene, LOX1, with appreciable homology to the cDNA clone. RNA blot analysis showed that the LOX1 gene is expressed in Arabidopsis leaves, roots, inflorescences, and young seedlings. LOXI expression levels were highest in roots and young seedlings. In mature plants, LOX1 mRNA levels increased upon treatment with the stress-related hormones abscisic acid and methyl jasmonate and remained high for at least 96 h. Expression of the LOX1 gene was examined following infiltration of leaves with virulent (Psm ES4326) and avirulent (Pst MM 1 065) strains of Pseudomonas syringae. LOX1 mRNA levels were induced approximately 6-fold by both virulent and avirulent strains; however, the response to avirulent strains was much more rapid. Infiltration of leaves with Pst MM1065 resulted in maximal induction within 12 h, whereas maximal induction by Psm ES4326 did not occur until 48 h. When a cloned avr gene, avrRpt2, was transferred to Psm ES4326, LOX1 mRNA accumulated in a pattern similar to that observed for the avirulent strain Pst MM1065. C1 WELLESLEY COLL,DEPT BIOL SCI,WELLESLEY,MA 02181. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. OHIO STATE UNIV,DEPT PLANT BIOL,COLUMBUS,OH 43210. OHIO STATE UNIV,CTR BIOTECHNOL,COLUMBUS,OH 43210. RI Davis, Keith/C-5623-2009; OI Davis, Keith/0000-0002-7432-8610; Melan, Melissa/0000-0001-6088-7801 FU NIGMS NIH HHS [GM45570] NR 61 TC 233 Z9 267 U1 0 U2 16 PU AMER SOC PLANT PHYSIOLOGISTS PI ROCKVILLE PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 SN 0032-0889 J9 PLANT PHYSIOL JI Plant Physiol. PD FEB PY 1993 VL 101 IS 2 BP 441 EP 450 DI 10.1104/pp.101.2.441 PG 10 WC Plant Sciences SC Plant Sciences GA KM094 UT WOS:A1993KM09400015 PM 7506426 ER PT J AU INOUE, G SUZUKI, K LEE, WPA AF INOUE, G SUZUKI, K LEE, WPA TI ARTERIALIZED VENOUS FLAP FOR TREATING MULTIPLE SKIN DEFECTS OF THE HAND SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Discussion ID ISLAND FLAPS; SURVIVAL; INFLOW; SYSTEM C1 MASSACHUSETTS GEN HOSP,DIV PLAST SURG,AMBULATORY CARE CTR 453,BOSTON,MA 02114. NR 19 TC 16 Z9 16 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD FEB PY 1993 VL 91 IS 2 BP 303 EP 306 DI 10.1097/00006534-199302000-00015 PG 4 WC Surgery SC Surgery GA KK118 UT WOS:A1993KK11800015 ER PT J AU MARKS, DR MARKS, LM AF MARKS, DR MARKS, LM TI FOOD ALLERGY - MANIFESTATIONS, EVALUATION, AND MANAGEMENT SO POSTGRADUATE MEDICINE LA English DT Article ID ADVERSE REACTIONS; INTOLERANCE AB Allergic reactions to food are more common among infants and children but occur in adults as well. Foods that are most often implicated in allergic reactions are eggs, cow's milk, nuts, wheat, soy products, whitefish, and crustacea. Gastrointestinal, respiratory tract, and dermatologic symptoms, as well as systemic anaphylaxis, may develop. In addition to history taking and physical examination, the workup may include skin testing, the radioallergosorbent test, and double-blind oral food challenge. Avoidance of off-ending antigens is the most important aspect of treatment. If exposure occurs, antihistamines and epinephrine may be needed for treatment of an acute reaction. C1 MASSACHUSETTS GEN HOSP,ALLERGY UNIT,BOSTON,MA 02114. RP MARKS, DR (reprint author), MASSACHUSETTS GEN HOSP,CLIN IMMUNOL UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 13 TC 16 Z9 16 U1 0 U2 1 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 0032-5481 J9 POSTGRAD MED JI Postgrad. Med. PD FEB 1 PY 1993 VL 93 IS 2 BP 191 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA KL527 UT WOS:A1993KL52700018 PM 8433953 ER PT J AU HAQQ, CM KING, CY DONAHOE, PK WEISS, MA AF HAQQ, CM KING, CY DONAHOE, PK WEISS, MA TI SRY RECOGNIZES CONSERVED DNA SITES IN SEX-SPECIFIC PROMOTERS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MULLERIAN INHIBITING SUBSTANCE; P450-AROMATASE; TRANSCRIPTION FACTORS; DNA-BINDING PROTEINS; SEXUAL DIMORPHISM ID MULLERIAN INHIBITING SUBSTANCE; TESTIS-DETERMINING GENE; DETERMINING REGION; Y-CHROMOSOME; EXPRESSION; PROTEIN; HORMONE; RAT; DIFFERENTIATION; ENCODES AB Formation of male-specific structures and regression of female primordia are regulated in early male embryogenesis by SRY, a single-copy gene on the Y chromosome. Assignment of SRY as the testis-determining factor in eutherian mammals is supported by molecular analysis of cytogenetic sex reversal (i.e., XX males and XY females) and by complementary studies of transgenic murine models. Here we characterize the putative DNA-binding domain of SRY, which contains a conserved sequence motif shared by high-mobility group nuclear proteins and a newly recognized class of transcription factors. The SRY DNA-binding domain specifically recognizes with nanomolar affinity proximal upstream elements (designated SRYe) in the promoters of the sex-specific genes encoding P450 aromatase and Mullerian inhibiting substance (MIS). P450 aromatase catalyzes the conversion of testosterone to estradiol, and in the male embryo its expression is down-regulated. Conversely, MIS is expressed in the male embryo to induce testicular differentiation and regression of female reproductive ducts. SRYe-binding activity is observed in nuclear extracts obtained from embryonic urogenital ridge immediately preceding morphologic testicular differentiation. Our results support the hypothesis that SRY directly controls male development through sequence-specific regulation of target genes. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT SURG,BOSTON,MA 02114. FU NCI NIH HHS [CA-17393, T32CA-09595]; NICHD NIH HHS [HD-26465] NR 29 TC 134 Z9 137 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 FEB 1 PY 1993 VL 90 IS 3 BP 1097 EP 1101 DI 10.1073/pnas.90.3.1097 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KK813 UT WOS:A1993KK81300067 PM 8430080 ER PT J AU KEYOMARSI, K PARDEE, AB AF KEYOMARSI, K PARDEE, AB TI REDUNDANT CYCLIN OVEREXPRESSION AND GENE AMPLIFICATION IN BREAST-CANCER CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MAMMARY EPITHELIAL-CELLS; MESSENGER-RNA; ONCOGENE; GROWTH; YEAST AB Cyclins are prime cell cycle regulators and are central to the control of major check points in eukaryotic cells. The aberrant expressions of two cyclins (i.e., cyclins A and D1) have been observed in some cancers, suggesting they may be involved in loss of growth control. However, in spite of these occasional changes involving only two cyclins, there.are no clear connections between general derangements of other cyclins or their dependent kinases in a single tumor type. We detected general cyclin overexpression in 3 of 3 breast tumor tissue samples. In addition, using proliferating normal vs. human tumor breast cells as a model system, we observed a number of alterations in cyclin expression: (i) an 8-fold amplification of cyclin E gene in one tumor line, a 64-fold overexpression of its mRNA, and altered expression of its protein; (ii) deranged expression of cyclin E protein in all (10 of 10) tumor cell lines studied; (iii) increased cyclin mRNA stability, resulting in (iv) general overexpression of RNAs and proteins for cyclins A and B and CDC2 in 9 of 10 tumor lines and (v) deranged order of appearance of cyclins in synchronized tumor vs. normal cells, with mitotic cyclins appearing prior to G1 cyclins. These multiple general derangements in cyclin expression in human breast cancer cells provide evidence linking aberrant cyclin expression to tumorigenesis. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP KEYOMARSI, K (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 22427, CA08949-01]; NCRR NIH HHS [S07RR05526-29] NR 32 TC 491 Z9 499 U1 2 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 1 PY 1993 VL 90 IS 3 BP 1112 EP 1116 DI 10.1073/pnas.90.3.1112 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KK813 UT WOS:A1993KK81300070 PM 8430082 ER PT J AU SIMON, MC AF SIMON, MC TI TRANSCRIPTION FACTOR GATA-1 AND ERYTHROID DEVELOPMENT SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Review ID DOMINANT CONTROL REGION; LOCUS-CONTROL REGION; DNA-BINDING FACTOR; BETA-GLOBIN GENE; EMBRYONIC-DEVELOPMENT; REGULATORY ELEMENT; TRANSGENIC MICE; MOUSE EMBRYOS; GAMMA-GLOBIN; FACTOR NF-E1 C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. NR 54 TC 20 Z9 20 U1 1 U2 3 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD FEB PY 1993 VL 202 IS 2 BP 115 EP 121 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KJ373 UT WOS:A1993KJ37300001 PM 8424101 ER PT J AU SCHILDBACH, JF NEAR, RI BRUCCOLERI, RE HABER, E JEFFREY, PD NOVOTNY, J SHERIFF, S MARGOLIES, MN AF SCHILDBACH, JF NEAR, RI BRUCCOLERI, RE HABER, E JEFFREY, PD NOVOTNY, J SHERIFF, S MARGOLIES, MN TI MODULATION OF ANTIBODY-AFFINITY BY A NONCONTACT RESIDUE SO PROTEIN SCIENCE LA English DT Article DE ANTIBODY; ANTIDIGOXIN; MOLECULAR MODELING; MUTAGENESIS; NONCONTACT RESIDUE ID 3-DIMENSIONAL STRUCTURE; MONOCLONAL-ANTIBODY; ANTIGEN-BINDING; COMPLEX; MUTATIONS; SITE; RESOLUTION; REGIONS; ENERGY; HEAVY AB Antibody LB4, produced by a spontaneous variant of the murine anti-digoxin monoclonal antibody 26-10, has an affinity for digoxin two orders of magnitude lower than that of the parent antibody due to replacement of serine with phenylalanine at position 52 of the heavy chain variable region (Schildbach, J.F., Panka, D.J., Parks, D.R., et al., 1991, J. Biol. Chem. 266, 4640-4647). To ''amine the basis for the decreased affinity, a panel of engineered antibodies with substitutions at position 52 was created, and their affinities for digoxin were measured. The antibody affinities decreased concomitantly with increasing size of the substituted side chains, although the shape of the side chains also influenced affinity. The crystal structure of the 26-10 Fab complexed with digoxin (P.D.J., R.K. Strong, L.C. Sieker, C. Chang, R.L. Campbell, G.A. Petsko, E.H., M.N.M., & S.S., submitted for publication) shows that the serine at heavy chain position 52 is not in contact with hapten, but is adjacent to a tyrosine at heavy chain position 33 that is a contact residue. The mutant antibodies were modeled by applying a conformational search procedure to position side chains, using the 26-10 Fab crystal structure as a starting point. The results suggest that each of the substituted side chains may be accommodated within the antibody without substantial structural rearrangement, and that none of these substituted side chains are able to contact hapten. These modeling results are consistent with the substituents at position 52 having only an indirect influence upon antibody affinity. The mutagenesis and modeling results suggest that even conservative replacements of non-contact residues can alter affinity indirectly through their impact on contact residue placement. C1 MASSACHUSETTS GEN HOSP,DEPT MED,JACKSON 1402,BOSTON,MA 02114. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,PRINCETON,NJ 08543. HARVARD UNIV,SCH PUBL HLTH,DIV BIOL SCI,CARDIOVASC BIOL LAB,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. HARVARD UNIV,GRAD SCH ARTS & SCI,PROGRAM IMMUNOL,CAMBRIDGE,MA 02138. FU NHLBI NIH HHS [P01 HL19259] NR 35 TC 51 Z9 51 U1 1 U2 5 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0961-8368 J9 PROTEIN SCI JI Protein Sci. PD FEB PY 1993 VL 2 IS 2 BP 206 EP 214 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KK363 UT WOS:A1993KK36300009 PM 8443598 ER PT J AU DAVIDSON, M KAHN, RS STERN, RG HIRSCHOWITZ, J APTER, S KNOTT, P DAVIS, KL AF DAVIDSON, M KAHN, RS STERN, RG HIRSCHOWITZ, J APTER, S KNOTT, P DAVIS, KL TI TREATMENT WITH CLOZAPINE AND ITS EFFECT ON PLASMA HOMOVANILLIC-ACID AND NOREPINEPHRINE CONCENTRATIONS IN SCHIZOPHRENIA SO PSYCHIATRY RESEARCH LA English DT Article DE ATYPICAL NEUROLEPTICS; TREATMENT-REFRACTORY SCHIZOPHRENIA; ALPHA(2)-ADRENERGIC RECEPTORS; DOPAMINE ID DOPAMINE METABOLISM; CATECHOLAMINE METABOLITES; BRAIN DOPAMINE; RECEPTORS; CHLORPROMAZINE; HALOPERIDOL; DEBRISOQUIN; SEROTONIN; DRUGS; POTENCIES AB Measurement of plasma concentrations of the dopamine metabolite, homovanillic acid (pHVA), is an indirect tool to assess changes in dopamine turnover. Levels of pHVA have been reported to decrease during treatment with conventional antidopaminergic, neuroleptics, with the decrement correlating with symptomatic improvement in schizophrenic symptoms. Clozapine, an atypical neuroleptic, is the only drug proved to be effective in treatment-refractory patients. However, the mechanism mediating this unique efficacy has not been fully elucidated. This study examined the effect of clozapine on pHVA concentrations in schizophrenic patients. Since clozapine potently binds to alpha2-adrenergic receptors, plasma norepinephrine (pNE) concentrations were also measured. Twenty-eight treatment-refractory schizophrenic patients (24 men, 4 women) were treated with clozapine (up to 600 mg/day) for 5 weeks, after a minimum 1-week drug-free period. Symptomatology and pHVA and pNE concentrations were measured at the last drug-free day and weekly for 5 weeks. Fourteen patients responded to clozapine treatment, while an equal number did not. Mean pHVA concentrations did not significantly change during treatment with clozapine. Although clozapine tended to lower pHVA concentrations in treatment responders, the effect was small and not significant. Clozapine treatment significantly raised pNE concentrations, but this did not differentiate responders from nonresponders to clozapine. These findings suggest that clozapine's effect on DA turnover is small and that clozapine may be effective in treatment-refractory schizophrenia by mechanisms other than, or in addition to, dopamine receptor blockade. However, since about one-third of NE is metabolized into HVA, the clozapine-induced increase in pNE may have overshadowed a possible lowering effect of clozapine on pHVA. C1 BRONX VET ADM MED CTR,CLIN RES UNIT,BRONX,NY. BRONX VET ADM MED CTR,HPLC LAB,BRONX,NY. CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. FU NIMH NIH HHS [R01 MH-37922-07] NR 43 TC 36 Z9 36 U1 1 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD FEB PY 1993 VL 46 IS 2 BP 151 EP 163 DI 10.1016/0165-1781(93)90017-B PG 13 WC Psychiatry SC Psychiatry GA KU969 UT WOS:A1993KU96900005 PM 8483974 ER PT J AU GROSS, TM JARVIK, ME ROSENBLATT, MR AF GROSS, TM JARVIK, ME ROSENBLATT, MR TI NICOTINE ABSTINENCE PRODUCES CONTENT-SPECIFIC STROOP INTERFERENCE SO PSYCHOPHARMACOLOGY LA English DT Article DE ABSTINENCE; INTRUSIVE THOUGHTS; NICOTINE; PRIMING; SEMANTIC ACTIVATION; STROOP INTERFERENCE ID POSTTRAUMATIC-STRESS-DISORDER; THREAT CUES; ANXIETY-STATES; INFORMATION; MEMORY AB Adult, male smokers were randomly assigned to be nicotine abstinent for 12 h (n = 10) or to smoke normally for the same period of time (n = 10). Performance on a modified version of the Stroop (1935) color-naming task, where subjects named the color of ink in which each of a series of words was written, showed that abstinent smokers took significantly longer to color-name words related to cigarette smoking (e.g., Lighter) than to color-name neutral control words (e.g., Pennant). Non-abstinent smokers showed a significant difference in the opposite direction. These results suggest that nicotine abstinence decreases the ability to ignore the meaning of smoking-related information, This finding supports the hypothesis that abstinence produces a content-specific shift in attentional focus. The present pattern of results cannot be explained by a general decrease in cognitive function due to nicotine abstinence. C1 W LOS ANGELES VA MED CTR,LOS ANGELES,CA 90073. RP GROSS, TM (reprint author), UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90024, USA. NR 16 TC 123 Z9 124 U1 0 U2 6 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD FEB PY 1993 VL 110 IS 3 BP 333 EP 336 DI 10.1007/BF02251289 PG 4 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KL525 UT WOS:A1993KL52500011 PM 7831427 ER PT J AU CLEARY, PD REILLY, DT GREENFIELD, S MULLEY, AG WEXLER, L FRANKEL, F MCNEIL, BJ AF CLEARY, PD REILLY, DT GREENFIELD, S MULLEY, AG WEXLER, L FRANKEL, F MCNEIL, BJ TI USING PATIENT REPORTS TO ASSESS HEALTH-RELATED QUALITY-OF-LIFE AFTER TOTAL HIP-REPLACEMENT SO QUALITY OF LIFE RESEARCH LA English DT Article DE HIP REPLACEMENT; HEALTH STATUS; RHEUMATOID ARTHRITIS; QUALITY OF LIFE ID OF-LIFE; DISABILITY; ARTHRITIS; OUTCOMES; VALIDITY; SCALES; CARE; QUESTIONNAIRE; ARTHROPLASTY; SENSITIVITY AB Data on disease severity, co-morbidity, and process of care were obtained from the medical records of 356 patients without rheumatoid arthritis undergoing a first unilateral total hip replacement at four teaching hospitals in California and Massachusetts. Socio-demographic characteristics, functional status prior and subsequent to hospitalization, and improvement in health status were measured with a patient questionnaire 12 months after discharge. Completed questionnaires were received from 284 patients, a reponse rate of 79.8%. The questionnaire was acceptable to patients, reliable, and had good construct validity. The data indicate substantial benefits from hip arthroplasty. As expected, pre-surgical functioning was a strong predictor of outcomes 1 year after surgery. Controlling for pre-surgical functioning, age was not related to outcomes. C1 HARVARD UNIV,SCH MED,DEPT ORTHOPED SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT HLTH CARE POLICY,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CTR COST EFFECT CARE,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NEW ENGLAND MED CTR,INST IMPROVEMENT MED CARE & HLTH,BOSTON,MA 02111. STANFORD UNIV,MED CTR,STANFORD,CA 94305. FU NIA NIH HHS [AG08331-01] NR 48 TC 39 Z9 40 U1 3 U2 5 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0962-9343 J9 QUAL LIFE RES JI Qual. Life Res. PD FEB PY 1993 VL 2 IS 1 BP 3 EP 11 DI 10.1007/BF00642884 PG 9 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA LF052 UT WOS:A1993LF05200001 PM 8490615 ER PT J AU STEARNS, N ROSS, DM AF STEARNS, N ROSS, DM TI CHANGING PATTERNS OF DOCTOR-PATIENT COMMUNICATION - THE PATIENT PERSPECTIVE SO QUALITY OF LIFE RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0962-9343 J9 QUAL LIFE RES JI Qual. Life Res. PD FEB PY 1993 VL 2 IS 1 BP 50 EP 50 PG 1 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA LF052 UT WOS:A1993LF05200010 ER PT J AU DATTA, R WEICHSELBAUM, R KUFE, DW AF DATTA, R WEICHSELBAUM, R KUFE, DW TI IONIZING-RADIATION DOWN-REGULATES HISTONE H1 GENE-EXPRESSION BY TRANSCRIPTIONAL AND POSTTRANSCRIPTIONAL MECHANISMS SO RADIATION RESEARCH LA English DT Article ID MESSENGER-RNA DEGRADATION; HELA-CELL CYCLE; PROTEIN-SYNTHESIS; DNA-REPLICATION; PROMOTER REGION; HUMAN H-1; KAPPA-B; 3' END; SEQUENCE; BINDING C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. PRITZKER SCH MED,CHICAGO,IL 60637. UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. FU NCI NIH HHS [CA55241, CA41068] NR 43 TC 14 Z9 14 U1 0 U2 0 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD FEB PY 1993 VL 133 IS 2 BP 176 EP 181 DI 10.2307/3578354 PG 6 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA KN250 UT WOS:A1993KN25000006 PM 8438058 ER PT J AU GOLDBERG, MA ROSENTHAL, DI CHEW, FS BLICKMAN, JG MILLER, SW MUELLER, PR AF GOLDBERG, MA ROSENTHAL, DI CHEW, FS BLICKMAN, JG MILLER, SW MUELLER, PR TI NEW HIGH-RESOLUTION TELERADIOLOGY SYSTEM - PROSPECTIVE-STUDY OF DIAGNOSTIC-ACCURACY IN 685 TRANSMITTED CLINICAL CASES SO RADIOLOGY LA English DT Article DE IMAGES, DISPLAY; IMAGES, TRANSMISSION; PICTURE ARCHIVING AND COMMUNICATION SYSTEM (PACS); RADIOLOGY AND RADIOLOGISTS, DESIGN OF RADIOLOGICAL FACILITIES; VIDEO SYSTEMS ID TOTAL DIGITAL RADIOLOGY; OBSERVER PERFORMANCE; SPATIAL-RESOLUTION; PROJECTION RADIOGRAPHY; CHEST RADIOGRAPHY; REQUIREMENTS; FILM; ROC; WORKSTATION; EXPERIENCE AB To compare the accuracy of interpretation of digitized radiographs with that of plain films, the authors prospectively evaluated the first 685 plain film cases (530 adult and 155 pediatric cases, each of which consisted of one or more images) transmitted from an outpatient center 18 miles (approximately 29 km) to a hospital radiology department by means of a high-speed teleradiology system. Plain films were digitized and transmitted via a T-1 (1.544 Mbit/sec) data link for display on high-resolution (2,560 x 2,048-pixel) workstations. Radiologists at the hospital used a copy of the radiology requisition that had been faxed from the remote center. Interpretation of the digital images was followed by review of the original plain radiographs within 1 working day. Discrepant interpretations occurred in 18 cases (2.6%) (sensitivity, 96%; specificity, 99%); an arbitration panel decided that they were associated with observer performance more than with the fidelity of the digital display. It is concluded that primary diagnosis without review of the original plain radiographs is feasible with state-of-the-art teleradiology systems. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP GOLDBERG, MA (reprint author), HARVARD UNIV,32 FRUIT ST,BOSTON,MA 02114, USA. OI Chew, Felix/0000-0003-2711-2013 NR 38 TC 69 Z9 69 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD FEB PY 1993 VL 186 IS 2 BP 429 EP 434 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KH843 UT WOS:A1993KH84300029 PM 8421746 ER PT J AU KINNEY, TB LEE, MJ FILOMENA, CA KREBS, TL DAWSON, SL SMITH, PL RAAFAT, N MUELLER, PR AF KINNEY, TB LEE, MJ FILOMENA, CA KREBS, TL DAWSON, SL SMITH, PL RAAFAT, N MUELLER, PR TI FINE-NEEDLE BIOPSY - PROSPECTIVE COMPARISON OF ASPIRATION VERSUS NONASPIRATION TECHNIQUES IN THE ABDOMEN SO RADIOLOGY LA English DT Article DE ABDOMEN, BIOPSY; ABDOMEN, CT; ABDOMEN, US; BIOPSIES, TECHNOLOGY ID CYTOLOGY AB A prospective study was designed to compare the aspiration (suction method) and nonaspiration (nonsuction method) techniques of fine-needle biopsy (FNB) in 50 consecutive patients with abdominal pathologic conditions. Sites of biopsy included liver (n = 24), retroperitoneum (n = 9), adrenal gland (n = 5), pancreas (n = 4), omentum (n = 4), and miscellaneous sites (n = 4). Aspiration and nonaspiration FNBs were performed in each lesion with 22-gauge needles, and results were interpreted by a single cytopathologist. Cytologic specimens obtained with each technique were analyzed for diagnostic accuracy, total number of cell clusters per biopsy (graded 0-10, 10-20, 20-30, and > 30), presence of crush artifact, and amount of blood present (graded from 0 to +3). No significant differences were seen between the aspiration and nonaspiration techniques with regard to number of cell clusters per biopsy (44 of 50 specimens vs 42 of 50) (P < .0003), amount of blood present (grade 2.3 vs 2.2) (P < .0003), and amount of crush artifact. The positive predictive value for the aspiration technique was 91.5% versus 74% for the nonaspiration technique. The aspiration technique of FNB appears superior to the nonaspiration technique in the abdomen. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 11 TC 25 Z9 25 U1 0 U2 2 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD FEB PY 1993 VL 186 IS 2 BP 549 EP 552 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KH843 UT WOS:A1993KH84300049 PM 8421763 ER PT J AU LEE, AH LEVINSON, AI SCHUMACHER, HR AF LEE, AH LEVINSON, AI SCHUMACHER, HR TI HYPOGAMMAGLOBULINEMIA AND RHEUMATIC DISEASE SO SEMINARS IN ARTHRITIS AND RHEUMATISM LA English DT Article DE HYPOGAMMAGLOBULINEMIA; AGAMMAGLOBULINEMIA; IMMUNE DEFICIENCY ID SYSTEMIC LUPUS-ERYTHEMATOSUS; COMMON VARIABLE HYPOGAMMAGLOBULINEMIA; SELECTIVE IGA DEFICIENCY; X-LINKED AGAMMAGLOBULINEMIA; UREAPLASMA-UREALYTICUM; GOLD THERAPY; MYCOPLASMA-PNEUMONIAE; SEPTIC ARTHRITIS; INFLAMMATORY POLYARTHRITIS; IMMUNOGLOBULIN DEFICIENCY C1 UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MED,DIV ALLERGY & IMMUNOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. NR 91 TC 75 Z9 78 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0049-0172 J9 SEMIN ARTHRITIS RHEU JI Semin. Arthritis Rheum. PD FEB PY 1993 VL 22 IS 4 BP 252 EP 264 DI 10.1016/0049-0172(93)80073-O PG 13 WC Rheumatology SC Rheumatology GA KN212 UT WOS:A1993KN21200004 PM 8484132 ER PT J AU BUJKO, K SUIT, HD SPRINGFIELD, DS CONVERY, K AF BUJKO, K SUIT, HD SPRINGFIELD, DS CONVERY, K TI WOUND-HEALING AFTER PREOPERATIVE RADIATION FOR SARCOMA OF SOFT-TISSUES SO SURGERY GYNECOLOGY & OBSTETRICS LA English DT Article ID LIMB-SPARING SURGERY; THERAPY; IRRADIATION; COMPLICATIONS; CHEMOTHERAPY; RESECTION; EXTREMITY; BRACHYTHERAPY; RADIOTHERAPY; SURVIVAL AB Morbidity from wound healing was retrospectively analyzed in a series of 202 consecutive patients with tumors of the soft tissue of die extremities, torso and head and neck region who were treated with preoperative irradiation and conservative operation at the Massachusetts General Hospital between january 1971 and June 1989. A radiation boost dose was given to 143 patients (71 percent) postoperatively. The overall wound complication rate was 37 percent. One patient died because of necrotizing fasciitis. In 33 instances (16.5 percent), secondary operation was necessary, including six patients (3 percent) who required amputation. The wounds in the remaining 40 patients (20 percent) were treated without operation. Multivariate analyses of the data showed the factors that were significantly associated with wound morbidity: tumor in the lower extremity (p<0.001), increasing age (p= 0.004) and postoperative boost with interstitial implant (p=0.016). Accelerated fractionation (BID, two fractions per day) reached borderline statistical significance (p=0.074). Two other factors showed association with wound morbidity by univariate analysis, but not in multivariate model: high pathologic grade (p=0.02) and estimated volume of resected specimen greater-than-or-equal-to 200 milliliters (p=0.065). Patient gender, intercurrent disease (diabetes or hypertension), obesity, maximal tumor size, primary versus recurrent tumor, duration of bed rest postoperatively, dose of postoperative boost radiation, the use of postoperative boost, the use of adjuvant chemotherapy and year of treatment did not show significant importance for wound morbidity. When the severe wound complications (defined as requiring secondary operation and including the patient who died because of necrotizing fasciitis) were considered, among all analyzed variables, only localization of tumor in the lower extremity as a single factor was significant (p<0.001). Techniques for managing the wound are considered which are judged likely to contribute to a decrease of the incidence of wound healing delays. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,COK 301,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED,BOSTON,MA 02114. NR 29 TC 94 Z9 97 U1 0 U2 0 PU FRANKLIN H MARTIN FOUNDATION PI CHICAGO PA 55 E ERIE ST, CHICAGO, IL 60611 SN 0039-6087 J9 SURG GYNECOL OBSTET JI Surg. Gynecol. Obstet. PD FEB PY 1993 VL 176 IS 2 BP 124 EP 134 PG 11 WC Obstetrics & Gynecology; Surgery SC Obstetrics & Gynecology; Surgery GA KK498 UT WOS:A1993KK49800005 PM 8421799 ER PT J AU KLAR, E MALL, G MESSMER, K HERFARTH, C RATTNER, DW WARSHAW, AL AF KLAR, E MALL, G MESSMER, K HERFARTH, C RATTNER, DW WARSHAW, AL TI IMPROVEMENT OF IMPAIRED PANCREATIC MICROCIRCULATION BY ISOVOLEMIC HEMODILUTION PROTECTS PANCREATIC MORPHOLOGY IN ACUTE BILIARY PANCREATITIS SO SURGERY GYNECOLOGY & OBSTETRICS LA English DT Article ID MOLECULAR WEIGHT DEXTRAN; BLOOD-FLOW; RAT AB Impairment of the pancreatic microcirculation is a characteristic finding in experimental biliary pancreatitis. Isovolemic hemodilution with dextran 60 has been proven to maintain pancreatic capillary perfusion. To evaluate the significance of this therapeutic approach with respect to histologic changes, intravital microscopic assessment of the microcirculation was combined with a morphometric analysis of the pancreas by means of light microscopy in rabbits (n=18). Pancreatic capillary perfusion was maintained in the rabbits subjected to hemodilution 30 minutes after the induction of pancreatitis with 54 percent of the capillaries still being perfused at 12 hours, compared with only 16 percent in the control group. The improved capillary perfusion resulted in a significant reduction of those changes considered potentially reversible (cell vacuolization and interstitial edema) that surround zones of necrosis. However, because of the early establishment of necrosis in this model, hemodilution was unsuccessful in preventing all cell death. Hemodilution can limit the progressive extension of pancreatic injury in this model of biliary pancreatitis. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,15 PARKMAN ST,SUITE 336,BOSTON,MA 02114. UNIV HEIDELBERG,DEPT GEN & EXPTL SURG,W-6900 HEIDELBERG,GERMANY. UNIV HEIDELBERG,DEPT PATHOL,W-6900 HEIDELBERG,GERMANY. NR 39 TC 51 Z9 53 U1 0 U2 0 PU FRANKLIN H MARTIN FOUNDATION PI CHICAGO PA 55 E ERIE ST, CHICAGO, IL 60611 SN 0039-6087 J9 SURG GYNECOL OBSTET JI Surg. Gynecol. Obstet. PD FEB PY 1993 VL 176 IS 2 BP 144 EP 150 PG 7 WC Obstetrics & Gynecology; Surgery SC Obstetrics & Gynecology; Surgery GA KK498 UT WOS:A1993KK49800008 PM 8421802 ER PT J AU SALAZAR, M DEULOFEUT, R YUNIS, JJ BING, DH YUNIS, EJ AF SALAZAR, M DEULOFEUT, R YUNIS, JJ BING, DH YUNIS, EJ TI A FAST PCR-SSP METHOD FOR HLA-DQ GENERIC TYPING SO TISSUE ANTIGENS LA English DT Note DE PCR; PCR-SSP; HLA-DQ GENETIC ID DNA C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP SALAZAR, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT IMMUNOGENET,ROOM 740,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 20531 HL 29583] NR 10 TC 18 Z9 19 U1 0 U2 1 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 FEB PY 1993 VL 41 IS 2 BP 102 EP 106 DI 10.1111/j.1399-0039.1993.tb01987.x PG 5 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA KR693 UT WOS:A1993KR69300008 PM 8475488 ER PT J AU WALLACE, EL SURGENOR, DM HAO, HS AN, J CHAPMAN, RH CHURCHILL, WH AF WALLACE, EL SURGENOR, DM HAO, HS AN, J CHAPMAN, RH CHURCHILL, WH TI COLLECTION AND TRANSFUSION OF BLOOD AND BLOOD COMPONENTS IN THE UNITED-STATES, 1989 SO TRANSFUSION LA English DT Article ID DONATION; DONORS AB To probe recent trends in transfusion practice and their effect on the adequacy of the national blood resource, transfusions and collections in the United States in 1989 were studied, by using data shared by the American Association of Blood Banks, the American Red Cross, and the Council of Community Blood Centers, together with results from a sample survey of the 3600 hospitals that were not members of the national organizations. Statistical methods were used to estimate national activities. The total US supply of blood in 1989 was 14,229,000 units, an increase of 1.2 percent over the supply in 1987. Red cell transfusions were 12,059,000 units. A total of 3,159,000 patients underwent transfusion with whole blood and/or red cells (mean, 3.8 units/patient). Preoperative autologous deposits of 655,000 units by 310,000 patients represented an increase of 65 percent over the level in 1987. However, only 356.000 units (54%) were transfused to the patients who preoperatively deposited them; of the remainder, 13,000 units were crossed over for transfusion to other patients, while 286,000 units were never used. Directed donations, 350,000 units, were provided for 130,000 intended recipients, but only 97,000 units (28%) were transfused to their intended recipients; of the balance, 59,000 units (17%) were crossed over and 194,000 units (55%) were never transfused. Total platelet transfusion were equivalent to 7,258,000 units in 1989, for an increase of 13.7 percent over totals in 1987. C1 CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV HEMATOL,BOSTON,MA 02115. SUNY BUFFALO,SCH MANAGEMENT,BUFFALO,NY 14260. CTR MANAGEMENT SYST,WILLIAMSVILLE,NY. FU NHLBI NIH HHS [HL-33774] NR 12 TC 130 Z9 132 U1 0 U2 3 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD FEB PY 1993 VL 33 IS 2 BP 139 EP 144 DI 10.1046/j.1537-2995.1993.33293158046.x PG 6 WC Hematology SC Hematology GA KM071 UT WOS:A1993KM07100009 PM 8430453 ER PT J AU HOSENPUD, JD SHIPLEY, GD MORRIS, TE HEFENEIDER, SH WAGNER, CR AF HOSENPUD, JD SHIPLEY, GD MORRIS, TE HEFENEIDER, SH WAGNER, CR TI THE MODULATION OF HUMAN AORTIC ENDOTHELIAL-CELL ICAM-1 (CD-54) EXPRESSION BY SERUM CONTAINING HIGH TITERS OF ANTI-HLA ANTIBODIES SO TRANSPLANTATION LA English DT Note ID ADHESION MOLECULE EXPRESSION; HEART-TRANSPLANTATION; LYMPHOCYTES-T; REJECTION; SURVIVAL; MHC AB Allograft recipients who have preformed antibodies to MHC determinants or develop these antibodies posttransplantation have a higher incidence of cellular rejection and graft loss. It is unclear whether this association is an etiologic one or whether the presence of these antibodies solely identifies individuals with a more pronounced alloimmunologic response. To determine whether antibodies to MHC determinants have a direct role in enhancing cell-mediated immunity, specifically in altering effector-target cell adhesion, the expression of endothelial cell surface intercellular adhesion molecule-1 (ICAM-1) in response to serum with high-titer anti-HLA antibodies was investigated. The target cells used were a pool of blood group 0 human aortic endothelial cells (HAECs) representing a wide range of HLA-A, B, C, and DR phenotypes. The test serum was serum pooled from 30 highly sensitized individuals (panel-reactive antibody 80%). Antibody binding to HAECs, and HAEC expression of class I and class II major histocompatibility (MHC) antigens and ICAM-1 were assessed by flow cytometry. General HAEC metabolic changes were assessed by H-3-uridine incorporation as a measure of RNA synthesis. Test serum resulted in almost a 14-fold increase in HAEC surface ICAM-1 expression compared with control serum, and titrations of test serum yielded a strong correlation between IgG bound to HAECs and HAEC ICAM-1 expression (r=0.92). Test serum induced no change in expression of HAEC class I or class Il MHC antigens, or H-3-uridine incorporation. The HAEC ICAM-1-inducing ability of the test serum was retained by concentrating the high molecular weight (>100 kilodaltons) fraction of the test serum, isolation and purification of IgG from the test serum, and lost by absorbing his fraction with pooled platelets, suggesting that the activity was mediated by antibodies directed against MHC class I determinants. These data suggest that the presence of anti-HLA antibodies is more than a marker for individuals with greater alloreactive responsiveness. Anti-HLA antibodies may directly and specifically alter adhesion of effector cells to the allograft. C1 OREGON CARDIAC TRANSPLANT PROGRAM,IMMUNOBIOL RES LAB,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,IMMUNOL RES LAB,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,DEPT MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,DEPT CELL BIOL & ANAT,PORTLAND,OR 97201. FU NHLBI NIH HHS [1-RO1-HL43369] NR 20 TC 21 Z9 21 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD FEB PY 1993 VL 55 IS 2 BP 405 EP 411 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN015 UT WOS:A1993KN01500032 PM 7679530 ER PT J AU HIRSCH, F PONCET, P FREEMAN, S GRESS, RE SACHS, DH DRUET, P HIRSCH, R AF HIRSCH, F PONCET, P FREEMAN, S GRESS, RE SACHS, DH DRUET, P HIRSCH, R TI ANTIFECTION - A NEW METHOD FOR TARGETED GENE TRANSFECTION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID CELLS; MOUSE C1 CHILDRENS HOSP MED CTR,DIV RHEUMATOL,ELLAND & BETHESDA AVES,CINCINNATI,OH 45229. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,BOSTON,MA. TULANE UNIV,NEW ORLEANS,LA 70118. HOP BROUSSAIS,INSERM,U28,F-75674 PARIS 14,FRANCE. NR 5 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 138 EP 139 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100047 PM 8438253 ER PT J AU EMERY, DW SMITH, CV SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C AF EMERY, DW SMITH, CV SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C TI EXPRESSION OF ALLOGENEIC CLASS-II CDNA IN SWINE PERIPHERAL-BLOOD MONONUCLEAR-CELLS FOLLOWING RETROVIRAL-MEDIATED GENE-TRANSFER INTO BONE-MARROW SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID TRANSPLANTATION C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. NHLBI,BETHESDA,MD 20892. NR 7 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 140 EP 141 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100048 PM 7679808 ER PT J AU FISHBEIN, JM GIANELLO, P NICKELEIT, V VITIELLO, D BLANCHO, G LATINNE, D NAKAJIMA, K ROSENGARD, B COLVIN, R SACHS, DH AF FISHBEIN, JM GIANELLO, P NICKELEIT, V VITIELLO, D BLANCHO, G LATINNE, D NAKAJIMA, K ROSENGARD, B COLVIN, R SACHS, DH TI INTERLEUKIN-2 REVERSES THE ABILITY OF CYCLOSPORINE TO INDUCE TOLERANCE TO CLASS-I DISPARATE KIDNEY ALLOGRAFTS IN MINIATURE SWINE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID MAJOR HISTOCOMPATIBILITY COMPLEX; TRANSPLANTATION C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA. FU NIAID NIH HHS [3R01 AI 31046-0251] NR 9 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 322 EP 323 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100117 PM 8438318 ER PT J AU LATINNE, D GIANELLO, P SMITH, CV NICKELEIT, V KAWAI, T BEADLE, M HAUG, C SYKES, M LEBOWITZ, E BAZIN, H COLVIN, R COSIMI, AB SACHS, DH AF LATINNE, D GIANELLO, P SMITH, CV NICKELEIT, V KAWAI, T BEADLE, M HAUG, C SYKES, M LEBOWITZ, E BAZIN, H COLVIN, R COSIMI, AB SACHS, DH TI XENOTRANSPLANTATION FROM PIG TO CYNOMOLGUS MONKEY - APPROACH TOWARD TOLERANCE INDUCTION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,TRANSPLANT UNIT,BOSTON,MA 02129. UNIV CATHOLIQUE LOUVAIN,EXPTL IMMUNOL UNIT,B-1200 BRUSSELS,BELGIUM. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02129. BIOTRANSPLANT INC,BOSTON,MA. NR 7 TC 25 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 336 EP 338 PN 1 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100123 PM 8438325 ER PT J AU SACHS, DH BODINE, DM MOULTON, AD PEARSON, DA NIENHUIS, AW SYKES, M AF SACHS, DH BODINE, DM MOULTON, AD PEARSON, DA NIENHUIS, AW SYKES, M TI TOLERANCE INDUCTION USING AUTOLOGOUS BONE-MARROW MODIFIED WITH AN ALLOGENEIC CLASS-I MHC GENE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID TRANSPLANTS C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. RP SACHS, DH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,MGH E,BLDG 149,BOSTON,MA 02129, USA. FU PHS HHS [N01-H1-19054] NR 5 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 348 EP 349 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100128 PM 8438329 ER PT J AU SMITH, CV FISHBEIN, J NAKAJIMA, K ROSENGARD, BR GUZZETTA, PC SACHS, DH AF SMITH, CV FISHBEIN, J NAKAJIMA, K ROSENGARD, BR GUZZETTA, PC SACHS, DH TI EFFECT OF TOLERANCE TO ALLOGENEIC MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS ON REJECTION ACROSS MINOR ANTIGEN DIFFERENCES SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID MINIATURE SWINE; TRANSPLANTATION C1 NCI,TRANSPLANTAT BIOL SECT,IMMUNOL BRANCH,BETHESDA,MD 20892. RP SMITH, CV (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH,BOSTON,MA 02129, USA. FU NIAID NIH HHS [IF32 AI08577-01, 5 R01 AI31046-02] NR 7 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 364 EP 365 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100136 PM 8438337 ER PT J AU BARRETT, LV RIMM, IJ WIENS, GR SEIDMAN, JG KIRKMAN, RL AF BARRETT, LV RIMM, IJ WIENS, GR SEIDMAN, JG KIRKMAN, RL TI INSIGHTS INTO THE MECHANISM OF ALLOGRAFT ACCEPTANCE IN T-CELL RECEPTOR (BETA-CHAIN) TRANSGENIC MICE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM C1 BRIGHAM & WOMENS HOSP,DEPT SURG,75 FRANCIS ST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 2 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 366 EP 367 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100137 PM 8438338 ER PT J AU DELMONICO, FL KNOWLES, RW COLVIN, RB CAVENDER, DE KAWAI, T BEDLE, M STROKA, D PREFFER, FI HAUG, C COSIMI, AB AF DELMONICO, FL KNOWLES, RW COLVIN, RB CAVENDER, DE KAWAI, T BEDLE, M STROKA, D PREFFER, FI HAUG, C COSIMI, AB TI IMMUNOSUPPRESSION OF CYNOMOLGUS RENAL-ALLOGRAFT RECIPIENTS WITH HUMANIZED OKT4A MONOCLONAL-ANTIBODIES SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN SURG SERV,TRANSPLANTAT UNIT,BOSTON,MA 02114. RW JOHNSON PHARMACEUT RES INST,RARITAN,NJ. RP DELMONICO, FL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114, USA. RI Stroka, Deborah/F-1806-2013 FU NHLBI NIH HHS [P01-HL-18646] NR 4 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 784 EP 785 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100300 PM 8438479 ER PT J AU WEE, S KAWAI, T KNOWLES, R COLVIN, R COSIMI, AB AF WEE, S KAWAI, T KNOWLES, R COLVIN, R COSIMI, AB TI POTENT CD8+ CTLS DETECTED IN ANTI-CD4 (OKT4A) MAB IMMUNOSUPPRESSED CYNOMOLGUS RECIPIENTS WITH PROLONGED ALLOGRAFT SURVIVAL SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM C1 MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. KW JOHNSON PHARMACEUT RES INST,RARITAN,NJ. RP WEE, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,TRANSPLANTAT UNIT,WHITE 546,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-18646] NR 6 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 794 EP 795 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100305 PM 8438484 ER PT J AU LEE, R GLIMCHER, LH AUCHINCLOSS, H AF LEE, R GLIMCHER, LH AUCHINCLOSS, H TI EVIDENCE THAT A 4-CELL CLUSTER MAY PRIME CYTOTOXIC T-CELLS DURING GRAFT-REJECTION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID SKIN ALLOGRAFT-REJECTION; INVIVO; MICE C1 MASSACHUSETTS GEN HOSP,DEPT SURG,TRANSPLANTAT UNIT,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL36372, HL18646]; NIAID NIH HHS [AI21569] NR 9 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 847 EP 849 PN 2 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200001 PM 8442245 ER PT J AU OHTANI, H STRAUSS, HW SOUTHERN, JF TAMATANI, T MIYASAKA, M ISOBE, M AF OHTANI, H STRAUSS, HW SOUTHERN, JF TAMATANI, T MIYASAKA, M ISOBE, M TI IMAGING OF INTERCELLULAR-ADHESION MOLECULE-1 INDUCTION IN REJECTING HEART - A NEW SCINTIGRAPHIC APPROACH TO DETECT EARLY ALLOGRAFT-REJECTION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID ENDOTHELIAL-CELLS; ICAM-1; INTERFERON; ADHERENCE C1 UNIV TOKYO,DEPT INTERNAL MED 3,BUNKYO KU,TOKYO 113,JAPAN. MASSACHUSETTS GEN HOSP,DIV NUCL MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TOKYO METROPOLITAN INST MED SCI,DEPT IMMUNOL,TOKYO 113,JAPAN. NR 16 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 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 867 EP 869 PN 2 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200008 PM 8095110 ER PT J AU VACANTI, CA KIM, W UPTON, J VACANTI, MP MOONEY, D SCHLOO, B VACANTI, JP AF VACANTI, CA KIM, W UPTON, J VACANTI, MP MOONEY, D SCHLOO, B VACANTI, JP TI TISSUE-ENGINEERED GROWTH OF BONE AND CARTILAGE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID ARTICULAR-CARTILAGE; CHONDROCYTES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PLAST SURG,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. CREIGHTON UNIV,DEPT PATHOL,OMAHA,NE 68178. MIT,DEPT CHEM ENGN,CAMBRIDGE,MA 02139. DEBORAH HEART & LUNG INST,DEPT PATHOL,RUTHERFORD,NJ. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. RP VACANTI, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,WHITE 5,BOSTON,MA 02114, USA. NR 15 TC 111 Z9 128 U1 3 U2 10 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 1019 EP 1021 PN 2 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200074 PM 8442027 ER PT J AU ISOBE, M IHARA, A AF ISOBE, M IHARA, A TI TOLERANCE INDUCTION AGAINST CARDIAC ALLOGRAFT BY ANTI-ICAM-1 AND ANTI-LFA-1 TREATMENT - T-CELLS RESPOND TO INVITRO ALLOSTIMULATION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC C1 MASSACHUSETTS GEN HOSP,PATHOL RES LAB,BOSTON,MA 02114. RP ISOBE, M (reprint author), UNIV TOKYO,DEPT INTERNAL MED 3,BUNKYO KU,TOKYO 113,JAPAN. NR 5 TC 30 Z9 30 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 1079 EP 1080 PN 2 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200098 PM 8095106 ER PT J AU FERRARA, JLM ABHYANKAR, S GILLILAND, DG AF FERRARA, JLM ABHYANKAR, S GILLILAND, DG TI CYTOKINE STORM OF GRAFT-VERSUS-HOST DISEASE - A CRITICAL EFFECTOR ROLE FOR INTERLEUKIN-1 SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID POLYMERASE CHAIN-REACTION; TUMOR NECROSIS FACTOR; RECEPTOR ANTAGONIST; MESSENGER-RNA; INVIVO; QUANTITATION; INHIBITION; MARROW; SKIN; DNA C1 CHILDRENS HOSP MED CTR,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP FERRARA, JLM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,ROOM 1640,44 BINNEY ST,BOSTON,MA 02115, USA. NR 13 TC 77 Z9 80 U1 1 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 1216 EP 1217 PN 2 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200156 PM 8442093 ER PT J AU SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA AF SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA TI SELECTIVE-INHIBITION OF CD4 GRAFT-VERSUS-HOST ACTIVITY IN IL-2-TREATED MICE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID DISEASE C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,BOSTON,MA 02129, USA. FU NCI NIH HHS [R01CA55290]; NIAID NIH HHS [R01AI31158] NR 6 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 1225 EP 1226 PN 2 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200159 PM 8442096 ER PT J AU LEE, LA SACHS, DH SYKES, M AF LEE, LA SACHS, DH SYKES, M TI EFFECT OF NATURAL-KILLER-CELL DEPLETION ON LONG-TERM MULTILINEAGE ALLOGENEIC BONE-MARROW ENGRAFTMENT SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID GRAFT-REJECTION; MICE RP LEE, LA (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129, USA. FU NCI NIH HHS [T32-CA09216]; PHS HHS [R01-55290, R01-31158] NR 5 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 1246 EP 1247 PN 2 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200168 PM 8442104 ER PT J AU CHOPEK, M ALOSCO, S SALAZAR, M YUNIS, EJ AF CHOPEK, M ALOSCO, S SALAZAR, M YUNIS, EJ TI UNRELATED DONOR MATCHING FOR BONE-MARROW TRANSPLANTATION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID MIXED-LYMPHOCYTE CULTURE; HLA-DR; DP; INDIVIDUALS; HLA-DR4 C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP CHOPEK, M (reprint author), AMER RED BLOOD SERV,NE REGION,180 RUSTCRAFT RD,DEDHAM,MA 02026, USA. NR 16 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 1255 EP 1258 PN 2 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200171 PM 8442106 ER PT J AU MOGIL, JS MAREK, P YIRMIYA, R BALIAN, H SADOWSKI, B TAYLOR, AN LIEBESKIND, JC AF MOGIL, JS MAREK, P YIRMIYA, R BALIAN, H SADOWSKI, B TAYLOR, AN LIEBESKIND, JC TI ANTAGONISM OF THE NONOPIOID COMPONENT OF ETHANOL-INDUCED ANALGESIA BY THE NMDA RECEPTOR ANTAGONIST MK-801 SO BRAIN RESEARCH LA English DT Note DE ETHANOL; NONOPIOID; MK-801; DIZOCILPINE; N-METHYL-D-ASPARTATE; STRESS-INDUCED ANALGESIA; GENETICS; SELECTIVE BREEDING ID STRESS-INDUCED ANALGESIA; BRAIN OPIATE RECEPTORS; RAT-BRAIN; CROSS-TOLERANCE; ALCOHOL; MORPHINE; BINDING; PAIN; MICE; SENSITIVITY AB Recent evidence from our laboratory suggests that the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (dizocilpine) selectively antagonizes non-opioid (i.e. naloxone-insensitive) mechanisms of stress-induced analgesia in mice. For example, we have recently demonstrated that a low dose of MK-801 (0.075 mg/kg, i.p.) antagonizes the non-opioid component of a mixed opioid/non-opioid swim stress-induced analgesia (SSIA) resulting from forced swimming for 3 min in 20-degrees-C water. Since ethanol-induced analgesia (EIA) has been found to be only partially attenuated by naloxone, we hypothesized that MK-801 would similarly block the non-opioid component of EIA. The effects of MK-801 and of the opioid receptor antagonist naloxone (10 mg/kg, i.p.) on analgesia produced by ethanol (2.5 g/kg in 20% vol/vol, i.p.) were studied in control mice and in mice selectively bred for high (HA) or low (LA) SSIA. HA mice showed significantly more, and LA mice significantly less, EIA than controls. Naloxone and MK-801 significantly attenuated EIA in control and HA mice, and in these lines the combined administration of both antagonists blocked EIA completely. In LA mice, which displayed very little EIA, naloxone but not MK-801 reversed EIA completely. These findings provide additional evidence for the role of the NMDA receptor in non-opioid mechanisms of analgesia. The finding that mice selectively bred for high and low SSIA also display high and low EIA suggests common mediation of the effects of stress and ethanol on antinociceptive processes. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90024. HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. POLISH ACAD SCI,INST GENET & ANIM BREEDING,DEPT BEHAV PHYSIOL,JASTRZEBIEC,POLAND. UNIV CALIF LOS ANGELES,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90024. W LOS ANGELES VAMC,BRENTWOOD DIV,LOS ANGELES,CA 90024. FU PHS HHS [N507628] NR 56 TC 20 Z9 20 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 JAN 29 PY 1993 VL 602 IS 1 BP 126 EP 130 DI 10.1016/0006-8993(93)90251-H PG 5 WC Neurosciences SC Neurosciences & Neurology GA KK302 UT WOS:A1993KK30200018 PM 8448649 ER PT J AU PRICE, RH HOLLINGSWORTH, Z YOUNG, AB PENNEY, JB AF PRICE, RH HOLLINGSWORTH, Z YOUNG, AB PENNEY, JB TI EXCITATORY AMINO-ACID RECEPTOR REGULATION AFTER SUBTHALAMIC NUCLEUS LESIONS IN THE RAT SO BRAIN RESEARCH LA English DT Note DE SUBTHALAMIC NUCLEUS; SUBSTANTIA NIGRA PARS RETICULATA; GLOBUS PALLIDUS; BASAL GANGLIA; EXCITATORY AMINO ACID; GLUTAMATE; RECEPTOR; AUTORADIOGRAPHY ID MONOAMINE-DEPLETED RATS; NIGRA PARS RETICULATA; SUBSTANTIA-NIGRA; GLOBUS-PALLIDUS; INTRACELLULAR ANALYSIS; BASAL GANGLIA; NEURONS; GLUTAMATE; CLONING; AMPA AB The subthalamic nucleus plays a pivotal role in the regulation of basal ganglia output. Recent electrophysiologic, lesion and immunocytochemical studies suggest that the subthalamic nucleus uses an excitatory amino acid as a neurotransmitter. After complete ablation of the subthalamic nucleus, we have examined the NMDA, AMPA, kainate and metabotropic subtypes of excitatory amino acid receptors in two major subthalamic projection areas (globus pallidus and substantia nigra pars reticulata) with quantitative autoradiography. Two weeks after ablation, binding sites for [H-3]AMPA and [H-3]kainate increased in substantia nigra pars reticulata ipsilateral to the lesion. In globus pallidus on the lesioned side, [H-3]glutamate binding to the NMDA recognition site decreased. The results suggest that glutamate receptors regulate after interruption of subthalamic nucleus output. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NINDS NIH HHS [NS19613] NR 26 TC 32 Z9 32 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 JAN 29 PY 1993 VL 602 IS 1 BP 157 EP 160 DI 10.1016/0006-8993(93)90257-N PG 4 WC Neurosciences SC Neurosciences & Neurology GA KK302 UT WOS:A1993KK30200024 PM 8383570 ER EF