FN Thomson Reuters Web of Science™ VR 1.0 PT J AU THALI, M FURMAN, C HO, DD ROBINSON, J TILLEY, S PINTER, A SODROSKI, J AF THALI, M FURMAN, C HO, DD ROBINSON, J TILLEY, S PINTER, A SODROSKI, J TI DISCONTINUOUS, CONSERVED NEUTRALIZATION EPITOPES OVERLAPPING THE CD4-BINDING REGION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GP120 ENVELOPE GLYCOPROTEIN SO JOURNAL OF VIROLOGY LA English DT Note ID HUMAN MONOCLONAL-ANTIBODY; CD4 RECEPTOR-BINDING; HTLV-III/LAV; T4 MOLECULE; HIV-1 GP120; AIDS; RETROVIRUS; INFECTION; CHIMPANZEES; SEQUENCE AB Monoclonal antibodies have been isolated from human immunodeficiency virus type 1 (HIV-1)-infected patients that recognize discontinuous epitopes on the gp120 envelope glycoprotein, that block gp120 interaction with the CD4 receptor, and that neutralize a variety of HIV-1 isolates. Using a panel of HIV-1 gp120 mutants, we identified amino acids important for precipitation of the gp120 glycoprotein by three different monoclonal antibodies with these properties. These amino acids are located within seven discontinuous, conserved regions of the gp120 glycoprotein, four of which overlap those regions previously shown to be important for CD4 recognition. The pattern of sensitivity to amino acid change in these seven regions differed for each antibody and also differed from that of the CD4 glycoprotein. These results indicate that the CD4 receptor and this group of broadly neutralizing antibodies recognize distinct but overlapping gp120 determinants. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10003. PUBL HLTH RES INST CITY NEW YORK INC,NEW YORK,NY 10016. LOUISIANA STATE UNIV,MED CTR,DEPT MICROBIOL IMMUNOL,NEW ORLEANS,LA 70112. FU NIAID NIH HHS [AI 31783, AI 24030, AI25541] NR 52 TC 194 Z9 197 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD SEP PY 1992 VL 66 IS 9 BP 5635 EP 5641 PG 7 WC Virology SC Virology GA JJ198 UT WOS:A1992JJ19800061 PM 1380099 ER PT J AU YANDAVA, CN SPECK, SH AF YANDAVA, CN SPECK, SH TI CHARACTERIZATION OF THE DELETION AND REARRANGEMENT IN THE BAMHI-C REGION OF THE X50-7 EPSTEIN-BARR-VIRUS GENOME, A MUTANT VIRAL STRAIN WHICH EXHIBITS CONSTITUTIVE BAMHI-W PROMOTER ACTIVITY SO JOURNAL OF VIROLOGY LA English DT Note ID NUCLEAR ANTIGEN-1; BURKITT-LYMPHOMA; INITIAL-STAGES; LYMPHOCYTES-B; DNA; EXPRESSION; INFECTION; CELLS; P3HR-1 AB Epstein-Barr virus infection of peripheral B lymphocytes predominantly results in a latent infection, with a concomitant growth transformation of the infected cells. These cells express six nuclear antigens (EBNAs) and three membrane antigens. Transcription of all the EBNA genes is driven by one of two promoters, Cp or Wp, located near the left end of the viral genome, and the activities of these promoters are mutually exclusive. We have previously shown that Wp is exclusively used during the initial stages of B-cell immortalization, followed by a switch to Cp usage. However, several cell lines which appear to have failed to switch from Wp to Cp usage and which exhibit constitutive Wp activity have been identified. In two cases, we have shown that this failure to switch is the result of a deletion of approximately 3.5 kb, spanning Cp. In this paper, we characterize the deletion in one of these cell lines, X50-7, and demonstrate not only that the viral genome in this cell line has sustained a deletion in the region of Cp, but also that there has been a rearrangement into the BamHI C region of viral sequences from the BamHI W and Y fragments. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 20 TC 19 Z9 19 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 SEP PY 1992 VL 66 IS 9 BP 5646 EP 5650 PG 5 WC Virology SC Virology GA JJ198 UT WOS:A1992JJ19800063 PM 1323716 ER PT J AU VANLINTHOUDT, D SCHUMACHER, HR BURUS, RB HINSHAW, KC PIERCE, V AF VANLINTHOUDT, D SCHUMACHER, HR BURUS, RB HINSHAW, KC PIERCE, V TI APATITE CRYSTAL DEPOSITION DISEASE IN A DIANA MONKEY (CERCOPITHECUS-DIANA-DIANA) SO JOURNAL OF ZOO AND WILDLIFE MEDICINE LA English DT Article DE APATITE CRYSTAL DEPOSITIONS; RENAL INSUFFICIENCY; DIANA MONKEY; CERCOPITHECUS-DIANA-DIANA ID CALCINOSIS-CIRCUMSCRIPTA; RHESUS-MONKEYS; CALCIUM AB A 16-year-old Diana monkey (Cercopithecus diana diana) with chronic renal insufficiency was evaluated for progressive weight loss. The examination revealed a subcutaneous mass on the left carpus. Fluid was aspirated and disclosed numerous, shiny, nonbirefringent particles that stained bright red with bright red S. The mineral present was identified as apatite by high resolution X-ray crystallographic analysis. Later, similar masses developed near the left ischium and the right tarsus. The monkey was euthanatized and a necropsy performed. The histological studies revealed profuse amounts of hematoxyphilic material surrounded by fibrosis, histiocytes, and multinucleated giant cells. Transmission electron microscopy showed clumps of intracellular fine needle-shaped crystals typical for apatite. These apatite deposits were probably related to an increased serum calcium x phosphorus product secondary to the renal disease. C1 UNIV PENN,VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. ZOOLOGICAL SOC PHILADELPHIA,PHILADELPHIA,PA. NR 25 TC 2 Z9 2 U1 0 U2 1 PU AMER ASSOC Z00 VETERINARIANS PI MEDIA PA 6 NORTH PENNELL ROAD, MEDIA, PA 19063 SN 1042-7260 J9 J ZOO WILDLIFE MED JI J. Zoo Wildl. Med. PD SEP PY 1992 VL 23 IS 3 BP 346 EP 352 PG 7 WC Veterinary Sciences SC Veterinary Sciences GA JP945 UT WOS:A1992JP94500011 ER PT J AU ANDERSON, RJ BRECKON, R AF ANDERSON, RJ BRECKON, R TI CYTOKINE REGULATION OF ADENYLATE-CYCLASE ACTIVITY IN LLC-PK1 CELLS SO KIDNEY INTERNATIONAL LA English DT Article ID TUMOR-NECROSIS-FACTOR; PROTEIN-KINASE-C; COLLECTING TUBULE CELLS; CANINE KIDNEY-CELLS; MESANGIAL CELLS; CYCLIC-AMP; SIGNAL TRANSDUCTION; GTP-BINDING; PROSTAGLANDIN BIOSYNTHESIS; HUMAN FIBROBLASTS AB Although several cytokines have been demonstrated to exert pleiotropic responses, there is little information on cytokine regulation of renal tubular epithelial cell function. In the present studies, we find that both T cell-derived (tumor necrosis factor-beta and interleukins 2 and 3) and monocyte/macrophage derived (tumor necrosis factor alpha and interleukin 1-beta) cytokines promote basal, arginine vasopressin- and forskolin-stimulated adenylate cyclase activity in cultured LLC-PK1 cells. No effect of TNF, IL-1-beta, and IL-2 to stimulate protein kinase C activity was observed. TNF-beta, IL-beta and IL-2 also modestly stimulated H-3 release from H-3-arachidonic acid labeled cells. Mepacrine, a phospholipase A inhibitor, prevented TNF-beta stimulation of H-3 release from H-3-arachidonic acid labeled cells and TNF-beta potentiation of adenylate cyclase activity. TNF-beta potentiation of adenylate cyclase activity and stimulation of H-3 release from H-3 arachidonic acid labeled cells was not prevented by pertussis toxin. These results demonstrate that several cytokines can stimulate adenylate cyclase activity while not affecting protein kinase C activity in cultured renal tubular epithelial cells. The effect of TNF-beta to stimulate adenylate cyclase appears to occur independent of pertussis toxin-sensitive substrate and may involve activation of phospholipase A. C1 UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80262. RP ANDERSON, RJ (reprint author), DENVER VET AFFAIRS MED CTR,DEPT MED,MED SERV 3,1055 CLERMONT ST,DENVER,CO 80220, USA. NR 46 TC 8 Z9 8 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD SEP PY 1992 VL 42 IS 3 BP 559 EP 566 DI 10.1038/ki.1992.319 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA JJ445 UT WOS:A1992JJ44500003 PM 1405334 ER PT J AU PANDOLFI, F ZAMBELLO, R CAFARO, A SEMENZATO, G AF PANDOLFI, F ZAMBELLO, R CAFARO, A SEMENZATO, G TI BIOLOGY OF DISEASE - BIOLOGIC AND CLINICAL HETEROGENEITY OF LYMPHOPROLIFERATIVE DISEASES OF PERIPHERAL MATURE LYMPHOCYTES-T SO LABORATORY INVESTIGATION LA English DT Article ID LARGE GRANULAR LYMPHOCYTES; CELL LEUKEMIA-LYMPHOMA; VIRUS TYPE-I; NATURAL-KILLER-CELLS; POLYMERASE CHAIN-REACTION; RECEPTOR GENE REARRANGEMENTS; LARGE ANTIGRANULOCYTES LYMPHOCYTES; ANTI-CD3 MONOCLONAL-ANTIBODY; ACUTE LYMPHOBLASTIC-LEUKEMIA; EXPANDED LGL POPULATIONS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. UNIV PADUA,DEPT CLIN MED,MED 1 CLIN,I-35100 PADUA,ITALY. UNIV PADUA,CLIN IMMUNOL SECT,I-35100 PADUA,ITALY. RP PANDOLFI, F (reprint author), UNIV ROME LA SAPIENZA,DEPT ALLERGY & CLIN IMMUNOL,I-00185 ROME,ITALY. RI Semenzato, Gianpietro/J-7727-2016; Cafaro, Aurelio/K-5314-2016 OI Semenzato, Gianpietro/0000-0002-6061-4595; NR 366 TC 15 Z9 15 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD SEP PY 1992 VL 67 IS 3 BP 274 EP 302 PG 29 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA JP572 UT WOS:A1992JP57200002 PM 1405488 ER PT J AU BARNHILL, RL FANDREY, K LEVY, MA MIHM, MC HYMAN, B AF BARNHILL, RL FANDREY, K LEVY, MA MIHM, MC HYMAN, B TI ANGIOGENESIS AND TUMOR PROGRESSION OF MELANOMA - QUANTIFICATION OF VASCULARITY IN MELANOCYTIC NEVI AND CUTANEOUS MALIGNANT-MELANOMA SO LABORATORY INVESTIGATION LA English DT Article DE MELANOCYTIC NEVI; DYSPLASTIC NEVI; NEOVASCULARIZATION ID SKIN AB BACKGROUND: The capacity of cutaneous malignant melanoma (CMM) to induce angiogenesis is well established. In addition, dysplastic melanocytic nevi (DMN) have been reported to display prominent vascularity relative to common acquired nevi; but this observation has never been verified objectively. EXPERIMENTAL DESIGN: In the following studies, papillary dermal or tumor vascularity was quantified in 10 examples of normal skin, and in a series of 18 melanocytic nevi, 29 DMN, 37 primary CMM and 5 melanoma metastases. Microvessels were identified with the lectin Ulex europaeus agglutinin I. The number of microvessels were counted with an ocular grid (area 7.84 x 10(-2) mm2) at x400 magnification, and the mean vascularity recorded for five fields for each specimen. RESULTS: Mean vascular counts were as follows: normal skin 5.9, common acquired nevus 9.1, nevus with features of DMN 10.3, DMN, slight atypia 11.8; DMN, moderate atypia 12.2; DMN, severe atypia 14.8; primary CMM 25.4; and metastatic melanoma 29.5). Significant differences were recorded for DMN, severe atypia versus melanoma (p < 0.01), DMN, severe versus common nevi (p < 0.02) and versus nevi with features of DMN (P < 0.05). When microvessel counts from CMM in the radial growth phase were compared with those from CMM in the vertical growth phase, or CMM < 1.0 mm versus those > 1.0 mm, no significant differences were found. However, CMM in radial growth did differ from severely atypical DMN (22.4 versus 14.8, p < 0.05). CONCLUSIONS: These results quantify for the first time a gradual rise in vascularity with tumor progression in the melanocytic system and onset of angiogenesis during the radial growth phase of CMM. Other than severely atypical DMN, DMN did not differ substantially from common nevi with reference to overall vascularity. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 20 TC 154 Z9 157 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD SEP PY 1992 VL 67 IS 3 BP 331 EP 337 PG 7 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA JP572 UT WOS:A1992JP57200006 PM 1383607 ER PT J AU WEDEEN, VJ AF WEDEEN, VJ TI MAGNETIC-RESONANCE-IMAGING OF MYOCARDIAL KINEMATICS - TECHNIQUE TO DETECT, LOCALIZE, AND QUANTIFY THE STRAIN RATES OF THE ACTIVE HUMAN MYOCARDIUM SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article ID VELOCITY; MOTION; HEART; PHASE RP WEDEEN, VJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-39371-04] NR 12 TC 92 Z9 92 U1 0 U2 1 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 SEP PY 1992 VL 27 IS 1 BP 52 EP 67 DI 10.1002/mrm.1910270107 PG 16 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JN166 UT WOS:A1992JN16600006 PM 1435210 ER PT J AU RATTNER, DW AF RATTNER, DW TI PANCREATIC-CANCER IN 1992 - HAS ANY PROGRESS BEEN NOTED SO MAYO CLINIC PROCEEDINGS LA English DT Editorial Material ID CARCINOMA; EXPERIENCE; MORTALITY; SURVIVAL; HEAD C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RATTNER, DW (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114, USA. NR 12 TC 8 Z9 8 U1 0 U2 0 PU MAYO CLINIC PROCEEDINGS PI ROCHESTER PA 660 SIEBENS BLDG MAYO CLINIC, ROCHESTER, MN 55905 SN 0025-6196 J9 MAYO CLIN PROC JI Mayo Clin. Proc. PD SEP PY 1992 VL 67 IS 9 BP 907 EP 909 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JL323 UT WOS:A1992JL32300015 PM 1434937 ER PT J AU ROSEN, AK GERACI, JM ASH, AS MCNIFF, KJ MOSKOWITZ, MA AF ROSEN, AK GERACI, JM ASH, AS MCNIFF, KJ MOSKOWITZ, MA TI POSTOPERATIVE ADVERSE EVENTS OF COMMON SURGICAL-PROCEDURES IN THE MEDICARE POPULATION SO MEDICAL CARE LA English DT Article ID TRANS-URETHRAL PROSTATECTOMY; NEW-YORK-STATE; HOSPITAL MORTALITY; ELDERLY PATIENTS; COMPLICATIONS; QUALITY; RATES; HEART; MEDISGROUPS; PREDICTORS AB Mortality rates are the most widely used measure in assessing patient outcome from hospitalization. However, they may be an insensitive measure of quality for surgical patients because death is a relatively rare outcome. A random sample of patient data (n = 8126) selected from the Medicare files of seven states was used to identify, through chart abstraction, clinical postoperative complications of surgery that could serve as measures of quality. Four surgical procedures were studied: 1) coronary artery bypass grafting; 2) coronary angioplasty; 3) cholecystectomy; and 4) prostatectomy. Severity at admission was controlled for using severity-of-illness models developed with chart-abstracted data to predict adverse events after these four procedures. 30-day mortality rates ranged from 1.0% to 6.6%, while the prevalence of postoperative adverse events identified from chart review was greater (6.9% to 33.3%). There were significant differences between patients with and without adverse events. For example, coronary artery bypass graft patients with adverse events had prolonged postsurgical lengths of stay (18.5 +/- 13.2 vs. 13.2 +/- 6.2, P < 0.001) and higher mortality rates (15.2% vs. 2.6%, P < 0.001). The R-square values using clinical indicators at admission to predict the occurrence of any adverse event ranged from 0.05 to 0.13. Clinically meaningful adverse events of surgery can be successfully identified through chart abstraction and appear to be valid measures of postoperative complications among surgical patients. Severity adjustment at admission only modestly predicts the occurrence of these adverse events. C1 HOUSTON VET AFFAIRS MED CTR,HOUSTON,TX. BAYLOR COLL MED,HOUSTON,TX 77030. BOSTON UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02118. RP ROSEN, AK (reprint author), BOSTON UNIV,MED CTR,EVANS MEM DEPT MED,GEN INTERNAL MED SECT,HLTH CARE RES UNIT,BOSTON,MA 02118, USA. NR 34 TC 40 Z9 41 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD SEP PY 1992 VL 30 IS 9 BP 753 EP 765 DI 10.1097/00005650-199209000-00001 PG 13 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA JN029 UT WOS:A1992JN02900001 PM 1518309 ER PT J AU ZAJAC, JD KEARNS, AK SKURAT, RM KRONENBERG, HM BRINGHURST, FR AF ZAJAC, JD KEARNS, AK SKURAT, RM KRONENBERG, HM BRINGHURST, FR TI REGULATION OF GENE-TRANSCRIPTION AND PROLIFERATION BY PARATHYROID-HORMONE IS BLOCKED IN MUTANT OSTEOBLASTIC CELLS RESISTANT TO CYCLIC-AMP SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE PARATHYROID HORMONE; CYCLIC AMP; OSTEOSARCOMA CELLS (RAT); SIGNAL TRANSDUCTION; PROLIFERATION; PROTEIN KINASE-A ID DEPENDENT PROTEIN-KINASE; OSTEO-SARCOMA CELLS; NUCLEAR FACTOR CREB; POSSIBLE INVOLVEMENT; SOMATOSTATIN GENE; RESPONSE ELEMENT; PHOSPHOLIPASE-C; BINDING PROTEIN; CAMP; STIMULATION AB We employed a cyclic AMP-resistant subclone of UMR 106-01 osteoblastic osteosarcoma cells (UMR 4-7) with a regulated, dominant-negative mutation of cyclic AMP-dependent protein kinase (PK-A), to examine the mechanism(s) whereby parathyroid hormone (PTH) regulates growth of these cells. Expression of a transiently transfected CAT reporter gene controlled by the cAMP response element of the rat somatostatin gene ('SST-CAT') was used to monitor PK-A activation in intact cells. Agonist-stimulated SST-CAT expression was specific for agents known to activate adenylate cyclase, required an intact cAMP response element and was specifically blocked following induction of the mutant cAMP-resistant phenotype in UMR 4-7 cells. Inhibition of the proliferation of UMR 106-01 cells by PTH, which is mimicked by forskolin and 8-bromo-cAMP, was blocked completely in mutant cyclic AMP-resistant UMR 4-7 cells. We conclude that control of proliferation in UMR 106-01 cells by PTH involves the cAMP messenger system and requires activation of PK-A. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,WELLMAN 5,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [P01-DK11794] NR 46 TC 8 Z9 8 U1 0 U2 1 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 SEP PY 1992 VL 87 IS 1-3 BP 69 EP 77 DI 10.1016/0303-7207(92)90234-W PG 9 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA JN574 UT WOS:A1992JN57400008 PM 1359985 ER PT J AU BACHINSKY, DR ZHENG, G ABBATE, M NILES, JL BROWN, D MCCLUSKEY, RT AF BACHINSKY, DR ZHENG, G ABBATE, M NILES, JL BROWN, D MCCLUSKEY, RT TI EVIDENCE OF 2 FORMS OF GP330, THE 3RD MEMBER OF THE LDL RECEPTOR GENE FAMILY AND AN AUTOANTIGEN IN HEYMANN NEPHRITIS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A296 EP A296 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501716 ER PT J AU BACIU, PC BINETTE, F GOETINCK, PF AF BACIU, PC BINETTE, F GOETINCK, PF TI GENOMIC ORGANIZATION AND EXPRESSION OF CHICKEN SYNDECAN-4 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A64 EP A64 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500372 ER PT J AU BAO, S LI, J BRUCATO, C PLATZ, J CHEN, LB AF BAO, S LI, J BRUCATO, C PLATZ, J CHEN, LB TI MOLECULAR-CLONING AND SEQUENCING OF A NOVEL 55/60-KDA FOCAL CONTACT PROTEIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A70 EP A70 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500404 ER PT J AU BINETTE, F CRAVENS, J GOETINCK, PF AF BINETTE, F CRAVENS, J GOETINCK, PF TI LINK PROTEIN IS A UBIQUITOUS STRUCTURAL COMPONENT OF NONCARTILAGINOUS TISSUES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract ID ACID-BINDING REGION; PROTEOGLYCAN; CARTILAGE C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. NR 5 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A224 EP A224 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501298 ER PT J AU BRUNKHORST, B LO, SH CHEN, LB AF BRUNKHORST, B LO, SH CHEN, LB TI TENSIN IS TRANSIENTLY DISPLACED FROM FOCAL CONTACTS BY ANTIPHOSPHOTYROSINE MONOCLONAL-ANTIBODY INVIVO SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A152 EP A152 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500881 ER PT J AU CHEN, YP LYNCH, DC AF CHEN, YP LYNCH, DC TI MECHANISM OF VONWILLEBRAND-FACTOR MULTIMERIZATION - STRUCTURAL ACTIVITY OF THE PROPEPTIDE-D1 AND PROPEPTIDE-D2 DOMAINS SO MOLECULAR BIOLOGY OF THE CELL 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 AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A69 EP A69 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500402 ER PT J AU CHUNGWELCH, N CAMBRIA, RP AF CHUNGWELCH, N CAMBRIA, RP TI CELL-PROLIFERATION AND COLLAGEN SECRETION IN NATIVE AND MODULATED HUMAN VASCULAR SMOOTH-MUSCLE CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG RES UNIT,VASC CELL BIOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A179 EP A179 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501036 ER PT J AU COSSETTE, LJ CHEN, LB AF COSSETTE, LJ CHEN, LB TI TYROSINE PHOSPHORYLATION OF TENSIN IS TRANSIENTLY INCREASED IN TGF-ALPHA-STIMULATED CHICK-EMBRYO FIBROBLASTS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A147 EP A147 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500851 ER PT J AU DEALMEIDA, JB DOHERTY, J NARULA, N BURKE, B MATLIN, K STOW, JL AF DEALMEIDA, JB DOHERTY, J NARULA, N BURKE, B MATLIN, K STOW, JL TI BINDING OF THE P200 COAT PROTEIN TO GOLGI MEMBRANES IS REGULATED BY PERTUSSIS TOXIN SENSITIVE G-PROTEINS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAT & CELL BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL & MOLEC PHYSIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A223 EP A223 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501291 ER PT J AU DEKKER, SK VINK, J PAVEL, S BRUIJN, JA MIHM, MC AF DEKKER, SK VINK, J PAVEL, S BRUIJN, JA MIHM, MC TI ROLE OF CYTOKINES ON THE MODULATION OF MELANOMA CELL MOTILITY AND INTEGRIN EXPRESSION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. LEIDEN UNIV,DEPT DERMATOL,2300 RA LEIDEN,NETHERLANDS. LEIDEN UNIV,DEPT PATHOL,2300 RA LEIDEN,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A127 EP A127 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500735 ER PT J AU FENDERSON, BA STAMENKOVIC, I ARUFFO, A AF FENDERSON, BA STAMENKOVIC, I ARUFFO, A TI DISTRIBUTION OF HYALURONAN IN POSTIMPLANTATION MOUSE EMBRYOS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 BRISTOL MYERS SQUIBB RES INST,DEPT CELLULAR INTERACT,SEATTLE,WA 98121. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. THOMAS JEFFERSON UNIV,DEPT PATHOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,DEPT CELL BIOL,PHILADELPHIA,PA 19107. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A105 EP A105 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500604 ER PT J AU GERECKE, D WAGMAN, D MCDONOUGH, M BURGESON, R AF GERECKE, D WAGMAN, D MCDONOUGH, M BURGESON, R TI CDNAS ENCODING FOR THE 3 CHAINS OF THE ANCHORING FILAMENT PROTEIN KALININ SHOW SIMILARITY TO THE LAMININ A, B1, AND B2 CHAINS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 1 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A1 EP A1 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500005 ER PT J AU LO, SH LIU, Y WONG, WK BRUNKHORST, B CHEN, LB AF LO, SH LIU, Y WONG, WK BRUNKHORST, B CHEN, LB TI STRUCTURAL-ANALYSIS OF TENSIN, A POTENTIAL INTEGRATOR FOR SIGNAL TRANSDUCTION AND THE CYTOSKELETON SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A267 EP A267 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501553 ER PT J AU LO, SH HARTWIG, JH JANMEY, PA CHEN, LB AF LO, SH HARTWIG, JH JANMEY, PA CHEN, LB TI TENSIN, AN SH2-CONTAINING PROTEIN, HAS ACTIN CAPPING AND BUNDLING ACTIVITIES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A41 EP A41 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500237 ER PT J AU MATLIN, KS ZUK, A ZINKL, G KENDALL, DM SCHOENENBERGER, CA AF MATLIN, KS ZUK, A ZINKL, G KENDALL, DM SCHOENENBERGER, CA TI ALTERATIONS OF INTEGRINS IN TRANSFORMED MDCK CELLS LACKING APICAL POLARITY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MAURICE MULLER INST,BASEL,SWITZERLAND. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAT & CELL BIOL,BOSTON,MA 02115. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A131 EP A131 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500756 ER PT J AU MAYSINGER, D PICCARDO, P GRCIC, J SHORT, MP BREAKEFIELD, XO CUELLO, AC AF MAYSINGER, D PICCARDO, P GRCIC, J SHORT, MP BREAKEFIELD, XO CUELLO, AC TI MICROENCAPSULATION OF GENETICALLY ENGINEERED FIBROBLASTS SECRETING NERVE GROWTH-FACTOR SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MCGILL UNIV,DEPT PHARMACOL & THERAPEUT,MONTREAL H3A 2T5,QUEBEC,CANADA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Cuello, A. Claudio/N-8211-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A330 EP A330 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501915 ER PT J AU NGUYEN, M WATANABE, H BUDSON, A RICHIE, JP HAYES, DF FOLKMAN, J AF NGUYEN, M WATANABE, H BUDSON, A RICHIE, JP HAYES, DF FOLKMAN, J TI BASIC FIBROBLAST GROWTH-FACTOR (BFGF) IS ELEVATED IN THE URINE OF PATIENTS WITH A WIDE VARIETY OF NEOPLASMS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TAKEDA CHEM IND LTD,OSAKA 532,JAPAN. NR 0 TC 12 Z9 12 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A234 EP A234 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501357 ER PT J AU NISHIYAMA, T MCDONOUGH, AM BURGESON, RE AF NISHIYAMA, T MCDONOUGH, AM BURGESON, RE TI THE GLOBULAR DOMAIN OF TYPE-XII OR TYPE-XIV COLLAGENS PROMOTES CONTRACTION OF COLLAGEN GELS BY DERMAL FIBROBLASTS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A74 EP A74 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500430 ER PT J AU PATTON, WF CHEN, A CHUNGWELCH, N CAMBRIA, RP MARKS, AR TAUBMAN, M TEMPST, P AF PATTON, WF CHEN, A CHUNGWELCH, N CAMBRIA, RP MARKS, AR TAUBMAN, M TEMPST, P TI SELECTIVE ALTERATIONS IN QUIESCENT SMOOTH-MUSCLE CELL POLYPEPTIDE EXPRESSION AFTER STIMULATION WITH SERUM, PDGF AND ANGIOTENSIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02129. MEM SLOAN KETTERING CANC CTR,MOLEC BIOL PROGRAM,NEW YORK,NY 10021. CUNY MT SINAI SCH MED,DEPT MOLEC MED,NEW YORK,NY 10029. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A179 EP A179 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501038 ER PT J AU PUDER, M BARNARD, GF MORI, M REDMAN, KL JESSUP, JM STEELE, GD CHEN, LB AF PUDER, M BARNARD, GF MORI, M REDMAN, KL JESSUP, JM STEELE, GD CHEN, LB TI THE UBIQUITIN-S27A FUSION PROTEIN IS OVEREXPRESSED IN HUMAN COLON-CARCINOMA BUT NOT GASTRIC-CARCINOMA SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A20 EP A20 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500111 ER PT J AU SANDERSON, IR OUELLETTE, AJ CARTER, EA WALKER, WA HARMATZ, PR AF SANDERSON, IR OUELLETTE, AJ CARTER, EA WALKER, WA HARMATZ, PR TI DIFFERENTIAL REGULATION OF B7 MESSENGER-RNA IN ENTEROCYTES AND LYMPHOID-CELLS - POTENTIAL MECHANISM FOR ORAL TOLERANCE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,MUCOSAL IMMUNOL LAB,BOSTON,MA 02129. SHRINERS BURNS RES CTR,CAMBRIDGE,MA 02142. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A277 EP A277 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501608 ER PT J AU SHAPIRO, F CAHILL, C NAYAK, RC AF SHAPIRO, F CAHILL, C NAYAK, RC TI IMMUNOGOLD TRANSMISSION ELECTRON-MICROSCOPIC DEMONSTRATION OF VIMENTIN IN OSTEOBLAST AND OSTEOCYTE CELL PROCESSES IN RAT BONE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,SKELETAL DISORDERS LAB,BOSTON,MA 02115. JOSLIN DIABET FDN INC,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A230 EP A230 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501333 ER PT J AU STAINIER, DYR LEE, RK FISHMAN, MC AF STAINIER, DYR LEE, RK FISHMAN, MC TI HEART DEVELOPMENT IN THE ZEBRAFISH EMBRYO SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A286 EP A286 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501659 ER PT J AU TONDRAVI, MM HAUDENSCHILD, D GOETINCK, PF AF TONDRAVI, MM HAUDENSCHILD, D GOETINCK, PF TI REGULATION OF COLLAGEN FIBRILLOGENESIS INVITRO BY CARTILAGE MATRIX PROTEIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. RI Haudenschild, Dominik/B-2381-2008 OI Haudenschild, Dominik/0000-0001-9947-9864 NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A223 EP A223 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501293 ER PT J AU VERTEL, BM WALTERS, LM GRIER, BL MAINE, N GOETINK, PF AF VERTEL, BM WALTERS, LM GRIER, BL MAINE, N GOETINK, PF TI NANOMELIC CHONDROCYTES SYNTHESIZE, BUT FAIL TO TRANSLOCATE, A TRUNCATED AGGRECAN PRECURSOR SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CHICAGO MED SCH,DEPT CELL BIOL & ANAT,N CHICAGO,IL 60064. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A222 EP A222 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501289 ER PT J AU VINK, J DEKKER, SK NOZ, K BRUIJN, JA MIHM, MC BYERS, HR AF VINK, J DEKKER, SK NOZ, K BRUIJN, JA MIHM, MC BYERS, HR TI ROLE OF BETA-1 INTEGRINS IN MELANOCYTE CELL SPREADING AND MIGRATION ON COLLAGEN TYPE-IV AND LAMININ SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A75 EP A75 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500435 ER PT J AU WATANABE, H NGUYEN, M SCHIZER, M LI, V HAYES, DF SALLAN, S FOLKMAN, J AF WATANABE, H NGUYEN, M SCHIZER, M LI, V HAYES, DF SALLAN, S FOLKMAN, J TI BASIC FIBROBLAST GROWTH-FACTOR IN HUMAN SERUM - A PROGNOSTIC TEST FOR BREAST-CANCER SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TAKEDA CHEM IND LTD,OSAKA 532,JAPAN. NR 0 TC 6 Z9 6 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A234 EP A234 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501359 ER PT J AU WILLIAMS, DB DEGEN, E MARGOLESE, L AHLUWALIA, N WANECK, GL AF WILLIAMS, DB DEGEN, E MARGOLESE, L AHLUWALIA, N WANECK, GL TI CHARACTERIZATION OF P88, A MOLECULAR CHAPERONE OF THE ENDOPLASMIC-RETICULUM SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV TORONTO,DEPT BIOCHEM,TORONTO M5S 1A8,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,SURG RES LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A5 EP A5 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500023 ER PT J AU YUE, B TWINING, SS ANDO, H ZHOU, X FINI, ME AF YUE, B TWINING, SS ANDO, H ZHOU, X FINI, ME TI MATRIX METALLOPROTEINASES AND PROTEASE INHIBITORS IN THE HUMAN AQUEOUS-HUMOR SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV ILLINOIS,DEPT OPHTHALMOL,CHICAGO,IL 60680. MED COLL WISCONSIN,DEPT BIOCHEM,MILWAUKEE,WI 53226. MED COLL WISCONSIN,DEPT OPHTHALMOL,MILWAUKEE,WI 53226. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A318 EP A318 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501848 ER PT J AU ZHANG, R HASEGAWA, H SKACH, W MA, T SHI, LB VERBAVETZ, JM BROWN, D BAKER, O VANHOEK, AN VERKMAN, AS AF ZHANG, R HASEGAWA, H SKACH, W MA, T SHI, LB VERBAVETZ, JM BROWN, D BAKER, O VANHOEK, AN VERKMAN, AS TI FUNCTIONAL-ANALYSIS OF A KIDNEY WATER CHANNEL HOMOLOGOUS TO CHIP28 - CDNA CLONING, EXPRESSION, PROTEIN RECONSTITUTION, FREEZE-FRACTURE EM AND INSITU HYBRIDIZATION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A302 EP A302 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501752 ER PT J AU BORSOOK, D ROSEN, H COLLARD, M DRESSLER, H HERRUP, K COMB, MJ HYMAN, SE AF BORSOOK, D ROSEN, H COLLARD, M DRESSLER, H HERRUP, K COMB, MJ HYMAN, SE TI EXPRESSION AND REGULATION OF A PROENKEPHALIN BETA-GALACTOSIDASE FUSION GENE IN THE REPRODUCTIVE-SYSTEM OF TRANSGENIC MICE SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID MOUSE SPERMATOGENIC CELLS; TESTICULAR GERM-CELLS; OPIOID PEPTIDE GENES; MESSENGER-RNA LEVELS; SOMATIC-CELLS; LEYDIG-CELLS; DIFFERENTIAL EXPRESSION; ENKEPHALIN PRECURSOR; CYCLIC AMP; RAT AB A fusion gene containing 3 kilobases of human proenkephalin 5'-flanking sequences and 1 kilobase of human proenkephalin 3'-flanking sequence and the easily visualized histochemical marker, Escherichia coli beta-galactosidase, was used to study the function of cis-regulatory elements within the human proenkephalin gene in transgenic mice. Here data are presented on expression and regulation of this fusion gene in the reproductive system of three independent lines of transgenic mice. Within the male reproductive system, the fusion gene is expressed in the proximal epididymis and in developing germinal cells but not in mature or elongating spermatids. In the female reproductive system, the transgene was expressed at low basal levels, but expression was dramatically stimulated in the ovary and oviduct by hormonal stimulation and pregnancy; additionally, expression was induced at the uteroplacental junction in pregnant mice. Taken together these observations suggest that critical sequences for expression and regulation of the proenkephalin gene within the reproductive system are contained within sequences of the construct. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT MOLEC VIROL,IL-91010 JERUSALEM,ISRAEL. UTAH STATE UNIV,TOXICOL & MOLEC BIOL PROGRAMS,LOGAN,UT 84322. EK SHRIVER CTR,DEPT DEV NEUROBIOL,WALTHAM,MA 02254. FU NIDA NIH HHS [DA-05706]; NIMH NIH HHS [MH-44160, MH-00892] NR 45 TC 31 Z9 31 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD SEP PY 1992 VL 6 IS 9 BP 1502 EP 1512 DI 10.1210/me.6.9.1502 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JR184 UT WOS:A1992JR18400017 PM 1435791 ER PT J AU KANDT, RS HAINES, JL SMITH, M NORTHRUP, H GARDNER, RJM SHORT, MP DUMARS, K ROACH, ES STEINGOLD, S WALL, S BLANTON, SH FLODMAN, P KWIATKOWSKI, DJ JEWELL, A WEBER, JL ROSES, AD PERICAKVANCE, MA AF KANDT, RS HAINES, JL SMITH, M NORTHRUP, H GARDNER, RJM SHORT, MP DUMARS, K ROACH, ES STEINGOLD, S WALL, S BLANTON, SH FLODMAN, P KWIATKOWSKI, DJ JEWELL, A WEBER, JL ROSES, AD PERICAKVANCE, MA TI LINKAGE OF AN IMPORTANT GENE LOCUS FOR TUBEROUS SCLEROSIS TO A CHROMOSOME 16 MARKER FOR POLYCYSTIC KIDNEY-DISEASE SO NATURE GENETICS LA English DT Article ID HYDROXYLASE PAH LOCUS; ABO BLOOD-GROUP; PCR DETECTION; V-ABL; HETEROGENEITY; RECOMBINATION; POLYMORPHISM; RFLP AB Tuberous sclerosis complex (TSC) is an autosomal dominant disorder of unknown aetiology that affects numerous body systems including skin, brain and kidneys. Some TSC has been linked to chromosome 9, additional TSC genes on chromosomes 11 and 12 have been proposed, but the majority of TSC families remain unlinked. Using TSC families in which data had excluded linkage to chromosome 9, we failed to detect linkage with loci on chromosomes 11, 12 and others. One marker examined was D16S283, the closest locus on the proximal side of the polycystic kidney disease type 1 (PKD1) gene. Linkage between TSC and D16S283 demonstrated a lod score of 9.50 at THETA = 0.02 with one family independently presenting a lod score of 4.44 at THETA = 0.05. These data reveal an important TSC locus near the region of PKD1 on chromosome 16p13. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,CHARLESTON,MA 02129. UNIV CALIF IRVINE,DEPT PEDIAT,IRVINE,CA 92717. UNIV TEXAS,SCH MED,DEPT PEDIAT,DIV MED GENET,HOUSTON,TX 77030. UNIV OTAGO,DEPT PEDIAT & CHILD HLTH,DUNEDIN,NEW ZEALAND. UNIV TEXAS,HLTH SCI CTR,SW MED SCH,DIV PEDIAT NEUROL,DALLAS,TX 75235. UNIV VIRGINIA,DEPT PEDIAT,CHARLOTTESVILLE,VA 22908. BRIGHAM & WOMENS HOSP,DIV EXPTL MED & HEMATOL ONCOL,BOSTON,MA 02115. MARSHFIELD MED RES FDN,MARSHFIELD,WI 54449. RP KANDT, RS (reprint author), UNIV N CAROLINA,MED CTR,DEPT PEDIAT,DIV NEUROL,DURHAM,NC 27710, USA. RI Roach, Ewell/E-3958-2011; Haines, Jonathan/C-3374-2012 NR 43 TC 230 Z9 234 U1 0 U2 5 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD SEP PY 1992 VL 2 IS 1 BP 37 EP 41 DI 10.1038/ng0992-37 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA JM646 UT WOS:A1992JM64600013 PM 1303246 ER PT J AU SUPER, M GILLIES, SD FOLEY, S SASTRY, K SCHWEINLE, JE SILVERMAN, VJ EZEKOWITZ, RAB AF SUPER, M GILLIES, SD FOLEY, S SASTRY, K SCHWEINLE, JE SILVERMAN, VJ EZEKOWITZ, RAB TI DISTINCT AND OVERLAPPING FUNCTIONS OF ALLELIC FORMS OF HUMAN MANNOSE BINDING-PROTEIN SO NATURE GENETICS LA English DT Article ID CARBOHYDRATE-RECOGNITION DOMAINS; CLASSICAL PATHWAY; HUMAN-SERUM; MANNAN; COMPLEMENT; IMMUNODEFICIENCY; SEQUENCE; LECTINS; ZYMOSAN; DEFECT AB Human mannose binding protein (MBP) is a C-type serum lectin involved in first-line host defense against a variety of bacterial, fungal and viral pathogens. Recently an association was found between low levels of serum MBP and an increased frequency of recurrent infections in infants. A particular genotype, in which glycine is substituted by aspartic acid at codon 54 of MBP in the fifth collagen repeat, shows apparent concordance with the clinical phenotype. We report, however, that this genotype occurs in 5% of the population and encodes a functional protein. Our results indicate that the Gly54Asp allele does not account for a deficiency state, but instead suggest that MBP may have two predominant allelic forms that have overlapping function and differ only in their ability to activate the classical pathway of complement. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. ABBOTT BIOTECH INC,NEEDHAM,MA. YALE UNIV,SCH MED,DEPT INTERNAL MED,DIV INFECT DIS,NEW HAVEN,CT 06510. BOSTON UNIV,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02118. RP SUPER, M (reprint author), HARVARD UNIV,CHILDRENS HOSP,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. NR 30 TC 130 Z9 133 U1 0 U2 1 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 SEP PY 1992 VL 2 IS 1 BP 50 EP 55 DI 10.1038/ng0992-50 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA JM646 UT WOS:A1992JM64600016 PM 1303250 ER PT J AU WHITE, RA PETERS, LL ADKISON, LR KORSGREN, C COHEN, CM LUX, SE AF WHITE, RA PETERS, LL ADKISON, LR KORSGREN, C COHEN, CM LUX, SE TI THE MURINE PALLID MUTATION IS A PLATELET STORAGE POOL DISEASE ASSOCIATED WITH THE PROTEIN 42 (PALLIDIN) GENE SO NATURE GENETICS LA English DT Article ID HUMAN-ERYTHROCYTE-MEMBRANE; CYTOPLASMIC DOMAIN; BAND 4.2; MOUSE MODEL; DEFICIENCY; ANKYRIN; CELLS; MICE AB Pallid is one of 12 independent murine mutations with a prolonged bleeding time that are models for human platelet storage pool deficiencies in which several intracellular organelles are abnormal. We have mapped the murine gene for protein 4.2 (Epb4.2) to chromosome 2 where it co-localizes with pallid. Southern blot analyses suggest that pallid is a mutation in the Epb4.2 gene. Northern blot analyses demonstrate a smaller than normal Epb4.2 transcript in affected pallid tissues, such as kidney and skin. This is the first gene defect to be associated with a platelet storage pool deficiency, and may allow the identification of a novel structure or biological pathway that influences granulogenesis. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MERCER UNIV,SCH MED,DEPT HUMAN GENET,MACON,GA 31207. TUFTS UNIV,SCH MED,BOSTON,MA 02115. ST ELIZABETH HOSP,DEPT BIOMED RES,BOSTON,MA 02115. RP WHITE, RA (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. NR 43 TC 93 Z9 94 U1 0 U2 1 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 SEP PY 1992 VL 2 IS 1 BP 80 EP 83 DI 10.1038/ng0992-80 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA JM646 UT WOS:A1992JM64600021 PM 1284644 ER PT J AU KOWALL, NW MCKEE, AC YANKNER, BA BEAL, MF AF KOWALL, NW MCKEE, AC YANKNER, BA BEAL, MF TI INVIVO NEUROTOXICITY OF BETA-AMYLOID [BETA(1-40)] AND THE BETA(25-35) FRAGMENT SO NEUROBIOLOGY OF AGING LA English DT Article DE BETA-AMYLOID; ALZHEIMERS DISEASE; NEUROTOXICITY; CYTOSKELETON; ALZ 50; TAU; PROTEIN; AGING; CELL DEATH; PRIMATE; RAT ID PRECURSOR PROTEIN GENE; ALZHEIMERS-DISEASE; HUNTINGTONS-DISEASE; CEREBRAL-CORTEX; SUBSTANCE-P; NEURONS; PATHOLOGY; LESIONS AB We examined the histological changes produced by injections of beta-amyloid [beta(1-40)], and control peptides in rat and monkey cerebral cortex. Beta(25-35) injections were also studied in rat cortex. Standard immunoperoxidase procedures were used to detect the distribution of tau, MAP2, beta(1-40) and ALZ 50 immunoreactivity. All injections produced localized necrosis at the injection site surrounded by a zone of neuronal loss and gliosis. In rat cortex, lesions produced by solubilized beta(1-40) and beta(25-35) in water were generally larger than those produced by control peptides. Tau and ALZ 50 antibodies labeled neurites and diffusely positive perikarya around beta(1-40) injections, whereas MAP2 staining was reduced, paralleling the distribution of neuronal loss and gliosis. In aged primate cortex, beta(1-40) lesion size was dose dependent. Hyalinized, ALZ 50 positive neurons, and abnormal neurites were prominent around the injection site. Although beta-amyloid is acutely neurotoxic in both rat and monkey cerebral cortex. neuronal degeneration in the primate more closely resembles that found in AD. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [AG 05134, AG09229]; NINDS NIH HHS [NS01240] NR 22 TC 212 Z9 218 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD SEP-OCT PY 1992 VL 13 IS 5 BP 537 EP 542 DI 10.1016/0197-4580(92)90053-Z PG 6 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA JT419 UT WOS:A1992JT41900002 PM 1461341 ER PT J AU ARRIAGADA, PV MARZLOFF, K HYMAN, BT AF ARRIAGADA, PV MARZLOFF, K HYMAN, BT TI DISTRIBUTION OF ALZHEIMER-TYPE PATHOLOGICAL-CHANGES IN NONDEMENTED ELDERLY INDIVIDUALS MATCHES THE PATTERN IN ALZHEIMERS-DISEASE SO NEUROLOGY LA English DT Article ID PAIRED HELICAL FILAMENTS; NEUROFIBRILLARY TANGLES; NEURITIC PLAQUES; SENILE PLAQUES; DIFFERENT AGES; DOWNS-SYNDROME; HUMAN-BRAIN; DEMENTIA; ALZ-50; TAU AB We studied the topographic distribution of Alzheimer's disease (AD)-type pathologic changes in the brains of 25 presumed nondemented elderly individuals. Neurofibrillary tangles (NFT) and senile plaques (SP) were evaluated quantitatively in nine to 20 cytoarchitectural fields using thioflavine S, Alz-50, and anti-beta/A4 amyloid immunohistochemistry. Our observations suggest that (1) most individuals over the age of 55 have at least a few NFT and SP; (2) the topographic distribution of NFT and SP in nondemented elderly individuals follows a consistent pattern of vulnerability in different cytoarchitectural areas; (3) NFT occur most frequently in the entorhinal and perirhinal cortices and the CA1/subiculum field of the hippocampus, while neocortical areas are less frequently affected; (4) immunohistochemically defined subtypes of SP have distinct patterns of distribution. Beta/A4 immunoreactive SP are present in neocortical areas >> limbic areas. Alz-50, immunoreactive SP are infrequent and limited to those areas that contain Alz-50-positive neurons and NFT. These patterns closely match the hierarchical topographic distribution of NFT and SP observed in AD, suggesting a commonality in the pathologic processes that lead to NFT and SP in both aging and AD. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROPATHOL,BOSTON,MA 02114. FU NIA NIH HHS [AG08487] NR 48 TC 443 Z9 449 U1 1 U2 8 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD SEP PY 1992 VL 42 IS 9 BP 1681 EP 1688 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA JM884 UT WOS:A1992JM88400007 PM 1307688 ER PT J AU OGAWA, T MATSON, WR BEAL, MF MYERS, RH BIRD, ED MILBURY, P SASO, S AF OGAWA, T MATSON, WR BEAL, MF MYERS, RH BIRD, ED MILBURY, P SASO, S TI KYNURENINE PATHWAY ABNORMALITIES IN PARKINSONS-DISEASE SO NEUROLOGY LA English DT Article ID QUINOLINIC ACID; HUNTINGTONS-DISEASE; RAT-BRAIN; L-DOPA; METABOLITE; NEUROTOXICITY; PROTECTION AB We measured metabolites of tyrosine and tryptophan (TRP) in the frontal cortex, putamen (PT), and pars compacta of the substantia nigra (SN) of control and Parkinson's disease (PD) brain tissues. Dopamine concentrations were significantly decreased in the PT and SN of PD tissue, regardless of L-dopa therapy. However, 3-O-methyldopa (3OMD) concentration showed a significant increase in each region of the PD group treated with L-dopa (PD[+]) as compared with both the control group and the PD group without L-dopa therapy (PD[-]). Therefore, 3OMD concentration appears to be a reliable marker of L-dopa therapy. Serotonin concentration was lower in each region of the PD groups than in the control group. Although the magnitude of decrease was greater in the PD(+) group, there was no statistical significance between the two PD groups. The same patterns of decrease were present in kynurenine (KYN) and kynurenic acid (KYA) concentrations, but the molar ratios of TRP to KYN and KYN to KYA were unchanged among three groups. In contrast, 3-hydroxykynurenine (3OHKY) concentration was increased in the PT and SN of both PD(-) and PD(+) groups, and the ratio of KYN to 3OHKY was significantly reduced in the PT of the PD(-) group and in three regions of the PD(+) group. Since the KYN pathway leads to formation of nicotinamide-adenine dinucleotide (NADH), the present results may be a further indication of a defect in NADH:ubiquinone oxidoreductase (complex I) in mitochondria in PD. C1 ESA INC,BELMONT,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. BOSTON UNIV,DEPT NEUROL,BOSTON,MA 02215. MIYAGI NATL HOSP,YAMAMOTO,JAPAN. RP OGAWA, T (reprint author), MCLEAN HOSP,CTR BRAIN TISSUE RESOURCE,115 MILL ST,BELMONT,MA 02178, USA. NR 28 TC 163 Z9 166 U1 0 U2 7 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD SEP PY 1992 VL 42 IS 9 BP 1702 EP 1706 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA JM884 UT WOS:A1992JM88400010 PM 1513457 ER PT J AU VANOVERLOOP, D SCHNELL, RR HARVEY, EA HOLMES, LB AF VANOVERLOOP, D SCHNELL, RR HARVEY, EA HOLMES, LB TI THE EFFECTS OF PRENATAL EXPOSURE TO PHENYTOIN AND OTHER ANTICONVULSANTS ON INTELLECTUAL FUNCTION AT 4 TO 8 YEARS OF AGE SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE ANTICONVULSANTS; COGNITIVE DYSFUNCTION ID MINOR PHYSICAL ANOMALIES; FETAL HYDANTOIN SYNDROME; PREDICTIVE VALUE; RATS; PERFORMANCE; CHILDREN; EPILEPSY; NEWBORN; GROWTH; FETUS AB Twenty phenytoin exposed children between 48 and 99 months of age had an evaluation of behavior and intelligence by a single examiner who was unaware of exposure status. The controls were 98 children identified at birth as having three or more minor anomalies. None of the children evaluated were mentally retarded. In both, a case-by-case comparison and a comparison of the two entire groups, the phenytoin-exposed children had significantly lower scores for both Performance IQ (PIQ), Full Scale IQ (FSIQ), and Visual Motor Integration Test (VMIT). Similar abnormalities have been found in studies of animals exposed to phenytoin in utero. These results suggest that the teratogenic effects of phenytoin may include an effect on cognitive function. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,EMBRYOL TERATOL UNIT,14 FRUIT ST,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEV EVALUAT CLIN,BOSTON,MA 02115. FU PHS HHS [10910] NR 28 TC 69 Z9 70 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0892-0362 J9 NEUROTOXICOL TERATOL JI Neurotoxicol. Teratol. PD SEP-OCT PY 1992 VL 14 IS 5 BP 329 EP 335 DI 10.1016/0892-0362(92)90039-D PG 7 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA JW784 UT WOS:A1992JW78400004 PM 1454041 ER PT J AU ISAACSON, K BHATTA, KM AF ISAACSON, K BHATTA, KM TI THE LASER-ASSISTED SCALPEL - INITIAL CLINICAL-EVALUATION OF ITS USE IN GYNECOLOGIC ENDOSCOPY SO OBSTETRICS AND GYNECOLOGY LA English DT Article AB The laser-assisted scalpel is a new disposable laparoscopic instrument that improves the precision and control of fiberoptic laser energy delivery and provides a means of tactile probing and blunt tissue dissection. The instrument simplifies laparoscopic technique by providing the surgeon with the ability to place tissue under tension when firing the laser, thus minimizing the need to exchange instruments. We describe the use and our impressions of the laser-assisted scalpel for six common human laparoscopic gynecologic procedures performed in 68 patients. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,WELLMAN LAB PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ISAACSON, K (reprint author), MASSACHUSETTS GEN HOSP,DEPT CARDIOVASC,ACC-231,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD SEP PY 1992 VL 80 IS 3 BP 469 EP 471 PN 1 PG 3 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA JJ702 UT WOS:A1992JJ70200031 PM 1386661 ER PT J AU TROPPMAIR, J BRUDER, JT APP, H HONG, C LIPTAK, L SZEBERENYI, J COOPER, GM RAPP, UR AF TROPPMAIR, J BRUDER, JT APP, H HONG, C LIPTAK, L SZEBERENYI, J COOPER, GM RAPP, UR TI RAS CONTROLS COUPLING OF GROWTH-FACTOR RECEPTORS AND PROTEIN-KINASE-C IN THE MEMBRANE TO RAF-1 AND B-RAF PROTEIN SERINE KINASES IN THE CYTOSOL SO ONCOGENE LA English DT Article ID STIMULATING FACTOR-I; SIGNAL TRANSDUCTION; PC12 CELLS; PHOSPHORYLATION; ONCOGENES; DIFFERENTIATION; ACTIVATION; INSULIN; TYROSINE; GENE AB A dominant negative mutant of Ras, M17 Ras, was used to study the role of Ras in receptor coupling of Raf-1 and B-Raf protein serine/threonine kinases (PSKs). We found that mutant Ras blocks serum- and 12-O-tetradecanoyl phorbol 13-acetate-induced activation of Raf-1 kinase in NIH3T3 cells and Raf-1 as well as B-Raf PSK stimulation by nerve growth factor (NGF) in PC12 pheochromocytoma cells. Mitogen stimulation of Raf kinase was measured by determination of Raf hyperphosphorylation and activity towards exogenous substrates and both of these events were inhibited in cells expressing M17 Ras. In contrast, tyrosine phosphorylation of a direct substrate of activated tyrosine kinase receptors, phospholipase C-gamma-1 (PLC-gamma-1), was unaffected. These data indicate that tyrosine phosphorylation of PLC-gamma-1 is not sufficient for growth induction in NIH3T3 cells and that Ras mediates signal transfer from activated membrane receptors to Raf kinases in the cytosol. As activated Raf induced differentiation in PC12 cells expressing M17 Ras we conclude that Raf kinase activation may be sufficient to account for this aspect of NGF function. C1 NCI,VIRAL CARCINOGENESIS LAB,VIRAL PATHOL SECT,FREDERICK,MD 21702. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 45 TC 116 Z9 116 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD SEP PY 1992 VL 7 IS 9 BP 1867 EP 1873 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA JJ376 UT WOS:A1992JJ37600024 PM 1386920 ER PT J AU TOWNSEND, DJ AF TOWNSEND, DJ TI EYELID REANIMATION FOR THE TREATMENT OF PARALYTIC LAGOPHTHALMOS - HISTORICAL PERSPECTIVES AND CURRENT APPLICATIONS OF THE GOLD WEIGHT IMPLANT SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article DE GOLD WEIGHTS; FACIAL NERVE PARALYSIS; EYELID REANIMATION; LID-LOADING; PARALYTIC ECTROPION AB Gold weight implants have been.used for over 30 years in the setting of eyelid rehabilitation following facial nerve paralysis; however, there has been a renewed interest by ophthalmologists in this reanimation technique in recent years. This article reviews the history of gold weight eyelid implantation and presents the results of gold weight eyelid implantation over a 15-month period in 23 patients. A 92% success rate was obtained (average follow-up, 12 months). Surgical technique and indications are discussed along with postoperative complications. RP TOWNSEND, DJ (reprint author), MASSACHUSETTS EYE & EAR INFIRM,100 CHARLES RIVER PLAZA,BOSTON,MA 02114, USA. NR 0 TC 32 Z9 33 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0740-9303 J9 OPHTHALMIC PLAST REC JI Ophthalmic Plast. Reconstr. Surg. PD SEP PY 1992 VL 8 IS 3 BP 196 EP 201 DI 10.1097/00002341-199209000-00006 PG 6 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA JM422 UT WOS:A1992JM42200006 PM 1390427 ER PT J AU ELNER, VM DUTT, S PAVILACK, MA SUGAR, A FOSTER, CS ELNER, SG AF ELNER, VM DUTT, S PAVILACK, MA SUGAR, A FOSTER, CS ELNER, SG TI INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) AND HLA-DR ANTIGENS IN HERPES KERATITIS SO OPHTHALMOLOGY LA English DT Article ID CLASS-II ANTIGENS; ENDOTHELIAL-CELLS; INTERFERON-GAMMA; LFA-1-DEPENDENT ADHESION; CORNEAL ENDOTHELIUM; ALLOGRAFT-REJECTION; CONTACT-DERMATITIS; STROMAL KERATITIS; T-CELLS; EXPRESSION AB Purpose: Intercellular adhesion molecule-1 (ICAM-1) is a cell surface glycoprotein that binds leukocyte function antigen-1 receptor on leukocytes, thereby regulating leukocyte trafficking and function at sites of inflammation. Recently, the authors demonstrated ICAM-1 in human corneas exposed to proinflammatory cytokines, but ICAM-1 has not been reported in corneal disease. In this study, the presence of ICAM-1 in human disciform herpes simplex virus (HSV) keratitis is investigated. Methods: Immunohistochemistry was performed for ICAM-1 on 4 keratoplasty specimens from patients with corneal scarring due to disciform HSV keratitis and 1 corneoscleral biopsy of a patient with active HSV keratoscleritis using specific, characterized monoclonal antibody to ICAM-1. Negative immunohistochemical controls included monoclonal antibodies to other vascular endothelial adhesion molecules or mouse Results: All 5 specimens demonstrated intense ICAM-1 immunoreactivity of keratinocytes, stromal keratocytes, and endothelial cells, predominantly in regions of leukocytic infiltration. Diffuse, intense HLA-DR positivity was detected throughout the corneas. The specimens failed to react with control antibodies. Conclusion: These results are the first to demonstrate ICAM-1 in human corneal disease and suggest important roles for ICAM-1 and HLA-DR co-expression in generating immune responses in HSV keratitis. Increased ICAM-1 expression in regions of leukocytic infiltration may regulate leukocyte-corneal cell binding, thereby promoting immune responses and damage by activated leukocytes. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. RP ELNER, VM (reprint author), UNIV MICHIGAN,WK KELLOGG EYE CTR,DEPT OPHTHALMOL,1000 WALL ST,ANN ARBOR,MI 48105, USA. FU NEI NIH HHS [EY-07003] NR 41 TC 31 Z9 32 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 SEP PY 1992 VL 99 IS 9 BP 1400 EP 1407 PG 8 WC Ophthalmology SC Ophthalmology GA JM227 UT WOS:A1992JM22700017 PM 1357614 ER PT J AU SHORE, JW CARVAJAL, J WESTFALL, CT AF SHORE, JW CARVAJAL, J WESTFALL, CT TI MINIPLATE RECONSTRUCTION OF THE LATERAL ORBITAL RIM AFTER ORBITAL DECOMPRESSION FOR GRAVES-DISEASE SO OPHTHALMOLOGY LA English DT Article ID IMPLANTS; BONE AB Background. Removal of lateral orbital bone with or without simultaneous removal of the lateral orbital rim is an accepted method of orbital decompression for Graves disease. Once removed, the bone is no longer available for reconstruction and secondary complications such as rounding of the canthal angle, canthal dystopia, and globe dystopia may result. Methods: The authors replaced the excised bone with a titanium miniplate to protect the globe and fixate the lateral canthal tendon in 18 patients (33 orbits). The orbital rim and lateral orbital wall were completely removed, and the inner aspect of the orbit was enlarged with a cutting burr. A standard titanium miniplate was then anchored to remaining bone, and soft tissue was secured to the miniplate to reconstruct the lateral canthus. Results: The results, as manifest by appearance of the lateral canthus and position of the eyelid in apposition to the globe, were graded as excellent in all patients and orbits. There were no early or late complications. Conclusion: Miniplate reconstruction of the lateral orbital rim after decompression for Graves disease allows the beneficial affect of lateral decompression and preserves the functional aspect of the lateral orbital wall. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CTR EYE PLAST & ORBIT,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 27 TC 5 Z9 6 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 SEP PY 1992 VL 99 IS 9 BP 1433 EP 1439 PG 7 WC Ophthalmology SC Ophthalmology GA JM227 UT WOS:A1992JM22700023 PM 1407976 ER PT J AU MELCHIOR, CL RITZMANN, RF AF MELCHIOR, CL RITZMANN, RF TI DEHYDROEPIANDROSTERONE ENHANCES THE HYPNOTIC AND HYPOTHERMIC EFFECTS OF ETHANOL AND PENTOBARBITAL SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE DEHYDROEPIANDROSTERONE; DEHYDROEPIANDROSTERONE SULFATE; NEUROSTEROID; ETHANOL; PENTOBARBITAL; HYPNOSIS; HYPOTHERMIA; GABA ID LACTATING FEMALE INTRUDERS; CASTRATED MALE-MICE; BRAIN; SULFATE; ANTAGONIST; RATS; NEUROSTEROIDS; RO15-4513; RECEPTOR; ATTACK AB Recent reports have indicated that the neurosteroid dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) interact with the GABA(A) receptor complex. Because many of the behavioral effects of ethanol and pentobarbital are due to activity at this complex, DHEA and DHEAS were tested for their ability to interact with the hypnotic and hypothermic effects of ethanol and pentobarbital. DHEA, but not DHEAS, causes a dose-dependent increase in the sleep time induced by either ethanol or pentobarbital. At 20 mg/kg, DHEA and DHEAS themselves cause a fall in body temperature. DHEA enhances the hypothermic effect of both ethanol and pentobarbital. DHEAS enhances the hypothermic effect of ethanol, but with pentobarbital it only delays the return of body temperature to baseline levels. Neither DHEA nor DHEAS affects the metabolism of ethanol. C1 W LOS ANGELES VET ADM,BRENTWOOD DIV RES,LOS ANGELES,CA 90073. FU NIAAA NIH HHS [AA08709] NR 23 TC 27 Z9 27 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD SEP PY 1992 VL 43 IS 1 BP 223 EP 227 DI 10.1016/0091-3057(92)90661-X PG 5 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA JK367 UT WOS:A1992JK36700028 PM 1409808 ER PT J AU TAKAHASHI, LK AF TAKAHASHI, LK TI ONTOGENY OF BEHAVIORAL-INHIBITION INDUCED BY UNFAMILIAR ADULT MALE CONSPECIFICS IN PREWEANLING RATS SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE PREWEANLING RATS; ULTRASONIC VOCALIZATIONS; FREEZING; BEHAVIORAL INHIBITION; DEVELOPMENT; BODY TEMPERATURE; CONSPECIFIC THREAT; SOCIAL ISOLATION ID DEFENSIVE REACTIONS; RATTUS-NORVEGICUS; MALLARD DUCKLINGS; 2-WEEK-OLD RATS; OLFACTORY CUES; RESPONSES; VOCALIZATIONS; ULTRASOUNDS; STRESS; PUPS AB Previous studies showed that when socially isolated at 22-degrees-C, postnatal day 14 rats. but not younger day 7 rats, reduce their emission of ultrasonic vocalizations when exposed to an unfamiliar adult male rat, a naturalistic threat. Because ultrasound production is associated with factors such as age and body temperature. this study examined in age-appropriate thermoneutral temperature ranges whether preweanling rats of different ages are equally capable of inhibiting their emission of ultrasounds when threatened. In Experiment 1, 7- and 14-day-old rats were socially isolated and exposed to unfamiliar anesthetized adult male rats in a thermoneutral environment. Only 14-day-old rats significantly reduced their emission of ultrasounds. This reduction in ultrasound production was accompanied by freezing. In Experiment 2, additional ages were examined under identical test conditions. At 3, 6, and 9 days of age, pups frequently emitted ultrasounds when exposed to the anesthetized male rat. However, at 12 days of age, rat pups responded to the anesthetized male rat by freezing and significantly reducing their emission of ultrasounds, Results indicate clearly that under the present testing conditions the ability of rat pups to inhibit ultrasounds and freeze when threatened is not present at birth but emerges by the end of the second postnatal week. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [MH-43986] NR 34 TC 76 Z9 77 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD SEP PY 1992 VL 52 IS 3 BP 493 EP 498 DI 10.1016/0031-9384(92)90336-Z PG 6 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA JL838 UT WOS:A1992JL83800012 PM 1409910 ER PT J AU DUMANIAN, GA DONAHOE, PK AF DUMANIAN, GA DONAHOE, PK TI BILATERAL ROTATED BUTTOCK FLAPS FOR VAGINAL ATRESIA IN SEVERELY MASCULINIZED FEMALES WITH ADRENOGENITAL SYNDROME SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID RECONSTRUCTION C1 MASSACHUSETTS GEN HOSP,DIV PEDIAT SURG,WARREN 11,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 8 TC 13 Z9 14 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 SEP PY 1992 VL 90 IS 3 BP 487 EP 491 PG 5 WC Surgery SC Surgery GA JL532 UT WOS:A1992JL53200022 PM 1513896 ER PT J AU SHIH, VE LAFRAMBOISE, R MANDELL, R PICHETTE, J AF SHIH, VE LAFRAMBOISE, R MANDELL, R PICHETTE, J TI NEONATAL FORM OF THE HYPERORNITHINEMIA, HYPERAMMONEMIA, AND HOMOCITRULLINURIA (HHH) SYNDROME AND PRENATAL-DIAGNOSIS SO PRENATAL DIAGNOSIS LA English DT Article DE PRENATAL DIAGNOSIS; AMINO ACID DISORDER; HYPERAMMONEMIA; INBORN ERROR OF METABOLISM ID TRANSPORT; ORNITHINE AB We describe here the first case of neonatal death due to the hyperornithinaemia, hyperammonaemia, and homocitrullinuria (HHH) syndrome and the first prenatal diagnosis of this disorder in a subsequent pregnancy in this family. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. CHU LAVAL,ST FOY,QUEBEC,CANADA. CHU LAVAL,DEPT PEDIAT,SERV MED GENET,QUEBEC CITY G1V 4G2,QUEBEC,CANADA. CHU LAVAL,DEPT PEDIAT,SERV NEONATAL,ST FOY,QUEBEC,CANADA. RP SHIH, VE (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BLDG 149,13TH ST,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS05096] NR 12 TC 9 Z9 9 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0197-3851 J9 PRENATAL DIAG JI Prenat. Diagn. PD SEP PY 1992 VL 12 IS 9 BP 717 EP 723 DI 10.1002/pd.1970120905 PG 7 WC Genetics & Heredity; Obstetrics & Gynecology SC Genetics & Heredity; Obstetrics & Gynecology GA JP747 UT WOS:A1992JP74700003 PM 1438066 ER PT J AU COLONNA, M SPIES, T STROMINGER, JL CICCONE, E MORETTA, A MORETTA, L PENDE, D VIALE, O AF COLONNA, M SPIES, T STROMINGER, JL CICCONE, E MORETTA, A MORETTA, L PENDE, D VIALE, O TI ALLOANTIGEN RECOGNITION BY 2 HUMAN NATURAL-KILLER-CELL CLONES IS ASSOCIATED WITH HLA-C OR A CLOSELY LINKED GENE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; BONE-MARROW; EXPRESSION; MICE; IDENTIFICATION; RESISTANCE; MOLECULES; REJECTION; CONTAINS; REGION AB Human natural killer (NK) cells with the CD3- CD16+ phenotype recognize allospecificities on normal T-cell blasts. The NK-defined specificity 1 (NK-1) is recessively inherited and has been mapped to the major histocompatibility complex between the complement gene cluster and HLA-A. A gene for NK-1, however, has not been identified. Here we demonstrate that NK-1 and the recently defined NK specificity 2 (NK-2) are reciprocally associated with homozygosity for a diallelic polymorphism at amino acid positions 77 and 80 in the putative peptide-binding site of HLA-C (P < 10(-5)). NK-cell recognition of allogeneic cells may, therefore, be controlled by HLA-C itself or by a closely linked gene(s), which dominantly prevents (resistance alleles) or recessively permits (susceptibility alleles) recognition of still-unknown target determinants. C1 IST NAZL RIC CANC,IMMUNOGENET LAB,I-16132 GENOA,ITALY. IST NAZL RIC CANC,IMMUNOPATHOL,I-16132 GENOA,ITALY. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. UNIV TURIN,DIPARTIMENTO MED & ONCOL SPERIMENTALE,I-10124 TURIN,ITALY. RP COLONNA, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115, USA. RI Pende, Daniela/J-7429-2016; OI Pende, Daniela/0000-0003-1565-451X; Colonna, Marco/0000-0001-5222-4987 FU NCI NIH HHS [CA-47554]; NIAID NIH HHS [AI-3058]; NIDDK NIH HHS [DK-30241] NR 23 TC 142 Z9 143 U1 0 U2 0 PU NATL ACAD PRESS 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 SEP 1 PY 1992 VL 89 IS 17 BP 7983 EP 7985 DI 10.1073/pnas.89.17.7983 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400028 PM 1518825 ER PT J AU DEMAY, MB KIERNAN, MS DELUCA, HF KRONENBERG, HM AF DEMAY, MB KIERNAN, MS DELUCA, HF KRONENBERG, HM TI SEQUENCES IN THE HUMAN PARATHYROID-HORMONE GENE THAT BIND THE 1,25-DIHYDROXYVITAMIN-D3 RECEPTOR AND MEDIATE TRANSCRIPTIONAL REPRESSION IN RESPONSE TO 1,25-DIHYDROXYVITAMIN-D3 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID RAT OSTEOCALCIN GENE; VITAMIN-D RECEPTOR; GLUCOCORTICOID RECEPTOR; NEGATIVE REGULATION; NUCLEOTIDE-SEQUENCE; 5'-FLANKING REGION; DNA-SEQUENCE; C-JUN; ELEMENT; PROTEIN AB 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], plays an important role in the regulation of mineral ion homeostasis. As well as being the major steroid hormone that regulates calcium metabolism, 1,25(OH)2D3 suppresses transcription of the gene encoding parathyroid hormone, a peptide that plays a dominant role in regulating extracellular calcium levels. To identify DNA sequences that may mediate this transcriptional repression, nuclear extracts containing the 1,25(OH)2D3 receptor were examined for binding to sequences in the 5'-flanking region of the human parathyroid hormone gene. A 25-base-pair (bp) oligonucleotide containing the sequences from -125 to -101 from the start of exon I binds nuclear proteins recognized by monoclonal antibodies against the 1,25(OH)2D3 receptor. The sequences in this region contain a single copy of a motif (AGGTTCA) homologous to the motifs repeated in the up-regulatory 1,25(OH)2D3-response elements. When placed upstream to a heterologous viral promoter, the sequences contained in this 25-bp oligonucleotide mediate transcriptional repression in response to 1,25(OH)2D3 in GH4C1 cells but not in ROS 17/2.8 cells. This down-regulatory element, therefore, differs from the up-regulatory 1,25(OH)2D3-response elements both in sequence composition and in the requirement for particular cellular factors other than the 1,25(OH)2D3 receptor for repressing transcription. C1 UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BIOCHEM,MADISON,WI 53706. RP DEMAY, MB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114, USA. FU NIADDK NIH HHS [AM-14881]; NIDDK NIH HHS [DK11794, DK36597] NR 28 TC 277 Z9 283 U1 0 U2 4 PU NATL ACAD PRESS 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 SEP 1 PY 1992 VL 89 IS 17 BP 8097 EP 8101 DI 10.1073/pnas.89.17.8097 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400052 PM 1325645 ER PT J AU FALO, LD COLARUSSO, LJ BENACERRAF, B ROCK, KL AF FALO, LD COLARUSSO, LJ BENACERRAF, B ROCK, KL TI SERUM PROTEASES ALTER THE ANTIGENICITY OF PEPTIDES PRESENTED BY CLASS-I MAJOR HISTOCOMPATIBILITY COMPLEX-MOLECULES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANTIGEN PRESENTATION; CYTOTOXIC LYMPHOCYTES-T; IMMUNOTHERAPY; VACCINE ID T-CELLS; MHC MOLECULES; BETA-2-MICROGLOBULIN; BINDING; REASSOCIATION; HYBRIDOMAS AB Any effect of serum on the antigenicity of peptides is potentially relevant to their use as immunogens in vivo, Here we demonstrate that serum contains distinct proteases that can increase or decrease the antigenicity of peptides. By using a functional assay, we show that a serum component other than beta-2-microglobulin enhances the presentation of ovalbumin peptides produced by cyanogen bromide cleavage. Three features of this serum activity implicate proteolysis: it is temperature dependent, it results in increased antigenicity in a low molecular weight peptide fraction, and it is inhibited by the protease inhibitor leupeptin. Conversely, presentation of the synthetic peptide OVA-(257-264) is inhibited by serum. This inhibition is unaffected by leupeptin but is blocked by bestatin, a protease inhibitor with distinct substrate specificities. Implications for peptide-based vaccine design and immunotherapy are discussed. C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP FALO, LD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-20248, AI-31337]; NIAMS NIH HHS [5-T32-AR-07098-17] NR 24 TC 65 Z9 65 U1 0 U2 1 PU NATL ACAD PRESS 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 SEP 1 PY 1992 VL 89 IS 17 BP 8347 EP 8350 DI 10.1073/pnas.89.17.8347 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400104 PM 1518868 ER PT J AU TYAN, ML AF TYAN, ML TI EFFECTS OF H-2 ON NEURAL-TUBE DEFECTS IN CONGENIC MICE SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID PERICONCEPTIONAL USE; RETINOIC ACID; SPINA-BIFIDA; MOUSE; SUPPLEMENTATION; PREGNANCY; MUTATION AB Pregnant mice congenic with C57BL/10 (B10.A, B10.BR, B10.D2, B10.A[2R], B10.A[5R], B10.A[15R], B10.A[1R], B10.A[18R], and B10.0L) were fed Purina Mouse Chow or the same diet plus 200 IU of vitamin A daily. The pregnant dams were sacrificed on the eighteenth day of gestation, and the fetuses were sexed and examined for defects in neural tube development. The frequency of neural tube defects was low (mean frequency of all strains, 0.36%) and was not affected by the addition of vitamin A (200 IU/day) to the diet. Twenty-seven of the 29 defects observed occurred in the anterior tube (exencephaly); fourteen were identified in female fetuses, but the sex could not be determined in the other 15 cases because of fetal death and early autolysis. Variations in frequency among the strains suggest that a locus between E(beta) and H-2D has a moderate influence on the occurrence of neural tube defects. Strains that had H-2d alleles in this segment of the H-2 complex had relatively high frequencies, and those with H-2b or H-2k alleles had significantly lower frequencies. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RP TYAN, ML (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,W 111M,LOS ANGELES,CA 90073, USA. NR 21 TC 6 Z9 6 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD SEP PY 1992 VL 200 IS 4 BP 487 EP 489 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA JK227 UT WOS:A1992JK22700006 PM 1508938 ER PT J AU WANG, CC BADYLAK, JA LUX, SE MORIYAMA, R DIXON, JE LOW, PS AF WANG, CC BADYLAK, JA LUX, SE MORIYAMA, R DIXON, JE LOW, PS TI EXPRESSION, PURIFICATION, AND CHARACTERIZATION OF THE FUNCTIONAL DIMERIC CYTOPLASMIC DOMAIN OF HUMAN ERYTHROCYTE BAND-3 IN ESCHERICHIA-COLI SO PROTEIN SCIENCE LA English DT Article DE BAND-3 CONFORMATION; CYTOPLASMIC DOMAIN OF BAND-3; INCLUSION BODY; PROTEIN EXPRESSION IN ESCHERICHIA-COLI; T7-PROMOTER ID ANKYRIN-BINDING SITE; TYROSINE PHOSPHORYLATION; MEMBRANE PROTEIN; RNA-POLYMERASE; CELL MEMBRANE; ASSOCIATION; HEMOGLOBIN; RECOVERY; ALDOLASE; LYSOZYME AB The cytoplasmic domain of the human erythrocyte membrane protein, band 3 (cdb3), contains binding sites for hemoglobin, several glycolytic enzymes, band 4. 1, band 4.2, and ankyrin, and constitutes the major linkage between the membrane skeleton and the membrane. Although erythrocyte cdb3 has been partially purified from proteolyzed red blood cells, further separation of the water-soluble 43-kDa and 41-kDa proteolytic fragments has never been achieved. In order to obtain pure cdb3 for crystallization and site-directed mutagenesis studies, we constructed an expression plasmid that has a tandemly linked T7 promoter placed upstream of the N-terminal 379 amino acids of the erythrocyte band 3 gene. Comparison of several Escherichia coli strains led to the selection of the BL21 (DE3) strain containing the pLysS plasmid as the best host for efficient production of cdb3. About 10 mg of recombinant cdb3 can be easily purified from 4 L of E. coli culture in two simple steps. Comparison of cdb3 released from the red blood cell by proteolysis with recombinant cdb3 reveals that both have the same N-terminal sequence, secondary structure, and pH-dependent conformational change. The purified recombinant cdb3 is also a soluble stable dimer with the same Stokes radius as erythrocyte cdb3. The affinities of the two forms of cdb3 for ankyrin are essentially identical; however, recombinant cdb3 with its unblocked N-terminus exhibits a slightly lower affinity for aldolase. C1 PURDUE UNIV,DEPT CHEM,W LAFAYETTE,IN 47907. PURDUE UNIV,DEPT BIOCHEM,W LAFAYETTE,IN 47907. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. OI Low, Philip/0000-0001-9042-5528 FU NIDDK NIH HHS [5R37-DK34083]; NIGMS NIH HHS [GM 24417, GM 40983] NR 36 TC 39 Z9 41 U1 0 U2 0 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 SEP PY 1992 VL 1 IS 9 BP 1206 EP 1214 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JR693 UT WOS:A1992JR69300013 PM 1304397 ER PT J AU TRESTMAN, RL LAWRENCE, TL COCCARO, EF HARVEY, P BERNSTEIN, D LAWRENCE, EK CONDELLO, V MAHON, T YANG, RK KNOTT, P HORVATH, TB SIEVER, LJ AF TRESTMAN, RL LAWRENCE, TL COCCARO, EF HARVEY, P BERNSTEIN, D LAWRENCE, EK CONDELLO, V MAHON, T YANG, RK KNOTT, P HORVATH, TB SIEVER, LJ TI NORADRENERGIC RESPONSES TO CLONIDINE IN ACUTE AND REMITTED DEPRESSED MALE-PATIENTS SO PSYCHIATRY RESEARCH LA English DT Article DE AFFECTIVE DISORDER; 3-METHOXY-4-HYDROXYPHENYLGLYCOL; MEAN ARTERIAL PRESSURE; HEART RATE ID GROWTH-HORMONE RESPONSE; PROLACTIN PLASMA-LEVELS; BLOOD-PRESSURE; ENDOGENOUS-DEPRESSION; LIQUID-CHROMATOGRAPHY; MHPG; NORADRENALINE; DISORDER; CORTISOL; TESTS AB To investigate noradrenergic function in depression, plasma 3-methoxy-4-hydroxyphenylglycol (MHPG), plasma norepinephrine (NE), mean arterial pressure (MAP), and heart rate responses to intravenous clonidine (2 mug/kg), an alpha2-adrenergic agonist, were measured in 27 acutely depressed patients, 18 remitted depressed patients, and 27 normal control subjects; a placebo infusion was administered to a subgroup. Clonidine compared with placebo, over a 150-minute time course, decreased plasma NE, MAP, and heart rate, but not plasma MHPG, in the control subjects. Plasma MHPG, plasma NE, MAP, and heart rate at baseline or in response to clonidine and placebo over 150 minutes did not indicate any group differences. The only significant plasma MHPG response to clonidine in the normal control subjects occurred 60 minutes after the infusion. A significantly diminished plasma MHPG response to clonidine at 60 minutes was found in the acutely depressed group compared with the normal control subjects. These results suggest that peripheral inhibitory noradrenergic responses to clonidine are normal in depressed patients, while plasma MHPG responses to clonidine, which have a limited central contribution, appear to be a weak reflection of central noradrenergic function and appear insufficiently robust for a meaningful evaluation of hypothetical group differences in central inhibitory alpha2-adrenergic activity in this population. C1 CUNY MT SINAI SCH MED,PSYCHIAT,NEW YORK,NY 10029. MED COLL PENN,EASTERN PENN PSYCHIAT INST,PHILADELPHIA,PA 19129. YESHIVA UNIV ALBERT EINSTEIN COLL MED,SCH MED,BRONX,NY 10461. SUNY DOWNSTATE MED CTR,BROOKLYN,NY 11203. RP TRESTMAN, RL (reprint author), BRONX VET AFFAIRS MED CTR,PSYCHIAT SERV,116A,1130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NCRR NIH HHS [RR00071]; NIMH NIH HHS [R01-MH41131] NR 46 TC 10 Z9 10 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 SEP PY 1992 VL 43 IS 3 BP 199 EP 213 DI 10.1016/0165-1781(92)90053-6 PG 15 WC Psychiatry SC Psychiatry GA JW645 UT WOS:A1992JW64500001 PM 1332095 ER PT J AU CRONINGOLOMB, A KOKODIS, A KEANE, MM CORKIN, S GROWDON, JH AF CRONINGOLOMB, A KOKODIS, A KEANE, MM CORKIN, S GROWDON, JH TI CATEGORY KNOWLEDGE IN ALZHEIMERS-DISEASE - NORMAL ORGANIZATION AND A GENERAL RETRIEVAL DEFICIT SO PSYCHOLOGY AND AGING LA English DT Article ID SEMANTIC MEMORY; DEMENTIA; ATTRIBUTES; IMPAIRMENT AB Three hypotheses that could account for deficits in the retrieval of category information in Alzheimer's disease (AD) were evaluated: abnormal organization, class- or category-specific vulnerability, and limitation by general factors, such as decreased processing speed. Relative to 18 elderly control subjects, 18 patients with AD produced fewer items in a category fluency task and had longer reaction times in a category decision task. The pattern of performance across categories on both tasks was normal in the AD group: The same categories elicited the most (or fastest) responses in both the control group and the AD group. AD patients showed normal performance in ranking of category exemplars by typicality. There was no evidence for differential accessibility by category or by class of information (animate vs. inanimate). The authors conclude that a general factor or factors limit(s) retrievability equally across all categories. C1 MIT,CLIN RES CTR,CAMBRIDGE,MA 02139. BOSTON UNIV,SCH PUBL HLTH,BOSTON,MA 02215. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP CRONINGOLOMB, A (reprint author), BOSTON UNIV,DEPT PSYCHOL,64 CUMMINGTON ST,BOSTON,MA 02215, USA. FU NCRR NIH HHS [RR00088]; NIA NIH HHS [AG5134, AG6605] NR 33 TC 33 Z9 33 U1 1 U2 3 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0882-7974 J9 PSYCHOL AGING JI Psychol. Aging PD SEP PY 1992 VL 7 IS 3 BP 359 EP 366 DI 10.1037//0882-7974.7.3.359 PG 8 WC Gerontology; Psychology, Developmental SC Geriatrics & Gerontology; Psychology GA JN086 UT WOS:A1992JN08600005 PM 1388856 ER PT J AU BELKIN, GS FLEISHMAN, JA STEIN, MD PIETTE, J MOR, V AF BELKIN, GS FLEISHMAN, JA STEIN, MD PIETTE, J MOR, V TI PHYSICAL SYMPTOMS AND DEPRESSIVE SYMPTOMS AMONG INDIVIDUALS WITH HIV-INFECTION SO PSYCHOSOMATICS LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY SYNDROME; CANCER-PATIENTS; HOMOSEXUAL MEN; PSYCHIATRIC-DISORDERS; DIAGNOSING DEPRESSION; MEDICAL ILLNESS; SOCIAL SUPPORT; AIDS; SUICIDE AB The authors investigate the importance of physical symptoms as a correlate of depressive symptoms and suicidal thoughts in a large (N = 881) community-based sample of persons infected with human immunodeficiency virus. The study overcomes limitations of prior research by minimizing overlap in measures of affective and physical symptoms, studying a more diverse population, and including correlates such as measures of social support, function, employment, insurance coverage, and cognitive impairment in the analysis. The authors' data support the notion that in diagnosing depression in the medically ill, concern over isolating physical symptoms as either "affective" or "physical" may be exaggerated. C1 BROWN UNIV,CTR GERONTOL & HLTH CARE RES,BOX G,PROVIDENCE,RI 02912. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,BOSTON,MA 02115. NR 59 TC 60 Z9 60 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD FAL PY 1992 VL 33 IS 4 BP 416 EP 427 PG 12 WC Psychiatry; Psychology SC Psychiatry; Psychology GA JQ781 UT WOS:A1992JQ78100007 PM 1461967 ER PT J AU CREMENS, MC FALK, WE AF CREMENS, MC FALK, WE TI THE DEMENTIAS - DIAGNOSIS AND MANAGEMENT - WEINER,MF SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,DIV AGING,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,GERIATR NEUROBEHAV CLIN,BOSTON,MA 02114. RP CREMENS, MC (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD FAL PY 1992 VL 33 IS 4 BP 466 EP 467 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA JQ781 UT WOS:A1992JQ78100015 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI PSYCHOSOMATIC SYNDROMES AND SOMATIC SYMPTOMS - KELLNER,R SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP GREENBERG, DB (reprint author), HARVARD UNIV,SCH MED,PSYCHIAT,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 FAL PY 1992 VL 33 IS 4 BP 467 EP 468 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA JQ781 UT WOS:A1992JQ78100017 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI SOMATIZATION DISORDER IN THE MEDICAL SETTING - SMITH,GR SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP GREENBERG, DB (reprint author), HARVARD UNIV,SCH MED,PSYCHIAT,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 FAL PY 1992 VL 33 IS 4 BP 467 EP 467 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA JQ781 UT WOS:A1992JQ78100016 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI CURRENT CONCEPTS OF SOMATIZATION - RESEARCH AND CLINICAL PERSPECTIVES, PROGRESS IN PSYCHIATRY .31. KIRMAYER,LJ, ROBBINS,JM SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP GREENBERG, DB (reprint author), HARVARD UNIV,SCH MED,PSYCHIAT,BOSTON,MA 02115, 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 FAL PY 1992 VL 33 IS 4 BP 468 EP 469 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA JQ781 UT WOS:A1992JQ78100018 ER PT J AU SILVA, JA LEONG, GB SAAB, S WINE, DB AF SILVA, JA LEONG, GB SAAB, S WINE, DB TI MISIDENTIFICATION SYNDROME, FACIAL MISRECOGNITION, AND DYSMORPHIC SYMPTOMS SO PSYCHOSOMATICS LA English DT Letter C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP SILVA, JA (reprint author), UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024, USA. NR 5 TC 5 Z9 5 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD FAL PY 1992 VL 33 IS 4 BP 471 EP 472 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA JQ781 UT WOS:A1992JQ78100020 PM 1461976 ER PT J AU KUTNER, NG ORY, MG BAKER, DI SCHECHTMAN, KB HORNBROOK, MC MULROW, CD AF KUTNER, NG ORY, MG BAKER, DI SCHECHTMAN, KB HORNBROOK, MC MULROW, CD TI MEASURING THE QUALITY-OF-LIFE OF THE ELDERLY IN HEALTH PROMOTION INTERVENTION CLINICAL-TRIALS SO PUBLIC HEALTH REPORTS LA English DT Article ID OF-LIFE; PERFORMANCE; DISEASE; ISSUES; STATE AB The Multicenter Trials of Frailty and Injuries: Cooperative Studies of Intervention Techniques (FICSIT) is a series of clinical trials Of biomedical, behavioral, and environmental interventions to reduce the risks of frailty and injury among the elderly. Reliable assessment of the quality of life reported by the subjects is a central issue in evaluating the interventions. An intervention may have a significant impact on an elderly person's sense of well-being, even though significant improvement is not observed in selected physical outcome measures. Elderly persons' compliance with particular intervention regimens may be influenced by the quality of life effects that they perceive in relation to the intervention. The researchers review the definition and measurement of quality of life in the trials, with particular attention to issues in determining common measures used at all study locations. considerations in the selection and use of quality of life measures in both community and institutional populations are addressed. Topics discussed include the interrelation of aging, functional capacities, and quality of life, the multi-dimensionality of quality of life in relation to differential intervention effects; and age-related issues in the collection of quality of life data. Preliminary observations are reviewed, and potential contributions of FICSIT to intervention-sensitive quality of life assessments among the elderly are noted. C1 NIA,SOCIAL SCI RES AGING,BETHESDA,MD 20892. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. UNIV OREGON,EUGENE,OR 97403. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP KUTNER, NG (reprint author), EMORY UNIV,SCH MED,1441 CLIFTON RD NE,ATLANTA,GA 30322, USA. FU NIA NIH HHS [U01-AG09089] NR 39 TC 30 Z9 30 U1 5 U2 6 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD SEP-OCT PY 1992 VL 107 IS 5 BP 530 EP 539 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JR213 UT WOS:A1992JR21300007 PM 1410233 ER PT J AU LEE, MJ MUELLER, PR DAWSON, SL MCLAUGHLIN, DT KINNEY, T HAHN, PF SAINI, S GAZELLE, GS AF LEE, MJ MUELLER, PR DAWSON, SL MCLAUGHLIN, DT KINNEY, T HAHN, PF SAINI, S GAZELLE, GS TI MEASUREMENT OF TISSUE CARCINOEMBRYONIC ANTIGEN LEVELS FROM FINE-NEEDLE BIOPSY SPECIMENS - TECHNIQUE AND CLINICAL USEFULNESS SO RADIOLOGY LA English DT Article DE ABDOMEN, BIOPSY; ABDOMEN, NEOPLASMS; BIOPSIES; CARCINOEMBRYONIC ANTIGEN (CEA); COLON, NEOPLASMS; LIVER NEOPLASMS, SECONDARY ID ASPIRATION BIOPSY; CARCINOMA; LOCALIZATION; DIAGNOSIS; CANCER AB Levels of tissue carcinoembryonic antigen (CEA) in 54 abdominal fine-needle biopsy specimens from 50 patients were measured to ascertain the use of tissue CEA levels in diagnosis of malignancy. Biopsy was performed in the following sites: liver (n = 34), retroperitoneum (n = 8), adrenal gland (n = 3), pancreas (n = 2), omentum (n = 2), pelvis (n = 2), spleen (n = 2), and stomach (n = 1). Histologic findings proved malignancy in 39 patients and benign disease in 11 patients. In these 11 patients, the mean levels of tissue CEA were lower than the normal level of serum CEA (3 ng/mL). Tissue CEA levels were higher than serum CEA levels in nine patients with colonic carcinoma and in 12 of 16 patients with noncolonic CEA-secreting malignancies. Four patients with noncolonic CEA-secreting malignancies had tissue CEA levels within the normal range (<3 ng/mL). Tissue CEA levels were also normal in 13 patients with various non-CEA-secreting tumors. Tissue CEA levels may prove useful in biopsy of necrotic or cystic lesions and assessment of response to ablative therapy for colon metastases. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP LEE, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 14 TC 3 Z9 3 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 SEP PY 1992 VL 184 IS 3 BP 717 EP 720 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JJ866 UT WOS:A1992JJ86600026 PM 1509055 ER PT J AU ROGOFF, PA HILGENBERG, AD MILLER, SL STEPHAN, SM AF ROGOFF, PA HILGENBERG, AD MILLER, SL STEPHAN, SM TI CEPHALIC MIGRATION OF THE BIRDS NEST INFERIOR VENA-CAVAL FILTER - REPORT OF 2 CASES SO RADIOLOGY LA English DT Article DE EMBOLISM, PULMONARY; INTERVENTIONAL PROCEDURES, COMPLICATIONS; VENAE-CAVAE, FILTERS; VENAE-CAVAE, INTERVENTIONAL PROCEDURE; VENAE-CAVAE, THROMBOSIS ID KIMRAY-GREENFIELD FILTER AB The Bird's Nest inferior vena caval filter (Cook, Bloomington, Ind) has been approved for clinical use since 1989. The authors report two cases of cephalic migration of the filter. Both cases of migration occurred in association with a massive thromboembolism after placement of the filter. It appears that a massive thromboembolism can cause this filter to migrate cephalad. The authors suggest that there is potential for nonsurgical management of the migrated filter. C1 NEWTON WELLESLEY HOSP,DEPT RADIOL,NEWTON,MA. MT AUBURN HOSP,DEPT CARDIOTHORAC SURG,CAMBRIDGE,MA 02238. MASSACHUSETTS GEN HOSP,DEPT CARDIOTHORAC SURG,BOSTON,MA 02114. RP ROGOFF, PA (reprint author), MT AUBURN HOSP,DEPT RADIOL,330 MT AUBURN ST,CAMBRIDGE,MA 02238, USA. NR 9 TC 17 Z9 17 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 SEP PY 1992 VL 184 IS 3 BP 819 EP 822 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JJ866 UT WOS:A1992JJ86600044 PM 1509073 ER PT J AU GIRARD, MJ HAHN, PF SAINI, S DAWSON, SL GOLDBERG, MA MUELLER, PR AF GIRARD, MJ HAHN, PF SAINI, S DAWSON, SL GOLDBERG, MA MUELLER, PR TI WALLSTENT METALLIC BILIARY ENDOPROSTHESIS - MR IMAGING CHARACTERISTICS SO RADIOLOGY LA English DT Note DE BILE DUCTS, MR; BILE DUCTS, PROSTHESES; MAGNETIC RESONANCE (MR), ARTIFACT; MAGNETIC RESONANCE (MR), SAFETY ID POTENTIAL HAZARDS; STENTS; IMPLANTS; OBSTRUCTION; STRICTURES; ARTIFACTS; DEVICES; SAFETY AB Image quality and safety of magnetic resonance (MR) imaging were evaluated in vitro and in eight patients with the most commonly employed metallic biliary endoprosthesis. In vitro, the stent produced no tip deflection at 0.6 or 1.5 T. Trace magnetic susceptibility artifact, similar to artifact from a column of air, paralleled the stent. In patients, image degradation was minimal with conventional pulse sequences. Middle-field-strength spin-echo images revealed minimal artifacts indistinguishable from those produced by pneumobilia. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 22 TC 17 Z9 17 U1 1 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 SEP PY 1992 VL 184 IS 3 BP 874 EP 876 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JJ866 UT WOS:A1992JJ86600055 PM 1509084 ER PT J AU OGAWA, M AF OGAWA, M TI IL6 AND HEMATOPOIETIC STEM-CELLS SO RESEARCH IN IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; MULTIPOTENTIAL HEMATOPOIETIC PROGENITORS; FACTOR-I; INTERLEUKIN-3-DEPENDENT PROLIFERATION; CULTURE; INTERLEUKIN-11; ENHANCEMENT; GROWTH; MICE; GM C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29401. RP OGAWA, M (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401, USA. NR 19 TC 11 Z9 11 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD SEP PY 1992 VL 143 IS 7 BP 749 EP 751 DI 10.1016/0923-2494(92)80016-E PG 3 WC Immunology SC Immunology GA JV754 UT WOS:A1992JV75400010 PM 1439149 ER PT J AU RYAN, L AF RYAN, L TI THE USE OF GENERALIZED ESTIMATING EQUATIONS FOR RISK ASSESSMENT IN DEVELOPMENTAL TOXICITY SO RISK ANALYSIS LA English DT Article DE QUASI-LIKELIHOOD; TERATOLOGY; BETA-BINOMIAL; DOSE-RESPONSE ID LONGITUDINAL DATA-ANALYSIS; TERATOLOGICAL EXPERIMENTS; RESPONSE MODEL; LINEAR-MODELS AB This paper reviews and compares several approaches to fitting dose-response models to developmental toxicity data. The main issue of interest is how to appropriately account for litter effects. Among the approaches reviewed are Beta Binomial models, models that attempt to characterize the litter effect through the use of covariates, and models that avoid the complication of correlated offspring by modeling "affected litter" rather than fetus-specific outcomes. Finally, we discuss our recommended approach, which is to use Generalized Estimating Equations, or quasi-likelihood. We give a number of reasons for preferring the latter and illustrate its application with an example. RP RYAN, L (reprint author), HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,DIV BIOSTAT,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [CA48061] NR 26 TC 34 Z9 35 U1 0 U2 4 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4332 J9 RISK ANAL JI Risk Anal. PD SEP PY 1992 VL 12 IS 3 BP 439 EP 447 DI 10.1111/j.1539-6924.1992.tb00696.x PG 9 WC Public, Environmental & Occupational Health; Mathematics, Interdisciplinary Applications; Social Sciences, Mathematical Methods SC Public, Environmental & Occupational Health; Mathematics; Mathematical Methods In Social Sciences GA JM260 UT WOS:A1992JM26000015 PM 1410710 ER PT J AU FISCHBACH, GD AF FISCHBACH, GD TI MIND AND BRAIN SO SCIENTIFIC AMERICAN LA English DT Article C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP FISCHBACH, GD (reprint author), HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115, USA. NR 0 TC 25 Z9 26 U1 0 U2 0 PU SCI AMERICAN INC PI NEW YORK PA 415 MADISON AVE, NEW YORK, NY 10017 SN 0036-8733 J9 SCI AM JI Sci.Am. PD SEP PY 1992 VL 267 IS 3 BP 48 EP 57 PG 10 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JK965 UT WOS:A1992JK96500007 PM 1502523 ER PT J AU MUELLER, PR AF MUELLER, PR TI FIBRINOLYSIS SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Editorial Material RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,INTERVENT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0739-9529 J9 SEMIN INTERVENT RAD JI Semin. Interv. Radiol. PD SEP PY 1992 VL 9 IS 3 BP 158 EP 158 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JM737 UT WOS:A1992JM73700010 ER PT J AU KAUFMAN, JA BETTMANN, MA AF KAUFMAN, JA BETTMANN, MA TI THROMBOLYSIS OF PERIPHERAL VASCULAR OCCLUSIONS WITH UROKINASE - A REVIEW OF THE CLINICAL LITERATURE SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Review RP KAUFMAN, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,GRAY 2,BOSTON,MA 02114, USA. NR 0 TC 6 Z9 6 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 SEP PY 1992 VL 9 IS 3 BP 159 EP 165 DI 10.1055/s-2008-1074683 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JM737 UT WOS:A1992JM73700002 ER PT J AU MOSKOWITZ, MA AF MOSKOWITZ, MA TI DISTRIBUTION OF THE 72-KD HEAT-SHOCK PROTEIN AS A FUNCTION OF TRANSIENT FOCAL CEREBRAL-ISCHEMIA IN RATS - EDITORIAL COMMENT SO STROKE LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MOSKOWITZ, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD SEP PY 1992 VL 23 IS 9 BP 1298 EP 1298 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA JK926 UT WOS:A1992JK92600016 ER PT J AU STOLER, JM HOLMES, LB AF STOLER, JM HOLMES, LB TI A CASE OF AGNATHIA, SITUS-INVERSUS, AND A NORMAL CENTRAL-NERVOUS-SYSTEM SO TERATOLOGY LA English DT Article ID MALFORMATIONS; ASSOCIATION AB We report here a premature female infant with agnathia, low-set but normally formed ears, a downward eye slant, choanal atresia and a cleft palate. She had severe respiratory distress and died despite maximum intervantion at 5 days of age. Autopsy revealed situs inversus totalis; crossed fused renal ectopia; agnathia; normal thyroid, larynx, trachea, and bronchi; incomplete lobation of the lungs; immature pulmonary development with early hyaline membranes; and a normal central nervous system. This lack of significant central nervous system abnormalities distinguishes this infant from the majority of previously reported infants with agnathia and situs inversus. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. RP STOLER, JM (reprint author), MASSACHUSETTS GEN HOSP,EMBRYOL TERATOL UNIT,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [5T32GM07748-13] NR 25 TC 21 Z9 21 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0040-3709 J9 TERATOLOGY JI Teratology PD SEP PY 1992 VL 46 IS 3 BP 213 EP 216 DI 10.1002/tera.1420460304 PG 4 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA JJ567 UT WOS:A1992JJ56700003 PM 1523578 ER PT J AU ROSS, DS AF ROSS, DS TI THYROID-HORMONE SUPPRESSIVE THERAPY OF SPORADIC NONTOXIC GOITER SO THYROID LA English DT Article ID FINE-NEEDLE ASPIRATION; THYROXINE TREATMENT; PROPHYLACTIC THYROXINE; MULTINODULAR GOITER; BENIGN SOLITARY; NODULAR GOITER; CLONAL ORIGIN; RECURRENCE; DIAGNOSIS; GROWTH AB Thyroid hormone has been used to reduce the size of sporadic nontoxic goiter since 1894. Noncontrolled clinical studies suggest that about two thirds of goiters respond to therapy, and a recent randomized clinical trial confirms the efficacy of suppressive therapy for sporadic nontoxic goiter. Efficacy is at least partly correlated with suppression of pituitary TSH production, response is usually evident by 3 months, relapse occurs when therapy is withdrawn, and nodular goiters may be less responsive than diffuse goiters. Some, but not all, series suggest that postoperative use of thyroid hormone suppressive therapy prevents recurrence of benign goiter. Three recent randomized trials suggest that thyroid hormone administered for 6 months to 3 years does not reduce the size of solitary thyroid nodules. About one third of nodules regressed in both treatment and placebo groups. Long-term studies are needed to define the effects of thyroid hormone suppressive therapy on the growth of goitrous lesions based on their underlying pathophysiology. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROSS, DS (reprint author), MASSACHUSETTS GEN HOSP,THYROID UNIT,BOSTON,MA 02114, USA. NR 52 TC 32 Z9 32 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD FAL PY 1992 VL 2 IS 3 BP 263 EP 269 DI 10.1089/thy.1992.2.263 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JR806 UT WOS:A1992JR80600013 PM 1422239 ER PT J AU SALAZAR, M YUNIS, JJ DELGADO, MB BING, D YUNIS, EJ AF SALAZAR, M YUNIS, JJ DELGADO, MB BING, D YUNIS, EJ TI HLA-DQB1 ALLELE TYPING BY A NEW PCR-RFLP METHOD - CORRELATION WITH A PCR-SSO METHOD SO TISSUE ANTIGENS LA English DT Article DE HLA-DQB1 TYPING; PCR-RFLP; PCR-SSO ID AMPLIFIED DNA; RESTRICTION ENDONUCLEASES; HLA-DQB; SUSCEPTIBILITY; DIGESTION AB We have developed a new PCR-RFLP method for HLA-DQB1 typing. This method was easy to follow, requiring only one DQB1 generic amplification and 5 endonucleases to assign 14 out of 15 HLA-DQBI alleles. In addition, we determined that by using one generic amplification and two enzymes (Sau96 I and Hae III) it was possible to type the generic specificities: DQw2, DQw4, DQw5, DQw6, and DQw7, DQw8-9, providing a practical alternative for serological HLA-DQ generic typing. We also performed a side-by-side correlation with a PCR-SSO typing method and found an almost 100% concordance between the methods. The limitations of these methods were: 1) the PCR-RFLP method did not allow the differentiation between the HLA-DQB1*0602 and *0603 alleles; 2) the PCR-SSO method gave crosshybridization signals in the detection of *0302 or *0303 alleles. Our results suggested that both methods. PCR-RFLP and PCR-SSO, are useful alternatives for HLA-DQBI typing. 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,44 BINNEY ST,ROOM 740,BOSTON,MA 02115, USA. NR 12 TC 32 Z9 32 U1 1 U2 2 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 SEP PY 1992 VL 40 IS 3 BP 116 EP 123 DI 10.1111/j.1399-0039.1992.tb02102.x PG 8 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA JP658 UT WOS:A1992JP65800002 PM 1359671 ER PT J AU DEVINE, P POSTOWAY, N HOFFSTADTER, L SURGENOR, DM LINDEN, JV HINES, D CHERNOFF, A CIAVARELLA, D BOVE, JR AF DEVINE, P POSTOWAY, N HOFFSTADTER, L SURGENOR, DM LINDEN, JV HINES, D CHERNOFF, A CIAVARELLA, D BOVE, JR TI BLOOD DONATION AND TRANSFUSION PRACTICES - THE 1990 AMERICAN-ASSOCIATION-OF-BLOOD-BANKS INSTITUTIONAL MEMBERSHIP QUESTIONNAIRE SO TRANSFUSION LA English DT Article AB Responses to the 1990 American Association of Blood Banks (AABB) Institutional Membership Questionnaire were submitted by 2126 regional blood centers, hospital-based blood banks, and transfusion facilities. Data from 2117 of these facilities were considered to be valid. The questionnaire included information on blood donor demographics, number of units collected, and collection procedures; services performed; usage of blood components; and transfusion-transmitted diseases reported during 1989. Institutional members collected 7.4 million whole blood units, of which 90.8 percent were donated for allogeneic use, 6.0 percent were donated for autologous use, and 3.2 percent were donated for directed use. Approximately 630,546 allogeneic and directed-use blood donors were deferred, most often for low hemoglobin or hematocrit values. Approximately 225,205 full allogeneic and directed-donor units were discarded, primarily for elevated alanine aminotransferase levels or the presence of hepatitis B core antibody. The 14.3 million transfused components included 56.7 percent red cell-containing components, 27.4 percent platelets, 11 percent fresh-frozen plasma, and 4.8 percent cryoprecipitate. Institutional members reported 1397 cases of transfusion-associated hepatitis. In this group, 921 patients were tested for hepatitis B surface antigen after the transfusion; 339 (36.8%) were found to be hepatitis B surface antigen positive. The AABB Institutional Questionnaire results provide recent data on blood donor and transfusion-related activities that are vital to the evaluation of current transfusion medicine practices. C1 SAN DIEGO BLOOD BANK,SAN DIEGO,CA 92103. CTR BLOOD RES,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,WADSWORTH CTR,ALBANY,NY 12201. VET ADM HINES MED CTR,HINES,IL. HUDSON VALLEY BLOOD CTR,VALHALLA,NY 10595. YALE NEW HAVEN MED CTR,NEW HAVEN,CT 06504. RP DEVINE, P (reprint author), HARVARD COMMUNITY HLTH PLAN,DEPT PATHOL & LAB MED,120 BROOKLINE AVE,BOSTON,MA 02215, USA. NR 0 TC 19 Z9 19 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD SEP PY 1992 VL 32 IS 7 BP 683 EP 687 DI 10.1046/j.1537-2995.1992.32792391046.x PG 5 WC Hematology SC Hematology GA JM761 UT WOS:A1992JM76100018 PM 1325695 ER PT J AU ROSENGARD, BR OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K BOORSTEIN, SM HILL, GS FISHBEIN, JM SACHS, DH AF ROSENGARD, BR OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K BOORSTEIN, SM HILL, GS FISHBEIN, JM SACHS, DH TI INDUCTION OF SPECIFIC TOLERANCE TO CLASS-I - DISPARATE RENAL-ALLOGRAFTS IN MINIATURE SWINE WITH CYCLOSPORINE SO TRANSPLANTATION LA English DT Article ID EXTRACTED HISTOCOMPATIBILITY ANTIGEN; LONG-TERM SURVIVAL; LUNG TRANSPLANTATION; SUPPRESSOR CELLS; HEART GRAFTS; A TREATMENT; LYMPHOCYTES; RATS; REJECTION; PROLONGATION AB Previous studies in miniature swine have suggested that the mechanism underlying the spontaneous development of tolerance in one third of one-haplotype class I disparate renal allografts (i.e., ag-->ad) involves a relative T cell help deficit at the time of first exposure to antigen. If this hypothesis were correct, then one might expect the administration of an immunosuppressive agent capable of inhibiting lymphokine production during this period to lead to the induction of tolerance to class I MHC antigens in two-haplotype class I mismatched renal allografts (i.e., gg-->dd), which are otherwise uniformly and acutely rejected. This hypothesis was tested in eight two-haplotype class I disparate, class II matched donor-recipient pairs, in which recipients were treated with cyclosporine 10 mg/kg, i.v. q.d. for 12 days. This protocol led to the induction of long-term (>100 days) specific tolerance in 100% of recipients, as compared with control animals that rejected grafts in 13.7 +/- 0.9 days (P<0.0001). The specificity of tolerance was assessed both in vivo with subsequent skin grafts and in vitro by mixed lymphocyte response (MLR) and cell-mediated lymphocytotoxicity (CML). Survival of donor-specific skin grafts was prolonged compared with skin grafts bearing third-party class I antigens (19.5+/-2.0 versus 11.5+/-2.0 days, n=4, P<0.05). Tolerant recipients had markedly diminished or absent anti-donor MLR and CML responses, but maintained normal reactivity to third party. Four of eight CsA-treated recipients showed detectable levels of anti-donor IgM, while none demonstrated the presence of anti-donor IgG, which was found in all rejecting controls. C1 NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. RP ROSENGARD, BR (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI-31046] NR 44 TC 135 Z9 135 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 SEP PY 1992 VL 54 IS 3 BP 490 EP 497 DI 10.1097/00007890-199209000-00020 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA JP018 UT WOS:A1992JP01800020 PM 1412729 ER PT J AU BALLEN, KK DONADIO, D BOULOUX, C MCCARTHY, P WEINSTEIN, H ANTIN, JH AF BALLEN, KK DONADIO, D BOULOUX, C MCCARTHY, P WEINSTEIN, H ANTIN, JH TI HERPES-SIMPLEX VIRUS AND NEUTROPENIA FOLLOWING BONE-MARROW TRANSPLANTATION SO TRANSPLANTATION LA English DT Note ID PROPHYLAXIS; INFECTIONS C1 HOP LARIBOISIERE,MALAD SANGUINE SERV,F-75475 PARIS 10,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CHILDRENS HOSP,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. RP BALLEN, KK (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-39542] NR 8 TC 4 Z9 4 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 SEP PY 1992 VL 54 IS 3 BP 553 EP 555 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA JP018 UT WOS:A1992JP01800032 PM 1412737 ER PT J AU KHAW, BA NARULA, J AF KHAW, BA NARULA, J TI ANTIMYOSIN SCINTIGRAPHY IN CARDIOVASCULAR-DISEASES SO TRENDS IN CARDIOVASCULAR MEDICINE LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; MYOSIN-SPECIFIC ANTIBODY; IN-111 MONOCLONAL ANTIMYOSIN; CARDIAC MYOSIN; HEART-TRANSPLANTATION; ENDOMYOCARDIAL BIOPSY; (FAB')2 FRAGMENTS; DIAGNOSIS; LOCALIZATION; EVOLUTION AB Antimyosin antibody is highly specific for in vivo delineation of acute myocyte necrosis as only irreversibly damaged myocytes with sarcolemmal disruption will enable access of the administered antibody to the once-privileged intracellular antigen-myosin. Thus, antimyosin radio-labeled with either indium-111 or technitium-99m has been used for the noninvasive diagnosis of myocyte necrosis associated with acute myocardial infarction, myocarditis, heart transplant rejection, as well as in other cardiac disorders such as rheumatic carditis or adriamycin cardiotoxicity. The sensitivity of antimyosin scintigraphy for these disorders has been reported to be 90%-100%. The final verdict on its full potential must await extensive clinical use. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,E CHARLESTOWN,MA 02129. NORTHEASTERN UNIV,BOUVE COLL PHARM & HLTH SCI,CTR DRUG TARGETING & ANAL,BOSTON,MA 02115. RP KHAW, BA (reprint author), MASSACHUSETTS GEN HOSP,DIV NUCL MED,E CHARLESTOWN,MA 02129, USA. NR 51 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 1050-1738 J9 TRENDS CARDIOVAS MED JI Trends Cardiovasc. Med. PD SEP-OCT PY 1992 VL 2 IS 5 BP 197 EP 204 DI 10.1016/1050-1738(92)90049-X PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JN057 UT WOS:A1992JN05700006 PM 21239254 ER PT J AU MAFUNE, K SAINI, KS RAVIKUMAR, TS CHEN, LB STEELE, GD THOMAS, P AF MAFUNE, K SAINI, KS RAVIKUMAR, TS CHEN, LB STEELE, GD THOMAS, P TI DIFFERENCES IN MESSENGER-RNA EXPRESSION OF CARCINOEMBRYONIC ANTIGEN IN SURGICAL SPECIMENS OF COLORECTAL-CARCINOMA SO TUMOR BIOLOGY LA English DT Article DE CARCINOEMBRYONIC ANTIGEN; COLORECTAL CANCER; MESSENGER RNA ID NORMAL COLON MUCOSA; CDNA SEQUENCE; GENE FAMILY; CEA; CANCER; RESECTION; ADHESION; MEMBERS; CLONES; TISSUE AB Carcinoembryonic antigen (CEA) is the most widely used tumor marker for colorectal cancer. Plasma CEA levels have been variably associated with prognosis. Since plasma CEA level is multifactorial, CEA gene expression in tumors may provide one precise mechanism to evaluate its functional role. This study evaluated CEA expression at the messenger RNA (mRNA) level in 22 human colorectal carcinomas and their adjacent normal mucosae by Northern blot hybridization using a P-32-labeled CEA probe (a loop-domain specific cDNA, LV7). Both tumor and normal mucosa displayed three mRNA species of 4.0, 3.6, and 3.0 kb in length. The expression of 3.6-kb mRNA which encodes for CEA was dominant and it was correlated with another 4.0-kb CEA mRNA expression. The expression of 3.0-kb mRNA which encodes for nonspecific cross-reacting antigen was weak and not detectable in 8 of 22 colon tumors and 12 of 22 normal colon mucosae. In only one tumor, a 4.5-kb mRNA (which might encode for a new family member of CEA) was expressed. A two- to fourfold higher expression of CEA mRNA (3.6 kb) was observed in 11 of 22 colorectal tumors (2 of 9 proximal colon tumors and 9 of 14 rectosigmoid tumors) when compared with morphologically normal adjacent mucosae. Preoperative plasma CEA levels and Dukes' staging had no correlation with this CEA mRNA expression. CEA mRNA did not appear to correlate with metastasis because its expression in the primary colon cancers with metastases (Dukes' stage D tumor) was not always increased. These data also imply that factors other than mRNA expression in tumor might be important in regulating plasma CEA levels. C1 NEW ENGLAND DEACONESS HOSP,DEPT SURG,CANC BIOL LAB,50 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. RI Saini, Kulvinder/G-4729-2013 FU NCI NIH HHS [CA44704, CA44583] NR 37 TC 13 Z9 13 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1010-4283 J9 TUMOR BIOL JI Tumor Biol. PD SEP-DEC PY 1992 VL 13 IS 5-6 BP 330 EP 337 PG 8 WC Oncology SC Oncology GA KM657 UT WOS:A1992KM65700011 PM 1290028 ER PT J AU MCKEATING, JA THALI, M FURMAN, C KARWOWSKA, S GORNY, MK CORDELL, J ZOLLAPAZNER, S SODROSKI, J WEISS, RA AF MCKEATING, JA THALI, M FURMAN, C KARWOWSKA, S GORNY, MK CORDELL, J ZOLLAPAZNER, S SODROSKI, J WEISS, RA TI AMINO-ACID-RESIDUES OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-I GP120 CRITICAL FOR THE BINDING OF RAT AND HUMAN NEUTRALIZING ANTIBODIES THAT BLOCK THE GP120-SCD4 INTERACTION SO VIROLOGY LA English DT Article ID HUMAN MONOCLONAL-ANTIBODY; ENVELOPE GLYCOPROTEIN; CD4 BINDING; SOLUBLE CD4; HIV-1; EPITOPE; SERA; SITE; AIDS C1 MED SCH NEW YORK,NEW YORK,NY 10016. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. VET AFFAIRS MED CTR,NEW YORK,NY 10010. NYU,DEPT PATHOL,NEW YORK,NY 10003. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP MCKEATING, JA (reprint author), INST CANC RES,CHESTER BEATTY LABS,FULHAM RD,LONDON SW3 6JB,ENGLAND. OI McKeating, Jane/0000-0002-7229-5886 NR 21 TC 64 Z9 64 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 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 134 EP 142 DI 10.1016/0042-6822(92)91199-5 PG 9 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900014 PM 1382339 ER PT J AU LO, KMS BIASOLO, MA DEHNI, G PALU, G HASELTINE, WA AF LO, KMS BIASOLO, MA DEHNI, G PALU, G HASELTINE, WA TI INHIBITION OF REPLICATION OF HIV-1 BY RETROVIRAL VECTORS EXPRESSING TAT-ANTISENSE AND ANTI-TAT RIBOZYME RNA SO VIROLOGY LA English DT Article ID TRANS-ACTIVATOR GENE; VIRUS TYPE-III; CELL-LINES; INFECTION; ENZYMES; REGION; AIDS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. UNIV PADUA,INST MICROBIOL,I-35100 PADUA,ITALY. FU NCI NIH HHS [P30CA06516]; PHS HHS [P30C128691, NCDDGA124845] NR 27 TC 105 Z9 106 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 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 176 EP 183 DI 10.1016/0042-6822(92)91203-7 PG 8 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900018 PM 1529527 ER PT J AU GOFF, BA BACHOR, R KOLLIAS, N HASAN, T AF GOFF, BA BACHOR, R KOLLIAS, N HASAN, T TI EFFECTS OF PHOTODYNAMIC THERAPY WITH TOPICAL APPLICATION OF 5-AMINOLEVULINIC ACID ON NORMAL SKIN OF HAIRLESS GUINEA-PIGS SO JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY LA English DT Article DE PHOTODYNAMIC THERAPY; 5-AMINOLEVULINIC ACID; PROTOPORPHYRIN-IX; STRATUM-CORNEUM; TAPE STRIPPED ID PROTOPORPHYRIN; FLUORESCENCE; SPECTRA AB Photodynamic therapy (PDT) is a relatively new approach to the treatment of neoplasms which involves the use of photoactivatable compounds to selectively destroy tumors. 5-Aminolevulinic acid (ALA) is an endogenous substance which is converted to protoporphyrin IX (PpIX) in the synthetic pathway to heme. PpIX is a very effective photosensitizer. The goal of this study was to evaluate the effect of PDT using topical ALA on normal guinea pig (g.p.) skin and g.p. skin in which the stratum corneum was removed by being tape-stripped (TS). Evaluation consisted of gross examination, PpIX fluorescence detection, reflectance spectroscopy, and histology. There was no effect from the application of light or ALA alone. Normal non-TS g.p. skin treated with ALA and light was unaffected unless high light and ALA doses were used. Skin from which the stratum corneum was removed was highly sensitive to treatment with ALA and light: 24 h after treatment, the epidermis showed full thickness necrosis, followed by complete repair within 7 d. Time-dependent fluorescence excitation and emission spectra were determined to characterize the chromophore and to demonstrate a build-up of the porphyrin in the skin. These data support the view that PDT with topical ALA is a promising approach for the treatment of epidermal cutaneous disorders. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,VINCENT GYNECOL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT UROL,BOSTON,MA 02114. FU NIAMS NIH HHS [R29 AR38918] NR 22 TC 66 Z9 66 U1 0 U2 5 PU ELSEVIER SCIENCE SA LAUSANNE PI LAUSANNE 1 PA PO BOX 564, 1001 LAUSANNE 1, SWITZERLAND SN 1011-1344 J9 J PHOTOCH PHOTOBIO B JI J. Photochem. Photobiol. B-Biol. PD AUG 31 PY 1992 VL 15 IS 3 BP 239 EP 251 DI 10.1016/1011-1344(92)85128-H PG 13 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JQ193 UT WOS:A1992JQ19300006 PM 1453276 ER PT J AU RUSKIN, JN GARAN, H AF RUSKIN, JN GARAN, H TI RADIOFREQUENCY CATHETER ABLATION OF A LEFT POSTERIOR ACCESSORY ATRIOVENTRICULAR CONNECTION IN A PATIENT WITH THE WOLFF-PARKINSON-WHITE SYNDROME SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note RP RUSKIN, JN (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 AUG 27 PY 1992 VL 327 IS 9 BP 613 EP 613 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JK204 UT WOS:A1992JK20400006 ER PT J AU CHRISTEN, WG MANSON, JE SEDDON, JM GLYNN, RJ BURING, JE ROSNER, B HENNEKENS, CH AF CHRISTEN, WG MANSON, JE SEDDON, JM GLYNN, RJ BURING, JE ROSNER, B HENNEKENS, CH TI A PROSPECTIVE-STUDY OF CIGARETTE-SMOKING AND RISK OF CATARACT IN MEN SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID POSTERIOR SUBCAPSULAR CATARACTS; LENS OPACITIES; NUCLEAR; PREVALENCE; ALCOHOL; PLASMA; EYES AB Objective.-To examine the association between cigarette smoking and the incidence of cataract. Design, Setting, and Participants.-The design was a prospective cohort study using data from the Physicians' Health Study, a randomized trial of aspirin and beta carotene among 22 071 US male physicians aged 40 to 84 years that began in 1982. This analysis includes the 17 824 physicians who did not report cataract at baseline and did provide complete risk factor information. Based on information reported at baseline, 10% were current smokers, 39% were past smokers, and 51% were never smokers. Main Outcome Measure.-An incident cataract was defined as a self-report confirmed by medical record review to have been first diagnosed after randomization, age-related in origin, and responsible for a decrease in best corrected visual acuity to 20/30 or worse. Main Results.-During 60 months of follow-up, 557 incident cataracts among 371 participants were confirmed. Compared with never smokers, current smokers of 20 or more cigarettes per day had a statistically significant increase in the risk of cataract (relative fisk [RR], 2.16; 95% confidence interval [CI], 1.46 to 3.20; P<.001). Similar results were obtained after simultaneously controlling for other potential cataract risk factors in a logistic regression model (RR, 2.05; 95% CI, 1.38 to 3.05; P<.001). Among the 557 eyes with cataract, nuclear sclerotic changes were present in 442 while posterior subcapsular changes were present in 204. After controlling for other potential cataract risk factors, current smokers of 20 or more cigarettes per day had statistically significant increases in nuclear sclerosis (RR, 2.24; 95% CI, 1.47 to 3.41; P<.001) and posterior subcapsular (RR, 3.17; 95% CI, 1.81 to 5.53; P<.001) cataract. Past smokers had an elevated risk of posterior subcapsular (RR, 1.44; 95% CI, 0.97 to 2.13; P=.07) but not nuclear sclerosis cataract. For current smokers of fewer than 20 cigarettes per day, no increased risks were observed of total, nuclear sclerosis, or posterior subcapsular cataract. Conclusions.-These data provide support for the hypothesis that cigarette smoking increases the risk of developing both nuclear sclerosis and posterior subcapsular cataract. C1 HARVARD UNIV,SCH MED,DEPT MED,CHANNING LAB,PHYSICIANS HLTH STUDY,900 COMMONWEALTH AVE E,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PREVENT MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,EPIDEMIOL UNIT,BOSTON,MA 02114. FU NEI NIH HHS [EY03355] NR 24 TC 98 Z9 98 U1 0 U2 4 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 AUG 26 PY 1992 VL 268 IS 8 BP 989 EP 993 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JK129 UT WOS:A1992JK12900022 PM 1501324 ER PT J AU HANKINSON, SE WILLETT, WC COLDITZ, GA SEDDON, JM ROSNER, B SPEIZER, FE STAMPFER, MJ AF HANKINSON, SE WILLETT, WC COLDITZ, GA SEDDON, JM ROSNER, B SPEIZER, FE STAMPFER, MJ TI A PROSPECTIVE-STUDY OF CIGARETTE-SMOKING AND RISK OF CATARACT-SURGERY IN WOMEN SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID POSTERIOR SUBCAPSULAR CATARACTS; EPIDEMIOLOGY; ALCOHOL; NUCLEAR; PLASMA AB Objective.-To examine prospectively the association between cigarette smoking and the risk of cataract extraction in women. Design.-Prospective cohort study beginning in 1980 with 8 years of follow-up. Setting.-United States, multistate. Participants.-Registered nurses 45 to 67 years of age and free of diagnosed cancer. There were 50 828 women included in 1980 and others were added as they became 45 years of age. Main Outcome Measure.-Incidence of senile cataract extraction. Results.-We documented 493 incident senile cataracts diagnosed and extracted during 470302 person-years of follow-up. The age-adjusted relative risk (RR) among women who smoked at least 65 pack-years was 1.63 (95% confidence interval [CI], 1.18 to 2.26; P for trend, .02). A similar increase in RR was noted when smoking was assessed in terms of number of cigarettes currently smoked or number of cigarettes smoked by past smokers. Results were also similar after adjusting for other potential risk factors for cataract. Smoking was also strongly associated with posterior subcapsular cataract specifically (RR, 2.59; 95% CI, 1.49 to 4.50 for greater-than-or-equal-to 65-pack-year smokers relative to nonsmokers). Conclusion.-Smoking appears to increase the risk of cataract extraction. C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP HANKINSON, SE (reprint author), HARVARD UNIV,SCH MED,CHANNING LAB,DEPT MED,180 LONGWOOD AVE,BOSTON,MA 02115, USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NCI NIH HHS [CA40356]; PHS HHS [5T32 E507069] NR 29 TC 117 Z9 117 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 AUG 26 PY 1992 VL 268 IS 8 BP 994 EP 998 DI 10.1001/jama.268.8.994 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JK129 UT WOS:A1992JK12900023 PM 1501325 ER PT J AU QIAN, XQ WEISS, MA AF QIAN, XQ WEISS, MA TI 2-DIMENSIONAL NMR-STUDIES OF THE ZINC FINGER MOTIF - SOLUTION STRUCTURES AND DYNAMICS OF MUTANT ZFY DOMAINS CONTAINING AROMATIC SUBSTITUTIONS IN THE HYDROPHOBIC CORE SO BIOCHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR-IIIA; DNA-BINDING DOMAIN; PROTEIN ZFY; ARCHITECTURAL RULES; SECONDARY STRUCTURE; COUPLING-CONSTANTS; HEN LYSOZYME; EVEN FINGER; RECOGNITION; H-1-NMR AB Solution structures of mutant Zn fingers containing aromatic substitutions in the hydrophobic core are determined by 2D-NMR spectroscopy and distance-geometry/simulated annealing (DG/SA). The wild-type domain (designated ZFY-6) is derived from the human male-associated protein ZFY and represents a sequence motif (Cys-X2-Cys-X-Ar-X7-Leu-X2-His-X4-His) that differs from the consensus (Cys-X2,4-Cys-X3-Phe-X5-Leu-X2-His-X3-His) in the location ("aromatic swap") and diversity (Ar = tyrosine, phenylalanine, or histidine) of the central aromatic residue (underlined). In a given ZFY domain the choice of a particular aromatic residue is invariant among vertebrates, suggesting that alternative "swapped" aromatic residues are functionally inequivalent. 2D-NMR studies of analogues containing tyrosine, phenylalanine, or histidine at the swapped site yield the following results. (i) The three DG/SA structures each retain the beta-beta-alpha motif and exhibit similar staggered-horizontal packing between the variant aromatic residue and the proximal histidine in the hydrophobic core. (ii) The structures and stabilities of the tyrosine and phenylalanine analogues are essentially identical, differing only by local exposure of polar (Tyr p-OH) or nonpolar (Phe p-H) surfaces. (iii) The dynamic stability of the histidine analogue is reduced as indicated by more rapid protein-deuterium exchange of hydrogen bonds related to secondary structure and amide-sulfur coordination (slowly exchanging amide resonances in D2O) and by more extensive averaging of main-chain dihedral angles (3J(alpha-NH) coupling constants). An aspartic acid in the putative DNA recognition surface, whose configuration is well-defined as a possible helix N-cap in the tyrosine and phenylalanine analogues, exhibits multiple weak main-chain contacts in the NOESY spectrum of the histidine analogue; such NOEs are geometrically inconsistent and so provide complementary evidence for structural fluctuations. (iv) Because the three DG ensembles have similar apparent precision, the finding of reduced dynamic stability in the histidine analogue emphasizes the importance of experiments that directly probe fluctuations at several time scales. Our results provide insight into the design of biological metal-binding sites and the relationship of protein sequence to structure and dynamics. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 41 TC 23 Z9 23 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD AUG 25 PY 1992 VL 31 IS 33 BP 7463 EP 7476 DI 10.1021/bi00148a006 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JK533 UT WOS:A1992JK53300006 PM 1510933 ER PT J AU FURUKAWA, Y UENOYAMA, S OHTA, M TSUNODA, A GRIFFIN, JD SAITO, M AF FURUKAWA, Y UENOYAMA, S OHTA, M TSUNODA, A GRIFFIN, JD SAITO, M TI TRANSFORMING GROWTH-FACTOR-BETA INHIBITS PHOSPHORYLATION OF THE RETINOBLASTOMA SUSCEPTIBILITY GENE-PRODUCT IN HUMAN MONOCYTIC LEUKEMIA-CELL LINE JOSK-I SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SV40 LARGE-T; FISSION YEAST; HISTONE-H1 KINASE; CONSTITUTIVE PRODUCTION; PROTEIN-KINASE; OSTEO-SARCOMA; S-TRANSITION; CDC2 PROTEIN; CYCLE; EXPRESSION AB Proliferation of the human monocytic leukemia cell line JOSK-I is inhibited by transforming growth factor-beta (TGF-beta). Growth inhibition by TGF-beta was not due to either a toxic effect or to induction of differentiation. TGF-beta induced a cell cycle arrest at late G1 phase and was not found to be inhibitory to JOSK-I cells in S phase or G2/M. This G1 cell cycle arrest was associated with an accumulation of the unphosphorylated form of the retinoblastoma susceptibility gene product (Rb) in good correlation with inhibition of DNA synthesis. In contrast to the effects of TGF-beta, two other agents which induced a G1 arrest of JOSK-I cells had a different effect on Rb. Aphidicolin blocked cells at G1/S but could not reduce Rb phosphorylation as great as that seen with TGF-beta. 12-O-Tetradecanoylphorbol-13-acetate, an inducer of differentiation, did reduce Rb phosphorylation, but not until 72 h, when differentiation had already occurred. The identities of the Rb kinases are unknown, but recent evidence suggests that the cdc2 gene product could participate in Rb phosphorylation. Although cdc2 mRNA and total protein levels were not affected, TGF-beta inhibited the rate of translation and kinase activity of cdc2 in JOSK-I cells. These results suggest that growth inhibition of hematopoietic cells by TGF-beta is linked to suppression of Rb phosphorylation to retain Rb in an unphosphorylated, growth-inhibitory state. The suppression of Rb phosphorylation is suggested to be mediated through inhibition of cdc2 kinase activity by TGF-beta. C1 JICHI MED SCH,INST HEMATOL,DIV HEMOPOIESIS,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 54 TC 64 Z9 64 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 AUG 25 PY 1992 VL 267 IS 24 BP 17121 EP 17127 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL053 UT WOS:A1992JL05300062 PM 1512249 ER PT J AU RUPRECHT, RM SOSA, MAG FAZELY, F KOCH, JA VERCELLOTTI, SV AF RUPRECHT, RM SOSA, MAG FAZELY, F KOCH, JA VERCELLOTTI, SV TI N-CARBOXYMETHYLCHITOSAN-N,O-SULFATE INHIBITS HIV-1 REPLICATION SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,BOSTON,MA 02115. V LABS INC,COVINGTON,LA 70433. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 9 EP CARB PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200576 ER PT J AU MADOFF, S FERRARO, MJ MERRILL, DP HIRSCH, MS AF MADOFF, S FERRARO, MJ MERRILL, DP HIRSCH, MS TI LACK OF ACTIVITY OF ZIDOVUDINE AGAINST UREAPLASMA-UREALYTICUM AND MYCOPLASMA-HOMINIS SO LANCET LA English DT Letter C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. RP MADOFF, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT MICROBIOL,BOSTON,MA 02114, USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD AUG 22 PY 1992 VL 340 IS 8817 BP 484 EP 484 DI 10.1016/0140-6736(92)91804-H PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JJ877 UT WOS:A1992JJ87700033 PM 1354810 ER PT J AU LIU, GT LESSELL, S AF LIU, GT LESSELL, S TI SPONTANEOUS VISUAL IMPROVEMENT IN CHIASMAL GLIOMAS SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID OPTIC-NERVE GLIOMAS; TERM FOLLOW-UP; LONG-TERM; HISTOCHEMICAL-OBSERVATIONS; SAN-FRANCISCO; MANAGEMENT; CHILDHOOD; PATHWAYS AB Three untreated patients with presumed chiasmal gliomas had spontaneous visual improvement, although serial magnetic resonance imaging in two of the patients showed the lesions to be unchanged. Two patients had evidence of neurofibromatosis. Three other patients with similar disease courses have been documented in the medical literature. These cases demonstrate that conservative management of optic chiasmal gliomas may sometimes be associated with favorable outcomes. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,HARVARD LONGWOOD NEUROL PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,NEUROOPHTHALMOL UNIT,BOSTON,MA 02115. NR 30 TC 51 Z9 51 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD AUG 15 PY 1992 VL 114 IS 2 BP 193 EP 201 PG 9 WC Ophthalmology SC Ophthalmology GA JH622 UT WOS:A1992JH62200011 PM 1642295 ER PT J AU MARCUS, DM MAWN, LA EGAN, KM ALBERT, DM AF MARCUS, DM MAWN, LA EGAN, KM ALBERT, DM TI NUCLEOLAR ORGANIZER REGIONS IN IRIS NEVI AND MELANOMAS SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID DIFFERENTIAL-DIAGNOSIS; MELANOCYTIC TUMORS; UVEAL MELANOMA; LESIONS; PATHOLOGY AB The silver staining of nucleolar organizer region-associated proteins is an objective method that has been used to differentiate benign from malignant neoplasms. Recently this method was used to distinguish benign choroidal nevi from malignant choroidal melanomas. We studied 24 iris melanocytic lesions to assess the applicability of this technique for differentiating benign from neoplastic iris tumors. Masked observers determined the number of silver-stained nucleolar organizer region dots per cell for silver-stained specimens. Iris nevi contained a mean of 1.6 silver-stained nucleolar organizer region dots per cell, whereas iris (spindle A and B, spindle B, epithelioid, mixed cell) malignant melanomas contained a mean of at least 3.5 silver-stained nucleolar organizer region dots per cell (P < .0001). All iris nevi demonstrated counts lower than 1.9, whereas all iris melanomas demonstrated counts greater than 2.8. Silver-stained nucleolar organizer region counts were also compared with the clinicopathologic variables of gender, age, and largest specimen dimension. Only the largest specimen dimension correlated with silver-stained nucleolar organizer region counts (P < .0029). The silver-stained nucleolar organizer region method is a simple technique for differentiating iris nevi from iris melanomas. The silver-stained nucleolar organizer region technique may aid in the assessment and treatment of iris lesions by confirming the malignancy of biopsy specimens. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DAVID G COGAN EYE PATHOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. FU NEI NIH HHS [EY01917] NR 20 TC 3 Z9 3 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD AUG 15 PY 1992 VL 114 IS 2 BP 202 EP 207 PG 6 WC Ophthalmology SC Ophthalmology GA JH622 UT WOS:A1992JH62200012 PM 1642296 ER PT J AU STOECKLE, JD REISER, S AF STOECKLE, JD REISER, S TI THE ETHOS OF DOCTORS AND CORPORATIONS - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD AUG 15 PY 1992 VL 117 IS 4 BP 348 EP 348 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JH464 UT WOS:A1992JH46400028 ER PT J AU ALDAHER, S DEGASPERI, R DANIEL, P HIRANI, S WARREN, C WINCHESTER, B AF ALDAHER, S DEGASPERI, R DANIEL, P HIRANI, S WARREN, C WINCHESTER, B TI SUBSTRATE-SPECIFICITY OF HUMAN LIVER NEUTRAL ALPHA-MANNOSIDASE SO BIOCHEMICAL JOURNAL LA English DT Article ID RAT-LIVER; OLIGOSACCHARIDES; SWAINSONINE; PURIFICATION; CATABOLISM; KIDNEY AB The digestion of radiolabelled natural oligosaccharide substrates by human liver neutral alpha-mannosidase has been studied by h.p.l.c. and h.p.t.l.c. The high-mannose oligosaccharides Man9GlcNAc and Man8GlcNAc are hydrolysed by the enzyme by two distinct non-random routes to a common product of composition Man6GlcNAc, which is then slowly converted into a unique Man5GlcNAc oligosaccharide, Man-alpha(1 --> 2)Man-alpha(1 --> 2)Man-alpha(1 --> 3)[Man-alpha(1 --> 6)] Man-beta(1 --> 4)GlcNAc. These pathways are different from the processing and lysosomal catabolic pathways for these structures. In particular, the alpha(1 --> 2)-linked mannose residues attached to the core alpha(1 --> 3)-linked mannose residue are resistant to hydrolysis. The key processing intermediate, Man-alpha(1 --> 3)[Man-alpha(1 --> 6)]Man-alpha(1 --> 6)[Man-alpha(1 --> 3)] Man-beta(1 --> 4)GlcNAc, is not produced in the digestion of high-mannose glycans by the neutral alpha-mannosidase, but it is hydrolysed by the enzyme by a non-random route to Man-beta(1 --> 4)GlcNAc via the core structure Man-alpha(1 --> 3)[Man-alpha(1 --> 6)]Man-beta(1 --> 4)GlcNAc. In contrast with its ready hydrolysis by lysosomal alpha-mannosidase, the core alpha(1 --> 3)-mannosidic linkage is quite resistant to hydrolysis by neutral alpha-mannosidase. The precise specificity of neutral alpha-mannosidase towards high-mannose oligosaccharides suggests that it has a role in the modification of such structures in the cytosol. C1 UNIV LONDON,INST CHILD HLTH,DIV BIOCHEM & METAB,ENZYMOL UNIT,30 GUILFORD ST,LONDON WC1N 1EH,ENGLAND. HARVARD UNIV,SCH MED,LOVETT LABS,CARBOHYDRATE UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA 02254. GENZYME,CAMBRIDGE,MA 02139. RI El-Daher, Samer/C-9499-2012 FU NICHD NIH HHS [HD-16942, HD-40930, HD-21087] NR 29 TC 15 Z9 15 U1 0 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD AUG 15 PY 1992 VL 286 BP 47 EP 53 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ767 UT WOS:A1992JJ76700009 PM 1520283 ER PT J AU DEGASPERI, R ALDAHER, S WINCHESTER, BG WARREN, CD AF DEGASPERI, R ALDAHER, S WINCHESTER, BG WARREN, CD TI SUBSTRATE-SPECIFICITY OF THE BOVINE AND FELINE NEUTRAL ALPHA-MANNOSIDASES SO BIOCHEMICAL JOURNAL LA English DT Article ID RAT-LIVER; URINARY OLIGOSACCHARIDES; ENDOPLASMIC-RETICULUM; CHROMATOGRAPHY; PURIFICATION; CATABOLISM; SEPARATION; GLYCANS; KIDNEY AB Neutral alpha-mannosidases were prepared from bovine and cat liver. The activities were distinguished from lysosomal and Golgi alpha-mannosidases by their neutral pH optima, relatively low K(m) for their synthetic substrate p-nitrophenyl alpha-D-mannoside, inhibition by Zn2+ and absence of inhibition by Co2+, EDTA, low concentrations of swainsonine, or deoxymannojirimycin. The cytosolic-alpha-mannosidases were not retained by concanavalin A-Sepharose. They were able to degrade efficiently a variety of oligosaccharides with structures corresponding to certain high-mannose glycans or the oligomannosyl parts of hybrid and complex glycans. However, unlike lysosomal alpha-mannosidases from the same species these enzymes were not able to degrade Man9GlcNAc2 efficiently, and the bovine neutral alpha-mannosidase was not able to degrade a hexasaccharide with a structure analogous to Man5GlcNAc2-PP-dolichol. Sharp differences were noted for the bovine and cat enzymes with regard to the specificity of degradation. The bovine neutral alpha-mannosidase degraded the substrates by defined pathways, but the cat neutral alpha-mannosidase often produced complex mixtures of products, especially from the larger oligosaccharides. Therefore the bovine enzyme resembled the rat and human cytosolic alpha-mannosidases, but the cat enzyme did not. The bovine and cat neutral alpha-mannosidases, unlike the corresponding lysosomal activities, did not show specificity for the hydrolysis of the (1 --> 3)- and (1 --> 6)-linked mannose residues in the N-linked glycan pentasaccharide core. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,LOVETT LABS,CARBOHYDRATE UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT MED,LOVETT LABS,CARBOHYDRATE UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. UNIV LONDON,INST CHILD HLTH,DIV BIOCHEM & METAB,LONDON WC1N 1EH,ENGLAND. RI El-Daher, Samer/C-9499-2012 FU NCRR NIH HHS [S07 RR0548-26]; NICHD NIH HHS [HD 21087]; NIDDK NIH HHS [DK 40930] NR 33 TC 15 Z9 15 U1 0 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD AUG 15 PY 1992 VL 286 BP 55 EP 63 PN 1 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ767 UT WOS:A1992JJ76700010 PM 1520284 ER PT J AU GROSSBARD, ML PRESS, OW APPELBAUM, FR BERNSTEIN, ID NADLER, LM AF GROSSBARD, ML PRESS, OW APPELBAUM, FR BERNSTEIN, ID NADLER, LM TI MONOCLONAL ANTIBODY-BASED THERAPIES OF LEUKEMIA AND LYMPHOMA SO BLOOD LA English DT Review ID BONE-MARROW TRANSPLANTATION; ACUTE LYMPHOBLASTIC-LEUKEMIA; CHRONIC LYMPHOCYTIC-LEUKEMIA; B-CELL LYMPHOMA; NON-HODGKINS-LYMPHOMA; VERSUS-HOST DISEASE; RICIN-A-CHAIN; PHASE-I TRIAL; TUMOR-CELLS; IDIOTYPE ANTIBODIES C1 FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT PEDIAT,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT BIOL STRUCT,SEATTLE,WA 98195. RP GROSSBARD, ML (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA34183, CA44991, CA55596] NR 105 TC 204 Z9 205 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD AUG 15 PY 1992 VL 80 IS 4 BP 863 EP 878 PG 16 WC Hematology SC Hematology GA JJ576 UT WOS:A1992JJ57600003 PM 1498329 ER PT J AU JANMEY, PA LAMB, JA EZZELL, RM HVIDT, S LIND, SE AF JANMEY, PA LAMB, JA EZZELL, RM HVIDT, S LIND, SE TI EFFECTS OF ACTIN-FILAMENTS ON FIBRIN CLOT STRUCTURE AND LYSIS SO BLOOD LA English DT Article ID D-BINDING-PROTEIN; FULMINANT HEPATIC-NECROSIS; VITAMIN-D; PLASMA GELSOLIN; PLASMINOGEN-ACTIVATOR; SKELETAL-MUSCLE; LUNG INJURY; HUMAN-SERUM; F-ACTIN; COMPLEXES C1 ROSKILDE UNIV CTR,DEPT CHEM,ROSKILDE,DENMARK. MASSACHUSETTS GEN HOSP,SURG SERV,SURG RES UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR BIOL,BOSTON,MA 02115. RP JANMEY, PA (reprint author), BRIGHAM & WOMENS HOSP,DIV EXPTL MED,221 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL42457]; NIAMS NIH HHS [AR38910] NR 47 TC 22 Z9 23 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD AUG 15 PY 1992 VL 80 IS 4 BP 928 EP 936 PG 9 WC Hematology SC Hematology GA JJ576 UT WOS:A1992JJ57600011 PM 1323346 ER PT J AU GRIBBEN, JG SAPORITO, L BARBER, M BLAKE, KW EDWARDS, RM GRIFFIN, JD FREEDMAN, AS NADLER, LM AF GRIBBEN, JG SAPORITO, L BARBER, M BLAKE, KW EDWARDS, RM GRIFFIN, JD FREEDMAN, AS NADLER, LM TI BONE MARROWS OF NON-HODGKINS-LYMPHOMA PATIENTS WITH A BCL-2 TRANSLOCATION CAN BE PURGED OF POLYMERASE CHAIN REACTION-DETECTABLE LYMPHOMA-CELLS USING MONOCLONAL-ANTIBODIES AND IMMUNOMAGNETIC BEAD DEPLETION SO BLOOD LA English DT Article ID SURFACE HAPTEN DENSITY; FOLLICULAR LYMPHOMAS; RESIDUAL CELLS; TRANSPLANTATION; ANTIGEN; T(14-18); DNA; AMPLIFICATION; COMPLEMENT; ACTIVATION RP GRIBBEN, JG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA34183, CA55207]; PHS HHS [04496] NR 25 TC 82 Z9 82 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 AUG 15 PY 1992 VL 80 IS 4 BP 1083 EP 1089 PG 7 WC Hematology SC Hematology GA JJ576 UT WOS:A1992JJ57600033 PM 1498325 ER PT J AU HABER, DA AF HABER, DA TI MULTIDRUG RESISTANCE (MDR1) IN ACUTE MYELOGENOUS LEUKEMIA - IS IT TIME TO TEST - RESPONSE SO BLOOD LA English DT Letter RP HABER, DA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA, 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 0006-4971 J9 BLOOD JI Blood PD AUG 15 PY 1992 VL 80 IS 4 BP 1094 EP 1095 PG 2 WC Hematology SC Hematology GA JJ576 UT WOS:A1992JJ57600036 ER PT J AU MAYER, DK AF MAYER, DK TI HAZARDS OF CHEMOTHERAPY - IMPLEMENTING SAFE HANDLING PRACTICES SO CANCER LA English DT Article; Proceedings Paper CT NATIONAL CONF ON NEW ONCOLOGIC AGENTS CY FEB 06-08, 1991 CL DALLAS, TX SP AMER CANC SOC, AMER COLL CLIN PHARM DE CHEMOTHERAPY; HAZARDS; SAFE HANDLING PRACTICES ID AGENTS; DRUGS; PERSONNEL; EXPOSURE; RISKS; LIFE AB Over the last decade, concerns about the hazards of handling cytotoxic chemotherapeutic agents increased as various studies were published. Analysis of these data suggest possible carcinogenic, teratogenic, and mutagenic risk for health professionals (predominantly nurses and pharmacists) that handle these drugs. However, the research is inconclusive. The nature of the problem, along with methodologic issues, may make it difficult or impossible to provide definitive data on the type and degree of risk for those exposed to chemotherapeutic agents. Guidelines and recommendations have been published by various groups including the Occupational Safety and Health Administration, the American Society of Hospital Pharmacists, the Oncology Nursing Society, and others. In essence, they recommend that only health professionals with specialized training should prepare or administer chemotherapeutic agents. In addition, equipment, unused drugs, and human excreta should be treated as chemically hazardous waste and disposed of according to the individual facility's policies and procedures. These guidelines should provide protection for those involved in preparing chemotherapy for administration, regardless of where this is done. Studies have shown differences in the degree and type of procedures followed and between existing procedures and actual practice. Some of these differences are based on the site of care (e.g., hospital [also influenced by bed size], private practice, or home care). Issues involved in implementing reasonable approaches to lower the relative risk for health-care professionals that handle cytotoxic chemotherapy will be discussed. RP MAYER, DK (reprint author), MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,GRAD PROGRAM NURSING,15 RIVER ST,BOSTON,MA 02108, USA. NR 34 TC 7 Z9 8 U1 3 U2 8 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 AUG 15 PY 1992 VL 70 IS 4 SU S BP 988 EP 992 PG 5 WC Oncology SC Oncology GA JJ558 UT WOS:A1992JJ55800014 PM 1638469 ER PT J AU CLAFFEY, KP WILKISON, WO SPIEGELMAN, BM AF CLAFFEY, KP WILKISON, WO SPIEGELMAN, BM TI VASCULAR ENDOTHELIAL GROWTH-FACTOR - REGULATION BY CELL-DIFFERENTIATION AND ACTIVATED 2ND MESSENGER PATHWAYS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; GLYCEROPHOSPHATE DEHYDROGENASE; PERMEABILITY FACTOR; ADIPOSE CONVERSION; ADIPOCYTE DEVELOPMENT; DEPENDENT PROTEINS; MOLECULAR-CLONING; 3T3 ADIPOCYTES; RNA CONTENT; AMINO-ACID AB Vascular endothelial growth factor (VEGF) is an angiogenic polypeptide that has been isolated from a variety of tumorigenic and nontransformed cell lines. Because of the importance of blood vessel growth to cell and tissue development, we have examined VEGF gene expression in a variety of mouse tissues and rodent models of cellular differentiation. Using a cloned murine VEGF cDNA we show that VEGF mRNA is expressed at relatively low levels in many adult mouse tissues examined. However, this message is dramatically induced in two models of cell differentiation: 3T3-adipose conversion and C2C12 myogenic differentiation. VEGF protein secretion is also induced in adipocyte differentiation. VEGF mRNA is markedly regulated in a pheochromocytoma (PC12) cell model of transformation and differentiation. The transformed undifferentiated cells express moderate levels of VEGF mRNA and this expression is virtually extinguished when cells differentiate into non-malignant neuron-like cells. Experiments employing phorbol esters and cAMP analogues indicate that VEGF mRNA expression is stimulated in preadipocytes by both protein kinase C and protein kinase A-mediated pathways. These results suggest that VEGF mRNA levels are closely linked to the process of cellular differentiation; they also clearly demonstrate that expression of this angiogenic factor is specifically regulated in a transformed cell line, possibly via aberrant activation of cellular second messenger pathways. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP CLAFFEY, KP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK 42420, DK08277, DK08278] NR 35 TC 305 Z9 310 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 AUG 15 PY 1992 VL 267 IS 23 BP 16317 EP 16322 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800052 PM 1644816 ER PT J AU WILDEN, PA KAHN, CR SIDDLE, K WHITE, MF AF WILDEN, PA KAHN, CR SIDDLE, K WHITE, MF TI INSULIN-RECEPTOR KINASE DOMAIN AUTOPHOSPHORYLATION REGULATES RECEPTOR ENZYMATIC FUNCTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH FACTOR-I; TYROSINE KINASE; BETA-SUBUNIT; PHOSPHORYLATION SITES; HYBRID RECEPTORS; SIGNAL TRANSDUCTION; TRANSFECTED CELLS; PROTEIN; REPLACEMENT; INVITRO AB We have studied a series of insulin receptor molecules in which the 3 tyrosine residues which undergo autophosphorylation in the kinase domain of the beta-subunit (Tyr1158, Tyr1162, and Tyr1163) were replaced individually, in pairs, or all together with phenylalanine or serine by in vitro mutagenesis. A single-Phe replacement at each of these three positions reduced insulin-stimulated autophosphorylation of solubilized receptor by 45-60% of that observed with wild-type receptor. The double-Phe replacements showed a 60-70% reduction, and substitution of all 3 tyrosine residues with Phe or Ser reduced insulin-stimulated tyrosine autophosphorylation by >80%. Phosphopeptide mapping each mutant revealed that all remaining tyrosine autophosphorylation sites were phosphorylated normally following insulin stimulation, and no new sites appeared. The single-Phe mutants showed insulin-stimulated kinase activity toward a synthetic peptide substrate of 50-75% when compared with wild-type receptor kinase activity. Insulin-stimulated kinase activity was further reduced in the double-Phe mutants and barely detectable in the triple-Phe mutants. In contrast to the wild-type receptor, all of the mutant receptor kinases showed a significant reduction in activation following in vitro insulin-stimulated autophosphorylation. When studied in intact Chinese hamster ovary cells, insulin-stimulated receptor autophosphorylation and tyrosine phosphorylation of the cellular substrate pp185 in the single-Phe and double-Phe mutants was progressively lower with increased tyrosine replacement and did not exceed the basal levels in the triple-Phe mutants. However, all the mutant receptors, including the triple-Phe mutant, retained the ability to undergo insulin-stimulated Ser and Thr phosphorylation. Thus, full activation of the insulin receptor tyrosine kinase is dependent on insulin-stimulated Tris phosphorylation of the kinase domain, and the level of autophosphorylation in the kinase domain provides a mechanism for modulating insulin receptor kinase activity following insulin stimulation. By contrast, insulin stimulation of receptor phosphorylation on Ser and Thr residues by cellular serine/threonine kinases can occur despite markedly reduced tyrosine autophosphorylation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02215. RP WILDEN, PA (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK 33201, DK 36836, DK 38712] NR 53 TC 115 Z9 115 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 15 PY 1992 VL 267 IS 23 BP 16660 EP 16668 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800102 PM 1322912 ER PT J AU SUGITA, K ROBERTSON, MJ TORIMOTO, Y RITZ, J SCHLOSSMAN, SF MORIMOTO, C AF SUGITA, K ROBERTSON, MJ TORIMOTO, Y RITZ, J SCHLOSSMAN, SF MORIMOTO, C TI PARTICIPATION OF THE CD27 ANTIGEN IN THE REGULATION OF IL-2-ACTIVATED HUMAN NATURAL-KILLER-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LYMPHOCYTE-T ACTIVATION; GROWTH-FACTOR RECEPTOR; TYROSINE PHOSPHORYLATION; FUNCTIONAL-PROPERTIES; EXPRESSION; PROTEIN; FAMILY; ENHANCEMENT; MOLECULES; INDUCTION AB The CD27 Ag is expressed by the majority of resting T lymphocytes and appears to play a crucial role in T cell activation. We found that some resting peripheral blood NK cells also express CD27. Furthermore, CD27 expression was up-regulated on NK cells stimulated by IL-2. The cytolytic activity of IL-2-activated, but not resting, NK cells was inhibited by an anti-CD27 mAb (anti-1A4). However, anti-1A4 did not affect conjugate formation between IL-2-activated NK cells and tumor cell targets. In contrast, anti-1A4 inhibited CD2-mediated calcium mobilization and the serine esterase activity of NK cell granules. These inhibitory effects could be mediated in part by increase in intracellular cAMP levels induced by anti-1A4. Our results suggest that the CD27 Ag plays an important role in the regulation of activated NK cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA-41619]; PHS HHS [A1-12069, A1-29530] NR 32 TC 61 Z9 62 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 AUG 15 PY 1992 VL 149 IS 4 BP 1199 EP 1203 PG 5 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200013 PM 1354231 ER PT J AU AVERY, RK BLEIER, KJ PASTERNACK, MS AF AVERY, RK BLEIER, KJ PASTERNACK, MS TI DIFFERENCES BETWEEN ATP-MEDIATED CYTOTOXICITY AND CELL-MEDIATED CYTOTOXICITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; INDUCE DNA FRAGMENTATION; NATURAL-KILLER CELLS; ADENOSINE 5'-TRIPHOSPHATE ATP; CYTOLYTIC LYMPHOCYTES; EXTRACELLULAR ATP; SERINE ESTERASE; TARGET-CELL; LYTIC GRANULES; CYTO-TOXICITY AB There has been considerable recent interest in the possible role of extracellular ATP in cell-mediated cytotoxicity. To investigate the similarities and differences between ATP-mediated lysis and CTL-mediated lysis, we studied in detail the ATP-mediated lysis of EL-4 cells, which are highly susceptible to lysis by extracellular ATP. ATP-mediated lysis was time and concentration dependent; most lysis occurred within 4 to 6 h of incubation. The kinetics of ATP- and cell-mediated lysis were similar. However, in contrast to CTL-mediated lysis, ATP-mediated lysis of EL-4 cells did not appear to be accompanied by characteristic chromosomal degradation (apoptosis). In order to compare these cytotoxic processes in greater detail, ATP-resistant clones were derived by growing EL-4 cells continuously in the presence of high concentrations of ATP. These cloned EL-4 lines showed marked resistance to ATP-mediated cytotoxicity across a wide range of concentrations but were as susceptible as the parent EL-4 cells to cell-mediated cytotoxicity by an alloreactive effector population from a MLC. Thus, there appear to be a number of differences between ATP-mediated and cell-mediated cytotoxicity in this system; most notable is the identification of cell lines that are resistant to ATP but susceptible to CTL-mediated lysis. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 50 TC 22 Z9 22 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 AUG 15 PY 1992 VL 149 IS 4 BP 1265 EP 1270 PG 6 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200023 PM 1500717 ER PT J AU SOBEL, RA KUCHROO, VK AF SOBEL, RA KUCHROO, VK TI THE IMMUNOPATHOLOGY OF ACUTE EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS INDUCED WITH MYELIN PROTEOLIPID PROTEIN - T-CELL RECEPTORS IN INFLAMMATORY LESIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; BASIC-PROTEIN; MULTIPLE-SCLEROSIS; BETA-CHAIN; MONOCLONAL-ANTIBODY; RHEUMATOID-ARTHRITIS; ENCEPHALITOGENIC DETERMINANT; LIMITED HETEROGENEITY; ANTIGEN-SPECIFICITY; SYNTHETIC PEPTIDES AB To determine whether there is predominance of T cells expressing a particular TCR V-beta-chain in the inflammatory lesions of an autoimmune disease model, TCR expression was analyzed in central nervous system (CNS) tissues of mice with experimental allergic encephalomyelitis (EAE). Acute EAE was induced in SJL/J mice either by sensitization with a synthetic peptide corresponding to myelin proteolipid protein residues 139-151 or by adoptive transfer of myelin proteolipid protein peptide 139-151-specific encephalitogenic T cell clones. Mice were killed when they showed clinical signs of EAE or by 40 days after sensitization or T cell transfer. Cryostat CNS and lymphoid tissue sections were immunostained with a panel of mAb to T cell markers and proportions of stained cells were counted in inflammatory foci. In mice with both actively induced and adoptively transferred EAE, infiltrates consisted of many CD3+, TCR-alpha-beta+, and CD4+ cells, fewer CD8+ cells, and small numbers of TCR-gamma-delta+ cells. Approximately 30% of CD45+ leukocytes in the inflammatory foci were T cells. Cells expressing TCR V-beta 2, 3, 4, 6, 7 and 14 were detected in the infiltrates, whereas TCR V-beta-8 and 11, which that are deleted in SJL mice, were absent. When EAE was induced by transfer of T cell clones that use either V-beta 2, 6, 10, or 17, there was also a heterogeneous accumulation of T cells in the lesions. Similar proportions of TCR V-beta+ and gamma-delta+ cells were detected in EAE lesions and in the spleens of the mice. Thus, at the time that clinical signs are present in acute EAE, peripherally derived, heterogeneous TCR V-beta+ cells are found in CNS lesions, even when the immune response is initiated to a short peptide Ag or by a T cell clone using a single TCR V-beta. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. EK SHRIVER CTR,DEPT BIOCHEM,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NICHD NIH HHS [HD 04147]; NINDS NIH HHS [NS 16945, NS 26773] NR 57 TC 63 Z9 63 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 AUG 15 PY 1992 VL 149 IS 4 BP 1444 EP 1451 PG 8 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200048 PM 1380045 ER PT J AU TOKSOZ, D ZSEBO, KM SMITH, KA HU, S BRANKOW, D SUGGS, SV MARTIN, FH WILLIAMS, DA AF TOKSOZ, D ZSEBO, KM SMITH, KA HU, S BRANKOW, D SUGGS, SV MARTIN, FH WILLIAMS, DA TI SUPPORT OF HUMAN HEMATOPOIESIS IN LONG-TERM BONE-MARROW CULTURES BY MURINE STROMAL CELLS SELECTIVELY EXPRESSING THE MEMBRANE-BOUND AND SECRETED FORMS OF THE HUMAN HOMOLOG OF THE STEEL GENE-PRODUCT, STEM-CELL FACTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID TYROSINE KINASE RECEPTOR; GROWTH-FACTOR; W-LOCUS; PROGENITOR CELLS; PROTO-ONCOGENE; SI-LOCUS; LIGAND; MOUSE; TRANSMEMBRANE; PURIFICATION AB The maintenance and differentiation of hematopoietic stem cells is influenced by cells making up the hematopoietic microenvironment (HM), including bone marrow-derived stromal cells. We and several other investigators have recently demonstrated the molecular basis of abnormal HM observed in the steel mutant mouse and cloned the normal cDNA products of this gene (termed SCF, KL, or MCF). In this report, we focus on the human counterpart of the mouse Steel (Sl) gene. Alternative splicing of the human SCF pre-mRNA transcript results in secreted and membrane-bound forms of the protein. To investigate the role of these two forms of human SCF, we targeted an immortalized stromal cell line derived from fetal murine homozygous (Sl/Sl) SCF-deficient embryos for gene transfer of various human cDNAs encoding SCF. We report that stable stromal cell transfectants can differentially process the two forms of human SCF protein product. We also demonstrate that both soluble SCF and membrane-bound SCF are active in increasing the number of human progenitor cells in the context of stromal cell cultures, although in a qualitatively different manner. Hence, the membrane-bound form of SCF may play an important role in the cell-cell interactions observed between stromal and hematopoietic cells both in vitro and in vivo. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. INDIANA UNIV,SCH MED,HOWARD HUGHES MED INST,HERMAN B WELLS CTR PEDIAT RES,INDIANAPOLIS,IN 46202. FU NHLBI NIH HHS [1 RO1 HL46528-01] NR 24 TC 258 Z9 259 U1 0 U2 0 PU NATL ACAD PRESS 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 AUG 15 PY 1992 VL 89 IS 16 BP 7350 EP 7354 DI 10.1073/pnas.89.16.7350 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100014 PM 1380155 ER PT J AU KRUEGER, NX SAITO, H AF KRUEGER, NX SAITO, H TI A HUMAN TRANSMEMBRANE PROTEIN-TYROSINE-PHOSPHATASE, PTP-ZETA, IS EXPRESSED IN BRAIN AND HAS AN N-TERMINAL RECEPTOR DOMAIN HOMOLOGOUS TO CARBONIC-ANHYDRASES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CDNA; DEPHOSPHORYLATION; NUCLEOTIDE SEQUENCE ID NERVOUS-SYSTEM AXONS; NUCLEOTIDE-SEQUENCE; DROSOPHILA; CLONING; FAMILY; GENE; CDNA; HYBRIDIZATION; CHROMOSOME; LAR AB Protein-tyrosine-phosphatases (PTPases, EC 3.1.3.48) play a crucial role in the regulation of protein tyrosine phosphorylation. Recently, it was found that the PTPase gene family exhibits a large variety of different functional domains associated with the PTPase catalytic domains. In this paper, we report the complete cDNA sequence of a human transmembrane PTPase, PTP-zeta, isolated from fetal brain cDNA libraries. The deduced amino acid sequence of human PTP-zeta is composed of a putative signal peptide of 19 amino acids, a very large extracellular domain of 1616 amino acids, a transmembrane peptide of 26 amino acids, and a cytoplasmic domain of 653 amino acids. The extracellular portion of human PTP-zeta contains two striking structural features: the N-terminal 280-amino acid sequence that is homologous to carbonic anhydrases (carbonate hydro-lyase, EC 4.2.1.1), and a sequence of 1048 amino acids without a cysteine residue. While it is unlikely that the carbonic anhydrase-like domain of PTP-zeta has any carbonic anhydrase activity, its three-dimensional structure may be quite similar to that of carbonic anhydrases, a structure that appears ideal for binding a small soluble ligand. The cytoplasmic portion of human PTP-zeta contains two repeated PTPase-like domains, which, when expressed in Escherichia coli, had PTPase activity in vitro. Mutational analyses indicate that only the membrane-proximal PTPase domain is catalytically active. Reverse transcription-polymerase chain reaction analyses indicate that human PTP-zeta is highly expressed in a glioblastoma cell line. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA51132]; NIAID NIH HHS [AI26598] NR 29 TC 200 Z9 201 U1 0 U2 4 PU NATL ACAD PRESS 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 AUG 15 PY 1992 VL 89 IS 16 BP 7417 EP 7421 DI 10.1073/pnas.89.16.7417 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100028 PM 1323835 ER PT J AU ROSS, SR CHOY, L GRAVES, RA FOX, N SOLEVJEVA, V KLAUS, S RICQUIER, D SPIEGELMAN, BM AF ROSS, SR CHOY, L GRAVES, RA FOX, N SOLEVJEVA, V KLAUS, S RICQUIER, D SPIEGELMAN, BM TI HIBERNOMA FORMATION IN TRANSGENIC MICE AND ISOLATION OF A BROWN ADIPOCYTE CELL-LINE EXPRESSING THE UNCOUPLING PROTEIN GENE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE FAT CELL; THERMOGENESIS; OBESITY ID BETA-ADRENERGIC AGONIST; T-ANTIGEN GENES; ADIPOSE-TISSUE; DIRECTS EXPRESSION; MESSENGER-RNA; ACINAR-CELLS; DIFFERENTIATION; MOUSE; INSULIN; THERMOGENESIS AB Transgenic mice were produced containing the adipocyte-specific regulatory region from the adipocyte P2 (aP2) gene linked to the simian virus 40 transforming genes. Most of the transgenic mice developed brown fat tumors (hibernomas) in their interscapular brown adipose tissue. Hibernoma formation was noticeable in some of the mice as early as 1 day after birth and most of the mice developed very large tumors by 1 month of age. All of the tumor tissue expressed the brown fat-specific uncoupling protein (UCP) gene as well as the aP2 gene. Several of the tumors have been used to establish cultured cell lines and at least one of these lines can be induced to differentiate into brown adipocytes. The cultured adipocytes express mRNA for UCP upon stimulation with N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate, norepinephrine, isoproterenol or D7114, a beta-3 adrenergic agonist. Thus, regulation of the key thermogenic gene UCP can now be studied in an established cell line. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. ELI LILLY & CO,LILLY RES LAB,DEPT CHEM & BIOTECHNOL RES,INDIANAPOLIS,IN 46285. CNRS,CTR RECH ENDOCRINOL MOLEC & DEV,F-92190 MEUDON,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ROSS, SR (reprint author), UNIV ILLINOIS,COLL MED,DEPT BIOCHEM MC 536,CHICAGO,IL 60612, USA. FU NIDDK NIH HHS [DK31405] NR 40 TC 100 Z9 100 U1 0 U2 1 PU NATL ACAD PRESS 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 AUG 15 PY 1992 VL 89 IS 16 BP 7561 EP 7565 DI 10.1073/pnas.89.16.7561 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100057 PM 1323843 ER PT J AU SLECKMAN, BP SHIN, JY IGRAS, VE COLLINS, TL STROMINGER, JL BURAKOFF, SJ AF SLECKMAN, BP SHIN, JY IGRAS, VE COLLINS, TL STROMINGER, JL BURAKOFF, SJ TI DISRUPTION OF THE CD4-P56(LCK) COMPLEX IS REQUIRED FOR RAPID INTERNALIZATION OF CD4 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-CELL ACTIVATION; RECEPTOR INTERNALIZATION; PROTEIN-TYROSINE KINASE ID PROTEIN-TYROSINE KINASE; PHORBOL-MYRISTATE ACETATE; GROWTH-FACTOR RECEPTOR; AMINO-TERMINAL DOMAIN; CYTOPLASMIC DOMAIN; INSULIN-RECEPTOR; T-CELLS; SIGNAL TRANSDUCTION; EGF RECEPTOR; P56LCK AB CD4 is a cell surface glycoprotein expressed by a subset of T lymphocytes and functions to enhance T-cell activation. CD4 is noncovalently associated via the cytoplasmic domain with the protein-tyrosine kinase p56lck, a member of the src protein-tyrosine kinase family. Upon activation of protein kinase C by phorbol ester, CD4 is phosphorylated on cytoplasmic serine residues and internalized from the cell surface, and disruption of the CD4-p56lck complex occurs. The exact relationship between these events is likely to be functionally significant, as cytoplasmic-domain serine phosphorylation and internalization have been shown to regulate the function of receptors that possess intrinsic protein-tyrosine kinase activity. Here we demonstrate that p56lck slows the rate of phorbol 12-myristate 13-acetate-induced internalization of CD4 in a manner that depends on a physical association between p56lck and CD4. This decreased rate is due at least in part to a requirement for disruption of the CD4-p56lck complex prior to internalization of CD4. Furthermore, disruption of the CD4-p56lck complex appears to depend on the integrity of the cytoplasmic-domain serine at position 408, probably due to a requirement for phosphorylation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP SLECKMAN, BP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA47554]; NIAID NIH HHS [AI15669, AI17258] NR 35 TC 67 Z9 68 U1 0 U2 1 PU NATL ACAD PRESS 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 AUG 15 PY 1992 VL 89 IS 16 BP 7566 EP 7570 DI 10.1073/pnas.89.16.7566 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100058 PM 1502168 ER PT J AU CALVO, V CREWS, CM VIK, TA BIERER, BE AF CALVO, V CREWS, CM VIK, TA BIERER, BE TI INTERLEUKIN-2 STIMULATION OF P70 S6 KINASE-ACTIVITY IS INHIBITED BY THE IMMUNOSUPPRESSANT RAPAMYCIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CYTOKINES; GROWTH FACTOR SIGNALING; SERINE; THEONINE KINASES ID RIBOSOMAL-PROTEIN S6; MOLECULAR-CLONING; RECEPTOR; PHOSPHORYLATION; EXPRESSION; ACTIVATION; COMPLEXES; PATHWAYS; SIGNALS; CDNAS AB Binding of interleukin 2 (IL-2) to its receptor generates intracellular signals, including the activation of tyrosine and serine/threonine kinases. In this study the activation of the serine/threonine-specific ribosomal protein S6 kinases in response to IL-2 was analyzed in the murine T-cell line CTLL-20, a model system of IL-2-dependent proliferation. Two major classes of S6 kinases have been characterized: the 90-kDa (rsk) family and the 70-kDa family. In response to the addition of recombinant IL-2, total S6 kinase activity was increased. This S6 kinase activity could not be immunoprecipitated by an antiserum specific for S6 kinases of the 90-kDa family, exhibited a chromatographic behavior characteristic of 70-kDa S6 kinases, and was recognized by a 70-kDa S6 kinase-specific antiserum. Thus, IL-2 binding to its receptor induces specific activation of the 70-kDa family of S6 kinases. Rapamycin, a macrolide immunosuppressant that inhibits IL-2-dependent proliferation, inhibited IL-2-stimulated 70-kDa S6 kinase activity subsequent to early increases in tyrosine kinase activity. These findings imply that the targets of rapamycin include molecules involved in the activation of 70-kDa S6 kinases. These observations further suggest that S6 kinases of the 70-kDa family participate in signal transmission pathways subsequent to IL-2 binding to its receptor. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & DEV BIOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP CALVO, V (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115, USA. RI Calvo, Victor/L-5024-2014 OI Calvo, Victor/0000-0002-5913-7058 NR 29 TC 181 Z9 182 U1 0 U2 1 PU NATL ACAD PRESS 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 AUG 15 PY 1992 VL 89 IS 16 BP 7571 EP 7575 DI 10.1073/pnas.89.16.7571 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100059 PM 1380162 ER PT J AU LATRON, F PAZMANY, L MORRISON, J MOOTS, R SAPER, MA MCMICHAEL, A STROMINGER, JL AF LATRON, F PAZMANY, L MORRISON, J MOOTS, R SAPER, MA MCMICHAEL, A STROMINGER, JL TI A CRITICAL ROLE FOR CONSERVED RESIDUES IN THE CLEFT OF HLA-A2 IN PRESENTATION OF A NONAPEPTIDE TO T-CELLS SO SCIENCE LA English DT Article ID ANTIGEN-BINDING SITE; TOXIC LYMPHOCYTES-T; HISTOCOMPATIBILITY ANTIGEN; PEPTIDE; RECOGNITION; MOLECULES AB The peptide binding cleft of the class I human histocompatibility antigen, HLA-A2, contains conserved amino acid residues clustered in the two ends of the cleft in pockets A and F as well as polymorphic residues. The function of two conserved tyrosines in the A pocket was investigated by mutating them to phenylalanines and of a conserved tyrosine and threonine in the F pocket by mutating them to phenylalanine and valine, respectively. Presentation of influenza virus peptides and of intact virus to cytolytic T lymphocytes (CTLs) was then examined. The magnitude of the reduction seen by the mutation of the two tyrosines in the A pocket suggests that hydrogen bonds involving them have a critical function in the binding of the NH2-terminal NH3+ of the peptide nonamer and possibly of all bound peptide nonamers. In contrast, the mutations in the F pocket had no effect on CTL recognition. C1 UNIV OXFORD,INST MOLEC MED,OXFORD OX3 9DU,ENGLAND. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. RP LATRON, F (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 47554]; NIAID NIH HHS [AI 20182] NR 21 TC 74 Z9 75 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 AUG 14 PY 1992 VL 257 IS 5072 BP 964 EP 967 DI 10.1126/science.1380181 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JH827 UT WOS:A1992JH82700035 PM 1380181 ER PT J AU LIANG, P PARDEE, AB AF LIANG, P PARDEE, AB TI DIFFERENTIAL DISPLAY OF EUKARYOTIC MESSENGER-RNA BY MEANS OF THE POLYMERASE CHAIN-REACTION SO SCIENCE LA English DT Article ID CELL-CYCLE; MOLECULAR-CLONING; CDNA SEQUENCES; KINASE; TUMOR; EXPRESSION; CANDIDATE; GENES; G1 AB Effective methods are needed to identify and isolate those genes that are differentially expressed in various cells or under altered conditions. This report describes a method to separate and clone individual messenger RNAs (mRNAs) by means of the polymerase chain reaction. The key element is to use a set of oligonucleotide primers, one being anchored to the polyadenylate tail of a subset of mRNAs, the other being short and arbitrary in sequence so that it anneals at different positions relative to the first primer. The mRNA subpopulations defined by these primer pairs were amplified after reverse transcription and resolved on a DNA sequencing gel. When multiple primer sets were used, reproducible patterns of amplified complementary DNA fragments were obtained that showed strong dependence on sequence specificity of either primer. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. RP LIANG, P (reprint author), HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. NR 21 TC 4503 Z9 5176 U1 16 U2 116 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD AUG 14 PY 1992 VL 257 IS 5072 BP 967 EP 971 DI 10.1126/science.1354393 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JH827 UT WOS:A1992JH82700036 PM 1354393 ER PT J AU PRICE, DJ GROVE, JR CALVO, V AVRUCH, J BIERER, BE AF PRICE, DJ GROVE, JR CALVO, V AVRUCH, J BIERER, BE TI RAPAMYCIN-INDUCED INHIBITION OF THE 70-KILODALTON S6 PROTEIN-KINASE SO SCIENCE LA English DT Article ID PEPTIDYL-PROLYL ISOMERASE; IMMUNOSUPPRESSANT FK506; RIBOSOMAL PROTEIN-S6; DISTINCT; PHOSPHORYLATION; ACTIVATION; CELLS; PURIFICATION; CYCLOSPORINE; CYCLOPHILIN AB The immunosuppressant rapamycin inhibited proliferation of the H4IIEC hepatoma cell line. Rapamycin, but not its structural analog FK506, also inhibited the basal and insulin-stimulated activity of the p70 ribosomal protein S6 kinase. By contrast, insulin stimulation of the p85 Rsk S6 kinase and mitogen-activated protein (MAP) kinase activity were unaffected by drug. Rapamycin treatment of COS cells transfected with recombinant p70 S6 kinase completely inhibited the appearance of the hyperphosphorylated form of p70 S6 kinase concomitant with the inhibition of enzyme activity toward 40S subunits. Thus, rapamycin inhibits a signal transduction element that is necessary for the activation of p70 S6 kinase and mitogenesis but unnecessary for activation of p85 Rsk S6 kinase or MAP kinase. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. RI Calvo, Victor/L-5024-2014 OI Calvo, Victor/0000-0002-5913-7058 FU NCI NIH HHS [P01 CA39542]; NIDDK NIH HHS [R01 DK17776] NR 35 TC 589 Z9 593 U1 1 U2 7 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD AUG 14 PY 1992 VL 257 IS 5072 BP 973 EP 977 DI 10.1126/science.1380182 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JH827 UT WOS:A1992JH82700038 PM 1380182 ER PT J AU HARRIS, JR LIPPMAN, ME VERONESI, U WILLETT, W AF HARRIS, JR LIPPMAN, ME VERONESI, U WILLETT, W TI BREAST-CANCER .3. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID ADJUVANT TAMOXIFEN THERAPY; FIBROBLAST GROWTH-FACTOR; SUBCUTANEOUS MASTECTOMY; FACTOR RECEPTOR; P53 MUTATIONS; TUMOR-GROWTH; FACTOR-BETA; ESTROGEN; CARCINOMAS; SURVIVAL C1 BETH ISRAEL HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RADIAT ONCOL,BOSTON,MA 02115. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. IST NAZL STUDIO & CURA TUMORI,I-20133 MILAN,ITALY. GEORGETOWN UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PHARMACOL,WASHINGTON,DC 20007. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CHANNING LAB,DEPT MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. RP HARRIS, JR (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT ONCOL,50 BINNEY ST,BOSTON,MA 02115, USA. NR 81 TC 197 Z9 198 U1 1 U2 3 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 AUG 13 PY 1992 VL 327 IS 7 BP 473 EP 480 DI 10.1056/NEJM199208133270706 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA JH340 UT WOS:A1992JH34000006 PM 1625737 ER PT J AU HENEY, NM MCGOVERN, FJ AF HENEY, NM MCGOVERN, FJ TI A 34-YEAR-OLD WOMAN WITH ENDOMETRIOSIS AND BILATERAL HYDRONEPHROSIS NEPHROLITHIASIS, BILATERAL, WITH URETERAL OBSTRUCTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP HENEY, NM (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 13 PY 1992 VL 327 IS 7 BP 481 EP 485 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JH340 UT WOS:A1992JH34000007 ER PT J AU KLEY, N CHUNG, RY FAY, S LOEFFLER, JP SEIZINGER, BR AF KLEY, N CHUNG, RY FAY, S LOEFFLER, JP SEIZINGER, BR TI REPRESSION OF THE BASAL C-FOS PROMOTER BY WILD-TYPE P53 SO NUCLEIC ACIDS RESEARCH LA English DT Article ID SIMIAN VIRUS-40; TRANSCRIPTIONAL ACTIVATION; MONOCLONAL-ANTIBODIES; RESPONSIVE ELEMENT; PROTO-ONCOGENE; PROTEINS BIND; GROWTH-FACTOR; GENE-PRODUCT; DNA; MUTANT AB Mutations in the p53 gene are the most common genetic alterations observed in many inherited and sporadic forms of human cancer. Recent studies indicate that wild-type p53 may be involved in the regulation of gene expression. In the present report we examined the effect of p53 on the human c-fos promoter. Using a transient co-transfection assay we show that wild-type human p53, but not a transforming mutant of p53, negatively regulates the activity of the c-fos promoter in a dose-dependent manner. Promoter deletion analysis maps a sequence confering p53 repression to the basal promoter region between nucleotides - 53 and + 42 relative to the cap site. In contrast, p53 strongly stimulates transcription when a sequence previously reported to bind p53 (TGCCT repeat) was inserted in front of the HSV-TK promoter driving CAT. These findings raise the question as to whether p53 may mediate its inhibitory effect on c-fos gene expression by interfering, directly or indirectly, with components of the basal transcriptional machinery. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. UNIV STRASBOURG 1,PHYSIOL GEN LAB,CNRS,URA 309,F-67070 STRASBOURG,FRANCE. RP KLEY, N (reprint author), MASSACHUSETTS GEN HOSP,CTR NEUROSCI,MOLEC NEUROONCOL LAB,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA 49455-03]; NIGMS NIH HHS [T32 GM007753, 2 T32 GMO7753-12] NR 38 TC 94 Z9 95 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD AUG 11 PY 1992 VL 20 IS 15 BP 4083 EP 4087 DI 10.1093/nar/20.15.4083 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ802 UT WOS:A1992JJ80200039 PM 1508692 ER PT J AU HANKINSON, SE STAMPFER, MJ SEDDON, JM COLDITZ, GA ROSNER, B SPEIZER, FE WILLETT, WC AF HANKINSON, SE STAMPFER, MJ SEDDON, JM COLDITZ, GA ROSNER, B SPEIZER, FE WILLETT, WC TI NUTRIENT INTAKE AND CATARACT-EXTRACTION IN WOMEN - A PROSPECTIVE-STUDY SO BMJ-BRITISH MEDICAL JOURNAL LA English DT Article ID FOOD FREQUENCY QUESTIONNAIRE; PLASMA BETA-CAROTENE; VITAMIN-C STATUS; CIGARETTE-SMOKING; ASCORBIC-ACID; NUTRITIONAL-STATUS; ALPHA-TOCOPHEROL; SENILE CATARACT; LENS; RISK AB Objective-To examine prospectively the association between dietary intake of vitamins C and E, carotene, and riboflavin and cataract extraction in women. Design-Prospective cohort study beginning in 1980 with eight years of follow up. Setting- 11 states of the United States. Participants - Female registered nurses who were 45 to 67 years of age. 50 828 women were included in 1980 and others were added as they became 45 years of age. Main outcome measure-Incidence of extraction of senile cataracts. Results-493 cataracts were extracted during 470 302 person years of follow up. Intake of carotene and vitamin A was inversely associated with cataract: in multivariate analyses, women in the highest fifth of total vitamin A intake (excluding supplements) had a 39% lower risk of cataract relative to women in the lowest fifth (relative risk 0.61; 95% confidence interval 0.45 to 0.81). Neither riboflavin nor dietary vitamins E or C were associated with cataract in a multivariate analysis. Among specific food items spinach (rather than carrots, the greatest source of beta-carotene) was most consistently associated with a lower relative risk. The risk of cataract was 45% lower among women who used vitamin C supplements for 10 or more years (relative risk 0.55 (0.32 to 0.96)), but no association was noted for multivitamin intake. Conclusion-Dietary carotenoids, although not necessarily beta-carotene, and long term vitamin C supplementation may decrease the risk of cataracts severe enough to require extraction. C1 BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. HARVARD UNIV, SCH PUBL HLTH, BOSTON, MA 02115 USA. MASSACHUSETTS EYE & EAR INFIRM, BOSTON, MA 02114 USA. RP HARVARD UNIV, SCH MED, CHANNING LAB, DEPT MED, 180 LONGWOOD AVE, BOSTON, MA 02115 USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NCI NIH HHS [CA40356]; PHS HHS [5T32 E507069] NR 45 TC 206 Z9 211 U1 0 U2 7 PU BMJ PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1756-1833 J9 BMJ-BRIT MED J JI BMJ-British Medical Journal PD AUG 8 PY 1992 VL 305 IS 6849 BP 335 EP 339 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JJ032 UT WOS:A1992JJ03200020 PM 1392884 ER PT J AU GADISSEUX, JF EVRARD, P MISSON, JP CAVINESS, VS AF GADISSEUX, JF EVRARD, P MISSON, JP CAVINESS, VS TI DYNAMIC CHANGES IN THE DENSITY OF RADIAL GLIAL FIBERS OF THE DEVELOPING MURINE CEREBRAL WALL - A QUANTITATIVE IMMUNOHISTOLOGICAL ANALYSIS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE GLIAL ANTIBODY; NEOCORTEX; HISTOGENESIS; ONTOGENIC COLUMNS; ARCHITECTONICS ID RECOMBINANT RETROVIRUS; NEURONAL MIGRATION; CELL LINEAGE; REELER MICE; NEOCORTEX; CORTEX; SYSTEM; MOUSE; ORGANIZATION AB The density of radial glial fibers in the developing murine cerebral wall decreases dramatically during the terminal week of gestation. The present analysis characterizes these variations of fiber density quantitatively. Radial glial fibers were stained with monoclonal antibody RC2. Fibers were counted in a standard area of 2,000-mu-m2, passing orthogonally to the fiber long axis. At E14, fiber density is maximum and relatively uniform throughout the full width of the cerebral wall. Subsequently, the overall glial fiber density decreases and fiber density gradients emerge in the transmural span of fibers. These radial fiber density gradients are marked by sharp declines at the level of the ventricular-subventricular zone and in the zone of transition between intermediate zone (IZ) and cortical plate. In the interval E14-P0, the decrease in densities of fibers crossing the IZ is commensurate with the predicted diluting effects of tissue expansion with growth. By contrast, the decrease in fiber densities in ascent across the cortical plate beyond E14 through E17 exceeds that predicted by growth. The observations suggest that a substantial population of radial glial fibers do not span the full ventricular zone to the cerebral surface. A major contingent appears to extend only as far as the external sagittal stratum/subplate through E16. Subsequently, at a time when supragranular cortical layers are being assembled, the full set of fibers appears to extend more uniformly through the cortical strata. The late surge of fibers would be appropriate to the intercalation of groupings of neurons of the supragranular layers. C1 CATHOLIC UNIV LOUVAIN,SCH MED,DEV NEUROBIOL UNIT,B-1200 BRUSSELS,BELGIUM. STATE UNIV LIEGE,SCH MED,PHYSIOL & DEV NEUROBIOL LAB,B-4000 LIEGE,BELGIUM. RP GADISSEUX, JF (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL DEV NEUROBIOL,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS 12005] NR 24 TC 21 Z9 21 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD AUG 8 PY 1992 VL 322 IS 2 BP 246 EP 254 DI 10.1002/cne.903220210 PG 9 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA JF952 UT WOS:A1992JF95200009 PM 1522252 ER PT J AU ZELEN, M AF ZELEN, M TI RANDOMIZED CONSENT TRIALS SO LANCET LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ZELEN, M (reprint author), HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115, USA. NR 1 TC 12 Z9 12 U1 1 U2 3 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD AUG 8 PY 1992 VL 340 IS 8815 BP 375 EP 375 DI 10.1016/0140-6736(92)91454-G PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JH125 UT WOS:A1992JH12500040 PM 1353840 ER PT J AU SWIERGIEL, AH TAKAHASHI, LK RUBIN, WW KALIN, NH AF SWIERGIEL, AH TAKAHASHI, LK RUBIN, WW KALIN, NH TI ANTAGONISM OF CORTICOTROPIN-RELEASING FACTOR RECEPTORS IN THE LOCUS-CERULEUS ATTENUATES SHOCK-INDUCED FREEZING IN RATS SO BRAIN RESEARCH LA English DT Article DE CORTICOTROPIN-RELEASING FACTOR ANTAGONIST; LOCUS-CERULEUS; FREEZING BEHAVIOR; RAT; STRESS; BARRINGTON NUCLEUS ID DORSOLATERAL PONTINE TEGMENTUM; SYMPATHETIC NERVOUS-SYSTEM; DIFFERENTIAL REGULATION; IMMUNOREACTIVE NEURONS; DEFENSIVE-WITHDRAWAL; BRAIN REGIONS; FACTOR CRF; STRESS; BEHAVIOR; LOCALIZATION AB Intracerebroventricularly administered alpha-helical CRF9-41, a corticotropin-releasing factor (CRF) receptor antagonist, is known to reduce a variety of stress-induced behavioral responses. This study examined in rats whether antagonism of CRF receptors in the region of locus coeruleus (LC) plays a role in reducing freezing induced by electric foot shock. Freezing is a well-characterized defensive response to stress and has been demonstrated to index an animal's degree of fear. A CRF-receptor antagonist, alpha-helical CRF9-41, bilaterally infused into the LC significantly reduced the duration of freezing at a dose as low as 0.20-mu-g. Additional experiments confirmed that 0.20-mu-g of alpha-helical CRF9-41 significantly reduced the duration of freezing only when cannulae were within the LC or in regions bordering the nucleus. Antagonist-treated rats with cannulae that did not impinge on the LC exhibited freezing at levels not different from vehicle-treated animals. These results strongly implicate CRF receptors located in the LC region in influencing the display of stress-induced behavior. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. RP SWIERGIEL, AH (reprint author), UNIV WISCONSIN, DEPT PSYCHIAT, 600 HIGHLAND AVE, MADISON, WI 53792 USA. FU NIMH NIH HHS [MH-40855] NR 42 TC 68 Z9 68 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 EI 1872-6240 J9 BRAIN RES JI Brain Res. PD AUG 7 PY 1992 VL 587 IS 2 BP 263 EP 268 DI 10.1016/0006-8993(92)91006-Z PG 6 WC Neurosciences SC Neurosciences & Neurology GA JK435 UT WOS:A1992JK43500012 PM 1326376 ER PT J AU ROSEN, FS AF ROSEN, FS TI ENCYCLOPEDIA OF IMMUNOLOGY - ROITT,IM, DELVES,PJ SO NATURE LA English DT Book Review RP ROSEN, FS (reprint author), CTR BLOOD RES INC,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 U1 1 U2 2 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD AUG 6 PY 1992 VL 358 IS 6386 BP 463 EP 464 DI 10.1038/358463b0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JG739 UT WOS:A1992JG73900036 ER PT J AU HARRIS, JR LIPPMAN, ME VERONESI, U WILLETT, W AF HARRIS, JR LIPPMAN, ME VERONESI, U WILLETT, W TI MEDICAL PROGRESS .2. BREAST-CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID DUCTAL CARCINOMA INSITU; INTRADUCTAL CARCINOMA; LOBULAR CARCINOMA; CONSERVING SURGERY; RADIATION-THERAPY; RANDOMIZED TRIAL; FOLLOW-UP; CONSERVATIVE MANAGEMENT; DEFINITIVE IRRADIATION; PRIMARY CHEMOTHERAPY C1 HARVARD UNIV,SCH MED,CHANNING LAB,DEPT MED,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RADIAT ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. IST NAZL STUDIO & CURA TUMORI,I-20133 MILAN,ITALY. GEORGETOWN UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PHARMACOL,WASHINGTON,DC 20007. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. RP HARRIS, JR (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT ONCOL,50 BINNEY ST,BOSTON,MA 02115, USA. NR 76 TC 178 Z9 181 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 AUG 6 PY 1992 VL 327 IS 6 BP 390 EP 398 DI 10.1056/NEJM199208063270606 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA JG356 UT WOS:A1992JG35600006 PM 1320737 ER PT J AU WEEKS, J AF WEEKS, J TI COST PER LIFE YEAR GAINED FOR SELECTED THERAPIES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material RP WEEKS, J (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD AUG 5 PY 1992 VL 84 IS 15 BP 1141 EP 1141 DI 10.1093/jnci/84.15.1141 PG 1 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700003 ER PT J AU LI, FP GARBER, JE FRIEND, SH STRONG, LC PATENAUDE, AF JUENGST, ET REILLY, PR CORREA, P FRAUMENI, JF AF LI, FP GARBER, JE FRIEND, SH STRONG, LC PATENAUDE, AF JUENGST, ET REILLY, PR CORREA, P FRAUMENI, JF TI RECOMMENDATIONS ON PREDICTIVE TESTING FOR GERM LINE P53 MUTATIONS AMONG CANCER-PRONE INDIVIDUALS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID HUNTINGTON DISEASE; FRAUMENI SYNDROME; BREAST-CANCER; FAMILIES; GENETICS; POLICY; GENES C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,EXECUT PLAZA N,RM 543,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MD ANDERSON CANC CTR,HOUSTON,TX. NATL CTR HUMAN GENOME RES,BETHESDA,MD. SHRIVER CTR MENTAL RETARDAT,WALTHAM,MA. LOUISIANA STATE UNIV,MED CTR,NEW ORLEANS,LA 70112. OI Juengst, Eric/0000-0002-8374-5774 NR 29 TC 121 Z9 121 U1 1 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD AUG 5 PY 1992 VL 84 IS 15 BP 1156 EP 1160 DI 10.1093/jnci/84.15.1156 PG 5 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700012 PM 1635084 ER PT J AU SEARLES, JS ALTERMAN, AI AF SEARLES, JS ALTERMAN, AI TI DIFFERENTIAL ATTRITION RATES IN ALCOHOL ABUSING AND NONABUSING SCHIZOPHRENIC INPATIENTS - A METHODOLOGICAL NOTE SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE SCHIZOPHRENIA; ALCOHOL ABUSE; ATTRITION RATES ID SUBSTANCE ABUSE; MAST AB This study investigates the impact of the screening process on the composition of the final sample of alcohol abusing and nonabusing hospitalized schizophrenics. The group of nonabusing schizophrenics had higher rates of study rejections by staff, refusals, inappropriate subjects, and a lower rate of study completers. The findings suggest that these differential attrition rates may have a significant impact on the interpretation of results of studies focusing on substance use in schizophrenic samples. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNIV PENN,PHILADELPHIA,PA 19104. FU NIDA NIH HHS [DA05186] NR 10 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD AUG PY 1992 VL 16 IS 4 BP 705 EP 707 DI 10.1111/j.1530-0277.1992.tb00665.x PG 3 WC Substance Abuse SC Substance Abuse GA JK612 UT WOS:A1992JK61200010 PM 1530133 ER PT J AU MALATY, H KLEIN, PD GRAHAM, DY AF MALATY, H KLEIN, PD GRAHAM, DY TI CEFPROZIL FOR THE ERADICATION OF HELICOBACTER-PYLORI INFECTION SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Article AB Helicobacter pylori infection has proven to be extraordinarily difficult to eradicate. Antimicrobial monotherapies have been particularly disappointing, with most eradication rates in the range of 0 to 15 %. We evaluated cefprozil (250 mg q.d.s. for 14 days) in 12 H. pylori-infected subjects. The C-13-urea breath test was used to evaluate effectiveness of therapy. Eradication was defined as a negative urea breath test 4 to 6 weeks after the end of treatment. Suppression of H. pylori was demonstrated in 4 of 12 (33 %) by a negative urea breath test two days after start of treatment. H pylori infection was not eradicated in any subject (0 %). Adverse events were intermittent and mild. Cefprozil does not appear to offer promise as monotherapy for the eradication of H. pylori. RP MALATY, H (reprint author), VET AFFAIRS MED CTR 111D,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NIDDK NIH HHS [DK 39919] NR 0 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-2813 J9 ALIMENT PHARM THERAP JI Aliment. Pharmacol. Ther. PD AUG PY 1992 VL 6 IS 4 BP 503 EP 506 PG 4 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA JG838 UT WOS:A1992JG83800012 PM 1420742 ER PT J AU DISLER, DG DELUCA, SA AF DISLER, DG DELUCA, SA TI TRAUMATIC RUPTURE OF THE DIAPHRAGM AND HERNIATION OF THE LIVER SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Injuries that result in a sudden increase in intra-abdominal pressure may cause a diaphragmatic tear and visceral herniation. Right-sided tears are significantly less likely than left-sided tears because of the protective effect of the liver. When diaphragmatic elevation persists in a post-trauma patient, or if unexplained acidosis or hypoxemia develops, herniation of abdominal contents should be suspected. This is particularly true when other signs of severe trauma are present, such as multiple rib fractures, laceration of the liver or spleen, or a history of deceleration injury. RP DISLER, DG (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD AUG PY 1992 VL 46 IS 2 BP 453 EP 456 PG 4 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA JG536 UT WOS:A1992JG53600014 PM 1636561 ER PT J AU SIU, SC NIDORF, SM GALAMBOS, GS WEYMAN, AE PICARD, MH AF SIU, SC NIDORF, SM GALAMBOS, GS WEYMAN, AE PICARD, MH TI THE EFFECT OF LATE PATENCY OF THE INFARCT-RELATED CORONARY-ARTERY ON LEFT-VENTRICULAR MORPHOLOGY AND REGIONAL FUNCTION AFTER THROMBOLYSIS SO AMERICAN HEART JOURNAL LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; TWO-DIMENSIONAL ECHOCARDIOGRAPHY; TISSUE PLASMINOGEN-ACTIVATOR; INTRACORONARY THROMBOLYSIS; REPERFUSION THERAPY; TRIAL; STREPTOKINASE; SURVIVAL; SIZE AB The use of early coronary angiography to assess the benefits of coronary patency on left ventricular size and function fails to account for subsequent reocclusion or spontaneous reperfusion. To investigate the relationship between late vessel patency and changes in left ventricular structure and function after thrombolysis, echocardiography was performed within 48 hours and at 6 to 12 weeks in 30 patients treated with intravenous thrombolysis. Left ventricular endocardial surface area index (ESA(i); cm2/m2) and extent of abnormal wall motion were quantitated in those with a patent (n = 20) and those with an occluded (n = 10) infarct-related artery on coronary angiography performed 8 +/- 6 days after thrombolysis. Mean ESA(i) increased from (53 +/- 7 to 61 +/- 10 cm2/m2; p < 0.02) in the occluded group during the follow-up period but remained unchanged (60 +/- 11 to 62 +/- 11 cm2/m2; p = NS) in the patent group. Mean percentage of abnormal wall motion decreased in the patent group (27 +/- 16% to 18 +/- 16%; p < 0.01), whereas no significant change was noted in the occluded group (20 +/- 13% to 23 +/- 17%; p = NS). Thus coronary patency at days after thrombolysis is associated with both improvement in regional left ventricular function and attentuated left ventricular dilatation. RP SIU, SC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC ULTRASOUND LAB,CARDIAC UNIT,FOUNDERS 8,BOSTON,MA 02114, USA. OI Picard, Michael/0000-0002-9264-3243 NR 21 TC 20 Z9 20 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 AUG PY 1992 VL 124 IS 2 BP 265 EP 272 DI 10.1016/0002-8703(92)90586-K PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JF915 UT WOS:A1992JF91500001 PM 1386181 ER PT J AU WEINRAUCH, LA DELIA, JA GLEASON, RE HAMPTON, LA SMITHOSSMAN, S DESILVA, RA NESTO, RW AF WEINRAUCH, LA DELIA, JA GLEASON, RE HAMPTON, LA SMITHOSSMAN, S DESILVA, RA NESTO, RW TI USEFULNESS OF LEFT-VENTRICULAR SIZE AND FUNCTION IN PREDICTING SURVIVAL IN CHRONIC DIALYSIS PATIENTS WITH DIABETES-MELLITUS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; STAGE RENAL-DISEASE; CONGESTIVE HEART-FAILURE; DILATED CARDIOMYOPATHY; SUDDEN-DEATH; HYPERTROPHY; TRANSPLANTATION; HEMODIALYSIS; ANGIOGRAPHY; ARRHYTHMIAS AB To identify patients at high risk for sudden death, a group of stable patients on maintenance dialysis with diabetes mellitus were studied for up to 135 months to determine if there were clinical, laboratory or echocardiographic predictors of high risk. Eighty-two patients on maintenance dialysis who underwent clinical, laboratory evaluation and echocardiography were enrolled and followed for a mean of 25 months for cardiac and noncardiac complications. Thirty-seven patients with normal wall motion and left ventricular (LV) internal diameter had a mean survival of 35.8 months; 28 patients survived > 12 months. Seven patients with normal LV wall motion and dilated LV cavities had a mean survival of 45.7 months; 7 patients survived > 12 months. Fifteen patients with abnormal LV wall motion and normal internal LV dimensions had a mean survival of 17 months; 7 patients survived > 12 months. Twenty-three patients with both abnormal LV wall motion and dilated LV cavities had a mean survival of 7.8 months; 5 patients survived > 12 months. Although echocardiographic abnormalities predicted cardiac mortality at 6 and 12 months, the combination of an abnormal standard electrocardiogram at baseline, clinical history of angina pectoris, and prior documented myocardial infarction or congestive heart failure did not. When the study group was divided by mode or duration of dialysis, presence or absence of diabetes, or use of cardioactive drugs, echocardiographic LV wall motion abnormalities remained the most important determinant of survival. C1 NEW ENGLAND DEACONESS HOSP,JOSLIN DIABET CTR,DEPT MED,JOHN COOK RENAL UNIT,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. OI Weinrauch, Larry/0000-0003-1357-9528 NR 26 TC 15 Z9 15 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD AUG 1 PY 1992 VL 70 IS 3 BP 300 EP 303 DI 10.1016/0002-9149(92)90608-2 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JE543 UT WOS:A1992JE54300006 PM 1632392 ER PT J AU FILOMENA, CA FILOMENA, AP HUDOCK, J BALLAS, SK AF FILOMENA, CA FILOMENA, AP HUDOCK, J BALLAS, SK TI EVALUATION OF SERUM IMMUNOGLOBULINS BY PROTEIN ELECTROPHORESIS AND RATE NEPHELOMETRY BEFORE AND AFTER THERAPEUTIC PLASMA-EXCHANGE SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE PLASMA EXCHANGE; PLASMAPHERESIS; IMMUNOGLOBULIN; MONOCLONAL GAMMOPATHY; SERUM PROTEIN ELECTROPHORESIS; IMMUNOEPHELOMETRY ID MULTIPLE-SCLEROSIS; PLASMAPHERESIS; NEUROPATHY AB One hundred fourteen pre- and postplasma exchange (PE) serum protein electrophoretograms and serum IgG, IgA, and IgM levels obtained during a 4-month period from 23 patients were evaluated. The interval between PE sessions varied from once daily to approximately once monthly. Typically, post-PE patterns had decreased alpha-1, decreased alpha-2, decreased beta, and decreased gamma fractions. The average percentage decreases of the immunoglobulins subsequent to PE were as follows: IgG, 52%; IgA, 55%; and IgM, 51%. There was a high linear correlation between the pre- and post-PE concentrations of IgG and IgA, whereas correlation of pre- and post-PE IgM concentrations was much lower. All IgG, IgA, and IgM levels (100%) returned to their respective reference intervals before subsequent PE when procedures were scheduled at least 2 weeks apart. When procedures occurred 1 week apart or less, only 1 IgG level (1%) returned to its reference interval, whereas 68 IgA (73%) and 74 IgM levels (80%) returned to their respective reference intervals. During this study, a faint monoclonal band was discovered in each of two patients. One had a normal baseline serum protein electrophoretogram before initiation of PE therapy, and the gammopathy was of uncertain significance. In the other patient, a vertebral plasmacytoma was discovered. It is concluded that PE reduces IgG, IgA, and IgM by approximately the same percentages; however, reference interval levels of IgA and IgM are restored more rapidly than IgG levels. Because monoclonal proteins may be present before or may appear during PE therapy, patients should be monitored by baseline and subsequent periodic serum protein electrophoresis. C1 HARVARD UNIV,BOSTON,MA 02115. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT MED,CARDEZA FDN HEMATOL RES,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT PATHOL & CELL BIOL,PHILADELPHIA,PA 19107. RP FILOMENA, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114, USA. NR 34 TC 3 Z9 3 U1 1 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 AUG PY 1992 VL 98 IS 2 BP 243 EP 248 PG 6 WC Pathology SC Pathology GA JK803 UT WOS:A1992JK80300020 PM 1510038 ER PT J AU TANZI, RE VAULA, G ROMANO, DM MORTILLA, M HUANG, TL TUPLER, RG WASCO, W HYMAN, BT HAINES, JL JENKINS, BJ KALAITSIDAKI, M WARREN, AC MCINNIS, MC ANTONARAKIS, SE KARLINSKY, H PERCY, ME CONNOR, L GROWDON, J CRAPPERMCLACHLAN, DR GUSELLA, JF STGEORGEHYSLOP, PH AF TANZI, RE VAULA, G ROMANO, DM MORTILLA, M HUANG, TL TUPLER, RG WASCO, W HYMAN, BT HAINES, JL JENKINS, BJ KALAITSIDAKI, M WARREN, AC MCINNIS, MC ANTONARAKIS, SE KARLINSKY, H PERCY, ME CONNOR, L GROWDON, J CRAPPERMCLACHLAN, DR GUSELLA, JF STGEORGEHYSLOP, PH TI ASSESSMENT OF AMYLOID BETA-PROTEIN PRECURSOR GENE-MUTATIONS IN A LARGE SET OF FAMILIAL AND SPORADIC ALZHEIMER-DISEASE CASES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID HEREDITARY CEREBRAL-HEMORRHAGE; LINKAGE ANALYSIS; CHROMOSOME-21; DUTCH; CDNA; MARKERS; DEFECT; EXONS; LOCUS AB A genetic locus associated with familial Alzheimer disease (FAD) and a candidate gene, APP, encoding the amyloid protein precursor have both been assigned previously to chromosome 21, and, in a few FAD families, mutations of APP have been detected. However, obligate crossovers between APP and FAD have also been reported in several FAD pedigrees, including FAD4, a large kindred showing highly suggestive evidence for linkage of the disorder to chromosome 21. In case the apparent APP crossover in FAD4 actually represented an intragenic recombination event or segregation of different mutations in different family branches, we have performed a more detailed assessment of APP as a candidate gene in this family. The entire coding region of the APP gene was sequenced for FAD4 and for FAD1, a second large kindred. No mutations were found, indicating that, in at least one chromosome 21-linked FAD pedigree, the gene defect is not accounted for by a mutation in the known coding region of the APP gene. A total of 25 well-characterized early- and late-onset FAD pedigrees were typed for genetic linkage to APP, to assess the percentage of FAD families predicted to carry mutations in the APP gene. None of the FAD families yielded positive lod scores at a recombination fraction of 0.0. To estimate the overall prevalence of FAD-associated mutations in the beta-A4 domain of APP, we sequenced exons 16 and 17 in 30 (20 early- and 10 late-onset) FAD kindreds and in 11 sporadic AD cases, and we screened 56 FAD kindreds and 81 cases of sporadic AD for the presence of the originally reported FAD-associated mutation, APP717 Val --> Ile (by BclI digestion). No APP gene mutations were found in any of the FAD families or sporadic-AD samples examined in this study, suggesting that the mutations in exons 16 and 17 are a rare cause of FAD. Overall, these data suggest that APP gene mutations account for a very small portion of FAD. C1 MASSACHUSETTS GEN HOSP, DEPT NEUROL, MOLEC NEUROGENET LAB, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, PROGRAM NEUROSCI, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT GENET, BOSTON, MA 02115 USA. UNIV TORONTO, DEPT MED, TORONTO M5S 1A1, ONTARIO, CANADA. UNIV TORONTO, DEPT NEUROL, TORONTO M5S 1A1, ONTARIO, CANADA. UNIV TORONTO, DEPT PSYCHIAT, TORONTO M5S 1A1, ONTARIO, CANADA. UNIV TORONTO, SURREY PL CTR OBSTET & GYNECOL, TORONTO M5S 1A1, ONTARIO, CANADA. JOHNS HOPKINS UNIV, SCH MED, CTR MED GENET, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT PSYCHIAT, BALTIMORE, MD 21205 USA. RI Haines, Jonathan/C-3374-2012; Tupler, Rossella/C-9500-2015; Antonarakis, Stylianos/N-8866-2014 OI Tupler, Rossella/0000-0002-3797-1789; Antonarakis, Stylianos/0000-0001-8907-5823 FU NHGRI NIH HHS [HG00317]; NIA NIH HHS [AG08487]; NINDS NIH HHS [NS30428] NR 42 TC 167 Z9 170 U1 1 U2 8 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 AUG PY 1992 VL 51 IS 2 BP 273 EP 282 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA JF776 UT WOS:A1992JF77600006 PM 1642228 ER PT J AU KASINATH, BS FRIED, TA DAVALATH, S MARSDEN, PA AF KASINATH, BS FRIED, TA DAVALATH, S MARSDEN, PA TI GLOMERULAR EPITHELIAL-CELLS SYNTHESIZE ENDOTHELIN PEPTIDES SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID MESANGIAL CELLS; RAT; LOCALIZATION; EXPRESSION AB Glomerular mesangial and endothelial cells have been reported to synthesize and secrete endothelin-1 (ET-1). Whether glomerular epithelial cells (GEC) have the ability to synthesize ET-peptides is not known. Employing immunocytochemistry we report that the GEC in vitro constitutively express ET-1 and ET-3. ET-1 synthesis by the GEC was further confirmed by detection of a specific 2.3kb mRNA that hybridizes with rat prepro ET-1 genomic DNA on Northern blot analysis. ET-1 is secreted into the medium in a time-dependent manner as measured by radioimmunoassay and radiobinding assay. Synthesis of endothelin peptides by the GEC may have important implications in the pathogenesis of glomerular diseases where GEC injury figures prominently. C1 ST MICHAELS HOSP,DEPT MED,TORONTO M5B 1W8,ONTARIO,CANADA. UNIV TORONTO,DEPT MED,TORONTO M5S 1A1,ONTARIO,CANADA. RP KASINATH, BS (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET ADM HOSP,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. RI Marsden, Philip/B-1441-2012 FU PHS HHS [R01-41517] NR 14 TC 59 Z9 59 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 AUG PY 1992 VL 141 IS 2 BP 279 EP 283 PG 5 WC Pathology SC Pathology GA JH625 UT WOS:A1992JH62500002 PM 1497086 ER PT J AU ELLIS, B SCHNEEBERGER, EE RABITO, CA AF ELLIS, B SCHNEEBERGER, EE RABITO, CA TI CELLULAR VARIABILITY IN THE DEVELOPMENT OF TIGHT JUNCTIONS AFTER ACTIVATION OF PROTEIN-KINASE-C SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE EPITHELIAL MEMBRANE; LLC-PK1 CELLS; MADIN-DARBY CANINE KIDNEY CELLS; PHORBOL ESTER; ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE ID PROXIMAL TUBULAR CELLS; TUMOR PROMOTERS; PHORBOL ESTERS; EPITHELIAL MEMBRANE; OCCLUDING JUNCTIONS; PERMEABILITY; LLC-PK1; LINE; DIACYLGLYCEROLS; ORGANIZATION AB Phorbol 12-myristate 13-acetate (PMA) decreases the tight junction conductance (TJC) during the reorganization of LLC-PK1A monolayers, but has the opposite effect in LLC-PK1B4, MDCK, and MDCK4 cells. Because no protein synthesis was required for the effects of PMA on the TJC of LLC-PK1A monolayers, we conclude that the regulation of the tight junction by protein kinase C (PKC) is a posttranslational event. In LLC-PK1A monolayers with existing tight junctions, PMA produced an initial increase in the TJC that reverted later to control values despite the continuous presence of PMA and cycloheximide. The inhibitory effect of PMA on the other cell lines was not revertible. A downregulation of total PKC activity and phorbol ester receptors was only observed during the reorganization of LLC-PK1A monolayers. PMA further increases this downregulation. This indicates that the peculiar response to PMA observed in LLC-PK1A monolayers is the result of two concurrent events: 1) the early activation of the enzyme just before the reorganization of the tight junctions begin, and 2) its late downregulation induced after prolonged exposure to phorbol esters. We conclude that PKC regulates the development of the occluding junctions, but through different mechanisms dependent on the characteristics of the cells. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-25822]; NIDDK NIH HHS [DK-27401] NR 34 TC 45 Z9 45 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 AUG PY 1992 VL 263 IS 2 BP F293 EP F300 PN 2 PG 8 WC Physiology SC Physiology GA JJ960 UT WOS:A1992JJ96000094 PM 1324609 ER PT J AU HUTCHISON, FN WEBSTER, SK AF HUTCHISON, FN WEBSTER, SK TI EFFECT OF ANG-II RECEPTOR ANTAGONIST ON ALBUMINURIA AND RENAL-FUNCTION IN PASSIVE HEYMANN NEPHRITIS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PROTEINURIA; NEPHROTIC SYNDROME; KALLIKREIN; CONVERTING ENZYME; DUP-753; LOSARTAN ID ANGIOTENSIN-CONVERTING-ENZYME; KALLIKREIN-KININ SYSTEM; DIETARY-PROTEIN; NEPHROTIC SYNDROME; RAT-KIDNEY; INHIBITION; CAPTOPRIL; RABBIT; MICROPUNCTURE; FILTRATION AB Angio-tensin-converting enzyme inhibitors reduce albuminuria in nephrotic subjects, but the hormonal mechanism of this effect is not known. To determine whether specific inhibition of angio-tensin (ANG) II activity would decrease albuminuria as occurs after converting enzyme inhibition, rats with passive Heymann nephritis received enalapril or the ANG II receptor antagonist losartan (6 mg.kg-1.day-1) for 4 days. Enalapril reduced both albuminuria (from 583 +/- 53 to 286 +/- 55 mg/day, P < 0.001) and the fractional clearance of albumin (FC(Alb)) each day after starting treatment but did not affect glomerular filtration rate (GFR). Losartan reduced albuminuria significantly only after 4 days of treatment, but this value was not different from controls. GFR significantly increased with losartan (from 1.24 +/-0.09 to 1.73 +/- 0.21 ml/min, P < 0.05) so that FC(Alb) was reduced (from 0.0134 +/- 0.0027 to 0.0080 +/- 0.0018, P < 0.05). Blood pressure decreased only in the enalapril group. Although plasma renin activity increased and the pressor response to ANG I was inhibited by both enalapril and losartan, suggesting effective peripheral blockade of ANG II activity, a third group of nephrotic rats was treated with losartan (18 mg.kg-1.day-1) to ensure that adequate ANG II blockade was achieved. Blood pressure decreased 10 mmHg, GFR increased from 1.35 +/- 0.14 to 1.79 +/- 0.12 ml/min (P < 0.01), but albuminuria and FC(Alb) did not change. Urinary total kallikrein excretion was increased only in nephrotic rats treated with enalapril. Although both enalapril and losartan reduce ANG II activity, only the converting enzyme inhibitor reduces albuminuria. These differences in effect on blood pressure, albuminuria, GFR, and urinary kallikrein excretion suggest that the beneficial effect of enalapril on albuminuria may not be due to inhibition of ANG II activity. C1 MED UNIV S CAROLINA,DIV NEPHROL,CHARLESTON,SC 29425. RP HUTCHISON, FN (reprint author), RALPH H JOHNSON VET AFFAIRS MED CTR,MED SERV,109 BEE ST,CHARLESTON,SC 29403, USA. FU NIDDK NIH HHS [DK-43186] NR 35 TC 36 Z9 36 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 AUG PY 1992 VL 263 IS 2 BP F311 EP F318 PN 2 PG 8 WC Physiology SC Physiology GA JJ960 UT WOS:A1992JJ96000096 PM 1510124 ER PT J AU TASDEMIROGLU, E MACFARLANE, R WEI, EP KONTOS, HA MOSKOWITZ, MA AF TASDEMIROGLU, E MACFARLANE, R WEI, EP KONTOS, HA MOSKOWITZ, MA TI PIAL VESSEL CALIBER AND CEREBRAL BLOOD-FLOW BECOME DISSOCIATED DURING ISCHEMIA-REPERFUSION IN CATS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GLOBAL CEREBRAL ISCHEMIA; HYPEREMIA; HYPOPERFUSION; VASCULAR RESISTANCE ID FOREBRAIN ISCHEMIA; PROLONGED ISCHEMIA; BRAIN; HYPEREMIA; CIRCULATION; METABOLISM; RADICALS; INJURY AB The relationship between pial arteriolar caliber and cerebral blood flow (CBF) was examined in 11 cats subjected to reperfusion for up to 120 min after 10 min of global cerebral ischemia induced by four-vessel occlusion and systemic hypotension. Thirty minutes after reperfusion CBF, as assessed by radiolabeled microsphere injection, had increased to 588% of control in middle cerebral artery (MSEC) cortical gray matter territory. The caliber of MSEC pial arterioles measured using the closed cranial window technique (>33 to <213-mu-m) increased to 172% of baseline. By 60 min of reperfusion, CBF was 76% of basal levels, but pial arterioles remained 133% of baseline. After 120 min, CBF approximated baseline values, but pial dilatation persisted (115% of control). Intracranial pressure measurements did not differ significantly from resting values. At 45 min and beyond, total cerebrovascular resistance did not differ from resting values. The coexistence of vasodilatation within pial arterioles and normal blood flow in cortical gray matter indicates that pial vessels (>33-mu-m) cannot be responsible for normal blood flow restoration following postocclusive hyperemia. Resistance during the posthyperemic phase must be increased selectively within parenchymal vessels to account for normal total cerebrovascular resistance, pial vessel dilatation, and normal-low parenchymal blood flow. Whether obstruction rather than vasoconstriction explains the resistance changes within intraparenchymal vessels remains for further study. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,STROKE RES LAB,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,BOSTON,MA 02114. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,DIV CARDIOL,RICHMOND,VA 23298. FU NINDS NIH HHS [NS-21558, NS-26361] NR 24 TC 28 Z9 28 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 AUG PY 1992 VL 263 IS 2 BP H533 EP H536 PN 2 PG 4 WC Physiology SC Physiology GA JJ960 UT WOS:A1992JJ96000031 PM 1510151 ER PT J AU ROLLINS, BJ AF ROLLINS, BJ TI OH, NO NOT ANOTHER CYTOKINE - MCP-1 AND RESPIRATORY-DISEASE SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Editorial Material ID PROTEIN-1; FAMILY; CELLS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROLLINS, BJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,44 BINNEY ST,BOSTON,MA 02115, USA. NR 7 TC 17 Z9 17 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD AUG PY 1992 VL 7 IS 2 BP 126 EP 127 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA KJ464 UT WOS:A1992KJ46400003 PM 1497901 ER PT J AU BROWN, JH CHEW, FS AF BROWN, JH CHEW, FS TI INVERTED PAPILLOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID SINUSES; NOSE C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 4 TC 4 Z9 4 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 AUG PY 1992 VL 159 IS 2 BP 278 EP 278 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JE567 UT WOS:A1992JE56700007 PM 1632339 ER PT J AU XU, XP CHRISTIANI, DC DOCKERY, DW WANG, LH AF XU, XP CHRISTIANI, DC DOCKERY, DW WANG, LH TI EXPOSURE-RESPONSE RELATIONSHIPS BETWEEN OCCUPATIONAL EXPOSURES AND CHRONIC RESPIRATORY ILLNESS - A COMMUNITY-BASED STUDY SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID COTTON TEXTILE WORKERS; GENERAL-POPULATION; SYMPTOMS; DISEASE AB Data from a random sample of 3,606 adults 40 to 69 yr of age residing in Beijing, China, were analyzed to investigate the association of reported occupational exposures to dusts and gases/fumes with the prevalence of chronic respiratory symptoms and level of pulmonary function. The prevalence of occupational dust exposure was 32%, and gas or fume exposure, 19%. After we adjusted for age, sex, area of residence, smoking status, coal stove heating, and education, an increased prevalence of chronic phlegm and breathlessness was significantly related to both types of exposures. Chronic cough was significantly related only to dust exposure, and persistent wheeze only to fume exposure. The global estimates of the relative odds of the four symptoms were 1.30 (95% CI [confidence interval] 1.09 to 1.48) and 1.27 (95% CI 1.09 to 1.48), respectively, for dusts and for gases/fumes. These two occupational exposures are associated with chronic respiratory symptoms independent of smoking, gender, and each other. There was an increasing prevalence of each symptom with increasing dust and fume exposure, represented by the index of cumulative exposure duration and exposure intensity. Linear trends for increased prevalence of chronic bronchitis and breathlessness were significant for both exposures, while the linear trend for wheeze was only significant for gases/fumes. Among subjects who did not report using coal stove heating, dust exposure was a significant predictor for FEV1, FEV1/FVC, FEF25-75, and peak expiratory flow rate (PEFR). There was also a significant decrease for FEV1 and FVC with increase of gas/fume exposure levels. Both current and former smokers appeared to be more susceptible to the effect of dusts than the never smokers. There was a significant interaction between smoking and dust exposure on FEV1/FVC and PEFR. In addition, dust exposure appears to interact with gases/fumes to reduce PEFR. These results from a Chinese population add to the body of evidence suggesting that nonspecific occupational dust and fume exposure is a risk for the development of chronic obstructive pulmonary disease. C1 BEIJING MED UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,BEIJING,PEOPLES R CHINA. MASSACHUSETTS GEN HOSP,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,DEPT ENVIRONM HLTH,BOSTON,MA 02115. RP XU, XP (reprint author), HARVARD UNIV,SCH PUBL HLTH,ENVIRONM EPIDEMIOL PROGRAM,655 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 22 TC 67 Z9 70 U1 0 U2 2 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD AUG PY 1992 VL 146 IS 2 BP 413 EP 418 PG 6 WC Respiratory System SC Respiratory System GA JP348 UT WOS:A1992JP34800025 PM 1489133 ER PT J AU ECKHARDT, WF PATAFIO, O CIGARROA, F AF ECKHARDT, WF PATAFIO, O CIGARROA, F TI PLUG IT IN - REPLY SO ANESTHESIA AND ANALGESIA LA English DT Letter RP ECKHARDT, WF (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD AUG PY 1992 VL 75 IS 2 BP 310 EP 310 DI 10.1213/00000539-199208000-00041 PG 1 WC Anesthesiology SC Anesthesiology GA JE573 UT WOS:A1992JE57300041 ER PT J AU MAROTA, JJA CROSBY, G UHL, GR AF MAROTA, JJA CROSBY, G UHL, GR TI SELECTIVE EFFECTS OF PENTOBARBITAL AND HALOTHANE ON C-FOS AND JUN-B GENE-EXPRESSION IN RAT-BRAIN SO ANESTHESIOLOGY LA English DT Article DE ANESTHESIA, GENERAL; ANESTHETICS, INTRAVENOUS, PENTOBARBITAL; ANESTHETICS, VOLATILE, HALOTHANE; BRAIN, METABOLISM; CELLS, METABOLISM; GENETIC FACTORS, C-FOS; JUN-B; PROTOONCOGENES; METABOLISM, DEOXYRIBONUCLEIC ACID; RIBONUCLEIC ACID ID IMMEDIATE EARLY GENES; SPINAL-CORD; NOXIOUS-STIMULATION; NERVOUS-SYSTEM; MESSENGER-RNA; PROTEIN; NEURONS; INDUCTION; PAIN; IMMUNOREACTIVITY AB The effects of pentobarbital and halothane anesthesia on the expression in brain of the immediate-early genes c-fos and jun-B were investigated. Pentobarbital-anesthetized rats (n = 10) received a single intraperitoneal injection of pentobarbital 65 mg/kg in a vehicle of 40% propylene glycol and 10% ethanol and then were placed in a plexiglass box flushed continuously with 100% oxygen at 5 l/min. Halothane-anesthetized rats (n = 10) received an intraperitoneal injection of vehicle only and were transferred to a box flushed continuously with oxygen plus 1.5% halothane. Unanesthetized control rats (n = 10) received an intraperitoneal injection of vehicle and were placed in a box flushed continuously with 100% oxygen. Four additional rats received no intraperitoneal injection but were handled and otherwise treated identically to the control group, and six others had a femoral arterial catheter inserted for blood pressure and blood gas measurements. Five animals from the control and both anesthetized groups were killed at 30 and 120 min postinjection and their brains rapidly removed and frozen. The messenger ribonucleic acid transcription products of the genes c-fos, jun-B, and beta-actin from whole cerebral hemispheres were analyzed autoradiographically after Northern blot hybridization with P-32-labeled deoxyribonucleic acid probes. Relative levels of c-fos and jun-B messenger ribonucleic acid were determined from optical density measurements of the autoradiographic bands, with beta-actin measurements being used to correct for sample-to-sample variation. Rats became immobile within minutes of drug administration and remained anesthetized until they were killed. The anesthetics had little effect on mean arterial blood pressure, rectal temperature, and Pa(O2); however, pentobarbital-anesthetized rats were hypercarbic at both 30 and 120 min. Because halothane also produced hypercarbia at 120 min, there were no physiologic differences between anesthetics at this later point. Handling of rats did not change c-fos or jun-B expression. Intraperitoneal injection produced a 2- to 3-fold increase i n the whole brain levels of c-fos and jun-B messenger ribonucleic acid (P < 0.01 for all comparisons) at 30 min versus 120 min. Neither anesthetic modified this increase in c-fos and jun-B expression at 30 min postinjection. At 120 min postinjection, selective anesthetic effects were apparent. Jun-B expression was 25% greater than that of control in pentobarbital-anesthetized rats (P < 0.05) and 38% lower in halothane-anesthetized rats (P < 0.01), but neither anesthetic affected c-fos expression. Because immediate-early genes are thought to play a pivotal role in neural mechanisms of stress, memory, and pain/analgesia, anesthetic-induced changes in jun-B expression may pertain to modifications that occur in these biological processes during the anesthetic state. In a broader sense, these data indicate that general anesthetics selectively alter expression of genes in the central nervous system. C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL LAB,BALTIMORE,MD. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. FU NIGMS NIH HHS [R01-GM 42466] NR 37 TC 38 Z9 40 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD AUG PY 1992 VL 77 IS 2 BP 365 EP 371 DI 10.1097/00000542-199208000-00021 PG 7 WC Anesthesiology SC Anesthesiology GA JG533 UT WOS:A1992JG53300021 PM 1642355 ER PT J AU SETHNA, NF SOCKIN, SM HOLZMAN, RS SLATER, JE AF SETHNA, NF SOCKIN, SM HOLZMAN, RS SLATER, JE TI LATEX ANAPHYLAXIS IN A CHILD WITH A HISTORY OF MULTIPLE ANESTHETIC DRUG ALLERGIES SO ANESTHESIOLOGY LA English DT Note DE ALLERGY, LATEX; ANESTHESIA, PEDIATRIC; BIRTH DEFECTS, MYELOMENINGOCELE ID INTRAOPERATIVE ANAPHYLAXIS; MUSCLE-RELAXANTS; SPINA-BIFIDA; RUBBER; HYPERSENSITIVITY; SENSITIVITY; CONTACT; SURGERY; GLOVES; IGE C1 MASSACHUSETTS GEN HOSP,CLIN IMMUNOL & ALLERGY UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. CHILDRENS HOSP,NATL MED CTR,DEPT ALLERGY & IMMUNOL,WASHINGTON,DC 20010. GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,WASHINGTON,DC 20052. RP SETHNA, NF (reprint author), CHILDRENS HOSP MED CTR,DEPT ANESTHESIA,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 24 TC 16 Z9 16 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD AUG PY 1992 VL 77 IS 2 BP 372 EP 375 DI 10.1097/00000542-199208000-00022 PG 4 WC Anesthesiology SC Anesthesiology GA JG533 UT WOS:A1992JG53300022 PM 1642356 ER PT J AU DENMAN, WT GOUDSOUZIAN, NG AF DENMAN, WT GOUDSOUZIAN, NG TI POSITION OF THE LARYNGEAL MASK AIRWAY SO ANESTHESIOLOGY LA English DT Letter RP DENMAN, WT (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD AUG PY 1992 VL 77 IS 2 BP 401 EP 402 DI 10.1097/00000542-199208000-00042 PG 2 WC Anesthesiology SC Anesthesiology GA JG533 UT WOS:A1992JG53300042 PM 1642371 ER PT J AU FAMULOK, M SZOSTAK, JW AF FAMULOK, M SZOSTAK, JW TI INVITRO SELECTION OF SPECIFIC LIGAND-BINDING NUCLEIC-ACIDS SO ANGEWANDTE CHEMIE-INTERNATIONAL EDITION IN ENGLISH LA English DT Article ID RANDOM-SEQUENCE OLIGONUCLEOTIDES; BACTERIOPHAGE-T4 DNA-POLYMERASE; COMPLEMENTARY-STRAND RNA; REV TRANS-ACTIVATOR; VIRAL MESSENGER-RNA; SELF-SPLICING RNA; GROUP-I INTRONS; INTERVENING SEQUENCE; TARGET SEQUENCE; GENE-PRODUCT AB In vitro selection is a method that allows the simultaneous screening of very large numbers of nucleic acid molecules for a wide range of properties from binding characteristics to catalytic properties; moreover, the isolation of the very rare functional molecules becomes possible. Binding sites between proteins and nucleic acids, for example, have been evaluated by this methodology in order to gain information about protein/nucleic acid interactions. Structure and function of catalytic RNA ("ribozymes") has been studied by in vitro selection and has led to new ribozymes with improved catalytic function. Substrate specificity of catalytic RNA has been changed and has led to a ribozyme that cleaves DNA. Other applications include the isolation of nucleic acids that bind specifically to small organic molecules and of RNA molecules that form triple helices with double-stranded DNA. In this article we discuss the background, design, and results of in vitro genetic experiments, which bridge biochemical/molecular biological and organic chemical approaches to molecular recognition. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP FAMULOK, M (reprint author), UNIV MUNICH,MAX PLANCK INST BIOCHEM,INST BIOCHEM,KLOPFERSPITZ 18A,W-8033 MARTINSRIED,GERMANY. NR 94 TC 63 Z9 63 U1 3 U2 9 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0570-0833 J9 ANGEW CHEM INT EDIT JI Angew. Chem.-Int. Edit. Engl. PD AUG PY 1992 VL 31 IS 8 BP 979 EP 988 DI 10.1002/anie.199209791 PG 10 WC Chemistry, Multidisciplinary SC Chemistry GA JP340 UT WOS:A1992JP34000003 ER PT J AU ACKERMAN, RH AF ACKERMAN, RH TI HAMMOND,GRAEME,M. AND THE ANA SO ANNALS OF NEUROLOGY LA English DT Item About an Individual C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. RP ACKERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 TC 3 Z9 3 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 AUG PY 1992 VL 32 IS 2 BP 224 EP 224 DI 10.1002/ana.410320217 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA JH162 UT WOS:A1992JH16200016 PM 1510363 ER PT J AU RAUCH, SD SANMARTIN, J MOSCICKI, RA AF RAUCH, SD SANMARTIN, J MOSCICKI, RA TI BOVINE TEMPORAL BONES AS A SOURCE OF INNER-EAR ANTIGEN SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE BOVINE ANIMAL MODEL; IMMUNOLOGY; INNER EAR; TEMPORAL BONE ID SENSORINEURAL HEARING-LOSS AB Modern immunologic techniques of immunostaining, immunoblotting, and creation of monoclonal antibodies are gaining wide application in studies of development, function, and pathology of the ear. These techniques require a source of inner ear tissue for production of antigen extract. Human tissue is not readily available, and other mammalian species common in auditory research are small in size. Bovine temporal bones are readily available. and the membranous portions of the inner ear are abundant and easily accessible. Herein we report our technique for acquisition and dissection of bovine temporal bones and preparation and preservation of inner ear antigen. RP RAUCH, SD (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 4 TC 6 Z9 6 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 AUG PY 1992 VL 101 IS 8 BP 688 EP 690 PG 3 WC Otorhinolaryngology SC Otorhinolaryngology GA JH737 UT WOS:A1992JH73700012 PM 1497277 ER PT J AU ROGGO, A OTTINGER, LW AF ROGGO, A OTTINGER, LW TI ACUTE SMALL-BOWEL VOLVULUS IN ADULTS - A SPORADIC FORM OF STRANGULATING INTESTINAL-OBSTRUCTION SO ANNALS OF SURGERY LA English DT Article ID CT DIAGNOSIS; MANAGEMENT AB Small bowel volvulus is an uncommon but important cause of small intestinal obstruction. It often results in ischemia or even infarction. Delay in diagnosis and surgical intervention increases morbidity and mortality rates. Based on cause, small bowel volvulus can be divided into primary and secondary type. Goals for treatment of small bowel volvulus should include physician awareness of this uncommon diagnosis, accurate workup, and advanced surgical intervention. The presentation and subsequent management of 35 patients with small bowel volvulus confirmed by laparotomy are reviewed and discussed. The incidence of small bowel volvulus in the adult European and North American is low. The resultant mortality rate, however, makes diagnosis critically important. The cardinal presenting symptom is abdominal pain. There is no single specific diagnostic clinical sign or abnormality in laboratory or radiologic finding. In practice, the diagnosis can only be made by laparotomy. The failure to perform an exploratory laparotomy cannot be justified. Early diagnosis and early surgery are the keys for successful management of strangulation obstruction of the small bowel. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN SURG SERV,ACC BLDG,4TH FLOOR,BOSTON,MA 02114. NR 43 TC 41 Z9 41 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 AUG PY 1992 VL 216 IS 2 BP 135 EP 141 DI 10.1097/00000658-199208000-00003 PG 7 WC Surgery SC Surgery GA JJ945 UT WOS:A1992JJ94500003 PM 1503517 ER PT J AU PERKINS, BA HAMILL, RJ MUSHER, DM OHARA, C AF PERKINS, BA HAMILL, RJ MUSHER, DM OHARA, C TI INVITRO ACTIVITIES OF STREPTOMYCIN AND 11 ORAL ANTIMICROBIAL AGENTS AGAINST CLINICAL ISOLATES OF KLEBSIELLA-RHINOSCLEROMATIS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note AB We tested in vitro the activities of streptomycin and tetracycline-antibiotics that have long been used to treat rhinoscleroma-as well as several newer oral agents by using 23 isolates of the causative organism Klebsiella rhinoscleromatis. All isolates were inhibited by clinically achievable concentrations of trimethoprim-sulfamethoxazole, amoxicillin-clavulanate, chloramphenicol, ciprofloxacin, cephalexin, cefuroxime, and cefpodoxime. C1 DEPT VET AFFAIRS MED CTR,MED SERV,INFECT DIS SECT,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,HOUSTON,TX 77030. CTR DIS CONTROL,NATL CTR INFECT DIS,HOSP INFECT PROGRAM,ANTIMICROB INVEST LAB,ATLANTA,GA 30333. NR 20 TC 16 Z9 19 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 AUG PY 1992 VL 36 IS 8 BP 1785 EP 1787 PG 3 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA JG147 UT WOS:A1992JG14700037 PM 1416867 ER PT J AU KOCH, JA RUPRECHT, RM AF KOCH, JA RUPRECHT, RM TI ANIMAL-MODELS FOR ANTI-AIDS THERAPY SO ANTIVIRAL RESEARCH LA English DT Review DE ANIMAL MODEL; ANTIVIRAL THERAPY; ANTI-AIDS THERAPY; DRUG DEVELOPMENT; TRANSGENIC MOUSE; CHIMERIC MOUSE ID HUMAN-IMMUNODEFICIENCY-VIRUS; LONG TERMINAL REPEAT; SCID-HU MOUSE; INFECTIOUS-ANEMIA VIRUS; PLACEBO-CONTROLLED TRIAL; MOLONEY LEUKEMIA-VIRUS; FOCUS-FORMING VIRUS; TRANSGENIC MICE; ANTIRETROVIRAL THERAPY; MOLECULAR-CLONING AB Primate and non-primate species have been used to study the pathobiology of the simian immunodeficiency virus (SIV) and of the human immunodeficiency virus type 1 (HIV-1), respectively, and to develop new therapeutic regimes. Transgenic mice which express either the entire HIV-1 provirus or subgenomic fragments have been used to analyze viral gene products in vivo and may serve as models for the development of agents targeted to select viral functions. Chimeric mice which were created by transplanting human hematolymphoid cells into mice suffering from congenital severe combined immunodeficiency (scid/scid or so called SCID mice), can be infected with HIV-1 and allow one to study the entire HIV-1 replicative cycle. Type C murine leukemia virus models have been used to develop new prophylactic and therapeutic strategies but their use is restricted to the evaluation of select antiviral drug inhibition, targeted to retroviral genes common to both Lentivirinae and Oncovirinae. The role of various animal model systems in the development of anti-HIV-1 and anti-AIDS therapies is summarized. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 151 TC 11 Z9 11 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD AUG PY 1992 VL 19 IS 2 BP 81 EP 109 DI 10.1016/0166-3542(92)90069-H PG 29 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA JP392 UT WOS:A1992JP39200001 PM 1444326 ER PT J AU XU, SH ROYCHOWDHURY, S GASKIN, F EPSTEIN, DL AF XU, SH ROYCHOWDHURY, S GASKIN, F EPSTEIN, DL TI ETHACRYNIC-ACID INHIBITION OF MICROTUBULE ASSEMBLY INVITRO SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID 2-(4-METHYL-1-PIPERAZINYLMETHYL) ACRYLOPHENONE DIHYDROCHLORIDE; TUBULIN; NEUROTUBULES; ABSENCE C1 UNIV VIRGINIA,HLTH SCI CTR,SCH MED,DEPT BEHAV MED & PSYCHIAT,BOX 203,CHARLOTTESVILLE,VA 22908. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NINDS NIH HHS [NS24489] NR 18 TC 16 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD AUG 1 PY 1992 VL 296 IS 2 BP 462 EP 467 DI 10.1016/0003-9861(92)90598-Q PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JD476 UT WOS:A1992JD47600014 PM 1352959 ER PT J AU DENKER, PS POLLOCK, VE AF DENKER, PS POLLOCK, VE TI FASTING SERUM-INSULIN LEVELS IN ESSENTIAL-HYPERTENSION - A METAANALYSIS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID STIMULATED-GLUCOSE-UPTAKE; BLOOD-PRESSURE; RESISTANCE; HYPERINSULINEMIA; METABOLISM; OBESE; INTOLERANCE; ETIOLOGY; SODIUM AB Background.-The role of insulin in the genesis of essential hypertension remains an area of intense controversy. Most clinical evidence suggests a definite association. Several pathophysiologic mechanisms have been proposed. However, current data remain disparate and contradictory. Methods.-Meta-analysis allows data pooling of primary study findings and subsequent integration into a statistically meaningful outcome. This method was used to study the relationship in euglycemic individuals between blood pressure and fasting serum insulin level, age, body mass index, and fasting plasma glucose level. Results.-A significant correlation was demonstrated between fasting serum insulin concentration and both systolic blood pressure and diastolic blood pressure. Age and body mass index also revealed meaningful associations. The meta-analytic correlation between plasma glucose level and both systolic blood pressure and diastolic blood pressure failed to achieve significance. Conclusions.-Data from a meta-analytic review examining fasting serum insulin levels in euglycemic individuals demonstrate a significant correlation with systolic and diastolic blood pressure. This study supports the role of hyperinsulinemia in the pathogenesis of essential hypertension. C1 JOSLIN DIABET CLIN,CLEARWATER,FL. UNIV S FLORIDA,DEPT INTERNAL MED,DIV ENDOCRINOL & METAB,TAMPA,FL 33620. UNIV SO CALIF,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90033. NR 27 TC 108 Z9 111 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD AUG PY 1992 VL 152 IS 8 BP 1649 EP 1651 DI 10.1001/archinte.152.8.1649 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JH363 UT WOS:A1992JH36300013 PM 1386725 ER PT J AU SAORNIL, MA EGAN, KM GRAGOUDAS, ES SEDDON, JM WALSH, SM ALBERT, DM AF SAORNIL, MA EGAN, KM GRAGOUDAS, ES SEDDON, JM WALSH, SM ALBERT, DM TI HISTOPATHOLOGY OF PROTON BEAM-IRRADIATED VS ENUCLEATED UVEAL MELANOMAS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID HELIUM ION THERAPY; MALIGNANT-MELANOMA; CHOROIDAL MELANOMA; CILIARY BODY; RADIATION-THERAPY; VASCULAR CHANGES; COMPLICATIONS; NECROSIS AB The histopathology of eyes with uveal melanoma was compared in a masked fashion in 47 eyes whose primary treatment was enucleation and a matched series of 47 eyes enucleated after proton beam irradiation. Irradiated tumors were more likely to show signs of necrosis (P<.001) and fibrosis (P=.005) and to have balloon cells present (P=.002). In the irradiated group, mitotic figures were fewer in 40 high-power fields (P=.020), and the prevalence of tumor blood vessel damage (P<.001) was higher. Changes in the retina were more common in the irradiated series, but damage was usually overlying or in close proximity to the tumor. Based on characteristic changes, the pathologist distinguished irradiated from nonirradiated eyes in 85% of the cases. These findings suggest that irradiation damages tumor cells and blood vessels, and alters the tumor's capacity for cellular reproduction. C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA UNIT,243 CHARLES ST,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,EYE PATHOL LAB,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,EPIDEMIOL UNIT,BOSTON,MA 02114. NR 36 TC 28 Z9 28 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 AUG PY 1992 VL 110 IS 8 BP 1112 EP 1118 PG 7 WC Ophthalmology SC Ophthalmology GA JH496 UT WOS:A1992JH49600025 PM 1323252 ER PT J AU ADCOCK, DM MARLAR, RA AF ADCOCK, DM MARLAR, RA TI ACTIVATED PARTIAL THROMBOPLASTIN TIME REAGENT SENSITIVITY TO THE PRESENCE OF THE LUPUS ANTICOAGULANT SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article AB The lupus anticoagulant (LA) is an acquired abnormality that is associated with a prolonged activated partial thromboplastin time (aPTT). It is one of the most frequent coagulation abnormalities seen in the routine clinical laboratory. The sensitivity of various commercial aPTT reagents varies in their ability to detect the LA. We undertook this evaluation by using a single coagulation instrument to determine the sensitivity of five different commercial aPTT reagents to the presence of the LA. We evaluated 23 patients with known LA using five different reagents, two of which were marketed as having enhanced LA sensitivity. All samples and testing were performed under the same conditions in a timely manner. Based on these data, essentially all of the commercial reagents that were tested could detect patients with known LA by at least minimally prolonging the aPTT. Some reagents were slightly better than others in their ability to detect the LA. For most hospitals, the detection of the LA is not the highest priority for the use of the aPTT assay. In most cases, heparin anticoagulation monitoring is the most common use of the aPTT assay. Since all five reagents are sensitive to the LA, then the best overall reagent will be the one with the best sensitivity to the most important need for the laboratory (usually heparin monitoring). Therefore, a reagent should be chosen based on the primary monitoring requirements of the aPTT assay, and greater than 90% of the patients with the LA will be detected. C1 DENVER VET AFFAIRS MED CTR,LAB SERV 113,1055 CLERMONT AVE,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DEPT PEDIAT,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT PATHOL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT BIOCHEM,DENVER,CO 80262. NR 17 TC 20 Z9 20 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 AUG PY 1992 VL 116 IS 8 BP 837 EP 840 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA JG534 UT WOS:A1992JG53400014 PM 1497465 ER PT J AU THORNBY, MA KREBS, DE AF THORNBY, MA KREBS, DE TI BIMANUAL SKILL DEVELOPMENT IN PEDIATRIC BELOW-ELBOW AMPUTATION - A MULTICENTER, CROSS-SECTIONAL STUDY SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article DE ACTIVITIES OF DAILY LIVING; AMPUTEE; DEVELOPMENTAL DELAY; PROSTHESIS ID CHILD AB The purpose of this study was to investigate the following in children with unilateral below-elbow amputation: (1) development of bimanual functional skills, (2) development patterns relative to able-bodied children, and (3) the relationship between duration of prosthetic wear and bimanual functional performance. Sixty-nine children with unilateral below-elbow amputation, all less than ten years old, were assessed on 14 prosthesis-assisted bimanual ADL, including play, feeding, dressing, and hygiene activities, which have been studied previously in able-bodied children. Bimanual ADL skill development was not delayed in five of the 14 comparisons to previously published standards, but most development patterns had multimodal, nonmonotonic performance profiles. Duration of prosthetic wear and other factors previously believed to contribute to good prosthetic function were not well correlated to ADL skills (r < .52). Although these children had no CNS dysfunction, it is apparent that below-elbow amputation impedes pediatric ADL skill development. The cause of these delays appears to be complex and is not expressed uniformly among all children; thus, the delays observed are not simply due to mechanical deficiencies of the prosthetic restoration. C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,15 RIVER ST,BOSTON,MA 02108. NYU,NEW YORK,NY 10003. NR 29 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD AUG PY 1992 VL 73 IS 8 BP 697 EP 702 PG 6 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA JG938 UT WOS:A1992JG93800001 PM 1642516 ER PT J AU JANG, IK GOLD, HK LEINBACH, RC FALLON, JT COLLEN, D WILCOX, JN AF JANG, IK GOLD, HK LEINBACH, RC FALLON, JT COLLEN, D WILCOX, JN TI ANTITHROMBOTIC EFFECT OF A MONOCLONAL-ANTIBODY AGAINST TISSUE FACTOR IN A RABBIT MODEL OF PLATELET-MEDIATED ARTERIAL THROMBOSIS SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE PLATELETS; ARTERIAL THROMBOSIS; TISSUE FACTOR ID PLASMINOGEN-ACTIVATOR; CORONARY THROMBOLYSIS; ANGIOPLASTY; INHIBITION; LOCALIZATION; HEMOSTASIS; LESIONS; PLAQUE; RICH AB Activation of the coagulation system by contact of circulating blood with tissue factor, a component of the extrinsic blood coagulation pathway that is produced in the vessel wall, may represent a pathway for the initiation of thrombosis in atherosclerotic vessels. This hypothesis was tested in vivo in a rabbit femoral artery eversion (inside-out) graft model, in which the adventitia, with its tissue factor, was exposed to circulating blood. Intra-arterial infusion of a neutralizing monoclonal antibody against tissue factor (D3) at a rate of 12 mg/kg over 15 minutes prevented thrombosis of a 7-8-mm eversion graft within a 2-hour observation period in four of five rabbits, whereas with a control antibody infusion (MA-15C5), occlusion occurred within 2 hours in five of six rabbits. In vitro immersion before reinsertion of the arterial segment in a solution containing 2 mg/ml of the control antibody for 30 minutes was associated with occlusion in all six rabbits, whereas pretreatment with D3 was associated with persistent patency in three of nine rabbits. Stepwise logistic-regression analysis of the results with perfusion status as the dependent variable and type of antibody (D3 or MA-15C5), application method (infusion versus immersion), and graft segment length as independent variables yielded a significant difference in frequency of occlusion with the two antibodies (p=0.016). It is concluded that exposure of tissue factor to flowing blood may constitute a trigger mechanism for platelet-mediated arterial thrombosis. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,ACC 4,SUITE 480,15 PARKMAN ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. GENENTECH INC,SAN FRANCISCO,CA 94080. FU NHLBI NIH HHS [HL-26205] NR 22 TC 45 Z9 46 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD AUG PY 1992 VL 12 IS 8 BP 948 EP 954 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA JG945 UT WOS:A1992JG94500010 PM 1637793 ER PT J AU ALEXANDERBRIDGES, M MUKHOPADHYAY, NK JHALA, U DENARO, M KONG, XF AVRUCH, J MALLER, J AF ALEXANDERBRIDGES, M MUKHOPADHYAY, NK JHALA, U DENARO, M KONG, XF AVRUCH, J MALLER, J TI GROWTH FACTOR-ACTIVATED KINASES PHOSPHORYLATE IRE-ABP SO BIOCHEMICAL SOCIETY TRANSACTIONS LA English DT Article; Proceedings Paper CT JOINT COLLOQUIUM OF SOCIETY / HOST / BIOENERGETICS GROUP ON MEMBRANE TRANSPORT, AT THE 642ND MEETING OF THE BIOCHEMICAL SOC CY APR 07-10, 1992 CL UNIV SOUTHAMPTON, SOUTHAMPTON, ENGLAND SP BIOCHEM SOC HO UNIV SOUTHAMPTON ID TESTIS-DETERMINING GENE; SEX-DETERMINING REGION; DNA-BINDING MOTIF; TRANSCRIPTION FACTOR; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; INSULIN REGULATION; TRANSGENIC MICE; PHORBOL ESTERS; ALPHA-ENHANCER; AMYLASE GENE C1 UNIV WASHINGTON,HOWARD HUGHES MED INST,SEATTLE,WA 98195. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,BOSTON,MA 02114. RP ALEXANDERBRIDGES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,DIABET UNIT,BOSTON,MA 02114, USA. NR 31 TC 6 Z9 6 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0300-5127 J9 BIOCHEM SOC T JI Biochem. Soc. Trans. PD AUG PY 1992 VL 20 IS 3 BP 691 EP 693 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JM261 UT WOS:A1992JM26100036 PM 1426612 ER PT J AU VANDEKAR, LD RITTENHOUSE, PA OCONNOR, P PALIONIS, T BROWNFIELD, MS LENT, SJ CARNES, M BETHEA, CL AF VANDEKAR, LD RITTENHOUSE, PA OCONNOR, P PALIONIS, T BROWNFIELD, MS LENT, SJ CARNES, M BETHEA, CL TI EFFECT OF COCAINE INJECTIONS ON THE NEUROENDOCRINE RESPONSE TO THE SEROTONIN AGONIST MK-212 SO BIOLOGICAL PSYCHIATRY LA English DT Article ID DORSAL RAPHE NUCLEUS; RENIN SECRETION; CORTICOSTERONE SECRETION; PROLACTIN SECRETION; CONSCIOUS RATS; MEDIOBASAL HYPOTHALAMUS; RECEPTOR ACTIVATION; 5-HT RECEPTOR; STIMULATION; NEURONS AB This study was undertaken to examine whether several of the hormones that can be released by activation of serotonin receptors will be affected by long-term cocaine administration. Male rats received cocaine injections (15 mg/kg, IP) twice daily for 7 days. Forty-two hr after the last cocaine injection, the rats were challenged with increasing doses (0, 1, 5, 10 mg/kg, IP) of the 5-HT1/5-HT2 agonist MK-212 (6-chloro-2-[1-piper-azinyl]-pyrazine). The following observations were made: (1) cocaine reduced the rate of body weight gain; (2) cocaine inhibited the stimulatory effect of MK-212 on plasma vasopressin, oxytocin, and prolactin concentrations and on plasma renin activity and concentration; (3) cocaine did not inhibit the stimulatory effect of MK-212 on plasma ACTH or corticosterone concentrations. The data indicate that a wide-spectrum 5-HT (serotonin) agonist such as MK-212 can reveal differential neuroendocrine responses. This effect could be related to cocaine-induced changes in the different 5-HT receptor subtypes that regulate the secretion of these hormones. C1 OREGON REG PRIMATE RES CTR,BEAVERTON,OR 97006. UNIV WISCONSIN,SCH VET MED,DEPT COMPARAT BIOSCI,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIATR SECT,MADISON,WI. RP VANDEKAR, LD (reprint author), LOYOLA UNIV,STRITCH SCH MED,DEPT PHARMACOL,2160 S 1ST AVE,MAYWOOD,IL 60153, USA. FU NIDA NIH HHS [DA04865]; NIMH NIH HHS [MH45812] NR 49 TC 14 Z9 14 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 AUG 1 PY 1992 VL 32 IS 3 BP 258 EP 269 DI 10.1016/0006-3223(92)90107-B PG 12 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JW492 UT WOS:A1992JW49200004 PM 1330009 ER PT J AU ORKIN, SH AF ORKIN, SH TI GATA-BINDING TRANSCRIPTION FACTORS IN HEMATOPOIETIC-CELLS SO BLOOD LA English DT Editorial Material ID PORPHOBILINOGEN DEAMINASE GENE; DOMINANT CONTROL REGION; GAMMA-GLOBIN PROMOTER; DNA-BINDING; ERYTHROID PROMOTER; REGULATORY ELEMENT; MAMMALIAN-CELLS; COMPLEX LOCUS; SCL GENE; EXPRESSION C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ORKIN, SH (reprint author), CHILDRENS HOSP MED CTR,DEPT HEMATOL,DIV HEMATOL ONCOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 55 TC 784 Z9 794 U1 0 U2 12 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 AUG 1 PY 1992 VL 80 IS 3 BP 575 EP 581 PG 7 WC Hematology SC Hematology GA JF855 UT WOS:A1992JF85500002 PM 1638017 ER PT J AU SYKES, M PEARSON, DA AF SYKES, M PEARSON, DA TI ALLOENGRAFTMENT IN IL-2-TREATED MICE SO BONE MARROW TRANSPLANTATION LA English DT Article ID VERSUS-HOST DISEASE; BONE-MARROW TRANSPLANTATION; NATURAL-KILLER-CELLS; II H-2 DIFFERENCES; T-CELLS; MONOCLONAL-ANTIBODIES; GRAFT-REJECTION; HISTOCOMPATIBILITY BARRIERS; ALLOGENEIC CHIMERISM; LYMPHOCYTES-T AB Despite major advances, graft-versus-host disease (GVHD) remains a major obstacle to clinical bone marrow transplantation. Prophylaxis by T cell depletion is associated with increased rates of engraftment failure and leukemic relapse. Treatment with high-dose IL-2 can markedly protect lethally irradiated mice from GVHD-related mortality, especially when T cell-depleted (TCD) syngeneic bone marrow cells (BMC) are co-administered. In these IL-2-protected animals, allogeneic reconstitution is observed, and a graft-versus-leukemia effect of allogeneic T cells is preserved. To determine whether IL-2 might increase alloresistance under conditions in which alloengraftment is more difficult to achieve, we have now evaluated the possible effect of IL-2 on: (1) competitive repopulation of lethally irradiated mice by mixtures of TCD allogeneic and TCD syngeneic BMC; (2) radiation protection by TCD allogeneic BMC; (3) timing of hematologic recovery; and (4) allogeneic engraftment in sublethally irradiated recipients. The results show that IL-2 has only a limited and strain-restricted effect on alloengraftment. This effect may reflect activation of alloresistant host natural killer cells, a cell population which is not essential for the protective effect of IL-2 against GVHD. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,MGH-E,BLDG 149,BOSTON,MA 02129, USA. FU NIAID NIH HHS [R01AI31158] NR 37 TC 13 Z9 13 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 AUG PY 1992 VL 10 IS 2 BP 157 EP 163 PG 7 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA JK705 UT WOS:A1992JK70500010 PM 1525605 ER PT J AU PRATHER, P ZURIF, E STERN, C ROSEN, TJ AF PRATHER, P ZURIF, E STERN, C ROSEN, TJ TI SLOWED LEXICAL ACCESS IN NONFLUENT APHASIA - A CASE-STUDY SO BRAIN AND LANGUAGE LA English DT Article ID COMPREHENSION; ACTIVATION C1 BOSTON UNIV,SCH MED,BOSTON VET ADM HOSP,APHASIA RES CTR,BOSTON,MA 02118. FRANCISCAN CHILDRENS HOSP,BOSTON,MA. BRANDEIS UNIV,WALTHAM,MA 02254. MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NINDS NIH HHS [NS06209, NS11408] NR 25 TC 66 Z9 67 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD AUG PY 1992 VL 43 IS 2 BP 336 EP 348 DI 10.1016/0093-934X(92)90134-Z PG 13 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA JK817 UT WOS:A1992JK81700008 PM 1393526 ER PT J AU AOBA, T MORENO, EC SHIMODA, S AF AOBA, T MORENO, EC SHIMODA, S TI COMPETITIVE ADSORPTION OF MAGNESIUM AND CALCIUM-IONS ONTO SYNTHETIC AND BIOLOGICAL APATITES SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE ADSORPTION; MAGNESIUM; CALCIUM; APATITE CRYSTALS; ENAMEL; DENTIN; BONE ID PORCINE AMELOGENESIS; CRYSTAL-GROWTH; TOOTH ENAMEL; FLUID; HYDROXYAPATITE; INHIBITORS; PHOSPHATE; PROTEINS; PRECIPITATION; PLASMA AB Magnesium (Mg) is a conspicuous constituent of hard tissues but its possible role in biomineralization is poorly understood. It is possible that Mg2+ adsorbed onto bioapatites may contribute to the modulation of crystal growth as such inhibitory activity has been reported for synthetic apatites, The present study was undertaken to determine the adsorption isotherms of Mg ions onto synthetic apatites and biominerals in tooth and bone tissues in the presence of other ions of natural occurrence. Synthetic crystals used as adsorbents were hydroxyapatite and, as a better prototype for the biomineral, Mg-containing carbonatoapatite. Human enamel and dentin materials were obtained from extracted, caries-free, permanent teeth. Porcine dentin materials at two developmental stages were obtained from erupted deciduous and unerupted permanent teeth of a 6-month-old slaughtered piglet. Porcine bone was obtained from the cortical portion of the mandible of the same animal. All biomineral samples were pulverized and then treated by plasma ashing (deproteination) at about 60-degrees-C. Each of the powdered samples was equilibrated in solutions containing various initial concentrations of Mg2+, Ca2+, and Na+ (or K+) as nitrate salts. Following equilibration, concentrations (and activities) of magnesium and calcium ions in the experimental solution were determined. The pH values of the equilibrium solutions were in the range of 6.2-6.5. Experimental data of the Mg adsorption onto hydroxyapatite were interpreted on the basis of a Langmuir-type model for binary systems assuming competition of Mg2+ and Ca2+ for the same adsorption sites on the crystal surfaces of the apatites. According to this model, the adsorbed Mg is expressed as a function of the ionic activity ratio (Mg2+)/(Ca2+) in the equilibrium solution. The model contains two parameters, the adsorption selectivity constant K(s) and the maximum number of adsorption sites N (mu-mol/g). The numerical values of K(s) were similar for all adsorbents used (synthetic and biological) and indicated the preferential adsorption of Ca2+ probably due to spacial restrictions extending to the very surface of the crystals. The initial level of Mg2+ in the surface pool was different in the various biominerals, probably reflecting the composition of fluid in which the biominerals were formed. Whereas the surface pool of Mg of human enamel was marginal, only 5% of the total Mg, significant fractions of the total Mg in human and porcine dentins (about 20-30%), and porcine bone (about 40%) existed on the crystal surfaces. There were significant differences in the total Mg and the value of the parameter N between young (unerupted) and mature (erupted) dentin minerals. It was ascertained that the occupancy of adsorption sites by Mg ions became greater with maturation of the dentin tissues. The overall results suggest that the Mg-mineral interaction in tooth and bone tissues may be a highly tissue-specific process, presumably reflecting differences in fluid composition (particularly Ca and Mg activities) responsible for biomineralization. C1 TSURUMI UNIV,SCH DENT,YOKOHAMA 230,JAPAN. RP AOBA, T (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE03187, DE07623, DE08670] NR 32 TC 44 Z9 44 U1 2 U2 13 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD AUG PY 1992 VL 51 IS 2 BP 143 EP 150 DI 10.1007/BF00298503 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JE090 UT WOS:A1992JE09000010 PM 1422954 ER PT J AU CONLON, MR CANNY, CLB AF CONLON, MR CANNY, CLB TI FAVORABLE OUTCOME IN A PATIENT WITH PENETRATING INTRAOCULAR BB PELLET INJURY SO CANADIAN JOURNAL OF OPHTHALMOLOGY-JOURNAL CANADIEN D OPHTALMOLOGIE LA English DT Article DE PELLET GUN; TRAUMA; WOUNDS AND INJURIES AB Intraocular BB pellet injuries are a devastating form of ocular trauma with a poor prognosis. The penetration of the eye by the pellet causes a marked disruption of the intraocular contents that in most cases leads to enucleation. We describe a 15-year-old boy who suffered a penetrating intraocular BB pellet injury to his right eye and underwent primary repair of the injury followed by secondary vitrectomy and prophylactic panretinal photocoagulation. The postoperative management was complicated by a retinal detachment; however, this responded to a scleral buckling procedure. Eighteen months after the injury the acuity in the affected eye was 20/30 with a contact lens. To our knowledge this is the first case in which useful vision has been recovered in this type of injury. C1 UNIV WESTERN ONTARIO,UNIV HOSP,339 WINDERMERE RD,LONDON N6A 5A5,ONTARIO,CANADA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 5 TC 1 Z9 1 U1 0 U2 0 PU CANADIAN OPHTHAL SOC PI OTTAWA PA 1525 CARLING AVE SUITE 610, OTTAWA ON K1Z 8R9, CANADA SN 0008-4182 J9 CAN J OPHTHALMOL JI Can. J. Opthalmol.-J. Can. Opthalmol. PD AUG PY 1992 VL 27 IS 5 BP 251 EP 253 PG 3 WC Ophthalmology SC Ophthalmology GA JP449 UT WOS:A1992JP44900011 PM 1393814 ER PT J AU JANOV, AJ ANDERSON, J CELLA, DF ZUCKERMAN, E KORNBLITH, AB HOLLAND, JC KANTOR, AF LI, FP AF JANOV, AJ ANDERSON, J CELLA, DF ZUCKERMAN, E KORNBLITH, AB HOLLAND, JC KANTOR, AF LI, FP TI PREGNANCY OUTCOME IN SURVIVORS OF ADVANCED HODGKIN DISEASE SO CANCER LA English DT Article DE HODGKIN DISEASE; PREGNANCY OUTCOME; SURVIVORS; LATE EFFECTS ID TERM FOLLOW-UP; OVARIAN-FUNCTION; WILMS TUMOR; COMBINATION CHEMOTHERAPY; GONADAL-FUNCTION; CANCER; WOMEN; CHILDHOOD; RADIATION; LEUKEMIA AB Background. Pregnancy outcome was reported by 139 survivors of advanced Hodgkin disease treated on nine protocols of Cancer and Leukemia Group B from 1966 to 1986. Methods. These patients provided data on 302 singleton pregnancies of a duration of at least 20 weeks that occurred before, during, or after treatment for Hodgkin disease (252, 26, and 24 pregnancies, respectively). Results. There were 4 perinatal deaths, as compared with 5.7 expected. Cancer subsequently developed in 2 offspring (expected, 1.2). However, 22 newborn infants had low a birth weight, exceeding the expected number of 13.7 (relative risk 1.6; 95% confidence interval, 1.0-2.4). The excess number of low weight births occurred primarily during the period of Hodgkin disease diagnosis and treatment but is based on small numbers. Conclusion. No increase in adverse outcome occurred in pregnancies that antedated the development of Hodgkin disease. C1 NCI,CLIN EPIDEMIOL BRANCH,CLIN STUDIES SECT,BETHESDA,MD 20892. UNIV NEBRASKA,MED CTR,CALGB BIOSTAT CTR,OMAHA,NE 68105. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. RP JANOV, AJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,ROOM M3A28,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA31946] NR 36 TC 8 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD AUG 1 PY 1992 VL 70 IS 3 BP 688 EP 692 DI 10.1002/1097-0142(19920801)70:3<688::AID-CNCR2820700325>3.0.CO;2-V PG 5 WC Oncology SC Oncology GA JF196 UT WOS:A1992JF19600022 PM 1623485 ER PT J AU BAILEY, H WILDING, G TUTSCH, KD ARZOOMANIAN, RZ ALBERTI, D TOMBES, MB GREM, JL SPRIGGS, DR AF BAILEY, H WILDING, G TUTSCH, KD ARZOOMANIAN, RZ ALBERTI, D TOMBES, MB GREM, JL SPRIGGS, DR TI A PHASE-I TRIAL OF 5-FLUOROURACIL, LEUCOVORIN, AND DIPYRIDAMOLE GIVEN BY CONCURRENT 120-H CONTINUOUS INFUSIONS SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE 5-FLUOROURACIL; LEUCOVORIN; DIPYRIDAMOLE; CONTINUOUS INFUSION ID COLON CANCER-CELLS; THYMIDYLATE SYNTHETASE; NUCLEOSIDE SALVAGE; COLORECTAL-CANCER; CYTO-TOXICITY; FOLINIC ACID; CHEMOTHERAPY; FLUOROURACIL; INHIBITION; DERIVATIVES AB A phase I trial of 5-fluorouracil (FUra) and leucovorin (LV) given with and without dipyridamole (DP) by concurrent 120-h continuous infusion was performed in 27 patients with advanced solid malignancies, 8 of whom had previously received FUra. The LV and DP doses were fixed at 500 mg/m2 daily and 7.7 mg/kg daily, respectively, whereas the FUra dose was escalated. Level 3 (450 mg/m2 FUra daily) represented the maximum tolerated dose for both FUra/LV + DP and FUra/LV. Dose-limiting stomatitis (greater-than-or-equal-to grade 3 or grade 2 occurring during the infusion) was encountered in 75% of the first courses given at level 4 (600 mg/m2 daily). Stomatitis was observed in 44/78 (56%) courses. Diarrhea was infrequent and mild. DP infusions were complicated by mild to moderate headache, which was controlled with narcotic analgesics, and mild to moderate nausea/vomiting. FUra-related toxicity was not enhanced by DP administration. Limited pharmacokinetic sampling at levels 3 and 4 revealed mean steady-state FUra concentrations of around 1.0-mu-M with infusions of FUra/LV + DP. Among three paired courses given with and without DP, no statistically significant difference was found in the total body clearance of FUra (P = 0.44). One partial response was seen in a patient with metastatic gastric carcinoma. For phase II trials, we recommend that concurrent 120-h continuous infusions of FUra (450 mg/m2 daily) and LV (500 mg/m2 daily) be given with and without DP (7.7 mg/kg daily) every 21 days. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. NCI,BETHESDA,MD 20892. RP BAILEY, H (reprint author), UNIV WISCONSIN,CTR CLIN CANC,K4-666,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [N01-CM-07306, N01-CM-57735]; NCRR NIH HHS [MO1 RR03186] NR 27 TC 3 Z9 3 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 AUG PY 1992 VL 30 IS 4 BP 297 EP 302 DI 10.1007/BF00686299 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA JF451 UT WOS:A1992JF45100009 PM 1643698 ER PT J AU YANG, KD STONE, RM LEE, CS CHAO, TY CHENG, SN SHAIO, MF AF YANG, KD STONE, RM LEE, CS CHAO, TY CHENG, SN SHAIO, MF TI EFFECT OF PICIBANIL (OK432) ON NEUTROPHIL-MEDIATED ANTITUMOR-ACTIVITY - IMPLICATION OF MONOCYTE-DERIVED NEUTROPHIL-ACTIVATING FACTORS SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Article DE OK432; NEUTROPHIL; ANTITUMOR ACTIVITY ID TUMOR-CELL DESTRUCTION; STREPTOCOCCAL PREPARATION OK-432; MALIGNANT ASCITES; POLYMORPHONUCLEAR LEUKOCYTES; CHEMOTACTIC PEPTIDE; ACTIN POLYMERIZATION; MOLECULAR-CLONING; NECROSIS FACTOR; CANCER ASCITES; MANAGEMENT AB Picibanil (OK432), an extract from streptococci, has been widely utilized to treat malignant ascites and pleural effusions. The antitumor mechanism is believed to include complement-mediated neutrophil activation. Employing a flow-cytometric analysis of actin polymerization as an indicator of cell activation as well as a tumor proliferation assay, we have found that monocyte-derived neutrophil-activating factors were involved in OK432-induced neutrophil activation as well as antitumor activity. OK432-stimulated (0.1 KE/ml; 0.01 mg/ml) monocyte supernatants (OKMS) induced neutrophil actin polymerization and chemotaxis. OKMS were responsible for neutrophil-mediated inhibition of human leukemic (CEM) cell proliferation and stimulated neutrophils to produce superoxide in the presence of CEM leukemic cells at an effector/target ratio higher than 20/1. In contrast, OK432 alone, OK432-stimulated lymphocyte supernatants, or OK432-stimulated neutrophil supernatants had no effect on neutrophil activation or suppression of tumor cell proliferation. OK432 in combination with mononuclear cells also had no effect on the inhibition of CEM cell proliferation. Pretreatment of OKMS at 56-degrees-C for 30 min did not affect its ability to activate neutrophils, implying that complement activation is not responsible for the neutrophil activation. Supernatants from OK432-stimulated mononuclear cells, as determined by enzyme-linked immunosorbent assays and radioimmunoassays, contained high levels of interleukin-8 (IL-8; 1567 +/- 145 pg/ml) and tumor necrosis factor (TNF-alpha; 2105 +/- 152 pg/ml), low levels of leukotriene B4 (800 +/- 45 pg/ml) and IL-1-beta (180 +/- 22 pg/ml), but interferon-gamma was not detectable. IL-1-beta, IL-8, and TNF-alpha transcripts, undetectable in untreated monocytes, increased significantly after 30-60 min exposure to OK432. These results suggest that neutrophil-activating factors from monocytes or resident macrophages may play an important role in the OK432-induced neutrophil activation and antitumor activity. C1 NATL DEF MED CTR,DEPT PEDIAT,TAIPEI,TAIWAN. NATL DEF MED CTR,DEPT PARASIT & TROP MED,TAIPEI,TAIWAN. NATL DEF MED CTR,DEPT MED,TAIPEI,TAIWAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. FU NCI NIH HHS [1K08-CA01 352] NR 33 TC 24 Z9 24 U1 2 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD AUG PY 1992 VL 35 IS 4 BP 277 EP 282 DI 10.1007/BF01789335 PG 6 WC Oncology; Immunology SC Oncology; Immunology GA JK233 UT WOS:A1992JK23300009 PM 1511463 ER PT J AU KAUFMAN, EN JAIN, RK AF KAUFMAN, EN JAIN, RK TI EFFECT OF BIVALENT INTERACTION UPON APPARENT ANTIBODY-AFFINITY - EXPERIMENTAL CONFIRMATION OF THEORY USING FLUORESCENCE PHOTOBLEACHING AND IMPLICATIONS FOR ANTIBODY-BINDING ASSAYS SO CANCER RESEARCH LA English DT Article ID MONOCLONAL-ANTIBODIES; IMMOBILIZED ANTIGEN; NORMAL-TISSUES; NUDE-MICE; TUMORS; TRANSPORT; CELLS; EXPRESSION; MODEL; MACROMOLECULES AB The affinity of a monoclonal antibody for its tumor-associated antigen is one of several parameters governing in vivo monoclonal antibody distribution. However, there is a lack of apparent correlation between the affinity of a bivalent monoclonal antibody measured using equilibrium binding experiments and its in vivo delivery. Furthermore, differences in the reported affinity for identical antibody/antigen pairs are quite common in the literature. In this paper, both of these discrepancies are addressed in terms of variation in avidity due to bivalent interaction. The enhancement of avidity afforded by bivalent attachment is addressed theoretically by extending the model of Crothers and Metzger (Immunochemistry, 9: 341-357, 1972). Theoretical assessment of Lineweaver-Burk, Scatchard, Steward-Petty, Langmuir, fluorescence recovery after photobleaching, and Sips models demonstrates quantitatively that the measured affinity using equilibrium binding experiments may vary over four orders of magnitude with similar variation in experimental cellular antigen density. Further, the measured affinity is a function of the experimental protocol. Predictions of avidity enhancement were confirmed experimentally using fluorescence recovery after photobleaching. These experiments measured the equilibrium binding constant and concentration of binding sites for an immunoglobulin G monoclonal antibody and its F(ab) fragment directed against the rabbit VX2 carcinoma cell line. Bivalent binding data agree quantitatively with those predicted by the bivalent model with no adjustable parameters. It is concluded that bivalent equilibrium binding constants are useful only in antibody screening, where experimental conditions are identical for all series. They must be used with caution in predicting in vivo antibody distribution, and it is recommended that the intrinsic, monovalent affinity be measured in tandem with any bivalent antibody study as a standard reference. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114. CARNEGIE MELLON UNIV,DEPT CHEM ENGN,PITTSBURGH,PA 15213. FU NCI NIH HHS [CA36902, CA49792] NR 65 TC 99 Z9 99 U1 0 U2 6 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 AUG 1 PY 1992 VL 52 IS 15 BP 4157 EP 4167 PG 11 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600016 PM 1638531 ER PT J AU GROSSBARD, ML LAMBERT, JM GOLDMACHER, VS BLATTLER, WA NADLER, LM AF GROSSBARD, ML LAMBERT, JM GOLDMACHER, VS BLATTLER, WA NADLER, LM TI CORRELATION BETWEEN INVIVO TOXICITY AND PRECLINICAL INVITRO PARAMETERS FOR THE IMMUNOTOXIN ANTI-B4-BLOCKED RICIN SO CANCER RESEARCH LA English DT Article ID RIBOSOME-INACTIVATING PROTEINS; CYTO-TOXICITY; PHASE-I; GELONIN; PURIFICATION; ANTIBODIES; CANCER; LECTIN; CELLS; SEEDS AB Anti-B4-blocked ricin (Anti-B4-bR) is an immunotoxin comprised of the anti-B4 monoclonal antibody and the protein toxin, "blocked ricin." In blocked ricin, the galactose-binding sites of the ricin B-chain which mediate nonspecific binding to cells are blocked by covalently linked affinity ligands prepared from N-linked oligosaccharides of fetuin. Blocked ricin consists of two species, one with two covalently attached ligands and one with three covalently attached ligands. In a Phase I dose escalation clinical trial, Anti-B4-bR was administered to patients with relapsed and refractory B-cell neoplasms by 7-day continuous infusion. Although several different lots of Anti-B4-bR had similar IC-37 values as determined by in vitro cytotoxicity testing on cultured human cell lines, these lots differed in their in vivo toxicity when administered to patients. Thus, IC37 values alone were not sufficient to predict in vivo toxicity. We report that the degree of cell kill at concentrations of drug that saturate the B4 antigen and murine 50% lethal dose values provide additional parameters that may be predictive of in vivo cytotoxicity. Furthermore, we performed detailed cytotoxicity studies of the ricin species containing two and three covalently attached ligands, respectively. In vitro cytotoxicity testing using these samples revealed that Anti-B4-bR made with blocked ricin containing two covalently attached ligands is capable of depleting five logs of target cells in an in vitro cytotoxicity assay, while Anti-B4-bR comprised of blocked ricin with three ligands can deplete only one log of cells. Log cell kill at antigen saturating concentration, murine 50% lethal dose and biochemical analysis of the composition of blocked ricin are therefore important considerations for establishing the potential efficacy and safety of Anti-B4-bR. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. IMMUNOGEN INC,CAMBRIDGE,MA 02139. RP GROSSBARD, ML (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA34183] NR 22 TC 35 Z9 35 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD AUG 1 PY 1992 VL 52 IS 15 BP 4200 EP 4207 PG 8 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600022 PM 1379121 ER PT J AU VONDEIMLING, A LOUIS, DN VONAMMON, K PETERSEN, I WIESTLER, OD SEIZINGER, BR AF VONDEIMLING, A LOUIS, DN VONAMMON, K PETERSEN, I WIESTLER, OD SEIZINGER, BR TI EVIDENCE FOR A TUMOR SUPPRESSOR GENE ON CHROMOSOME-19Q ASSOCIATED WITH HUMAN ASTROCYTOMAS, OLIGODENDROGLIOMAS, AND MIXED GLIOMAS SO CANCER RESEARCH LA English DT Note ID DELETIONS AB Previous studies have shown frequent allelic losses of chromosomes 9p, 10, 17p, and 22q in glial tumors. Other researchers have briefly reported that glial tumors may also show allelic losses of chromosome 19, suggesting a putative tumor suppressor gene locus on this chromosome (D. T. Ransom et al., Proc. Am. Assoc. Cancer Res., 32: 302, 1991). To evaluate whether loss of chromosome 19 alleles is common in glial tumors of different types and grades, we performed Southern blot restriction fragment length polymorphism analysis for multiple chromosome 19 loci in 122 gliomas from 116 patients. Twenty-nine tumors had loss of constitutional heterozygosity of 19q, and four tumors had partial deletions of 19q. Allelic losses on 19q were restricted to grade III anaplastic astrocytomas (4/9) and grade IV glioblastomas (11/46), grade II oligodendrogliomas (2/5) and grade III anaplastic oligodendrogliomas ( 2/2), and grade II (5/8) and grade III (5/7) mixed oligoastrocytomas. These data demonstrate genetic similarities between astrocytomas, oligodendrogliomas, and mixed glial tumors and indicate the presence of a glial tumor suppressor gene on chromosome 19q. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV ZURICH,DEPT NEUROSURG,CH-8091 ZURICH,SWITZERLAND. UNIV ZURICH,DEPT PATHOL,NEUROPATHOL LAB,CH-8091 ZURICH,SWITZERLAND. RP VONDEIMLING, A (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BLDG 19,FLOOR 6W,BOSTON,MA 02129, USA. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [CA09144] NR 25 TC 173 Z9 174 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 AUG 1 PY 1992 VL 52 IS 15 BP 4277 EP 4279 PG 3 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600035 PM 1353411 ER PT J AU KALINOSKI, DL JOHNSON, LC BRYANT, BP BRAND, JG AF KALINOSKI, DL JOHNSON, LC BRYANT, BP BRAND, JG TI SELECTIVE INTERACTIONS OF LECTINS WITH AMINO-ACID TASTE RECEPTOR-SITES IN THE CHANNEL CATFISH SO CHEMICAL SENSES LA English DT Article ID PURIFICATION; SPECIFICITY; SENSATION; PROTEINS; BINDING AB Five lectins of varying carbohydrate specificities. Dolichos biflorus (DBA). jacalin, Phaseolus vulgaris (PHA), Pisum sativum (PSA) and Ricinus communis (RCA 1), were used to extend characterization of the glycoprotein nature of taste plasma membranes and to differentially affect the binding of two taste StiMUli, L-alanine and L-arginine, to their respective taste receptor sites in the cutaneous taste system of the channel catfish (Ictalurus punctatus). The binding of the taste stimulus L-arginine to a partial membrane fraction (P-) from taste epithelium was inhibited by 68 and 74% by preincubation in the presence of the unconjugated lectins PHA and RCA I respectively. A corresponding level of inhibition of L-alanine binding was seen in the presence of RCA I (76%); however, PHA had little effect upon L-alanine binding. DBA appeared to selectively inhibit L-alanine but not L-arginine binding (60 versus 8 % respectively) while jacalin moderately inhibited the binding of both stimuli to fraction P2. PSA had little effect upon the binding of either L-alanine or i.-arginine (4 and 5 % inhibition respectively). Inhibition of taste receptor binding by all lectins was time- and dose-dependent, and was fully abolished by incubation in the presence of the appropriate hapten sugar. The biotinylated lectins DBA, jacalin. PHA, RCA I and concanavalin A (Con A) were used to identify the glycoprotein components of the chemosensory plasma membranes after polyacrylamide gel electrophoresis. As previously shown, numerous protein components were labeled by Con A. In contrast, only a few minor protein components were labeled by PHA, DBA and RCA I. This differential labeling of the taste membranes and the differential inhibition of receptor binding by lectins suggest that they may prove useful as tools in the isolation and purification of taste receptor proteins. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. UNIV PENN,SCH DENT MED,DEPT BIOCHEM,PHILADELPHIA,PA 19104. RP KALINOSKI, DL (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. NR 30 TC 8 Z9 8 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0379-864X J9 CHEM SENSES JI Chem. Senses PD AUG PY 1992 VL 17 IS 4 BP 381 EP 390 DI 10.1093/chemse/17.4.381 PG 10 WC Behavioral Sciences; Food Science & Technology; Neurosciences; Physiology SC Behavioral Sciences; Food Science & Technology; Neurosciences & Neurology; Physiology GA JL988 UT WOS:A1992JL98800002 ER PT J AU SPIELMAN, AI RICKETTSFOOT, DA BRAND, JG AF SPIELMAN, AI RICKETTSFOOT, DA BRAND, JG TI HIGH-RESOLUTION SCANNING ELECTRON MICROGRAPHIC STUDY OF DISSOCIATED MOUSE TASTE CELLS SO CHEMICAL SENSES LA English DT Note ID BUD CELLS; ULTRASTRUCTURE AB New techniques for enzymatic dissociation of mammalian taste cells allowed us to study, for the first time, the morphology of murine taste receptor cells using high resolution scanning electron microscopy. Cell shape varied from spindle to bipolar to lamellar, similar to shapes previously described in cells from amphibian taste buds. Cell length varied from 19 to 65-mu-m (39 +/- 19-mu-m), with width averaging 6 +/- 3.4-mu-m. A rare picture of the apical microvilli of a taste receptor cell, and a view of microvilli within a taste pore. suggest that at any given time, five to eight taste cells may be exposed to the oral cavity. Assuming a cell life-span of 10 days, and 50 cells per bud, all of which eventually reach the taste pore, one can calculate that the average cell is exposed to the oral environment for approximately 4-5 h. After this time, these cells may fuse into the surrounding epithelium and slough off into the oral cavity where secretions of the major or von Ebner's salivary glands remove them. C1 UNIV PENN, RES STRUCT MATTER LAB, PHILADELPHIA, PA 19104 USA. MONELL CHEM SENSES CTR, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA 19104 USA. RP NYU, COLL DENT, DEPT ORAL MED & PATHOL, 345 E 24TH ST, NEW YORK, NY 10010 USA. NR 23 TC 7 Z9 7 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0379-864X EI 1464-3553 J9 CHEM SENSES JI Chem. Senses PD AUG PY 1992 VL 17 IS 4 BP 451 EP 460 DI 10.1093/chemse/17.4.451 PG 10 WC Behavioral Sciences; Food Science & Technology; Neurosciences; Physiology SC Behavioral Sciences; Food Science & Technology; Neurosciences & Neurology; Physiology GA JL988 UT WOS:A1992JL98800008 ER PT J AU PANDOLFI, F TRENTIN, L MARTIN, JES WONG, JT KURNICK, JT MOSCICKI, RA AF PANDOLFI, F TRENTIN, L MARTIN, JES WONG, JT KURNICK, JT MOSCICKI, RA TI T-CELL HETEROGENEITY IN PATIENTS WITH COMMON VARIABLE IMMUNODEFICIENCY AS ASSESSED BY ABNORMALITIES OF T-CELL SUBPOPULATIONS AND T-CELL RECEPTOR GENE ANALYSIS SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE COMMON VARIABLE IMMUNODEFICIENCY; T-CELL RECEPTOR; LYMPHOCYTES-T; HYPOGAMMAGLOBULINEMIA; GENE REARRANGEMENTS ID INFECTIOUS-MONONUCLEOSIS; HELPER-INDUCER; LYMPHOCYTES-T; ACQUIRED AGAMMAGLOBULINEMIA; VARIED IMMUNODEFICIENCY; MONOCLONAL-ANTIBODIES; HYPOGAMMAGLOBULINEMIA; DIFFERENTIATION; EXPRESSION; POPULATIONS AB T lymphocyte regulation of immunoglobulin production may be abnormal in some patients with common variable immunodeficiency (CVI). Phenotypic analysis of peripheral blood T lymphocytes from nine patients with CVI was conducted to examine whether an abnormal distribution could be detected in a functionally distinct T lymphocyte subpopulation. The percentage of CD8+ lymphocytes proved to be increased in some patients and decreased in others. In comparison with normal controls, many patients with CVI had reduced percentages of lymphocytes expressing both CD4 and CD45RA, a phenotype associate with naive CD4+ cells. There was no significant difference in CD4+ populations bearing CD29 or leucocyte adhesion molecule-1 (LAM-1) antigens. The pattern of gene rearrangement of the T cell antigen receptor (TCR) was studied using peripheral blood lymphocytes from these patients with CVI. Genomic DNA from freshly isolated lymphocytes as well as from selectively propagated CD4+ or CD8+ populations were examined using Southern blot analysis and a probe for the beta-chain of the TCR. A polyclonal pattern of TCR gene rearrangement, without the appearance of dominant non-germline bands, was demonstrated in all patient samples. These data suggest that the T lymphocytes in patients with CVI have a polyclonal pattern of TCR rearrangement despite an abnormal distribution of T cell subpopulations in some patients. 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,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN MED SERV,CLIN IMMUNOL & ALLERGY UNIT,BOSTON,MA 02114. RP PANDOLFI, F (reprint author), UNIV ROME,DEPT ALLERGY & CLIN IMMUNOL,VIALE UNIV 37,I-00185 ROME,ITALY. RI TRENTIN, LIVIO/J-7676-2016 OI TRENTIN, LIVIO/0000-0003-1222-6149 FU NCI NIH HHS [CA44324]; NIAMS NIH HHS [AR39993] NR 33 TC 16 Z9 16 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD AUG PY 1992 VL 89 IS 2 BP 198 EP 203 PG 6 WC Immunology SC Immunology GA JF054 UT WOS:A1992JF05400007 PM 1638763 ER PT J AU GRUNEWALD, J JEDDITEHRANI, M DERSIMONIAN, H ANDERSSON, R WIGZELL, H AF GRUNEWALD, J JEDDITEHRANI, M DERSIMONIAN, H ANDERSSON, R WIGZELL, H TI A PERSISTENT T-CELL EXPANSION IN THE PERIPHERAL-BLOOD OF A NORMAL ADULT MALE - A NEW CLINICAL ENTITY SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE T-CELL RECEPTOR; T-CELL EXPANSION ID V-GENE USAGE; MONOCLONAL-ANTIBODY; EXPRESSION; ARTHRITIS; LEUKEMIA; CD4+ AB A dramatic and persistent T cell expansion in a healthy adult male was initially identified, using anti-T cell receptor for antigen (TCR)-specific MoAbs. The expanded T cells were found to be expressing TCR containing V-alpha 12.1 and V-beta 5.2, and they composed approximately one third of all the CD8+ T cells. The cells were shown to be not only non-activated (HLA-DR-, IL-2R-) but also of 'virgin' cell type (CD45RA +/CD45RO-) and they persisted over the observation period of more than one and a half years. Various T and B cell markers, and all other laboratory and physical parameters analysed, were normal. The expanded CD8+ T cells were further characterized by polymerase chain reaction (PCR) amplification, using V-beta- and C-beta-specific primers, followed by hybridization with J-beta-specific probes. Close to 90% of the V-alpha-12.1+ V-beta-5.2+ T cells were found to utilize the J-beta 2.5 gene segment, thus strongly suggesting the expanded T cells to be monoclonal. The condition may constitute a T cell counterpart to 'monoclonal gammopathy of undetermined significance' (MGUS), and by analogy we suggest it should be designated 'monoclonal T cell expansion of undertermined significance' (MTUS). C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,BOSTON,MA 02115. RP GRUNEWALD, J (reprint author), KAROLINSKA INST,DEPT IMMUNOL,BOX 60400,S-10401 STOCKHOLM 60,SWEDEN. NR 25 TC 52 Z9 52 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD AUG PY 1992 VL 89 IS 2 BP 279 EP 284 PG 6 WC Immunology SC Immunology GA JF054 UT WOS:A1992JF05400020 PM 1386298 ER PT J AU HARRER, T WOLF, B NAGER, W SCHWARZ, W BERGNER, D KALDEN, JR AF HARRER, T WOLF, B NAGER, W SCHWARZ, W BERGNER, D KALDEN, JR TI INVITRO ACTIVATION OF PERIPHERAL MONONUCLEAR-CELLS BY ZINC IN HIV-INFECTED PATIENTS AND HEALTHY CONTROLS SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE AIDS; HIV; LYMPHOCYTE ACTIVATION; ZINC ID ACQUIRED IMMUNODEFICIENCY SYNDROME; HUMAN LYMPHOCYTES; ABNORMALITIES; HOMOSEXUALS; DEFICIENCY AB Zinc is a mitogen for peripheral blood mononuclear cells (PBMC). The optimal mitogenic concentration was found to be 0.05 mmol/l (327-mu-g/dl), four times higher than physiological serum levels. Maximal proliferation was observed after 6 days. Limited dilution technique revealed a frequency of zinc reactive cells of 1:3467 (median; range 1:16235). Cord blood mononuclear cells from four of six healthy children could be stimulated to proliferate by zinc. A normal zinc-induced proliferative response could be demonstrated in all six HIV-infected patients in the Walter-Reed-stage I, in nine of 11 patients in Walter-Reed II and in only two of five patients in Walter-Reed III. In Walter-Reed IV to VI all eight patients showed a weak response to zinc (< 50% of the healthy day control). Decreased zinc serum levels were found in 10 of 28 patients and in one of 16 controls. There was a significant correlation of a diminished zinc-induced proliferation with lower serum levels of zinc and a reduced proportion of CD4 helper cells in HIV-1 infected men. Because of a suppression of mitogenesis by high dose of zinc an excessive intake of zinc as used by some HIV-1-infected patients can presently not be recommended. The value of zinc-induced proliferation for monitoring HIV-infected patients has still to be established. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,FRUITST,BOSTON,MA 02114. UNIV ERLANGEN NURNBERG,DEPT INTERNAL MED 3,W-8520 ERLANGEN,GERMANY. UNIV ERLANGEN NURNBERG,INST CLIN IMMUNOL & RHEUMATOL,W-8520 ERLANGEN,GERMANY. UNIV ERLANGEN NURNBERG,ZENT LAB,W-8520 ERLANGEN,GERMANY. NR 32 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD AUG PY 1992 VL 89 IS 2 BP 285 EP 289 PG 5 WC Immunology SC Immunology GA JF054 UT WOS:A1992JF05400021 PM 1638772 ER PT J AU LEES, S AF LEES, S TI MECHANICAL EFFECTS OF SODIUM-FLUORIDE ON BOVINE CORTICAL BONE SO CLINICAL BIOMECHANICS LA English DT Letter RP LEES, S (reprint author), FORSYTH DENT CTR,DEPT BIOENGN,140 FENWAY,BOSTON,MA 02115, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0268-0033 J9 CLIN BIOMECH JI Clin. Biomech. PD AUG PY 1992 VL 7 IS 3 BP 187 EP 187 DI 10.1016/0268-0033(92)90036-4 PG 1 WC Engineering, Biomedical; Orthopedics; Sport Sciences SC Engineering; Orthopedics; Sport Sciences GA JF050 UT WOS:A1992JF05000010 PM 23915729 ER PT J AU PINS, MR COMPTON, CC SOUTHERN, JF RATTNER, DW LEWANDROWSKI, KB AF PINS, MR COMPTON, CC SOUTHERN, JF RATTNER, DW LEWANDROWSKI, KB TI CILIATED ENTERIC DUPLICATION CYST PRESENTING AS A PANCREATIC CYSTIC NEOPLASM - REPORT OF A CASE WITH CYST FLUID ANALYSIS SO CLINICAL CHEMISTRY LA English DT Article DE CANCER; CARCINOEMBRYONIC ANTIGEN; CA-125; AMYLASE ID CARCINOEMBRYONIC ANTIGEN; CYSTADENOCARCINOMA; DIAGNOSIS AB Pancreatic cysts include inflammatory pseudocysts, cystic tumors (serous and mucinous), and various rare cystic lesions. We report a case of a ciliated enteric duplication cyst that presented on computed tomographic scan as a pancreatic cystic neoplasm. Cyst fluid analysis revealed markedly increased concentrations of carcinoembryonic antigen and CA 125 and increased fluid viscosity. These features are typical for a mucinous cystic neoplasm of the pancreas and demonstrate a potential pitfall associated with the diagnosis of pancreatic cysts by chemical analyses. Enteric duplications involving the pancreas are rare, usually of gastric origin, and usually communicate with their enteric source. Morphological and histochemical analysis suggest that this cyst was of caudal foregut origin. This is the first reported case of a ciliated foregut cyst involving the pancreas. The chemical characteristics of the cyst fluid of these lesions have not been described previously. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,CLIN CHEM LAB,GRAY 5,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 17 TC 32 Z9 32 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD AUG PY 1992 VL 38 IS 8 BP 1501 EP 1503 PN 1 PG 3 WC Medical Laboratory Technology SC Medical Laboratory Technology GA JH683 UT WOS:A1992JH68300024 PM 1643723 ER PT J AU MALONEY, WJ DAVEY, JR HARRIS, WH AF MALONEY, WJ DAVEY, JR HARRIS, WH TI BEAD LOOSENING FROM A POROUS-COATED ACETABULAR COMPONENT - A FOLLOW-UP NOTE SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article AB Beaded porous-coated implants are commonly used in total joint arthroplasty. In this study, the authors extended the follow-up period for the Davey and Harris1 study of bead loosening in beaded cementless acetabular components. When 56 primary total hip arthroplasties were first reviewed, at an average of 2.5 years after surgery, the incidence of bead loosening was 8.9%. Reevaluation at a mean of 4.5 years after surgery revealed that the incidence of loosening had increased to 19.6%. Bead loosening was associated with acetabular migration in one component and a broken screw in a second. In the absence of loose beads, there were no broken fixation screws or socket migration. Radiolucencies at the bone-implant interface were seen in association with loose beads in only one case. Although long-term implications of bead loosening are not clear, bead migration may increase the possibility of macrophage response to metallic debris. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MALONEY, WJ (reprint author), PALO ALTO MED CLIN,300 HOMER AVE,PALO ALTO,CA 94301, USA. NR 12 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD AUG PY 1992 IS 281 BP 112 EP 114 PG 3 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JG977 UT WOS:A1992JG97700019 PM 1499196 ER PT J AU CHERTKOW, H BUB, D CAPLAN, D AF CHERTKOW, H BUB, D CAPLAN, D TI CONSTRAINING THEORIES OF SEMANTIC MEMORY PROCESSING - EVIDENCE FROM DEMENTIA SO COGNITIVE NEUROPSYCHOLOGY LA English DT Article ID OPTIC APHASIA; ALZHEIMERS-DISEASE; VISUAL INFORMATION; LANGUAGE FUNCTION; PICTURES; WORDS; REPRESENTATIONS; SYSTEMS; OBJECT; COMPREHENSION AB In this paper we analyse the performance of ten patients with Dementia of the Alzheimer's Type (D.A.T.) who show a pattern of performance suggesting a deficit at the level of semantic memory in the face of normal visual perceptual processing. We use the results of their performance on probe questions for pictures and words to evaluate several hypotheses arising from recent theories concerning semantic memory. We assess whether these patients demonstrate better performance on pictures than words (they do), and whether this can be explained away as a by-product of the perceptual nature of the items tested; pictures whose items have many discernible object parts would tend to contact more residual information in semantic memory, thus producing apparent superior performance from pictures. In fact, we find no support for this explanation. Rather, we are able to demonstrate, in the semantic category of animals, that it is only the items that are correctly identified (as a whole) that will give rise to evidence of better performance on pictures. C1 CENT HOSP COTES DE NEIGES,MONTREAL,QUEBEC,CANADA. MONTREAL NEUROL HOSP & INST,MONTREAL H3A 2B4,QUEBEC,CANADA. MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,BOSTON,MA 02114. RP CHERTKOW, H (reprint author), SIR MORTIMER B DAVIS JEWISH HOSP,LADY DAVIS INST MED RES,3755 COTE ST CATHERINE RD,MONTREAL H3T 1E2,QUEBEC,CANADA. NR 54 TC 92 Z9 92 U1 0 U2 2 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE, EAST SUSSEX, ENGLAND BN3 2FA SN 0264-3294 J9 COGNITIVE NEUROPSYCH JI Cogn. Neuropsychol. PD AUG PY 1992 VL 9 IS 4 BP 327 EP 365 DI 10.1080/02643299208252064 PG 39 WC Psychology; Psychology, Experimental SC Psychology GA JH600 UT WOS:A1992JH60000003 ER PT J AU HUQUE, T BRAND, JG RABINOWITZ, JL AF HUQUE, T BRAND, JG RABINOWITZ, JL TI METABOLISM OF INOSITOL-1,4,5-TRISPHOSPHATE IN THE TASTE ORGAN OF THE CHANNEL CATFISH, ICTALURUS-PUNCTATUS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY LA English DT Article ID INOSITOL 1,4,5-TRISPHOSPHATE PHOSPHATASE; TRISPHOSPHATE KINASE; BOVINE BRAIN; RAT-BRAIN; 3-KINASE; CA-2+; TETRAKISPHOSPHATE; CALMODULIN; ACTIVATION; MEMBRANES AB 1. The metabolism of inositol-1,4,5-trisphosphate was studied in the taste organ (barbel) of the channel catfish, Ictalurus punctatus. 2. Homogenates of epithelial barbel scrapings were incubated with [H-3]-1,4,5-IP3, whose dephosphorylation or phosphorylation was assayed under first-order conditions by measuring the production of either [H-3]-1,4-IP2 (representing the activity of IP3-5-phosphatase) or [H-3]-1,3,4,5-IP4 (representing the activity of IP3-3-kinase). 3. Both enzymes were predominantly cytosolic, magnesium-dependent and maximally active at pH 6.4. For IP3-phosphatase, K(m) = 6-mu-M and V(max) = 10.5 nmol/min/mg. For IP3-kinase, K(m) = 0.23-mu-M and V(max) = 0.05 nmol/min/mg. 4. Neither enzyme was significantly affected by the presence of taste stimuli (amino acids), GTP-gamma-S, cAMP or phorbol esters. 5. In the presence of physiological levels of free calcium (0.05-12-mu-M) IP3-phosphatase was moderately activated whereas IP3-kinase was moderately inhibited. 6. IP3-phosphatase was moderately activated by Mn2+, unaffected by LiCl, and strongly inhibited by 2,3-diphosphoglycerate, Na-pyrophosphate, CdCl2, HgCl2, CUCl2, FeCl3 and ZnSO4 7. IP3-kinase was strongly activated by 2,3-diphosphoglycerate, Na-pyrophosphate, CdCl2, HgCl2, FeCl3 and LiCl and inhibited by ZnSO4 and Mn2+. 8. IP3-kinase was significantly activated in a calcium-dependent manner by exogenously-added phosphatidylcholine and sphingomyelin, and to a lesser extent by diacylglycerol. IP3-phosphatase, was unaffected by exogenously-added lipids. 9. IP3-phosphatase may participate in taste transduction since calculations based on the first-order rate constant (6.9 sec-1) indicate that it is capable of dephosphorylating basal levels of IP3 with a half-life of 0.1 sec. C1 UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. UNIV PENN,SCH DENT MED,DEPT BIOCHEM,PHILADELPHIA,PA 19104. RP HUQUE, T (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. FU NCRR NIH HHS [SO7RR05825]; NIDCD NIH HHS [DC-00327, DC-00356] NR 37 TC 5 Z9 5 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0305-0491 J9 COMP BIOCHEM PHYS B JI Comp. Biochem. Physiol. B-Biochem. Mol. Biol. PD AUG PY 1992 VL 102 IS 4 BP 833 EP 839 DI 10.1016/0305-0491(92)90088-9 PG 7 WC Biochemistry & Molecular Biology; Zoology SC Biochemistry & Molecular Biology; Zoology GA JH263 UT WOS:A1992JH26300028 PM 1327660 ER PT J AU STRAWDERMAN, RL MEHTA, C AF STRAWDERMAN, RL MEHTA, C TI ON THE VALIDATION OF EXACT TESTS FOR NONPARAMETRIC-INFERENCE SO COMPUTATIONAL STATISTICS & DATA ANALYSIS LA English DT Article ID CONTINGENCY-TABLES AB Exact nonparametric tests have gained widespread acceptance, and new algorithms are being developed at a rapid pace. Because of the computational complexity of these algorithms, the numerical results from software based on these new algorithms are difficult to verify independently. This paper provides a library of "gold standard" data sets and exact test results, independently validated through various means, for thirteen major exact nonparametric tests. We consider this library to be expandable, and suggest a mechanism for accessing and augmenting it. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. NR 10 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-9473 J9 COMPUT STAT DATA AN JI Comput. Stat. Data Anal. PD AUG PY 1992 VL 14 IS 2 BP 263 EP 266 DI 10.1016/0167-9473(92)90178-I PG 4 WC Computer Science, Interdisciplinary Applications; Statistics & Probability SC Computer Science; Mathematics GA JL513 UT WOS:A1992JL51300010 ER PT J AU CIMINO, C BARNETT, GO AF CIMINO, C BARNETT, GO TI ANALYSIS OF PHYSICIAN QUESTIONS IN AN AMBULATORY CARE SETTING SO COMPUTERS AND BIOMEDICAL RESEARCH LA English DT Article ID INFORMATION NEEDS C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT NEUROL,BRONX,NY 10461. MASSACHUSETTS GEN HOSP,COMP SCI LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP CIMINO, C (reprint author), YESHIVA UNIV ALBERT EINSTEIN COLL MED,OFF EDUC,BRONX,NY 10461, USA. FU NLM NIH HHS [2-T15-LM07037-04, N01-LM-8-3513] NR 15 TC 6 Z9 6 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0010-4809 J9 COMPUT BIOMED RES JI Comput. Biomed. Res. PD AUG PY 1992 VL 25 IS 4 BP 366 EP 373 DI 10.1016/0010-4809(92)90026-7 PG 8 WC Computer Science, Interdisciplinary Applications; Medical Informatics SC Computer Science; Medical Informatics GA JH894 UT WOS:A1992JH89400005 PM 1511597 ER PT J AU SINGER, DE KISTLER, JP HUGHES, RA AF SINGER, DE KISTLER, JP HUGHES, RA TI PREVENTING STROKE IN ATRIAL-FIBRILLATION SO CORONARY ARTERY DISEASE LA English DT Article DE ATRIAL FIBRILLATION; STROKE; ANTICOAGULATION; WARFARIN ID RISK-FACTORS; THROMBOEMBOLIC COMPLICATIONS; WARFARIN; ASPIRIN; INFARCTION; THERAPY; TRIAL AB Epidemiologic studies have shown that atrial fibrillation raises the risk of stroke approximately fivefold, and that, because atrial fibrillation is so common among the stoke-prone elderly, it accounts for a substantial fraction of all strokes. The set of five recently completed randomized trials have established that warfarin, at low dose, can prevent most of the additional stroke risk caused by atrial fibrillation. The trials have also demonstrated that warfarin therapy can be safe if careful monitoring is implemented. The trials have not, however, settled the anticoagulation decision for all patients. Warfarin remains a demanding and risky therapy, which many patients and physicians do not find attractive. This review analyzes the epidemiologic observations and randomized trials that provide our new understanding of atrial fibrillation and stroke. It also reviews possible risk factors for stroke in atrial fibrillation and alternative antithrombotic regimens such as aspirin. At the present time, low-dose warfarin should be considered for all patients with chronic atrial fibrillation. Younger patients with no other clinical heart disease may be at such low risk for stroke that warfarin might be avoided. The evidence is not substantial that aspirin is an effective alternative. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,STROKE SERV,BOSTON,MA 02114. RP SINGER, DE (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,GEN INTERNAL MED UNIT,BULFINCH 1,BOSTON,MA 02114, USA. NR 33 TC 3 Z9 3 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD AUG PY 1992 VL 3 IS 8 BP 753 EP 760 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JL873 UT WOS:A1992JL87300013 ER PT J AU RINKES, IHMB TONER, M EZZELL, RM TOMPKINS, RG YARMUSH, ML AF RINKES, IHMB TONER, M EZZELL, RM TOMPKINS, RG YARMUSH, ML TI EFFECTS OF DIMETHYL-SULFOXIDE ON CULTURED RAT HEPATOCYTES IN SANDWICH CONFIGURATION SO CRYOBIOLOGY LA English DT Article ID CRYOPRESERVATION; DIMETHYLSULFOXIDE; CRYOPROTECTANTS; ACTIN; PERMEABILITY; ORGANIZATION; TRANSPORT; RECOVERY; EMBRYOS C1 RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. RP RINKES, IHMB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02114, USA. NR 30 TC 13 Z9 13 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0011-2240 J9 CRYOBIOLOGY JI Cryobiology PD AUG PY 1992 VL 29 IS 4 BP 443 EP 453 PG 11 WC Biology; Physiology SC Life Sciences & Biomedicine - Other Topics; Physiology GA JG974 UT WOS:A1992JG97400002 ER PT J AU JANG, IK GOLD, HK FUSTER, V AF JANG, IK GOLD, HK FUSTER, V TI BASIC STUDIES ON THROMBOSIS AND FIBRINOLYSIS SO CURRENT OPINION IN CARDIOLOGY LA English DT Article AB Thrombosis is the main cause of various cardiovascular diseases, such as coronary artery disease, cerebral infarction and transient ischemic attack, and pulmonary embolism. The thrombus results from an imbalance between the endogenous fibrinolytic system and the clotting mechanism, although platelets also play a critical role. Various therapeutic modalities have been developed for the treatment of thrombosis, particularly for coronary artery thrombosis. These include plasminogen activators of the first, second, and third generation, selective thrombin inhibitors, such as hirudin and argatroban, and platelet inhibitors, such as an antibody or peptide against platelet receptor glycoprotein IIb/IIIa. RP JANG, IK (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BUL 105,12 FRUIT ST,BOSTON,MA 02114, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 0 TC 0 Z9 0 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0268-4705 J9 CURR OPIN CARDIOL JI Curr. Opin. Cardiol. PD AUG PY 1992 VL 7 IS 4 BP 546 EP 552 DI 10.1097/00001573-199208000-00003 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JD867 UT WOS:A1992JD86700003 ER PT J AU CHATZIPANTELI, K RUDOLPH, S AXELROD, L AF CHATZIPANTELI, K RUDOLPH, S AXELROD, L TI COORDINATE CONTROL OF LIPOLYSIS BY PROSTAGLANDIN-E2 AND PROSTACYCLIN IN RAT ADIPOSE-TISSUE SO DIABETES LA English DT Article ID FATTY-ACID REESTERIFICATION; FUNCTIONAL VASODILATATION; DIABETIC-KETOACIDOSIS; HUMAN ADIPOCYTES; INDOMETHACIN; INSULIN; CELLS; PATHOGENESIS; INHIBITION; PGI2 AB PGE2 is a potent antilipolytic agent produced by adipose tissue, but its role as a physiological regulator of triglyceride lipolysis is controversial because inhibitors of prostaglandin synthesis have not enhanced hormone-stimulated lipolysis in adipose tissue consists. Adipose tissue also produces PGl2, but this eicosanoid has not had a demonstrated effect on lipolysis under physiological conditions previously. We investigated both PGE2 and PGl2 production and their effects on lipolysis in rat adipose tissue. We found that 1) EPI-stimulated PGE2 production (like PGl2 production) requires the cooperation of adipocytes and endothelial cells, 2) adipose tissue produces PGE2 and PGl2 at comparable rates, 3) indomethacin inhibits EPI-induced PGE2 and PGl2 production and has no effect on EPI-stimulated lipolysis when added to a mixture of adipocytes and endothelial cells or to intact epididymal fat pads, 4) PGl2 is a potent lipolytic agent when added to isolated adipocytes in the absence of endothelial cells under physiological conditions, 5) the magnitudes and the ED50s of the antilipolytic effect of PGE2 and the lipolytic effect of PGl2 in isolated adipocytes in the absence of endothelial cells are comparable, 6) PGl2 antagonizes the antilipolytic effect of PGE2 in isolated adipocytes in the absence of endothelial cells in a dosage-related manner, and 7) the antilipolytic effect of added PGE2 in isolated adipocytes is greater in the absence of endothelial cells than in their presence, suggesting that endogenous eicosanoid production reduces the effectiveness of added PGE2. These studies demonstrate that catecholamine-induced lipolysis is under the coordinate control of PGE2, a potent antilipolytic agent, and PGl2, a potent lipolytic agent. The failure of PGH synthase inhibition to affect lipolysis can be explained by concurrent PGE2 and PGl2 inhibition. The existence of this mechanism for coordinate control of lipolysis may have broad implications for the function of adipose tissue in health and disease. C1 MASSACHUSETTS GEN HOSP, DIABET UNIT, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-39249] NR 32 TC 44 Z9 44 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD AUG PY 1992 VL 41 IS 8 BP 927 EP 935 DI 10.2337/diabetes.41.8.927 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JE969 UT WOS:A1992JE96900006 PM 1628767 ER PT J AU PUGH, JA WAGNER, ML SAWYER, J RAMIREZ, G TULEY, M FRIEDBERG, SJ AF PUGH, JA WAGNER, ML SAWYER, J RAMIREZ, G TULEY, M FRIEDBERG, SJ TI IS COMBINATION SULFONYLUREA AND INSULIN THERAPY USEFUL IN NIDDM PATIENTS - A METAANALYSIS SO DIABETES CARE LA English DT Article ID DEPENDENT DIABETES-MELLITUS; SECONDARY DRUG FAILURE; DOUBLE-BLIND; FOLLOW-UP; GLIBENCLAMIDE; GLYBURIDE; TERM; GLUCOREGULATION; REQUIREMENT; METABOLISM AB OBJECTIVE - To assess the efficacy of combination of therapy with sulfonylurea in the treatment of NIDDM. RESEARCH DESIGN AND METHODS - Studies published between January 1966 and January 1991 were identified through a computerized Medline search and by hand searching the bibliographies of identified articles. We identified 17 eligible randomized, controlled trials of combination therapy in NIDDM. These trials had a minimum duration of 8 wk and at least one of three outcome measures (fasting glucose, HbA1, or C-peptide) with SD or SE of the mean reported to do metaanalysis. With standardized forms, three independent reviewers abstracted measures of study quality and specific descriptive information about population, intervention, and outcome measurements. RESULTS - We calculated effect size and weighted mean changes of the three outcome measures for control and treatment groups. In the treatment group, the fasting plasma glucose decreased from a mean of 11.4 mM (206 mg/dl) at baseline to a mean of 9.16 mM (165 mg/dl) posttreatment, whereas the control group decreased from (11.3 to 10.8 mM) (204 to 194 mg/dl) (effect size 0.39, P < 0.0001). For HbA1, the treatment group decreased from a baseline of 11.0 to 10.2% compared to 11.0 and 11.2% in the control group (effect size 0.43, P < 0.0001). For fasting C-peptide, the treatment group increased from 0.49 to 0.58 nM (1.45 to 1.75 ng/ml) compared with 0.47 and 0.43 (1.42 and 1.30) for the control group (effect size 0.26, P < 0.017). CONCLUSIONS - Combined insulin-sulfonylurea therapy leads to modest imporvement in glycemic control compared with insulin therapy alone. With combined therapy, lower insulin doses may be used to achieve similar control. Obese patients with higher fasting C-peptides may be more likely to respond than others. RP PUGH, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. OI Pugh, Jacqueline/0000-0003-4933-141X NR 38 TC 74 Z9 74 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD AUG PY 1992 VL 15 IS 8 BP 953 EP 959 DI 10.2337/diacare.15.8.953 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JF369 UT WOS:A1992JF36900002 PM 1387073 ER PT J AU ALARCON, C LINCOLN, B RHODES, CJ AF ALARCON, C LINCOLN, B RHODES, CJ TI BIOSYNTHESIS AND PROTEOLYTIC PROCESSING OF PC1 AND PC2 ENDOPEPTIDASES IN PANCREATIC-BETA-CELLS SO DIABETOLOGIA LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 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 AUG PY 1992 VL 35 SU 1 BP A67 EP A67 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500255 ER PT J AU LALIC, NM ZAMAKLAR, M SIMONSON, DC JACKSON, R DORDEVIC, PB AF LALIC, NM ZAMAKLAR, M SIMONSON, DC JACKSON, R DORDEVIC, PB TI IMPAIRMENTS IN GLUCOSE DISPOSAL IN PATIENTS WITH RECENT-ONSET TYPE-1 (INSULIN-DEPENDENT) DIABETES SO DIABETOLOGIA LA English DT Meeting Abstract C1 INST ENDOCRINOL,BELGRADE,YUGOSLAVIA. JOSLIN DIABET FDN INC,BOSTON,MA 02215. NR 0 TC 0 Z9 0 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 AUG PY 1992 VL 35 SU 1 BP A106 EP A106 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500405 ER PT J AU MARTIN, BC WARRAM, JH BERGMAN, RN SOELDNER, JS KROLEWSKI, AS AF MARTIN, BC WARRAM, JH BERGMAN, RN SOELDNER, JS KROLEWSKI, AS TI EFFECTS OF EXPOSURE TO MATERNAL TYPE-I DIABETES INUTERO ON GLUCOSE DISPOSAL AND INSULIN-SECRETION IN THE CHILDREN SO DIABETOLOGIA LA English DT Meeting Abstract C1 UNIV ZURICH,SCH MED,INST SOCIAL & PREVENT MED,CH-8006 ZURICH,SWITZERLAND. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. JOSLIN DIABET CTR,DIV RES,BOSTON,MA. NR 0 TC 0 Z9 0 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 AUG PY 1992 VL 35 SU 1 BP A182 EP A182 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500703 ER PT J AU MARTIN, S KOLB, H ROTHLEIN, R MAINOLFI, EA KISHIMOTO, TK BERTRAMS, J LAMPETER, EF AF MARTIN, S KOLB, H ROTHLEIN, R MAINOLFI, EA KISHIMOTO, TK BERTRAMS, J LAMPETER, EF TI ELEVATED CIRCULATING ADHESION MOLECULES IN TYPE-1 DIABETES AND SUBJECTS AT RISK OF DIABETES SO DIABETOLOGIA LA English DT Meeting Abstract C1 BOEHRINGER INGELHEIM PHARMACEUT INC,RIDGEFIELD,CT. ELISABETH HOSP,ESSEN,GERMANY. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. UNIV DUSSELDORF,DIABET RES INST,W-4000 DUSSELDORF 1,GERMANY. NR 0 TC 0 Z9 0 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 AUG PY 1992 VL 35 SU 1 BP A33 EP A33 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500120 ER PT J AU MONTANA, E BONNERWEIR, S WEIR, GC AF MONTANA, E BONNERWEIR, S WEIR, GC TI TRANSPLANTED BETA-CELL MASS DOUBLED AFTER 95-PERCENT PANCREATECTOMY SO DIABETOLOGIA LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1992 VL 35 SU 1 BP A187 EP A187 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500722 ER PT J AU PREVITI, M DOTTA, F TIBERTI, C LENTI, L EISENBARTH, GS ANDREANI, D DIMARIO, U AF PREVITI, M DOTTA, F TIBERTI, C LENTI, L EISENBARTH, GS ANDREANI, D DIMARIO, U TI BIOCHEMICAL-CHARACTERIZATION OF A PROPOSED ISLET TARGET ANTIGEN - THE GM2-1 ISLET GANGLIOSIDE SO DIABETOLOGIA LA English DT Meeting Abstract C1 UNIV RC CATANZARO,DEPT EXPTL & CLIN MED,CATANZARO,ITALY. UNIV ROME LA SAPIENZA,DEPT ENDOCRINOL,I-00185 ROME,ITALY. UNIV ROME LA SAPIENZA,DEPT EXPTL MED,I-00185 ROME,ITALY. JOSLIN DIABET CTR,BOSTON,MA. RI Dotta, Francesco/H-3788-2012 NR 0 TC 0 Z9 0 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 AUG PY 1992 VL 35 SU 1 BP A42 EP A42 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500154 ER PT J AU BRAUNHUT, SJ DAMORE, PA GUDAS, LJ AF BRAUNHUT, SJ DAMORE, PA GUDAS, LJ TI THE LOCATION AND EXPRESSION OF FIBROBLAST GROWTH-FACTOR (FGF) IN F9 VISCERAL AND PARIETAL EMBRYONIC-CELLS AFTER RETINOIC ACID-INDUCED DIFFERENTIATION SO DIFFERENTIATION LA English DT Article ID SUBENDOTHELIAL EXTRACELLULAR-MATRIX; HEPARIN-LIKE MOLECULES; EARLY XENOPUS EMBRYOS; ENDOTHELIAL-CELLS; TERATOCARCINOMA CELLS; TGF-BETA; CARCINOMA-CELLS; STEM-CELLS; BINDING; MESODERM AB It is well-established that fibroblast growth factors (FGFs) participate in mesoderm formation and patterning in the developing embryo. To identify cells in mammalian embryos that produce and/or respond to FGFs, we utilized the F9 teratocarcinoma cell system. Undifferentiated F9 cells resemble inner cell mass (ICM) cells of the mouse blastocyst by several criteria including having a characteristic high nuclear to cytoplasmic ratio and by their expression of stage-specific embryonic antigens. F9 stem cells differ from ICM cells by their low spontaneous rate of differentiation and their differentiation potential. ICM cells are heterogeneous with a proportion of the cells maintaining totipotency. In contrast, F9 stem cells appear capable of forming only endodermal derivatives. Retinoic acid (RA) treatment of F9 stem cells is required for them to differentiate, and under different culturing conditions the F9 cells will form either extraembryonic parietal or visceral endoderm. We have previously shown that FGF is synthesized by F9 parietal endoderm, but not by F9 stem cells. Our present study demonstrates that F9 aggregate cultures that contain visceral endoderm cells produce cell-associated-heparin-binding mitogens for 3T3 and endothelial cells, factors with characteristics of FGFs. Furthermore, our studies detect endothelial cell-mitogens within the extracellular matrix (ECM) of F9 parietal endoderm cells, not detected within F9 stem cell 'matrices'. Parietal endoderm cell matrix mitogens could be removed by prior treatment of the ECM with buffers containing heparin or 2 M NaCl, and could be neutralized by basic FGF antibodies. Additional studies indicate that fully-differentiated F9 parietal endodermal cells proliferate in response to FGF. In contrast, F9 stem cells do not respond to FGF, with or without added soluble heparin. Thus, FGF made by differentiating visceral and parietal endodermal cells of the early mouse blastocyst may act in an autocrine fashion to support the expansion of these cell populations. Further, matrix-associated FGF, synthesized by endodermal cells, could act on other embryonic cells in the immediate vicinity that are susceptible to the mitogenic or morphogenic action of FGFs. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT OPHTHALMOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BRAUNHUT, SJ (reprint author), CHILDRENS HOSP MED CTR,DEPT SURG,SURG RES LAB,JOHN ENDERS PEDIAT RES BLDG,RM 1061,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY-05985, EY-06726]; NICHD NIH HHS [R01-HD-24319] NR 53 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD AUG PY 1992 VL 50 IS 3 BP 141 EP 152 DI 10.1111/j.1432-0436.1992.tb00669.x PG 12 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA JJ783 UT WOS:A1992JJ78300002 PM 1426701 ER PT J AU KIRSH, I THORNTON, A BURKARD, R HALPIN, C AF KIRSH, I THORNTON, A BURKARD, R HALPIN, C TI THE EFFECT OF COCHLEAR HEARING-LOSS ON AUDITORY BRAIN-STEM RESPONSE LATENCY SO EAR AND HEARING LA English DT Article ID AUDIOGRAM AB The effect of audiometric configuration on the auditory brain stem response was studied in a large patient sample, and wave I latencies, wave V latencies, and the I-V interwave intervals were compared to those from a previous report. Patients with notched hearing losses showed longer wave V latencies and I-V interwave intervals than those with other audiometric configurations, but the magnitude of the effect was relatively small, and the confidence limit for cochlear diagnosis was essentially the same as that based upon a cochlear hearing loss population without regard to audiometric configuration. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT AUDIOL,243 CHARLES ST,BOSTON,MA 02114. GARDEN STATE REHABIL HOSP,TOMS RIVER,NJ. BOSTON UNIV,BOSTON,MA 02215. NR 9 TC 2 Z9 2 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-0202 J9 EAR HEARING JI Ear Hear. PD AUG PY 1992 VL 13 IS 4 BP 233 EP 235 DI 10.1097/00003446-199208000-00004 PG 3 WC Audiology & Speech-Language Pathology; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Otorhinolaryngology GA JK060 UT WOS:A1992JK06000004 PM 1397765 ER PT J AU MEYERSON, M ENDERS, GH WU, CL SU, LK GORKA, C NELSON, C HARLOW, E TSAI, LH AF MEYERSON, M ENDERS, GH WU, CL SU, LK GORKA, C NELSON, C HARLOW, E TSAI, LH TI A FAMILY OF HUMAN CDC2-RELATED PROTEIN-KINASES SO EMBO JOURNAL LA English DT Article DE CDC2-RELATED GENES; CDK3; CELL CYCLE; PROTEIN KINASES ID CELL-CYCLE CONTROL; SACCHAROMYCES-CEREVISIAE; FISSION YEAST; MESSENGER-RNA; CDC2 PROTEIN; M-PHASE; GENE; HOMOLOG; MITOSIS; DNA AB The p34cdc2 protein kinase is known to regulate important transitions in the eukaryotic cell cycle. We have identified 10 human protein kinases based on their structural relation to p34cdc2. Seven of these kinases are novel and the products of five share > 50% amino acid sequence identity with p34cdc2. The seven novel genes are broadly expressed in human cell lines and tissues with each displaying some cell type or tissue specificity. The cdk3 gene, like cdc2 and cdk2, can complement cdc28 mutants of Saccharomyces cerevisiae, suggesting that all three of these protein kinases can play roles in the regulation of the mammalian cell cycle. The identification of a large family of cdc2-related kinases opens the possibility of combinatorial regulation of the cell cycle together with the emerging large family of cyclins. C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. RP MEYERSON, M (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129, USA. RI Meyerson, Matthew/E-7123-2012 NR 88 TC 808 Z9 835 U1 1 U2 9 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 AUG PY 1992 VL 11 IS 8 BP 2909 EP 2917 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JE537 UT WOS:A1992JE53700017 PM 1639063 ER PT J AU HIROBE, S HE, WW LEE, MM DONAHOE, PK AF HIROBE, S HE, WW LEE, MM DONAHOE, PK TI MULLERIAN INHIBITING SUBSTANCE MESSENGER-RIBONUCLEIC-ACID EXPRESSION IN GRANULOSA AND SERTOLI CELLS COINCIDES WITH THEIR MITOTIC-ACTIVITY SO ENDOCRINOLOGY LA English DT Article ID SEX-DETERMINING REGION; EPIDERMAL GROWTH-FACTOR; OOCYTE MATURATION; INSITU HYBRIDIZATION; TESTICULAR DESCENT; Y-CHROMOSOME; RAT OVARY; GENE; BOVINE; ONTOGENY AB In males, Mullerian inhibiting substance (MIS) mRNA was first detected on the medial aspect of the urogenital ridge early on the morning of day 13 of gestation before testicular differentiation was evident, and localized to the more obvious Sertoli cells later on embryonic day 13. MIS transcripts remained at maximal levels between 14.5 and 17.5 days gestation, while the Mullerian duct involutes, and remained high until birth. MIS gene expression decreased progressively after birth and, as germ cell meiosis increased, became barely detectable in the Sertoli cells of the seminiferous tubules. In female rats, MIS mRNA was first detected in the single layer of cuboidal granulosa cells surrounding larger primary follicles 3 days after birth, coincident with the initiation of follicular growth. As follicular growth progressed, MIS mRNA expression was high in preantral and small antral follicles, especially in those granulosa cells closest to the oocyte. MIS mRNA expression decreased gradually in larger antral follicles, remaining prominent only in the cumulus cells and the dividing population of granulosa cells closest to the lumen. MIS gene expression was absent in follicles with features of atresia and in the larger antral follicles. The expression of MIS mRNA in actively dividing Sertoli and granulosa cells correlates with the stages of germ cell division. These findings are suggestive of a role for MIS in the control of germ cell maturation. C1 MASSACHUSETTS GEN HOSP,DIV PEDIAT SURG,PEDIAT SURG RES LABS,WARREN BLDG,ROOM 1133,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PEDIAT ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. OI Lee, Mary/0000-0002-7204-4884 FU NCI NIH HHS [CA-17393] NR 43 TC 129 Z9 132 U1 0 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 AUG PY 1992 VL 131 IS 2 BP 854 EP 862 DI 10.1210/en.131.2.854 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JG581 UT WOS:A1992JG58100046 PM 1639028 ER PT J AU VIDARD, L ROCK, KL COUDERC, J MOUTON, D BENACERRAF, B AF VIDARD, L ROCK, KL COUDERC, J MOUTON, D BENACERRAF, B TI PROCESSING AND PRESENTATION OF OVALBUMIN IN MICE GENETICALLY SELECTED FOR ANTIBODY-RESPONSE SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Note ID B-CELLS; INVIVO; H-2; RESPONSIVENESS; POLYMORPHISM; MACROPHAGES; LINES; GENES AB Lines of mice selected for high or low antibody production to sheep red blood cells (H-I and L-I) were studied for their ability to process and present ovalbumin to a panel of 12 T-T hybridomas in two different H-2 haplotypes. When H-I and L-I spleen cells were used as antigen-presenting cells, no difference could be observed in the peptide generation by these mice compared to H-2-compatible B.10.Q and B.10.S spleen cells, respectively. Neither normal splenic L-1 B-cells nor L-I thioglycolate-induced peritoneal macrophages were defective at presenting native ovalbumin, to six and eight different I-A(s)-restricted T-T hybrids, respectively. Altogether, these results differ from previous findings which had indicated a deficiency in the processing and presentation of antigen by the low line, L-I. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. INST CURIE,CNRS,URA 1413,F-75231 PARIS 05,FRANCE. FU NCI NIH HHS [CA 46967]; NIAID NIH HHS [AI 20248] NR 18 TC 2 Z9 2 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD AUG PY 1992 VL 22 IS 8 BP 2165 EP 2168 DI 10.1002/eji.1830220831 PG 4 WC Immunology SC Immunology GA JH919 UT WOS:A1992JH91900030 PM 1379188 ER PT J AU MOLEA, N CALLAHAN, RJ WILKINSON, RA TSAI, E BRADY, TJ STRAUSS, HW PAPISOV, MI AF MOLEA, N CALLAHAN, RJ WILKINSON, RA TSAI, E BRADY, TJ STRAUSS, HW PAPISOV, MI TI BIODISTRIBUTION AND IMAGING STUDIES OF A NEW RADIOPHARMACEUTICAL FOR LYMPH-NODE IMAGING FOLLOWING INTRAVENOUS ADMINISTRATION SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PD AUG PY 1992 VL 19 IS 8 BP 590 EP 590 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JL496 UT WOS:A1992JL49600080 ER PT J AU ELMALEH, DR MELTZER, PC MADRAS, B LIANG, AY BROWNELL, AL HANTRAYE, P ISACSON, O SHOUP, T FICSHMAN, AJ BROWNELL, GL STRAUSS, HW AF ELMALEH, DR MELTZER, PC MADRAS, B LIANG, AY BROWNELL, AL HANTRAYE, P ISACSON, O SHOUP, T FICSHMAN, AJ BROWNELL, GL STRAUSS, HW TI PET IMAGING PROBES FOR THE COCAINE RECEPTORS - A VALIDATION-STUDY IN A NONHUMAN PRIMATE MODEL SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ORGANIX,WOBURN,MA 01801. NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PD AUG PY 1992 VL 19 IS 8 BP 734 EP 734 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JL496 UT WOS:A1992JL49600651 ER PT J AU BURKE, JF AF BURKE, JF TI CURRENT CONCEPTS IN PEDIATRIC BURN CARE - ARTIFICIAL SKIN - ITS PLACE IN THE SYSTEM OF PEDIATRIC BURN CARE SO EUROPEAN JOURNAL OF PEDIATRIC SURGERY LA English DT Article; Proceedings Paper CT 21ST ANNUAL CONGRESS OF THE SWISS ASSOC OF PEDIATRIC SURGERY CY SEP 05-06, 1991 CL ZURICH, SWITZERLAND SP SWISS ASSOC PEDIAT SURG DE ARTIFICIAL SKIN; PEDIATRIC BURN CARE ID PROMPT ESCHAR EXCISION; DESIGN; MORTALITY; CHILDREN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA. FU NIGMS NIH HHS [GM 21700] NR 10 TC 1 Z9 1 U1 1 U2 1 PU HIPPOKRATES VERLAG GMBH PI STITTGART PA PO BOX 30 05 04 RUDIGERSTRASSE 14, 70469 STITTGART, GERMANY SN 0939-7248 J9 EUR J PEDIATR SURG JI Eur. J. Pediatr. Surg. PD AUG PY 1992 VL 2 IS 4 BP 205 EP 206 DI 10.1055/s-2008-1063441 PG 2 WC Pediatrics; Surgery SC Pediatrics; Surgery GA JN159 UT WOS:A1992JN15900003 PM 1390546 ER PT J AU COMPTON, CC AF COMPTON, CC TI CURRENT CONCEPTS IN PEDIATRIC BURN CARE - THE BIOLOGY OF CULTURED EPITHELIAL AUTOGRAFTS - AN 8-YEAR STUDY IN PEDIATRIC BURN PATIENTS SO EUROPEAN JOURNAL OF PEDIATRIC SURGERY LA English DT Article DE CULTURED EPITHELIUM; AUTOGRAFTS; BURNS; SKIN REGENERATION; DERMIS; WOUND HEALING; CHILDREN ID AUTOLOGOUS EPIDERMAL-CELLS; SURFACE-AREA WOUNDS; MONOCLONAL-ANTIBODY; KERATIN EXPRESSION; ANCHORING FIBRILS; MOLECULAR MARKERS; MOUSE SKIN; GROWTH; DIFFERENTIATION; TRANSPLANTATION AB An 8-year histopathological study of skin regeneration and wound healing in 22 pediatric patients treated with cultured epithelial autografts (CEA) grafted to full-thickness bum wounds excised to muscle fascia is reported. Biopsies of CEA have been analyzed by light microscopic, immunohistochemical, morphometric, electron microscopic and ultrastructural immunolabelling techniques and compared to controls of meshed split-thickness autograft (MSTA) interstices at comparable times postgrafting. At transplantation, CEA are undifferentiated and lack both granular and cornified cell layers. By 6 days postgrafting, CEA differentiate all normal epidermal strata but lack rete ridges. De novo formation of a confluent basal lamina and mature hemidesmosomes is complete by about 3 weeks. Anchoring fibrils appear sparse and immature (as in MSTA controls) compared to normal skin until about 6-12 months. CEA develop rete ridges and a neodermis with normal stromal and vascular organization at about 6-12 months, whereas MSTA interstice controls do not. At 4-5 years, elastin expression is also observed in the CEA neodermis, completing the dermal regeneration process. Normal epidermal differentiation is maintained long-term. These long-term results indicate that CEA regenerate a stable normal epidermis and are capable of inducing dermal regeneration from wound bed connective tissue. C1 SHRINERS BURN INST,DEPT PATHOL,BOSTON,MA. RP COMPTON, CC (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [R01-GM35242] NR 50 TC 44 Z9 46 U1 1 U2 3 PU HIPPOKRATES VERLAG GMBH PI STITTGART PA PO BOX 30 05 04 RUDIGERSTRASSE 14, 70469 STITTGART, GERMANY SN 0939-7248 J9 EUR J PEDIATR SURG JI Eur. J. Pediatr. Surg. PD AUG PY 1992 VL 2 IS 4 BP 216 EP 222 DI 10.1055/s-2008-1063444 PG 7 WC Pediatrics; Surgery SC Pediatrics; Surgery GA JN159 UT WOS:A1992JN15900006 PM 1390549 ER PT J AU ISACSON, O SOFRONIEW, MV AF ISACSON, O SOFRONIEW, MV TI NEURONAL LOSS OR REPLACEMENT IN THE INJURED ADULT CEREBRAL NEOCORTEX INDUCES EXTENSIVE REMODELING OF INTRINSIC AND AFFERENT NEURAL SYSTEMS SO EXPERIMENTAL NEUROLOGY LA English DT Article ID NERVE GROWTH-FACTOR; ACID-LESIONED STRIATUM; ALZHEIMERS-DISEASE; CHOLINERGIC NEURONS; IBOTENIC ACID; BASAL NUCLEUS; HUNTINGTONS-DISEASE; RETROGRADE DEGENERATION; CELL DEGENERATION; CAUDATE-PUTAMEN C1 HARVARD UNIV,MCLEAN HOSP,SCH MED,PROGRAM NEUROSCI,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CAMBRIDGE,DEPT ANAT,CAMBRIDGE,ENGLAND. HARVARD UNIV,MCLEAN HOSP,SCH MED,DEPT NEUROL,BELMONT,MA 02178. FU NINDS NIH HHS [NS29178]; Wellcome Trust NR 84 TC 46 Z9 47 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD AUG PY 1992 VL 117 IS 2 BP 151 EP 175 DI 10.1016/0014-4886(92)90123-8 PG 25 WC Neurosciences SC Neurosciences & Neurology GA JH927 UT WOS:A1992JH92700005 PM 1379936 ER PT J AU GUELRUD, M ROSSITER, A SOUNEY, PF ROSSITER, G FANIKOS, J MUJICA, V AF GUELRUD, M ROSSITER, A SOUNEY, PF ROSSITER, G FANIKOS, J MUJICA, V TI THE EFFECT OF VASOACTIVE INTESTINAL POLYPEPTIDE ON THE LOWER ESOPHAGEAL SPHINCTER IN ACHALASIA SO GASTROENTEROLOGY LA English DT Article ID VIP-IMMUNOREACTIVE NERVES; GASTROINTESTINAL-TRACT; HIRSCHSPRUNGS-DISEASE; REGULATORY PEPTIDES; HEALTHY-SUBJECTS; PRESSURE; INNERVATION; STIMULATION; RELAXATION; NEUROTRANSMITTER C1 HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DEPT PHARM, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. RP HOSP GEN OESTE, POLICLIN METROPOLITANA, DEPT GASTROENTEROL, URB CAURIMARE, CARACAS, VENEZUELA. NR 40 TC 21 Z9 21 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 EI 1528-0012 J9 GASTROENTEROLOGY JI Gastroenterology PD AUG PY 1992 VL 103 IS 2 BP 377 EP 382 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JF014 UT WOS:A1992JF01400003 PM 1634056 ER PT J AU LIVINGSTON, EH PASSARO, EP MILLER, J GUTH, PH AF LIVINGSTON, EH PASSARO, EP MILLER, J GUTH, PH TI SPECTRUM OF INJURY PRODUCED IN THE DUODENUM BY PERFUSION WITH LUMINAL ACID IN THE RAT SO GASTROENTEROLOGY LA English DT Article ID ALKALINE SECRETION; HCO3 TRANSPORT; PH GRADIENT; SURFACE; MUCOSA; INVIVO; MECHANISMS; INVITRO; DAMAGE C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,MED SERV,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,RES SERV,LOS ANGELES,CA 90024. CTR ULCER RES & EDUC,LOS ANGELES,CA. RP LIVINGSTON, EH (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SURG SERV,691-151H,BLDG 115,LOS ANGELES,CA 90024, USA. NR 14 TC 20 Z9 20 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 AUG PY 1992 VL 103 IS 2 BP 481 EP 489 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JF014 UT WOS:A1992JF01400016 PM 1634066 ER PT J AU ALTHERR, MR PLUMMER, S BATES, G MACDONALD, M TAYLOR, S LEHRACH, H FRISCHAUF, AM GUSELLA, JF BOEHNKE, M WASMUTH, JJ AF ALTHERR, MR PLUMMER, S BATES, G MACDONALD, M TAYLOR, S LEHRACH, H FRISCHAUF, AM GUSELLA, JF BOEHNKE, M WASMUTH, JJ TI RADIATION HYBRID MAP SPANNING THE HUNTINGTON DISEASE GENE REGION OF CHROMOSOME-4 SO GENOMICS LA English DT Article ID LONG ARM; LOCUS C1 UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA 02114. UNIV MICHIGAN,DEPT BIOSTAT,ANN ARBOR,MI 48109. RI Bates, Gillian/E-1146-2012 OI Bates, Gillian/0000-0002-4041-6305 FU NHGRI NIH HHS [HG00320]; NINDS NIH HHS [NS16367, NS25631] NR 21 TC 20 Z9 20 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 AUG PY 1992 VL 13 IS 4 BP 1040 EP 1046 DI 10.1016/0888-7543(92)90017-M PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800017 PM 1387106 ER PT J AU DANIEL, PF EVANS, JE DEGASPERI, R WINCHESTER, B WARREN, CD AF DANIEL, PF EVANS, JE DEGASPERI, R WINCHESTER, B WARREN, CD TI A HUMAN LYSOSOMAL ALPHA(1-]6)-MANNOSIDASE ACTIVE ON THE BRANCHED TRIMANNOSYL CORE OF COMPLEX GLYCANS SO GLYCOBIOLOGY LA English DT Article DE HUMAN FIBROBLASTS; LYSOSOMES; ALPHA(1-]6)-MANNOSIDASE; ALPHA-MANNOSIDOSIS; SWAINSONINE ID ALPHA-D-MANNOSIDASES; URINARY OLIGOSACCHARIDES; SUBSTRATE-SPECIFICITY; GLYCOPROTEIN CATABOLISM; LIQUID-CHROMATOGRAPHY; METHYLATION ANALYSIS; SWAINSONINE; BIOSYNTHESIS; INHIBITION; FELINE AB Normal human fibroblasts and fibroblasts from a patient with alpha-mannosidosis were grown in the presence or absence of 100-mu-M swainsonine for 7 days. Accumulated oligosaccharides were isolated and analysed by high performance liquid chromatography (HPLC) and methylation analysis. Man-alpha-1 --> 3Man-beta-1 --> 4GlcNAc and Man-alpha-1 --> 2Man-alpha-1 --> 3Man-beta-1 --> 4GlcNAc (where Man is D-mannose and GlcNAc is N-acetyl-D-glucosamine) comprised > 80% of the total oligosaccharides in untreated mannosidosis cells. However, Man-alpha-1 --> 6[Man-alpha-1 --> 3]Man-beta-1 --> 4GlcNAc was the major Man3GlcNAc isomer present after 7 days of swainsonine treatment. No mannose-containing oligosaccharides were detected in control fibroblasts in the absence of swainsonine but, in its presence, oligosaccharides containing 2-9 mannose residues accumulated. Man-alpha-1 --> 6[Man-alpha-1 --> 3]Man-alpha-1 --> 6[Man-alpha-1 --> 3]Man-beta-1 --> 4GlcNAc and Man-alpha-1--> 6[Man-alpha-1 --> 3]Man-beta-1 --> 4GlcNAc were the major components (67%). Surprisingly, Man-alpha-1 --> 3Man-beta-1 --> 4GlcNAc was only observed in swainsonine-treated control cells during the recovery period after removal of swainsonine. These studies suggest the presence of a second lysosomal alpha-mannosidase activity which is unaffected in genetic alpha-mannosidosis, but is inhibited by swainsonine. This enzyme would cleave the alpha(1 --> 6)-linked mannose residue from branched Man3GlcNAc to form Man-alpha-1 --> 3Man-beta-1 --> 4GlcNAc. To confirm this hypothesis, fractions from ce-mannosidosis and control fibroblasts that bound to concanavalin A (ConA)-Sepharose and were eluted with 0.5 M alpha-methyl mannoside were incubated at pH 4.0 with Man-alpha-1 --> 6[Man-alpha-1 --> 3]Man-beta-1 --> 4GlcNAc. As anticipated, Man-alpha-1 --> 3Man-beta-1 --> 4GlcNAc was the sole product using enzyme from mannosidosis fibroblasts, while the major product from control fibroblasts was Man-alpha-1 --> 6Man-beta-1 --> 4GlcNAc. This confirmed the presence of a swainsonine-inhibitable alpha(1 --> 6)-mannosidase activity unaffected by the disease. The differing substrate specificities of the alpha(1 --> 6)-mannosidase and the major lysosomal alpha-mannosidase indicate that the alpha(1 --> 6)-mannosidase plays an important role in the generation of the oligosaccharides accumulated in alpha-mannosidosis patients. C1 HARVARD UNIV,SCH MED,WALTHAM,MA 02254. SHRIVER CTR MENTAL RETARDAT,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,LOVETT LABS CARBOHYDRATE UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. UNIV LONDON,INST CHILD HLTH,DEPT CLIN BIOCHEM,LONDON WC1N 1EH,ENGLAND. RP DANIEL, PF (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,200 TRAPELO RD,WALTHAM,MA 02254, USA. FU NCRR NIH HHS [SO7 RR 05486-28]; NICHD NIH HHS [HD 16942]; NIDDK NIH HHS [DK 40930] NR 38 TC 22 Z9 22 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0959-6658 J9 GLYCOBIOLOGY JI Glycobiology PD AUG PY 1992 VL 2 IS 4 BP 327 EP 336 DI 10.1093/glycob/2.4.327 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JK168 UT WOS:A1992JK16800009 PM 1421754 ER PT J AU RICE, LW LAGE, JM BERKOWITZ, RS GOODMAN, A MUTO, MG KNAPP, RC BELL, DA AF RICE, LW LAGE, JM BERKOWITZ, RS GOODMAN, A MUTO, MG KNAPP, RC BELL, DA TI PREOPERATIVE SERUM CA-125 LEVELS IN BORDERLINE TUMORS OF THE OVARY SO GYNECOLOGIC ONCOLOGY LA English DT Article ID MONOCLONAL-ANTIBODY; CLINICAL BEHAVIOR; EPITHELIAL TUMORS; CANCER; CARCINOMA; RADIOIMMUNOASSAY; MALIGNANCY C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,VINCENT GYNECOL SERV,BOSTON,MA 02114. RP RICE, LW (reprint author), BRIGHAM & WOMENS HOSP,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,BOSTON,MA 02115, USA. NR 19 TC 30 Z9 30 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 AUG PY 1992 VL 46 IS 2 BP 226 EP 229 DI 10.1016/0090-8258(92)90260-P PG 4 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA JK855 UT WOS:A1992JK85500017 PM 1500026 ER PT J AU LEE, WPA MAY, JW AF LEE, WPA MAY, JW TI NEUROSENSORY FREE FLAPS TO THE HAND - INDICATIONS AND DONOR SELECTION SO HAND CLINICS LA English DT Article RP LEE, WPA (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE 453,BOSTON,MA 02114, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0749-0712 J9 HAND CLIN JI Hand Clin. PD AUG PY 1992 VL 8 IS 3 BP 465 EP 477 PG 13 WC Orthopedics SC Orthopedics GA JG565 UT WOS:A1992JG56500007 PM 1400601 ER PT J AU YOUNG, RH SCULLY, RE AF YOUNG, RH SCULLY, RE TI PATHOLOGY OF EPITHELIAL TUMORS SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID SEROUS BORDERLINE TUMORS; CLEAR-CELL-CARCINOMA; SURFACE PAPILLARY CARCINOMA; MALIGNANT POTENTIAL TUMORS; OVARIAN BRENNER TUMORS; MUCINOUS TUMORS; CLINICOPATHOLOGICAL ANALYSIS; ENDOMETRIOID CARCINOMA; PERITONEAL IMPLANTS; HISTOLOGIC FEATURES C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,FRUIT ST,BOSTON,MA 02114, USA. NR 71 TC 7 Z9 7 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD AUG PY 1992 VL 6 IS 4 BP 739 EP 760 PG 22 WC Oncology; Hematology SC Oncology; Hematology GA JG438 UT WOS:A1992JG43800003 PM 1500384 ER PT J AU LEWANDROWSKI, K WARSHAW, A COMPTON, C AF LEWANDROWSKI, K WARSHAW, A COMPTON, C TI MACROCYSTIC SEROUS CYSTADENOMA OF THE PANCREAS - A MORPHOLOGICAL VARIANT DIFFERING FROM MICROCYSTIC ADENOMA SO HUMAN PATHOLOGY LA English DT Article DE PANCREAS TUMORS; MICROCYSTIC ADENOMA; SEROUS CYSTADENOMA; GLYCOGEN-RICH ADENOMA ID CYSTIC NEOPLASMS; CYSTADENOCARCINOMA C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 8 TC 114 Z9 120 U1 0 U2 0 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 AUG PY 1992 VL 23 IS 8 BP 871 EP 875 DI 10.1016/0046-8177(92)90397-L PG 5 WC Pathology SC Pathology GA JH943 UT WOS:A1992JH94300006 PM 1644432 ER PT J AU SHUSTER, E AF SHUSTER, E TI WHEN GENES DETERMINE MOTHERHOOD - PROBLEMS IN GESTATIONAL SURROGACY SO HUMAN REPRODUCTION LA English DT Article DE SURROGACY; LAW AB Gestational surrogacy in which a commissioning couple's egg and spermatozoon are united in vitro and the resulting embryo is implanted in a woman's uterus is, of all the new methods for overcoming infertility, the most genetically appealing. This is because the genes are often perceived as determining all aspects of human health, disease and even behaviour. Having a child with the genes of both parents has become far more attractive to most infertile couples than having one who is only genetically related to the father. However, gestational surrogacy has created a situation where one child has two mothers, each one claiming to be the 'true' mother having exclusive parental rights. Surrogacy arrangements also raise the question of the meaning of motherhood. RP SHUSTER, E (reprint author), VET AFFAIRS MED CTR,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 0 TC 9 Z9 10 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0268-1161 J9 HUM REPROD JI Hum. Reprod. PD AUG PY 1992 VL 7 IS 7 BP 1029 EP 1033 PG 5 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA JK922 UT WOS:A1992JK92200030 PM 1430122 ER PT J AU COX, RA SUN, SH DOLAN, MJ HARRISON, JL AF COX, RA SUN, SH DOLAN, MJ HARRISON, JL TI LOCALIZATION OF THE TUBE PRECIPITIN AND COMPLEMENT-FIXATION ANTIGENS OF COCCIDIOIDES-IMMITIS BY IMMUNOELECTRON MICROSCOPY WITH MURINE MONOCLONAL-ANTIBODIES SO INFECTION AND IMMUNITY LA English DT Article ID WALL FRACTION; REACTIVITY; PROTEIN AB The cellular localization of the tube precipitin (TP) and complement fixation (CF) antigens of Coccidioides immitis was examined by immunoelectron microscopy with murine immunoglobulin G1 monoclonal antibodies directed against the TP and CF antigens, respectively. Immunoelectron microscopic analyses of saprobic- and parasitic-phase cells showed that the TP antigen is present at a high concentration within the inner cell wall layer and along the plasma membrane. The antigen was also detected, at a lesser concentration, within cytoplasmic vacuoles. In contrast to the predominant localization of the TP antigen in the cell walls, the CF antigen resides primarily within the cytoplasm, where it appears to be dispersed throughout the cytoplasm rather than associated with a specific cytoplasmic organelle. A sparse amount of the CF antigen within the inner cell walls was also demonstrable. The localization of the TP and CF antigens throughout the morphogenetic phases of C. immitis has important implications in antigen production and in analyses of host response in coccidioidomycosis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,LACKLAND AFB,TX 78236. RP COX, RA (reprint author), SAN ANTONIO STATE CHEST HOSP,DEPT RES IMMUNOL,SAN ANTONIO,TX 78223, USA. FU NIAID NIH HHS [AI21431] NR 25 TC 4 Z9 4 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD AUG PY 1992 VL 60 IS 8 BP 3315 EP 3324 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JG023 UT WOS:A1992JG02300041 PM 1639499 ER PT J AU EISENHAUER, PB LEHRER, RI AF EISENHAUER, PB LEHRER, RI TI MOUSE NEUTROPHILS LACK DEFENSINS SO INFECTION AND IMMUNITY LA English DT Note ID PURIFICATION; EXPRESSION; PEPTIDES AB Defensins are broad-spectrum antimicrobial peptides that are abundant in human, rat, and rabbit neutrophils. We now report that neutrophils from nine strains of mice lacked appreciable defensin content. Mice may therefore be imperfect experimental surrogates for humans or rats in models of infection in which neutrophil function is significant. C1 W LOS ANGELES VET ADM HOSP,LOS ANGELES,CA 90073. RP LEHRER, RI (reprint author), UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT MED,LOS ANGELES,CA 90024, USA. FU NIAID NIH HHS [AI-29595, AI22839] NR 16 TC 152 Z9 155 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD AUG PY 1992 VL 60 IS 8 BP 3446 EP 3447 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JG023 UT WOS:A1992JG02300059 PM 1639513 ER PT J AU LIU, H LAMPE, MA IREGUI, MV CANTOR, H AF LIU, H LAMPE, MA IREGUI, MV CANTOR, H TI CLONAL UNRESPONSIVENESS RESULTS FROM AN INTERACTION BETWEEN STAPHYLOCOCCAL-ENTEROTOXIN B-CELLS AND T-CELLS EXPRESSING UNEXPECTED V-BETA ELEMENTS SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE CD4+ T-CELL CLONE; T-CELL UNRESPONSIVENESS; V-BETA USAGE; STAPHYLOCOCCAL ENTEROTOXIN-B; SUPERANTIGEN ID INCOMPATIBLE STRAIN C3H; HUMAN LYMPHOCYTES-T; CONVENTIONAL ANTIGEN; NON-H-2 ANTIGENS; IMMUNE-RESPONSE; MICE; INDUCTION; RECEPTOR; STIMULATION; ACTIVATION AB The ability of staphylococcal toxins to stimulate large numbers of T cells has led to their designation as a superantigen. Previous studies have indicated that activation of T cells bearing particular V(beta) elements may be responsible for the toxic effects of these bacterial products. However, the widespread expression of functionally similar proteins by unrelated bacterial species suggests the possibility that these products may represent a successful microbial strategy for subversion of the host antibacterial response. We have examined the effects of the staphylococcal enterotoxin B (SEB) on T cell clones that express different V(beta) elements. We note that SEB stimulates clones bearing previously defined V(beta) elements to proliferate and to produce cytokines. In addition, we demonstrate that an interaction between SEB and the TCR of clones that express additional V(beta) elements, including V(beta)2 and V(beta)6, results in a sterile form of immunological activation. This activation phenotype is characterized by proliferation without detectable cytokine production and is followed by profound immunological unresponsiveness in vitro and in vivo. We propose that reduced levels of antibacterial responses resulting from this form of T cell unresponsiveness may account for the highly conserved expression of superantigens by diverse bacterial species. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOPATHOL LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI-13600, AI-12184] NR 44 TC 11 Z9 11 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD AUG PY 1992 VL 4 IS 8 BP 851 EP 859 DI 10.1093/intimm/4.8.851 PG 9 WC Immunology SC Immunology GA JH232 UT WOS:A1992JH23200003 PM 1358187 ER PT J AU MOINGEON, P LUCICH, JL REINHERZ, EL AF MOINGEON, P LUCICH, JL REINHERZ, EL TI CHARACTERIZATION OF FC-EPSILON-RI-GAMMA IN HUMAN NATURAL-KILLER-CELLS SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE FC RECEPTORS; NATURAL KILLER CELLS; SIGNAL TRANSDUCTION ID T-CELL; RECEPTOR COMPLEX; LYMPHOCYTES-T; EXPRESSION; CD3-ZETA; SUBUNIT; MEMBRANE; PATHWAYS; FAMILY; CHAIN AB We report the characterization of the Fc-epsilon-RI-gamma chain which associates with the transmembrane form of CD16 to form the low affinity receptor for IgG (Fc-gamma-RIII) expressed on human natural killer (NK) cells. cDNA cloning and sequence analysis of Fc-epsilon-RI-gamma from a polyclonal CD3-CD16+ NK line established that this molecule is identical to Fc-epsilon-RI-gamma previously identified in human basophils as part of a high affinity receptor for IgE. Polymerase chain reaction analysis of Fc-epsilon-RI-gamma-gene expression in a series of CD3+CD16- and CD3-CD16+ NK clones reveals that Fc-epsilon-RI-gamma is not directly linked to NK activity since clones of the CD3+CD16- phenotype lack Fc-epsilon-RI-gamma RNA but nevertheless mediate cytotoxicity. Taken together, these results demonstrate that the Fc-epsilon-RI-gamma molecule is expressed in various types within the hematopoietic system as part of multimeric surface receptors involved in different biological functions. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP MOINGEON, P (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115, USA. NR 24 TC 6 Z9 6 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD AUG PY 1992 VL 4 IS 8 BP 955 EP 958 DI 10.1093/intimm/4.8.955 PG 4 WC Immunology SC Immunology GA JH232 UT WOS:A1992JH23200015 PM 1419960 ER PT J AU SCHMIDT, J LEWANDROWSI, K WARSHAW, AL COMPTON, CC RATTNER, DW AF SCHMIDT, J LEWANDROWSI, K WARSHAW, AL COMPTON, CC RATTNER, DW TI MORPHOMETRIC CHARACTERISTICS AND HOMOGENEITY OF A NEW MODEL OF ACUTE-PANCREATITIS IN THE RAT SO INTERNATIONAL JOURNAL OF PANCREATOLOGY LA English DT Article DE ACUTE PANCREATITIS; EXPERIMENTAL; HOMOGENEITY; NECROSIS; HISTOPATHOLOGY; MODEL ID BILE-INDUCED PANCREATITIS; HEMORRHAGIC-PANCREATITIS; PRESSURE; DUCT AB Extreme maldistribution and immediate establishment of severe cellular injury are typical features of traditional bile salt models of acute pancreatitis; both factors complicate assessment and interpretation of therapeutic benefits in trials of experimental therapy. Even more important, both are indications not of the desired induction of pancreatitis but rather of local injury by barotrauma and noxious chemicals. This study contrasts the severity and regional variability of cellular injury in traditional high-dose bile salt models with that seen in a new preparation employing the combination of intravenous (iv) caerulein (CAE) and intraductal (id) low-dose glycodeoxycholic acid (GDOC). Thirty-six male Sprague-Dawley rats (350-450 g) were induced with (group A) high-dose GDOC id (34 mmol/L), low-dose GDOC id (10 mmol/L) (group B), or low-dose GDOC id combined with caerulein iv for 6 b (group C). The regional distribution of histopathologic injury within the pancreas was assessed in 20 fields/organ by two pathologists unaware of the induction technique used. High-dose GDOC id (group A) resulted in extremely heterogenous distribution of injury for all variables (edema, p = 0.001; acinar necrosis, p = 0.0001; inflammation, p = 0.0001; and hemorrhage p = 0.001). The lesions were confined to the head of the pancreas, which showed large areas of necrosis involving entire lobules, whereas adjacent areas were unaffected. Low-dose GDOC id (group B) was more homogenously distributed, but the injury was mild and regional variability (edema, p= 0.0001; acinar necrosis, p < 0.04; inflammation, p = 0.0001; and hemorrhage p < 0.05) was still demonstrable. In contrast, low-dose GDOC id combined with CAE iv (group C) produced moderately severe pancreatitis, which equally affected all areas of the gland. There were no geographical differences in acinar necrosis or inflammation. This feature of the new model provides a desirable prerequisite for accurate and reproducible assessment of histopathology in studies aimed at detecting effects of therapy. We suggest that it replace traditional id bile salt infusion models. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,ACC 337,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. NR 25 TC 68 Z9 128 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0169-4197 J9 INT J PANCREATOL JI Int. J. Pancreatol. PD AUG PY 1992 VL 12 IS 1 BP 41 EP 51 PG 11 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA KE559 UT WOS:A1992KE55900006 PM 1527449 ER PT J AU HUI, KY SIRAGY, HM HABER, E AF HUI, KY SIRAGY, HM HABER, E TI DESIGN OF POTENT SUBSTRATE-ANALOG INHIBITORS OF CANINE RENIN SO INTERNATIONAL JOURNAL OF PEPTIDE AND PROTEIN RESEARCH LA English DT Article DE CANINE RENIN; INHIBITORS ID PEPTIDES; ANGIOTENSINOGEN; SUBNANOMOLAR; PEPSTATIN; SEQUENCE; STATINE AB Through a systematic study of structure-activity relationships, we designed potent renin inhibitors for use in dog models. In assays against dog plasma renin at neutral pH, we found that, as in previous studies of rat renin inhibitors, the structure at the P2 position appears to be important for potency. The substitution of Val for His at this position increases potency by one order of magnitude. At the P3 position, potency appears to depend on a hydrophobic side chain that does not necessarilv have to be aromatic. Our results also support the approach of optimizing potency in a renin inhibitor bv introducing a moiety that promotes aqueous solubility (an amino group) at the C-terminus of the substrate analogue. In the design of potent dog plasma renin inhibitors, the influence of the transition-state residue 4(S)-amino-3(S)-hydroxy-5-cyclohexylpentanoic acid (ACHPA) - commonly used as a substitute for the scissile-bond dipeptide to boost potency - is not obvious, and appears to be sequence dependent. The canine renin inhibitor Ac-paF-Pro-Phe-Val-statine-Leu-Phe-paF-NH2 (compound 15; IC50 of 1.7 nm against dog plasma renin at pH 7.4; statine, 4(S)-amino-3(S)-hydroxy-6-methylheptanoic acid; paF, para-aminophenylalanine) had a potent hypotensive effect when infused intravenously into conscious, sodium-depleted, normotensive dogs. Also, compound 15 concurrently inhibited plasma renin activity and had a profound diuretic effect. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. UNIV VIRGINIA,MED CTR,SCH MED,CHARLOTTESVILLE,VA 22901. RP HUI, KY (reprint author), LILLY CORP CTR,LILLY RES LABS,INDIANAPOLIS,IN 46285, USA. NR 37 TC 4 Z9 4 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0367-8377 J9 INT J PEPT PROT RES JI Int. J. Pept. Protein Res. PD AUG PY 1992 VL 40 IS 2 BP 152 EP 160 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JQ312 UT WOS:A1992JQ31200012 PM 1446972 ER PT J AU GONG, JX ROSNER, B REES, DG BERSON, EL WEIGELDIFRANCO, CA SCHAEFER, EJ AF GONG, JX ROSNER, B REES, DG BERSON, EL WEIGELDIFRANCO, CA SCHAEFER, EJ TI PLASMA DOCOSAHEXAENOIC ACID LEVELS IN VARIOUS GENETIC FORMS OF RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE RETINITIS-PIGMENTOSA; DOCOSAHEXAENOIC ACID (22/6-OMEGA-3 4,7,10,13,16,19-DOCOSAHEXAENOIC ACID); FATTY ACIDS; RETINAL DEGENERATIONS; PLASMA ID FATTY-ACID; DEFICIENCY; MEMBRANES; PHOSPHOLIPIDS; METABOLISM; VITAMIN; LIPIDS; BRAIN; LIVER AB In 188 patients from separate families with various forms of retinitis pigmentosa (RP) and 91 normal subjects, plasma fatty acids were measured as a percentage of total plasma fatty acids, and their concentrations were determined using capillary-column gas-liquid chromatography. After controlling for the effects of age and gender, those with RP had significantly lower (P < 0.01) mean plasma percentages and concentrations of the omega-3 fatty acids: 18:3-omega-3 (alpha-linolenic acid), 22:3-omega-3 (13,16,19 docosatriaenoic acid), and 22:6-omega-3 (docosahexaenoic acid, DHA) compared with the group of normal subjects. The mean percentages were reduced 15%, 14%, and 10%, respectively, below the mean percentages in normal subjects. Analysis by genetic type revealed that the X-linked and isolate forms of RP had significantly lower (P < 0.01) mean percentage values for DHA (18% and 17%, respectively). Dominant and recessive forms of RP had DHA levels close to normal. Mean absolute plasma DHA concentrations in X-linked RP were not significantly different from the concentrations in the control subjects, although these levels were significantly lower in patients with isolate RP. These data identify the possibility that some forms of RP may have alterations in plasma omega-3 fatty acid metabolism resulting in decreased plasma DHA content. These observations await additional confirmation using an analysis of the fatty acid content of specific erythrocyte phospholipid classes. C1 TUFTS UNIV,SCH MED,LIPID METAB LAB,711 WASHINGTON ST,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. FU NEI NIH HHS [P50EY02014] NR 36 TC 53 Z9 53 U1 0 U2 2 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 AUG PY 1992 VL 33 IS 9 BP 2596 EP 2602 PG 7 WC Ophthalmology SC Ophthalmology GA JG614 UT WOS:A1992JG61400003 PM 1386350 ER PT J AU SCOTT, JA PALMER, EL FISCHMAN, AJ STRAUSS, HW AF SCOTT, JA PALMER, EL FISCHMAN, AJ STRAUSS, HW TI METEOROLOGICAL INFLUENCES ON THE FREQUENCY OF PULMONARY-EMBOLISM SO INVESTIGATIVE RADIOLOGY LA English DT Article DE BAROMETRIC PRESSURE; ENVIRONMENT; LUNGS; METEOROLOGY; PULMONARY EMBOLISM AB RATIONALE AND OBJECTIVES. Reports published earlier this century suggested that meteorologic factors influence the incidence of pulmonary embolism. These observations were based on few patients and often lacked rigorous standards of evidence. In the current study, the authors evaluate the association between barometric pressure changes and pulmonary embolism using radionuclide ventilation-perfusion (V/Q) scan data. METHODS. Daily interpretation data for V/Q lung scans were correlated retrospectively with daily local barometric pressure changes over a 7-year period. RESULTS. The incidence of pulmonary embolic disease was significantly related to a decrease in barometric pressure during the 3 days preceding clinical presentation. CONCLUSIONS. Meteorologic factors are less important than better-known risk factors for pulmonary embolism; however, their effect is demonstrable in a large data sample. This work confirms previously published associations between barometric pressure changes and the incidence of pulmonary embolism. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP SCOTT, JA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114, USA. NR 13 TC 15 Z9 15 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD AUG PY 1992 VL 27 IS 8 BP 583 EP 586 DI 10.1097/00004424-199208000-00005 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JH649 UT WOS:A1992JH64900004 PM 1428735 ER PT J AU RUNGE, VM BRONEN, RA DAVIS, KR AF RUNGE, VM BRONEN, RA DAVIS, KR TI EFFICACY OF GADOTERIDOL FOR MAGNETIC-RESONANCE-IMAGING OF THE BRAIN AND SPINE SO INVESTIGATIVE RADIOLOGY LA English DT Article DE BRAIN, MAGNETIC RESONANCE STUDIES; GADOLINIUM; GADOTERIDOL; MAGNETIC RESONANCE, CONTRAST ENHANCEMENT; SPINE, MAGNETIC RESONANCE STUDIES ID GADOLINIUM-DTPA; GD-DTPA; MR; DISEASE; TUMORS AB RATIONALE AND OBJECTIVES. The efficacy of gadoteridol for contrast enhancement of central nervous system pathology was assessed in a multicenter clinical trial involving 411 patients suspected of having intracranial or spinal pathology. METHODS. Magnetic resonance imaging was performed before and after intravenous administration of 0.10 mmol/kg gadoteridol. Two groups of images were interpreted by one of two neuroradiologists blinded to patient history. The results were analyzed separately. RESULTS. Patients with radiologic evidence of disease demonstrated enhancement of intracranial pathologic lesions in 44 of 63 (70%) and in 91 of 111 (82%) cases, respectively, whereas enhancement of spinal lesions was observed in 36 of 58 (62%) and in 65 of 78 (83%) cases, respectively. Subjectively, postcontrast scans provided more information than precontrast images in 37 of 63 (59%) and 84 of 111 (76%) intracranial cases, respectively, and in 25 of 58 (43%) and 55 of 78 (71%) spinal cases, respectively. Additional information included the subjective sense that there was improved visualization of pathology and definition of lesion borders. CONCLUSIONS. Subjective assessment of magnetic resonance scans suggest gadoteridol is an effective intravenous contrast agent for magnetic resonance imaging. C1 YALE UNIV,DEPT DIAGNOST RADIOL,NEW HAVEN,CT 06520. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT DIAGNOST RADIOL,BOSTON,MA 02114. RP RUNGE, VM (reprint author), UNIV KENTUCKY,CTR MAGNET RESONANCE IMAGING & SPECT,DEPT RADIOL,HM103 MED CTR,LEXINGTON,KY 40536, USA. NR 11 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD AUG PY 1992 VL 27 SU 1 BP S22 EP S32 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JH663 UT WOS:A1992JH66300006 PM 1506150 ER PT J AU SAINI, S AF SAINI, S TI FUTURE APPLICATIONS OF MAGNETIC-RESONANCE CONTRAST AGENTS IN THE ABDOMEN SO INVESTIGATIVE RADIOLOGY LA English DT Article ID CT; LIVER; TUMOR C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SAINI, S (reprint author), HARVARD UNIV,SCH MED,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02115, USA. NR 17 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD AUG PY 1992 VL 27 SU 1 BP S61 EP S63 DI 10.1097/00004424-199208001-00012 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JH663 UT WOS:A1992JH66300012 PM 1506156 ER PT J AU KAUFMANN, R LAROCHE, D BUCHNER, K HUCHO, F RUDD, C LINDSCHAU, C LUDWIG, P HOER, A OBERDISSE, E KOPP, J KORNER, IJ REPKE, H AF KAUFMANN, R LAROCHE, D BUCHNER, K HUCHO, F RUDD, C LINDSCHAU, C LUDWIG, P HOER, A OBERDISSE, E KOPP, J KORNER, IJ REPKE, H TI THE HIV-1 SURFACE PROTEIN GP120 HAS NO EFFECT ON TRANSMEMBRANE SIGNAL TRANSDUCTION IN T-CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1; CD4; GP120; CALCIUM; INOSITOL PHOSPHATES; ARACHIDONIC ACID; PROTEIN KINASE-C; TYROSINE PHOSPHORYLATION ID HUMAN-IMMUNODEFICIENCY-VIRUS; HUMAN LYMPHOCYTES-T; ENVELOPE GLYCOPROTEIN; CD4; ACTIVATION; TYPE-1; RECEPTOR; BINDING; ASSOCIATION; INHIBITION AB The ability of HIV-1 envelope glycoprotein gp120 to induce transmembrane signaling processes in human T cells and tumor T-cell lines was investigated. Differently glycosylated gp120 preparations were characterized with respect to their purity, the fraction of native gp120, and the affinity of the gp120-CD4 interaction. These data were used to establish experimental conditions that allow a substantial fraction of the CD4 receptor to be complexed with gp120 in the course of the experiments. The results are in contrast to several previous studies since no effect of gp120 on the intracellular Ca2+ concentration, the metabolism of inositol phosphates and arachidonic acid, protein kinase C translocation, and tyrosine phosphorylation was found. Cross-linking of the gp120:CD4 complex by anti-gp120 antibodies did not elicit additional effects. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. HUMBOLDT UNIV,INST PHARMACOL & TOXICOL,O-1086 BERLIN,GERMANY. HUMBOLDT UNIV,INST PHYSIOL & BIOL CHEM,O-1086 BERLIN,GERMANY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV TUMOR IMMUNOL,BOSTON,MA 02115. FREE UNIV BERLIN,KLINIKUM STEGLITZ,INST BIOCHEM,W-1000 BERLIN 45,GERMANY. FREE UNIV BERLIN,KLINIKUM STEGLITZ,INST PHARMACOL,W-1000 BERLIN 45,GERMANY. FREE UNIV BERLIN,KLINIKUM STEGLITZ,MED KLIN,W-1000 BERLIN 45,GERMANY. CTR MOLEC MED,BERLIN,GERMANY. RI Lindschau, Carsten/G-1798-2011 OI Lindschau, Carsten/0000-0003-1960-099X FU NCI NIH HHS [P30 CA 06516]; NIAID NIH HHS [AI24845] NR 35 TC 10 Z9 10 U1 0 U2 2 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 AUG PY 1992 VL 5 IS 8 BP 760 EP 770 PG 11 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JE582 UT WOS:A1992JE58200002 PM 1325556 ER PT J AU FAVA, M ROSENBAUM, JF COHEN, L REITER, S MCCARTHY, M STEINGARD, R CLANCY, K AF FAVA, M ROSENBAUM, JF COHEN, L REITER, S MCCARTHY, M STEINGARD, R CLANCY, K TI HIGH-DOSE FLUOXETINE IN THE TREATMENT OF DEPRESSED-PATIENTS NOT RESPONSIVE TO A STANDARD DOSE OF FLUOXETINE SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Article DE DEPRESSION; FLUOXETINE; TREATMENT REFRACTORY ID ANTIDEPRESSANT; SEROTONIN AB In a four-week, open label study of major depression, 15 patients who had failed to respond to a trial of fluoxetine 20 mg/day of 8-12 weeks duration were then treated with fluoxetine 40 mg/day for one week and then, if tolerated, with either 60 or 80 mg/day. The mean HAM-D-17 and CGIS scores of these 15 patients decreased significantly at the end of 4 weeks on a higher dosage of fluoxetine (60 or 80 mg/day) with respect to the beginning of the four-week study. No significant side-effects were noted. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,ACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 14 TC 39 Z9 39 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0327 J9 J AFFECT DISORDERS JI J. Affect. Disord. PD AUG PY 1992 VL 25 IS 4 BP 229 EP 234 DI 10.1016/0165-0327(92)90080-P PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JN272 UT WOS:A1992JN27200003 PM 1430659 ER PT J AU LEFEBVRE, XP YOGANATHAN, AP LEVINE, RA AF LEFEBVRE, XP YOGANATHAN, AP LEVINE, RA TI INSIGHTS FROM INVITRO FLOW VISUALIZATION INTO THE MECHANISM OF SYSTOLIC ANTERIOR MOTION OF THE MITRAL-VALVE IN HYPERTROPHIC CARDIOMYOPATHY UNDER STEADY FLOW CONDITIONS SO JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME LA English DT Article; Proceedings Paper CT SYMP ON HEMODYNAMICS AND THE ARTERIAL WALL CY SEP 02-04, 1990 CL LA JOLLA, CA ID EXTENT; SHAPE AB Hypertrophic obstructive cardiomyopathy is a heart disease characterized by a thickened interventricular septum which narrows the left ventricular outflow tract, and by systolic anterior motion (SAM) of the mitral value which can contact the septum and create dynamic subaortic obstruction. The most common explanation for SAM has been the Venturi mechanism which postulates that septal hypertrophy, by narrowing the outflow tract, produces high velocities and thus low pressure between the mitral valve and the septum, causing the valve leaflets to move anteriorly. This hypothesis, however, fails to explain why SAM often begins early in systole, when outflow tract velocities are low or negligible or why it may occur in the absence of septal hypertrophy. The goal of this study was therefore to investigate an alternative hypothesis in which structural abnormalities of the papillary muscles act as a primary cause of SAM by altering valve restraint and thereby changing the geometry of the closed mitral apparatus and its relationship to the surrounding flow field. In order to test this hypothesis, an in vitro model of the left ventricle which included an explanted human mitral valve with intact chords and papillary muscle apparatus was constructed. Flow visualization was used to observe the ventricular flow field and the mitral valve geometry. Displacing the papillary muscles anteriorly and closer to each other, as observed clinically in patients with cardiomyopathy and obstruction produced SAM in the absence of septal hypertrophy. Flow could be seen impacting on the upstream (posterior) surface of the leaflets; suchflow is capable of producing form drag forces which can initiate and maintain SAM. In contrast, increasing septal hypertrophy to narrow the outflow tract and create velocities as high as 3.3 m/s did not produce SAM in the absence of papillary muscle displacement, despite an increase in the calculated lift forces. Therefore, primary abnormalities of the papillary muscle-mitral valve apparatus can alter the relationship of the mitral valve to the surrounding flow field in such a way that SAM is generated, whereas the Venturi mechanism, induced by septal hypertrophy alone, is insufficient to do so with a normally positioned and tethered valve. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC ULTRASOUND LAB,BOSTON,MA 02114. RP LEFEBVRE, XP (reprint author), GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID DYNAM LAB,ATLANTA,GA 30332, USA. FU NHLBI NIH HHS [HL-34392, R29HL-38176] NR 21 TC 20 Z9 21 U1 0 U2 1 PU ASME-AMER SOC MECHANICAL ENG PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 SN 0148-0731 J9 J BIOMECH ENG-T ASME JI J. Biomech. Eng.-Trans. ASME PD AUG PY 1992 VL 114 IS 3 BP 406 EP 413 DI 10.1115/1.2891402 PG 8 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA JK893 UT WOS:A1992JK89300020 PM 1387919 ER PT J AU TANZER, M DRUCKER, D JASTY, M MCDONALD, M HARRIS, WH AF TANZER, M DRUCKER, D JASTY, M MCDONALD, M HARRIS, WH TI REVISION OF THE ACETABULAR COMPONENT WITH AN UNCEMENTED HARRIS-GALANTE POROUS-COATED PROSTHESIS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID TOTAL HIP-REPLACEMENT; 10-YEAR FOLLOW-UP; METAL; BONE AB One hundred and forty revisions for loosening of the acetabular component were performed in 124 patients, with the use of an uncemented Harris-Galante acetabular prosthesis. A component was considered loose if there was a change in its position or vertical or horizontal migration, or both, of four millimeters or more, as demonstrated on serial radiographs. All patients were followed prospectively for a mean of forty-one months (range, twenty-four to seventy-six months). Bone-grafting was performed at the time of the revision in 127 of the hips. Identifiable failure of fixation of the acetabular component occurred in only two hips (1 per cent), which had both severe acetabular bone loss and pelvic discontinuity. In one of these hips, fixation of the component could not be achieved during the revision, and the component subsequently migrated. No other components migrated. Only one patient had a revision of the index acetabular operation. A continuous radiolucency developed at the bone-mesh interface of five acetabular components, and in one other hip a small portion of the mesh separated. This hip was reoperated on for a problem with the femur, and the socket was found to be rigidly fixed. No other evidence of loosening was identified. All of the bone grafts united, but partial resorption of the graft occurred in thirty-nine hips. Although there were substantial osseous defects that necessitated major bone-grafting, revision with the uncemented Harris-Galante porous-coated acetabular component provided superior fixation compared with that reported in other series in which cemented acetabular components were used for revision. Of the 140 hips, eighty-nine (64 per cent) had a postoperative score of good or excellent, according-to the Harris hip-rating system. Twenty-eight (70 per cent) of the forty hips that had revision of the acetabular component alone were rated as good or excellent. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. NR 34 TC 123 Z9 124 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 AUG PY 1992 VL 74A IS 7 BP 987 EP 994 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JN515 UT WOS:A1992JN51500005 PM 1522106 ER PT J AU ENGH, CA MCGOVERN, TF BOBYN, JD HARRIS, WH AF ENGH, CA MCGOVERN, TF BOBYN, JD HARRIS, WH TI A QUANTITATIVE-EVALUATION OF PERIPROSTHETIC BONE-REMODELING AFTER CEMENTLESS TOTAL HIP-ARTHROPLASTY SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID DUAL PHOTON-ABSORPTIOMETRY; LUMBAR SPINE; REPLACEMENT; DESIGN AB Dual-energy x-ray absorptiometry analysis was used to determine the periprosthetic bone-mineral content of ten femora that had been obtained at the autopsies of rive elderly patients who had had an AML (anatomic medullary locking) prosthesis in situ for seventeen to eighty-four months. Clinical radiographs showed resorptive remodeling changes characteristic of femora containing this implant. Before the absorptiometry was performed, an identical prosthesis had been inserted into the contralateral, normal femur of each cadaver. The mean difference in the periprosthetic bone-mineral content between the remodeled femora and the femora in which the prosthesis had been implanted post mortem ranged from 7 to 52 per cent, with the bone-mineral content always less in the remodeled femora. The greatest mean decrease in bone-mineral content (45 per cent) occurred adjacent to the proximal one-third of the remodeled femora. The percentage decrease in periprosthetic bone-mineral content in the remodeled femora had an inverse linear relationship with the corresponding bone-mineral content of the contralateral control femora. Preoperative analysis of bone density may therefore be useful for prediction of the extent of resorptive bone-remodeling after total hip replacement. C1 MONTREAL GEN HOSP,MONTREAL H3G 1A4,QUEBEC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP ENGH, CA (reprint author), ANDERSON ORTHOPAED RES INST,2445 ARMY NAVY DR,ARLINGTON,VA 22206, USA. NR 25 TC 234 Z9 237 U1 1 U2 11 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 AUG PY 1992 VL 74A IS 7 BP 1009 EP 1020 PG 12 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JN515 UT WOS:A1992JN51500007 PM 1522088 ER PT J AU ARNOLD, A BROWN, M URENA, P DRUEKE, T SARFATI, E AF ARNOLD, A BROWN, M URENA, P DRUEKE, T SARFATI, E TI X-INACTIVATION ANALYSIS OF CLONALITY IN PRIMARY AND SECONDARY PARATHYROID HYPERPLASIA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HOP NECKER ENFANTS MALAD,F-75730 PARIS 15,FRANCE. HOP ST LOUIS,F-75010 PARIS,FRANCE. NR 0 TC 5 Z9 5 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S153 EP S153 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500241 ER PT J AU BAUER, RL HAFFNER, SM AF BAUER, RL HAFFNER, SM TI AXIAL SKELETAL BONE-DENSITY IN MEXICAN-AMERICAN (MA) AND NON-HISPANIC WHITE (NHW) WOMEN SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 5 Z9 5 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S195 EP S195 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500410 ER PT J AU BIANCHI, S FABIANI, S ARNOLD, A BRANDI, ML AF BIANCHI, S FABIANI, S ARNOLD, A BRANDI, ML TI CALCIUM MODULATES THE EXPRESSION OF CYCLIN-D1 IN A PARATHYROID CELL-LINE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV FLORENCE,I-50121 FLORENCE,ITALY. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S242 EP S242 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500597 ER PT J AU BRINGHURST, FR ABOUSAMRA, AB JUPPNER, H SEGRE, GV AF BRINGHURST, FR ABOUSAMRA, AB JUPPNER, H SEGRE, GV TI PTH REGULATES PHOSPHATE-UPTAKE IN PTH RECEPTOR-TRANSFECTED LLC-PK1 CELLS INDEPENDENTLY OF CYCLIC-AMP, PHOSPHOLIPASE-C OR CALCIUM SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S145 EP S145 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500210 ER PT J AU BYRNE, MH WU, H BIRKHEAD, JR GOLDRING, MB JAENISCH, R KRANE, SM AF BYRNE, MH WU, H BIRKHEAD, JR GOLDRING, MB JAENISCH, R KRANE, SM TI SLIDING THE COLLAGENASE CLEAVAGE SITE IN THE ALPHA-1(I) CHAIN OUT OF PHASE WITH THE ALPHA-2(I) CHAIN CONFERS COLLAGENASE RESISTANCE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MIT,WHITEHEAD INST,CAMBRIDGE,MA 02142. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S131 EP S131 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500155 ER PT J AU CHOREV, M CAULFIELD, MP LEU, CT LEVY, JL FLANNERY, M GOLDRING, SR ROSENBLATT, M AF CHOREV, M CAULFIELD, MP LEU, CT LEVY, JL FLANNERY, M GOLDRING, SR ROSENBLATT, M TI DESIGN AND EVALUATION OF NOVEL CALCITONIN LIGANDS TO STUDY THE CONTACT POINTS BETWEEN CALCITONIN AND ITS CLONED RECEPTOR SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. MERCK SHARP & DOHME LTD,W POINT,PA 19486. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S243 EP S243 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500600 ER PT J AU CRYNS, VL ARNOLD, A AF CRYNS, VL ARNOLD, A TI RETINOBLASTOMA TUMOR SUPPRESSOR GENE DELETIONS IN HUMAN PARATHYROID NEOPLASIA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S101 EP S101 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500036 ER PT J AU DEMAY, M KIERNAN, MS KRONENBERG, HM AF DEMAY, M KIERNAN, MS KRONENBERG, HM TI CHARACTERIZATION OF SEQUENCES IN THE HUMAN PARATHYROID-HORMONE GENE THAT MEDIATE TRANSCRIPTIONAL REPRESSION IN RESPONSE TO 1,25-DIHYDROXYVITAMIN-D(3) SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S145 EP S145 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500212 ER PT J AU FINKELSTEIN, J MITLAK, B SLOVIK, D NEER, R AF FINKELSTEIN, J MITLAK, B SLOVIK, D NEER, R TI A NOVEL AND IMPROVED METHOD FOR CALIBRATING DUAL ENERGY X-RAY DENSITOMETERS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S191 EP S191 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500396 ER PT J AU FREYALDENHOVENKITTEN, AM KATZ, MS AF FREYALDENHOVENKITTEN, AM KATZ, MS TI BIDIRECTIONAL MODULATION OF PARATHYROID HORMONE-RESPONSIVE ADENYLATE-CYCLASE BY PROTEIN-KINASE-C SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S104 EP S104 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500048 ER PT J AU GOLDRING, SR FLANNERY, MS MANNING, CA GORN, AH AF GOLDRING, SR FLANNERY, MS MANNING, CA GORN, AH TI ANALYSIS OF THE MECHANISMS INVOLVED IN THE UNIQUE INTERACTION OF CALCITONIN (CT) WITH ITS RECEPTOR SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S239 EP S239 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500587 ER PT J AU JUPPNER, H GARDELLA, T LEE, CW SCHIPANI, E NUSSBAUM, S KRONENBERG, HM ABOUSAMRA, AB SEGRE, GV AF JUPPNER, H GARDELLA, T LEE, CW SCHIPANI, E NUSSBAUM, S KRONENBERG, HM ABOUSAMRA, AB SEGRE, GV TI MAPPING OF A LIGAND-BINDING DOMAIN BY USING MUTANT PTH PTHRP RECEPTORS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S93 EP S93 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500002 ER PT J AU KARAPLIS, AC TYBULEWICZ, V MULLIGAN, RC KRONENBERG, HM AF KARAPLIS, AC TYBULEWICZ, V MULLIGAN, RC KRONENBERG, HM TI DISRUPTION OF PARATHYROID HORMONE-RELATED PEPTIDE GENE LEADS TO A MULTITUDE OF SKELETAL ABNORMALITIES AND PERINATAL-MORTALITY SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. NR 0 TC 9 Z9 9 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S93 EP S93 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500001 ER PT J AU KRANE, SM CONCA, W AOUNWATHNE, M AURON, PE AF KRANE, SM CONCA, W AOUNWATHNE, M AURON, PE TI SEPARATE EVENTS ARE REQUIRED FOR OPTIMAL INDUCTION OF LATE GENES IN FIBROBLASTS BY INTERLEUKIN-1-BETA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ARTHRITIS UNIT,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S131 EP S131 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500154 ER PT J AU LEE, K WEAVER, DR BOND, AT SEGRE, GV AF LEE, K WEAVER, DR BOND, AT SEGRE, GV TI LOCALIZATION OF PTHRP AND PTH PTHRP RECEPTOR MESSENGER-RNAS IN THE RAT CENTRAL-NERVOUS-SYSTEM BY INSITU HYBRIDIZATION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEV CHRONOBIOL LAB,BOSTON,MA 02114. NR 1 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S246 EP S246 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500613 ER PT J AU LEE, K KARAPLIS, A BOND, AT SEGRE, GV AF LEE, K KARAPLIS, A BOND, AT SEGRE, GV TI EXPRESSION OF PTHRP AND PTH PTHRP RECEPTOR TRANSCRIPTS IS NOT SPATIALLY OR TEMPORALLY CORRELATED IN RAT FETAL DEVELOPMENT SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S134 EP S134 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500166 ER PT J AU LEE, K BOND, AT SAITO, H CHIBA, S SEGRE, GV AF LEE, K BOND, AT SAITO, H CHIBA, S SEGRE, GV TI VISUALIZATION OF PTH ACTION IN INTACT BONE - DIFFERENTIAL INDUCTION OF THE PROTOONCOGENE C-FOS BY PTH SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S107 EP S107 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500058 ER PT J AU LI, YP STASHENKO, P AF LI, YP STASHENKO, P TI MAPPING STUDIES OF A TUMOR-NECROSIS-FACTOR RESPONSIVE ELEMENT IN THE OSTEOCALCIN 5'-FLANKING REGION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S131 EP S131 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500156 ER PT J AU ORLOFF, JJ URENA, P SCHIPANI, E RIBAUDO, AE MILSTONE, LM PHILBRICK, WM ABOUSAMRA, AB SEGRE, GV JUEPPNER, H AF ORLOFF, JJ URENA, P SCHIPANI, E RIBAUDO, AE MILSTONE, LM PHILBRICK, WM ABOUSAMRA, AB SEGRE, GV JUEPPNER, H TI HUMAN SQUAMOUS CARCINOMA-CELLS AND NORMAL HUMAN KERATINOCYTES EXPRESS MESSENGER-RNAS RELATED TO BUT DISTINCT FROM HUMAN PTH RECEPTOR MESSENGER-RNA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,W HAVEN,CT 06516. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S230 EP S230 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500552 ER PT J AU PEACOCK, M JOHNSTON, CC LONGCOPE, C MCCLINTOCK, R CLEMENS, D HILL, CS AF PEACOCK, M JOHNSTON, CC LONGCOPE, C MCCLINTOCK, R CLEMENS, D HILL, CS TI BIOMARKERS OF BONE TURNOVER - RELATIVE VALUE IN RELATION TO ESTROGEN STATUS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 INDIANA UNIV,SCH MED,INDIANAPOLIS,IN 46202. OSTEX INT,SEATTLE,WA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HYBRITECH INC,SAN DIEGO,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S326 EP S326 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500932 ER PT J AU PIROLA, CJ WANG, HM WU, S OKANO, K JUPPNER, H ABOUSAMRA, AB SEGRE, GV FORRESTER, JS FAGIN, JA CLEMENS, TL AF PIROLA, CJ WANG, HM WU, S OKANO, K JUPPNER, H ABOUSAMRA, AB SEGRE, GV FORRESTER, JS FAGIN, JA CLEMENS, TL TI REGULATED EXPRESSION OF PARATHYROID HORMONE-RELATED PROTEIN AND ITS RECEPTOR MESSENGER-RNA IN RAT AORTIC SMOOTH-MUSCLE CELLS SUGGESTS AN AUTOCRINE VASOACTIVE ROLE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S144 EP S144 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500207 ER PT J AU REDDY, SV KUZHANDAIVELU, N TAKAHASHI, S HOSKING, D SINGER, FR ROODMAN, GD AF REDDY, SV KUZHANDAIVELU, N TAKAHASHI, S HOSKING, D SINGER, FR ROODMAN, GD TI PARAMYXOVIRAL TRANSCRIPTS ARE EXPRESSED IN FRESHLY ISOLATED MARROW-CELLS AND MARROW-DERIVED MULTINUCLEATED CELLS (MNC) FROM PAGETS PATIENTS BUT NOT FROM NORMALS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. CITY HOSP NOTTINGHAM,NOTTINGHAM NG5 1PD,ENGLAND. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S115 EP S115 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500091 ER PT J AU REDDY, SV SCARCEZ, T WINDLE, J LEACH, R ROBERTS, M CHOU, J ROODMAN, GD AF REDDY, SV SCARCEZ, T WINDLE, J LEACH, R ROBERTS, M CHOU, J ROODMAN, GD TI FUNCTIONAL-CHARACTERIZATION OF THE 5' FLANKING SEQUENCE FOR MURINE TARTRATE RESISTANT ACID-PHOSPHATASE (TRAP) SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S111 EP S111 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500076 ER PT J AU SCHIPANI, E KARGA, H KARAPLIS, AC HELLMAN, P XIE, LY POTTS, JT KRONENBERG, HM ABOUSAMRA, AB SEGRE, GV JUPPNER, H AF SCHIPANI, E KARGA, H KARAPLIS, AC HELLMAN, P XIE, LY POTTS, JT KRONENBERG, HM ABOUSAMRA, AB SEGRE, GV JUPPNER, H TI CHARACTERIZATION OF THE CDNA-ENCODING THE HUMAN PTH/PTHRP RECEPTOR SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S246 EP S246 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500612 ER PT J AU SLOVIK, D MINASSIAN, P AF SLOVIK, D MINASSIAN, P TI FUNCTIONAL OUTCOME IN ELDERLY HIP FRACTURE PATIENTS TREATED IN A REHABILITATION HOSPITAL SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 SPAULDING REHABIL HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S330 EP S330 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500945 ER PT J AU TAKAHASHI, S REDDY, S ROODMAN, GD AF TAKAHASHI, S REDDY, S ROODMAN, GD TI DEVELOPMENT OF A HUMAN MARROW STROMAL CELL-LINE THAT ENHANCES OSTEOCLAST-LIKE MULTINUCLEATED CELL (MNC) FORMATION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S315 EP S315 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500888 ER PT J AU THIEDE, MA PETERSEN, DN GRASSER, WA JUEPPNER, H ABOUSAMRA, AB SEGRE, GV AF THIEDE, MA PETERSEN, DN GRASSER, WA JUEPPNER, H ABOUSAMRA, AB SEGRE, GV TI COEXPRESSION OF PTHRP AND PTH/PTHRP RECEPTOR MESSENGER-RNA IN VASCULATURE SUPPORTS A LOCAL MECHANISM OF ACTION IN CARDIOVASCULAR TISSUES SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 PFIZER INC,CENT RES,GROTON,CT 06340. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 6 Z9 6 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S240 EP S240 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500590 ER PT J AU URENA, P LEE, K WEAVER, D KONG, XF BROWN, D BOND, AT ABOUSAMRA, AB SEGRE, GV AF URENA, P LEE, K WEAVER, D KONG, XF BROWN, D BOND, AT ABOUSAMRA, AB SEGRE, GV TI PTH PTHRP RECEPTOR MESSENGER-RNA EXPRESSION AS ASSESSED BY NORTHERN BLOT AND INSITU HYBRIDIZATION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S118 EP S118 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500103 ER PT J AU URENA, P IIDAKLEIN, A KONG, XF ABOUSAMRA, AB SEGRE, GV AF URENA, P IIDAKLEIN, A KONG, XF ABOUSAMRA, AB SEGRE, GV TI REGULATION OF THE PTH PTHRP RECEPTOR MESSENGER-RNA BY GLUCOCORTICOIDS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S125 EP S125 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500131 ER PT J AU YAMIN, R FUKUO, K BIRKHEAD, JR GOLDRING, MB AF YAMIN, R FUKUO, K BIRKHEAD, JR GOLDRING, MB TI REGULATION OF EARLY GENE-EXPRESSION IN HUMAN CHONDROCYTES - SPECIFIC INDUCTION OF EGR-1 MESSENGER-RNA BY INTERLEUKIN-1 SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S120 EP S120 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500109 ER PT J AU YEH, CK HYMER, TK KATZ, MS AF YEH, CK HYMER, TK KATZ, MS TI LACK OF PARATHYROID-HORMONE RESPONSE IN RAT MANDIBULAR BONE-CELLS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT DENT DIAG SCI,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S205 EP S205 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500450 ER PT J AU ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA AF ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA TI COMPARISON OF THE CARDIAC AND HEMODYNAMIC-EFFECTS OF LISINOPRIL AND ATENOLOL IN PATIENTS WITH HYPERTENSION - THERAPEUTIC IMPLICATIONS SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE DIASTOLIC FUNCTION; RADIONUCLIDE CINEANGIOGRAPHY; EXERCISE; LUSITROPY ID LEFT-VENTRICULAR HYPERTROPHY; ANTIHYPERTENSIVE THERAPY; DIASTOLIC FUNCTION; PROPRANOLOL; REGRESSION; CAPTOPRIL; ENALAPRIL; EXERCISE; DISEASE AB The antihypertensive and hemodynamic effects of lisinopril and atenolol were evaluated in 21 patients with mild-to-moderate essential hypertension. Left ventricular systolic and diastolic performances were assessed prior to and following treatment by first-pass radionuclide cineangiography at rest and during peak upright bicycle exercise. Both lisinopril and atenolol treatment significantly reduced the blood pressure. Lisinopril therapy was associated with a reduction in systemic vascular resistance and left ventricular end-diastolic and end-systolic volumes but no change in stroke volume, cardiac output, peak ejection rate, peak filling rate, time to peak ejection rate, or time to peak filling rate. In contrast, atenolol therapy was associated with an increase in end-diastolic volume and stroke volume but no change in cardiac output; the left ventricular peak ejection and peak filling rates were decreased by atenolol treatment. Although both lisinopril and atenolol each significantly reduced the blood pressure, lisinopril had no effect on left ventricular systolic or diastolic performance; in contrast, atenolol decreased both systolic and diastolic parameters of ventricular performance. Left ventricular function may be affected in significantly different ways despite apparent similarities in blood pressure control in patients who respond to angiotensin converting enzyme inhibition or beta-adrenergic receptor blockade. Differences in hemodynamic response to an antihypertensive agent may be important in the selection of a drug for the treatment of subsets of patients with cardiac function abnormalities. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZUSMAN, RM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,DIV HYPERTENS & VASC MED,CARDIAC UNIT,BOSTON,MA 02114, USA. NR 28 TC 7 Z9 8 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PD AUG PY 1992 VL 20 IS 2 BP 216 EP 222 DI 10.1097/00005344-199208000-00006 PG 7 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA JE853 UT WOS:A1992JE85300006 PM 1381012 ER PT J AU BACKER, JM SHOELSON, SE WEISS, MA HUA, QX CHEATHAM, RB HARING, E CAHILL, DC WHITE, MF AF BACKER, JM SHOELSON, SE WEISS, MA HUA, QX CHEATHAM, RB HARING, E CAHILL, DC WHITE, MF TI THE INSULIN-RECEPTOR JUXTAMEMBRANE REGION CONTAINS 2 INDEPENDENT TYROSINE BETA-TURN INTERNALIZATION SIGNALS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID HUMAN TRANSFERRIN RECEPTOR; DENSITY-LIPOPROTEIN RECEPTOR; CYTOPLASMIC DOMAIN; COATED PITS; MEDIATED INTERNALIZATION; RAPID ENDOCYTOSIS; KINASE-ACTIVITY; DOWN-REGULATION; AMINO-ACIDS; MUTATION AB We have investigated the role of tyrosine residues in the insulin receptor cytoplasmic juxtamembrane region (Tyr953 and Tyr960) during endocytosis. Analysis of the secondary structure of the juxtamembrane region by the Chou-Fasman algorithms predicts that both the sequences GPLY953 and NPEY960 form tyrosine-containing beta-turns. Similarly, analysis of model peptides by 1-D and 2-D NMR show that these sequences form beta-turns in solution, whereas replacement of the tyrosine residues with alanine destabilizes the beta-turn. CHO cell lines were prepared expressing mutant receptors in which each tyrosine was mutated to phenylalanine or alanine, and an additional mutant contained alanine at both positions. These mutations had no effect on insulin binding or receptor autophosphorylation. Replacements with phenylalanine had no effect on the rate of [I-125]insulin endocytosis, whereas single substitutions with alanine reduced [I-125]insulin endocytosis by 40-50%. Replacement of both tyrosines with alanine reduced internalization by 70%. These data suggest that the insulin receptor contains two tyrosine/beta-turns which contribute independently and additively to insulin-stimulated endocytosis. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP BACKER, JM (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK-36836, DK-38712] NR 50 TC 105 Z9 105 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 AUG PY 1992 VL 118 IS 4 BP 831 EP 839 DI 10.1083/jcb.118.4.831 PG 9 WC Cell Biology SC Cell Biology GA JJ106 UT WOS:A1992JJ10600006 PM 1500426 ER PT J AU SELSTED, ME MILLER, SI HENSCHEN, AH OUELLETTE, AJ AF SELSTED, ME MILLER, SI HENSCHEN, AH OUELLETTE, AJ TI ENTERIC DEFENSINS - ANTIBIOTIC PEPTIDE COMPONENTS OF INTESTINAL HOST DEFENSE SO JOURNAL OF CELL BIOLOGY LA English DT Article ID SALMONELLA-TYPHIMURIUM VIRULENCE; PANETH CELLS; NEUTROPHIL DEFENSIN; PHOP-PHOQ; MOUSE; EPITHELIUM; RESISTANCE; PROTEINS; LYSOZYME; LOCUS AB Five intestinal defensins, termed cryptdins 1-5, have been purified from mouse small bowel, sequenced, and localized to the epithelium by immunohistochemistry. Although identified as members of th defensin peptide family by peptide sequencing, enteric defensins are novel in that four cryptdins have amino termini which are three to six residues longer than those of leukocyte-derived defensins. A fifth cryptdin is the first defensin to diverge from the previously invariant spacing of cysteines in the peptide structure. The most abundant enteric defensin, cryptdin-1, had antimicrobial activity against an attenuated phoP mutant of Salmonella typhimurium but was not active against the virulent wild-type parent. Immunohistochemical localization demonstrated that cryptdin-1, and probably cryptdins 2 and 3, occur exclusively in Paneth cells, where the peptides appear to be associated with cytoplasmic granules. Biochemical and immunologic analysis of the luminal contents of the small intestine suggest that cryptdin peptides are secreted into the lumen, similar to Paneth cell secretion of lysozyme. The presence of several enteric defensins in the intestinal epithelium, evidence of their presence in the lumen, and the antibacterial activity of cryptdin-1 suggest that these peptides contribute to the antimicrobial barrier function of the small bowel mucosa. C1 SHRINERS BURN INST,CELL BIOL UNIT,BOSTON,MA 02114. UNIV CALIF IRVINE,DEPT MOLEC BIOL & BIOCHEM,IRVINE,CA 92717. MASSACHUSETTS GEN HOSP,MED SERV,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. RP SELSTED, ME (reprint author), UNIV CALIF IRVINE,CALIF COLL MED,DEPT PATHOL,IRVINE,CA 92717, USA. FU NIAID NIH HHS [AI22931, AI29595, AI30479] NR 36 TC 256 Z9 275 U1 2 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD AUG PY 1992 VL 118 IS 4 BP 929 EP 936 DI 10.1083/jcb.118.4.929 PG 8 WC Cell Biology SC Cell Biology GA JJ106 UT WOS:A1992JJ10600014 PM 1500431 ER PT J AU THOMAS, L BYERS, HR VINK, J STAMENKOVIC, I AF THOMAS, L BYERS, HR VINK, J STAMENKOVIC, I TI CD44H REGULATES TUMOR-CELL MIGRATION ON HYALURONATE-COATED SUBSTRATE SO JOURNAL OF CELL BIOLOGY LA English DT Article ID HOMING RECEPTOR; LYMPH-NODE; GLYCOPROTEIN; ADHESION; MEMBRANE; MOLECULE; BINDING; RECOGNITION; ANTIBODIES; EXPRESSION AB CD44 is a broadly distributed cell surface glycoprotein expressed in different isoforms in various tissues and cell lines. One of two recently characterized human isoforms, CD44H, is a cell surface receptor for hyaluronate, suggesting a role in the regulation of cell-cell and cell-substrate interactions as well as of cell migration. While CD44H has been shown to mediate cell adhesion, direct demonstration that CD44H expression promotes cell motility has been lacking. In this work we show that a human melanoma cell line, stably transfected with CD44H, displays enhanced motility on hyaluronate-coated surfaces while transfectants expressing an isoform that does not bind hyaluronate, CD44E, fail to do so. Migration of CD44H-expressing transfectants is observed to be blocked by a soluble CD44-immunoglobulin fusion protein as well as by anti-CD44 antibody, and to depend on the presence of the cytoplasmic domain of CD44. However, cells expressing CD44H cytoplasmic deletion mutants retain significant binding capacity to hyaluronate-coated substrate. Taken together, our results provide direct evidence that CD44H plays a major role in regulating cell migration on hyaluronate-coated substrate. C1 MASSACHUSETTS GEN HOSP, DIV DERMATOPATHOL, BOSTON, MA 02129 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02129 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02129 USA. RP THOMAS, L (reprint author), MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02129 USA. FU NCI NIH HHS [CA-45587, CA-55735]; NIGMS NIH HHS [GM-43257] NR 44 TC 305 Z9 306 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD AUG PY 1992 VL 118 IS 4 BP 971 EP 977 DI 10.1083/jcb.118.4.971 PG 7 WC Cell Biology SC Cell Biology GA JJ106 UT WOS:A1992JJ10600018 PM 1380003 ER PT J AU TEIXIDO, J HEMLER, ME GREENBERGER, JS ANKLESARIA, P AF TEIXIDO, J HEMLER, ME GREENBERGER, JS ANKLESARIA, P TI ROLE OF BETA-1-INTEGRINS AND BETA-2-INTEGRINS IN THE ADHESION OF HUMAN CD34HI STEM-CELLS TO BONE-MARROW STROMA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ADHESION; CD34HI; INTEGRINS; STROMA ID HEMATOPOIETIC PROGENITOR CELLS; VASCULAR ENDOTHELIAL-CELLS; SURFACE HETERODIMER VLA-4; CHRONIC MYELOID-LEUKEMIA; C-KIT PROTOONCOGENE; MONOCLONAL-ANTIBODY; INTEGRIN VLA-4; GROWTH-FACTOR; FIBRONECTIN RECEPTOR; ALPHA-4-BETA-1 INTEGRIN AB Hematopoietic stem cell interaction with elements of the underlying stroma is essential for sustained normal hematopoiesis. Here we have determined that adhesion receptors in the integrin family play a role in promoting adhesion of human hematopoietic stem cells to cultured human marrow stromal cells. Enriched CD34hi progenitor cells expressed VLA-4, VLA-5, and at least one or more beta-2 integrins. Homogeneous marrow stromal cell monolayers capable of supporting proliferation of cocultivated CD34hi cells expressed VCAM-1 and fibronectin (ligands for VLA-4 and VLA-5) as well as ICAM-1 (ligand for LFA-1 and Mac-1). Adhesion-blocking experiments indicated that VLA-4/VCAM-1, VLA-5/fibronectin, and beta-2-integrin/ICAM-1 pathways all are important for CD34hi cell attachment to stromal cells. Consistent with this suggestion, IL-1 stimulation of stromal cells caused both increased VCAM-1 and ICAM-1 expression and increased attachment by CD34hi bone marrow cells. In addition, CD34hi cells utilized VLA-4 to adhere to purified VCAM-1 and employed VLA-5 (and to a lesser extent VLA-4) to adhere to purified fibronectin. Together these results suggest that CD34hi stem cells may utilize multiple integrin-mediated adhesion pathways to localize within specialized microenvironmental niches created by marrow stromal cells. C1 UNIV MASSACHUSETTS, CTR MED, DEPT RADIAT ONCOL, 55 LAKE AVE N, WORCESTER, MA 01655 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT TUMOR VIROL, BOSTON, MA 02115 USA. RI Teixido, Joaquin/J-8543-2014 OI Teixido, Joaquin/0000-0002-3177-4151 FU NCI NIH HHS [CA-39851, CA42368]; NIDCR NIH HHS [DE-08798] NR 83 TC 334 Z9 344 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD AUG PY 1992 VL 90 IS 2 BP 358 EP 367 DI 10.1172/JCI115870 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA JH801 UT WOS:A1992JH80100009 PM 1379610 ER PT J AU MASSACESI, L JOSHI, N LEEPARRITZ, D ROMBOS, A LETVIN, NL HAUSER, SL AF MASSACESI, L JOSHI, N LEEPARRITZ, D ROMBOS, A LETVIN, NL HAUSER, SL TI EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN CYNOMOLGUS MONKEYS - QUANTITATION OF T-CELL RESPONSES IN PERIPHERAL-BLOOD SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MULTIPLE SCLEROSIS; MYELIN BASIC PROTEIN ID MYELIN BASIC-PROTEIN; MULTIPLE-SCLEROSIS; LYMPHOCYTES-T; PROTEOLIPID PROTEIN; LEWIS RAT; DISEASE; RECOGNITION; INVITRO; MICE AB Chronic relapsing-remitting experimental allergic encephalomyelitis (EAE) was induced in cynomolgus monkeys by a single immunization with a homogenate of human brain white matter (BH) in adjuvant. Proliferative T lymphocyte responses to BH, to myelin basic protein (MBP), but not to proteolipid protein, were detected in peripheral blood mononuclear cells (PBMC) of all animals and persisted until their death or, in surviving animals, for > 10 mo postimmunization. Responses of higher magnitude tended to be associated with fatal, compared with nonfatal episodes of clinical EAE. The frequency of MBP-reactive T cells in PBMC of animals with acute EAE was quantitated with a soft agar colony system; the ratio of T cells that proliferated specifically to MBP was estimated at between 5 and 20 per 10(6) PBMC. A similar frequency of peptide-specific T cells was estimated from PBMC of monkeys immunized with a synthetic 14-mer peptide corresponding to a region near the carboxy terminus of MBP. Thus, autoantigen-reactive T cells can be detected in the circulation throughout the course of chronic EAE, are predictive of disease severity, and occur at a frequency similar to that estimated to be present in humans with multiple sclerosis. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROIMMUNOL UNIT,WARREN 324,BOSTON,MA 02114. NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. RI Hauser, Stephen/J-2978-2016; OI Massacesi, Luca/0000-0001-5083-372X NR 39 TC 26 Z9 29 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD AUG PY 1992 VL 90 IS 2 BP 399 EP 404 DI 10.1172/JCI115874 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA JH801 UT WOS:A1992JH80100013 PM 1379611 ER PT J AU DUPUY, PM SHORE, SA DRAZEN, JM FROSTELL, C HILL, WA ZAPOL, WM AF DUPUY, PM SHORE, SA DRAZEN, JM FROSTELL, C HILL, WA ZAPOL, WM TI BRONCHODILATOR ACTION OF INHALED NITRIC-OXIDE IN GUINEA-PIGS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE BRONCHOCONSTRICTION; METHACHOLINE; PULMONARY RESISTANCE; PULMONARY COMPLIANCE ID SELECTIVE PULMONARY VASODILATOR; ACTIVATES GUANYLATE CYCLASE; SMOOTH-MUSCLE; GLYCERYL TRINITRATE; SODIUM-NITROPRUSSIDE; TISSUE PREPARATIONS; ORGANIC NITRATES; S-NITROSOTHIOLS; RELAXATION; 3',5'-MONOPHOSPHATE AB The effects of inhaling nitric oxide (NO) on airway mechanics were studied in anesthetized and mechanically ventilated guinea pigs. In animals without induced bronchoconstriction, breathing 300 ppm NO decreased baseline pulmonary resistance (R(L)) from 0.138+/-0.004 (mean+/-SE) to 0.125+/-0.002 cmH2O/ml.s (P < 0.05). When an intravenous infusion of methacholine (3.5-12-mu-g/kg.min) was used to increase R(L) from 0.143+/-0.008 to 0.474+/-0.041 cmH2O/ml.s (P < 0.05), inhalation of 5-300 ppm NO-containing gas mixtures produced a dose-related, rapid, consistent, and reversible reduction of R(L) and an increase of dynamic lung compliance. The onset of bronchodilation was rapid, beginning within 30 s after commencing inhalation. An inhaled NO concentration of 15.0+/-2.1 ppm was required to reduce R(L) by 50% of the induced bronchoconstriction. Inhalation of 100 ppm NO for 1 h did not produce tolerance to its bronchodilator effect nor did it induce substantial methemoglobinemia (< 2%). The bronchodilating effects of NO were additive with the effects of inhaled terbutaline, irrespective of the sequence of NO and terbutaline administration. Inhaling aerosol generated from S-nitroso-N-acetylpenicillamine also induced a rapid and profound decrease of R(L) from 0.453+/-0.022 to 0.287+/-0.022 cmH2O/ml.s, which lasted for over 15 min in guinea pigs bronchoconstricted with methacholine. Our results indicate that low levels of inhaled gaseous NO, or an aerosolized NO-releasing compound are potent bronchodilators in guinea pigs. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,RESP BIOL PROGRAM,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-19170, HL-42397] NR 43 TC 279 Z9 282 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 AUG PY 1992 VL 90 IS 2 BP 421 EP 428 DI 10.1172/JCI115877 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA JH801 UT WOS:A1992JH80100016 PM 1644915 ER PT J AU FELIX, CA DAMICO, D MITSUDOMI, T NAU, MM LI, FP FRAUMENI, JF COLE, DE MCCALLA, J REAMAN, GH WHANGPENG, J KNUTSEN, T MINNA, JD POPLACK, DG AF FELIX, CA DAMICO, D MITSUDOMI, T NAU, MM LI, FP FRAUMENI, JF COLE, DE MCCALLA, J REAMAN, GH WHANGPENG, J KNUTSEN, T MINNA, JD POPLACK, DG TI ABSENCE OF HEREDITARY P53 MUTATIONS IN 10 FAMILIAL LEUKEMIA PEDIGREES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE ACUTE LYMPHOBLASTIC LEUKEMIA; GERMLINE MUTATION; SOMATIC MUTATION; TUMOR SUPPRESSOR GENE ID ACUTE LYMPHOBLASTIC-LEUKEMIA; TUMOR SUPPRESSOR GENE; CELL LUNG-CANCER; T-CELL; CHROMOSOME-CHANGES; MUTANT P53; SARCOMAS; NEOPLASMS; CHILDHOOD; ONCOGENE AB Germline p53 mutations have been identified in the Li-Fraumeni syndrome but the role of such mutations in familial leukemia is not established. The p53 gene was examined by single-strand conformation polymorphism analysis of exons 4-8 in 10 families with multiple members affected with leukemia. The diagnoses included acute and chronic leukemias and Hodgkin's disease. Identified in two families were p53 mutations that were nonhereditary. These included a 2-bp deletion in exon 6 found in the lymphoblast DNA of one child whose sibling, cousin, and several adult relatives had acute leukemia. The other nonhereditary p53 mutation was a transition at codon 248 (CGG to CAG, arginine to glutamine) found in the lymphoblasts of a patient with a preleukemic syndrome and acute lymphoblastic leukemia (ALL) whose brother is a long-term survivor of ALL. Thus, p53 mutations were found to occur in two families but both were nonhereditary. Moreover, in the remaining eight families no p53 mutation was identified in the regions of p53 where most mutations have been found in other cancers. Although p53 mutations sometimes may be present, they do not appear to be a primary event responsible for hereditary susceptibility to familial leukemia. This study suggests involvement of other genes or mechanisms. C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20892. NCI,EPIDEMIOL BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,NATL CANC INST,BOSTON,MA 02115. GEORGE WASHINGTON UNIV,CHILDRENS NATL MED CTR,DIV HEMATOL ONCOL,WASHINGTON,DC 20010. UNIV TEXAS,SW MED CTR,SIMMONS CANC RES CTR,DALLAS,TX 75235. RP FELIX, CA (reprint author), CHILDRENS HOSP PHILADELPHIA,DEPT PEDIAT,DIV ONCOL,ROOM 9093,34TH ST & CIV CTR BLVD,PHILADELPHIA,PA 19104, USA. OI Mitsudomi, Tetsuya/0000-0001-9860-8505 NR 31 TC 42 Z9 42 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 AUG PY 1992 VL 90 IS 2 BP 653 EP 658 DI 10.1172/JCI115907 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA JH801 UT WOS:A1992JH80100046 PM 1644930 ER PT J AU JORGENSEN, JH BARRY, AL DOERN, GV FERRARO, MJ MURRAY, PR AF JORGENSEN, JH BARRY, AL DOERN, GV FERRARO, MJ MURRAY, PR TI DEVELOPMENT OF REVISED QUALITY-CONTROL LIMITS FOR DISK DIFFUSION SUSCEPTIBILITY TESTS OF SELECTED CEPHEM ANTIBIOTICS WITH HAEMOPHILUS-INFLUENZAE AND DESCRIPTION OF A NEW CONTROL STRAIN SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID MUELLER-HINTON AGAR; HEMOPHILUS-INFLUENZAE; STAPHYLOCOCCUS-AUREUS; AMPICILLIN; RESISTANCE AB Inconsistent quality control results in disk diffusion testing of cefaclor, cefamandole, cefonicid, and cefuroxime with Haemophilus influenzae ATCC 49247 and Haemophilus test medium (HTM) prompted a search for an alternative control strain that would provide more reliable results. A five-laboratory study was conducted to evaluate two candidate H. influenzae strains as possible alternatives to the aforementioned strain. Repetitive testing of the candidate strains and H. influenzae ATCC 49247 over several days with a total of six different lots of HTM documented consistent performance of the two candidate strains and confirmed inconsistent results for some of the antibiotics with H. influenzae ATCC 49247. In particular, certain lots of HTM failed to yield cefaclor and cefamandole zone sizes within the quality control range advocated by the National Committee for Clinical Laboratory Standards. Because of the greater consistency offered by the new strains, one was selected (now designated H. influenzae ATCC 49766) to be recommended for routine quality control testing of cefaclor, cefamandole, cefonicid, cefuroxime, and the related carbacephem loracarbef. The new control strain and zone size ranges proposed here have been approved by the National Committee for Clinical Laboratory Standards in place of the previously recommended strain and zone size limits for testing of these five cephem antibiotics. C1 CLIN MICROBIOL INST INC,TUALATIN,OR 97062. UNIV MASSACHUSETTS,MED CTR,DEPT CLIN MICROBIOL,WORCESTER,MA 01655. MASSACHUSETTS GEN HOSP,MICROBIOL LAB,BOSTON,MA 02114. WASHINGTON UNIV,DEPT LAB MED,ST LOUIS,MO 63110. RP JORGENSEN, JH (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284, USA. NR 15 TC 7 Z9 7 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 AUG PY 1992 VL 30 IS 8 BP 2029 EP 2032 PG 4 WC Microbiology SC Microbiology GA JD594 UT WOS:A1992JD59400023 PM 1500510 ER PT J AU LI, FP FRAUMENI, JF AF LI, FP FRAUMENI, JF TI PREDICTIVE TESTING FOR INHERITED MUTATIONS IN CANCER-SUSCEPTIBILITY GENES SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID HUMAN GENOME PROJECT; LI-FRAUMENI SYNDROME C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. RP LI, FP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 13 TC 15 Z9 15 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 AUG PY 1992 VL 10 IS 8 BP 1203 EP 1204 PG 2 WC Oncology SC Oncology GA JF661 UT WOS:A1992JF66100001 PM 1634911 ER PT J AU AISNER, J GOUTSOU, M MAURER, LH COOPER, R CHAHINIAN, P CAREY, R SKARIN, A SLAWSON, R PERRY, MC GREEN, MR AF AISNER, J GOUTSOU, M MAURER, LH COOPER, R CHAHINIAN, P CAREY, R SKARIN, A SLAWSON, R PERRY, MC GREEN, MR TI INTENSIVE COMBINATION CHEMOTHERAPY, CONCURRENT CHEST IRRADIATION, AND WARFARIN FOR THE TREATMENT OF LIMITED-DISEASE SMALL-CELL LUNG-CANCER - A CANCER AND LEUKEMIA GROUP-B PILOT-STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID RADIATION-THERAPY; RANDOMIZED TRIAL; CARCINOMA; ETOPOSIDE; CISPLATIN; CYCLOPHOSPHAMIDE; ANTICOAGULATION; RADIOTHERAPY; ADRIAMYCIN; VP-16 C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,NORRIS COTTON CANC CTR,HANOVER,NH 03756. MT SINAI HOSP,NEW YORK,NY. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC 27103. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MISSOURI,COLUMBIA,MO 65201. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. RP AISNER, J (reprint author), UNIV MARYLAND,CTR CANC,22 S GREENE ST,BALTIMORE,MD 21201, USA. FU NCI NIH HHS [CA-31983, CA-04326, CA-33601] NR 25 TC 29 Z9 30 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD AUG PY 1992 VL 10 IS 8 BP 1230 EP 1236 PG 7 WC Oncology SC Oncology GA JF661 UT WOS:A1992JF66100006 PM 1321892 ER PT J AU STRAUSS, GM HERNDON, JE SHERMAN, DD MATHISEN, DJ CAREY, RW CHOI, NC REGE, VB MODEAS, C GREEN, MR AF STRAUSS, GM HERNDON, JE SHERMAN, DD MATHISEN, DJ CAREY, RW CHOI, NC REGE, VB MODEAS, C GREEN, MR TI NEOADJUVANT CHEMOTHERAPY AND RADIOTHERAPY FOLLOWED BY SURGERY IN STAGE-IIIA NON-SMALL-CELL CARCINOMA OF THE LUNG - REPORT OF A CANCER AND LEUKEMIA GROUP-B PHASE-II STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID RADIATION; CISPLATIN; THERAPY; SYSTEM C1 HARVARD COMMUNITY HLTH PLAN,DEPT ONCOL,BOSTON,MA. ST JOSEPHS HOSP,DEPT RADIAT ONCOL,MILWAUKEE,WI. FRONTIER SCI & TECHNOL RES FDN INC,AMHERST,NY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,DIV THORAC SURG,MED ONCOL UNIT,BOSTON,MA 02114. DUKE UNIV,SCH MED,CANC CTR BIOSTAT,DURHAM,NC 27706. RHODE ISL HOSP,DEPT MED ONCOL,PROVIDENCE,RI 02902. UNIV CALIF SAN DIEGO,MED CTR,DIV HEMATOL ONCOL,SAN DIEGO,CA 92103. RP STRAUSS, GM (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV HEMATOL ONCOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA12449, CA32291, CA33601] NR 20 TC 186 Z9 187 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD AUG PY 1992 VL 10 IS 8 BP 1237 EP 1244 PG 8 WC Oncology SC Oncology GA JF661 UT WOS:A1992JF66100007 PM 1321893 ER PT J AU SALASCHE, SJ ORENGO, IF AF SALASCHE, SJ ORENGO, IF TI TUMORS OF THE NAIL UNIT SO JOURNAL OF DERMATOLOGIC SURGERY AND ONCOLOGY LA English DT Article ID SQUAMOUS-CELL CARCINOMA; SUBUNGUAL MALIGNANT-MELANOMA; TENDON SHEATH; MYXOID CYSTS; NODULAR TENOSYNOVITIS; RECALCITRANT WARTS; MUCOUS CYSTS; EXOSTOSES; BED AB Tumors of the nail unit are often initially misdiagnosed or diagnosed later in their course than their skin counterparts. This is probably because the nail can obscure the lesion or many nail tumors mimic inflammatory dermatoses of the nail unit. Both benign and malignant tumors the nail unit are described. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL SURG,BOSTON,MA 02114. NR 53 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0148-0812 J9 J DERMATOL SURG ONC PD AUG PY 1992 VL 18 IS 8 BP 691 EP 700 PG 10 WC Oncology; Dermatology; Surgery SC Oncology; Dermatology; Surgery GA JH991 UT WOS:A1992JH99100005 PM 1644941 ER PT J AU PERRIN, JM MACLEAN, WE GORTMAKER, SL ASHER, KN AF PERRIN, JM MACLEAN, WE GORTMAKER, SL ASHER, KN TI IMPROVING THE PSYCHOLOGICAL STATUS OF CHILDREN WITH ASTHMA - A RANDOMIZED CONTROLLED TRIAL SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE PSYCHOLOGICAL STATUS; ASTHMA; STRESS; EDUCATION ID LIFE EVENTS; CHRONIC ILLNESS; SOCIAL SUPPORT; ADOLESCENTS; THERAPY; HEALTH AB Children with asthma are at special risk for problems in psychological functioning, as are children with other chronic illnesses. We conducted a controlled trial of a combined education and stress management program among children ages 6 to 14 years with asthma. Eighty-one children were randomly assigned to an intervention or a control group; 56 children completed data collection, 29 intervention and 27 control. Psychological status was assessed by the Child Behavior Checklist (CBCL) before and after the intervention, as were children's knowledge of asthma, stress (as measured by children's life events), and functional status (as indicated by such activities as school attendance, time playing with friends, and daily chore performance). Children in the intervention group had a significant improvement in the total Behavior Problems score (p < .04) and Internalizing scale (p < .01) on the CBCL and a significant increase in daily chores (p < .04) compared with the control group. Before intervention, the two groups had statistically significant positive relationships between negative life events and behavior problem scores. After intervention, children in the control group still demonstrated a significant relationship between negative life events and total and Internalizing Behavior Problem scores, although participation in the intervention group negated that relationship. Children in the intervention group whose knowledge of asthma increased were more likely to report an increase in daily chores (p < .02). We conclude that the intervention had a beneficial effect on psychological status and on children's daily activities. The effect may have occurred in part by decreasing the likelihood that perceived stress from negative life events led to poorer adjustment. C1 VANDERBILT UNIV,GEORGE PEABODY COLL TEACHERS,DEPT PSYCHOL,NASHVILLE,TN 37203. HARVARD UNIV,SCH PUBL HLTH,DEPT BEHAV SCI,BOSTON,MA 02115. ASSOCIATES DEV PEDIAT,SEATTLE,WA. RP PERRIN, JM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,CHILDRENS SERV,WACC 715,BOSTON,MA 02114, USA. RI MacLean, William/H-1387-2013 NR 34 TC 39 Z9 42 U1 1 U2 7 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD AUG PY 1992 VL 13 IS 4 BP 241 EP 247 PG 7 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA JH137 UT WOS:A1992JH13700001 PM 1506461 ER PT J AU RUBIN, DS ARNETT, HL PERRIN, J LAPEY, A JELLINEK, M AF RUBIN, DS ARNETT, HL PERRIN, J LAPEY, A JELLINEK, M TI THE INFLUENCE OF PARENTAL PERCEPTIONS OF UNCERTAINTY ON THE PSYCHOSOCIAL HEALTH OF THEIR CHILDREN WITH CHRONIC ASTHMA SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 4 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD AUG PY 1992 VL 13 IS 4 BP 304 EP 304 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA JH137 UT WOS:A1992JH13700018 ER PT J AU MOEBIUS, U CLAYTON, LK ABRAHAM, S HARRISON, SC REINHERZ, EL AF MOEBIUS, U CLAYTON, LK ABRAHAM, S HARRISON, SC REINHERZ, EL TI THE HUMAN IMMUNODEFICIENCY VIRUS-GP120 BINDING-SITE ON CD4 - DELINEATION BY QUANTITATIVE EQUILIBRIUM AND KINETIC BINDING-STUDIES OF MUTANTS IN CONJUNCTION WITH A HIGH-RESOLUTION CD4 ATOMIC-STRUCTURE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TOXIC LYMPHOCYTES-T; CLASS-II MHC; CELL ANTIGEN RECEPTOR; HTLV-III/LAV; ENVELOPE GLYCOPROTEIN; MONOCLONAL-ANTIBODY; VIRUS; HIV; ACTIVATION; MOLECULE AB The first immunoglobulin V-like domain of CD4 contains the binding site for human immunodeficiency virus gp120. Guided by the atomic structure of a two-domain CD4 fragment, we have examined gp120 interaction with informative CD4 mutants, both by equilibrium and kinetic analysis. The binding site on CD4 appears to be a surface region of about 900 angstrom2 on the C" edge of the domain. It contains an exposed hydrophobic residue, Phe43, on the C" strand and four positively charged residues, Lys29, Lys35, Lys46, and Arg59, on the C, C', C", and D strands, respectively. Replacement of Phe43 with Ala or Ile reduces affinity for gp120 by more than 500-fold; Tyr, Trp, and Leu substitutions have smaller effects. The four positively charged side chains each make significant contributions (7-50-fold). This CD4 site may dock into a conserved hydrophobic pocket bordered by several negatively charged residues in gp120. Class II major histocompatibility complex binding includes the same region on CD4; this overlap needs to be considered in the design of inhibitors of the CD4-gp120 interaction. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,HOWARD HUGHES MED INST,CAMBRIDGE,MA 02138. RP MOEBIUS, U (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-27336, AI-30361, P30 AI-28691] NR 46 TC 145 Z9 147 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 AUG 1 PY 1992 VL 176 IS 2 BP 507 EP 517 DI 10.1084/jem.176.2.507 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA JF803 UT WOS:A1992JF80300020 PM 1500858 ER PT J AU ELGHORR, AA GORDON, DA GEORGE, K MARATOSFLIER, E AF ELGHORR, AA GORDON, DA GEORGE, K MARATOSFLIER, E TI REGULATION OF EXPRESSION OF THE REOVIRUS RECEPTOR ON DIFFERENTIATED HL-60-CELLS SO JOURNAL OF GENERAL VIROLOGY LA English DT Article ID BETA-ADRENERGIC-RECEPTOR; PROMYELOCYTIC LEUKEMIA-CELLS; MAMMALIAN REOVIRUS; ATTACHMENT PROTEIN; SURFACE RECEPTOR; TYPE-3; BINDING; VIRUS; INFECTION; DOMAINS AB The reovirus receptor on mammalian cells has not been fully characterized and controversy exists over the nature of this receptor. We report here that the expression of this receptor is dependent on the differentiation status of a human promyelocytic leukaemia cell line (HL60). Phorbol treatment of HL60 cells for 24 h, at a concentration range of 160 nm down to 1 nm, led to differentiation of these cells towards monocytes and a loss of approximately 80% of their ability to bind reovirus in a fluorescence assay. These cells also lost their susceptibility to TI and T3 reovirus infection. DMSO treatment for 24 h at a concentration of 1.25% (v/v) led to differentiation towards granulocytes. This was accompanied by an increase of approximately 15% in binding of reovirus to these cells. After being infected by TI or T3 reovirus, the granulocytes produced higher titres of progeny virus than did untreated HL60 cells. Similar differences were noted when virus binding to HL60 cells was assayed using radiolabelled reovirus. These effects were not detected when murine L fibroblasts were treated with DMSO or phorbol. ATCC-derived murine R1. 1 cells did not bind reovirus. Competition data indicated that there may be two reovirus receptors on HL60 cells, and that T1 can bind to only one receptor whereas T3 can bind to both receptors. Our data also suggested that the beta-adrenergic receptor was unlikely to act as the reovirus receptor on HL60 cells. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,ELLIOTT P JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02115. FU NIAID NIH HHS [AI 28971]; NIDDK NIH HHS [DK36836] NR 29 TC 6 Z9 6 U1 0 U2 0 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1317 J9 J GEN VIROL JI J. Gen. Virol. PD AUG PY 1992 VL 73 BP 1961 EP 1968 DI 10.1099/0022-1317-73-8-1961 PN 8 PG 8 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA JG774 UT WOS:A1992JG77400010 PM 1645137 ER PT J AU GREER, JM KUCHROO, VK SOBEL, RA LEES, MB AF GREER, JM KUCHROO, VK SOBEL, RA LEES, MB TI IDENTIFICATION AND CHARACTERIZATION OF A 2ND ENCEPHALITOGENIC DETERMINANT OF MYELIN PROTEOLIPID PROTEIN (RESIDUES 178-191) FOR SJL MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; T-CELL RECEPTORS; MAJOR HISTOCOMPATIBILITY COMPLEX; BASIC-PROTEIN; IMMUNODOMINANT EPITOPE; ANTIGEN RECOGNITION; EXPRESSION; PEPTIDE; LINES AB We previously described a synthetic peptide of myclin proteolipid protein (PLP), peptide 139-151, which induces experimental allergic encephalomyelitis in SJL/J (H-2s) mice. We have now identified an additional determinant, PLP residues 178-191, that is also a potent encephalitogen in this strain. When PLP peptide 178-191 was compared with peptide 139-151 on an equimolar basis, the day of onset of disease induced by PLP 178-191 was earlier, but the incidence, severity, and histologic features were indistinguishable. Lymph node cells from animals immunized with the whole PLP molecule responded to both PLP 178-191 and 139-151, suggesting immunologic codominance of the two epitopes. PLP 178-191 elicited stronger proliferative responses and this may relate to the earlier onset of disease induced with this peptide. Two CD4+, peptide-specific, I-A(s)-restricted T cell lines, selected by stimulation of lymph node cells with either PLP 178-191 or 139-151, were each encephalitogenic in naive syngeneic mice. The presence of multiple encephalitogenic codominant PLP epitopes within a single mouse strain emphasizes the complexity of the immune response to PLP and its potential as a target Ag in autoimmune demyelinating diseases. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP GREER, JM (reprint author), EK SHRIVER CTR,DEPT BIOCHEM,200 TRAPELO RD,WALTHAM,MA 02254, USA. RI Greer, Judith/C-4945-2009 OI Greer, Judith/0000-0003-4440-4309 FU NINDS NIH HHS [NS 16954, NS 26773] NR 35 TC 114 Z9 115 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 AUG 1 PY 1992 VL 149 IS 3 BP 783 EP 788 PG 6 WC Immunology SC Immunology GA JF474 UT WOS:A1992JF47400006 PM 1378866 ER PT J AU HIRSCH, F GERMANA, S GUSTAFSSON, K PRATT, K SACHS, DH LEGUERN, C AF HIRSCH, F GERMANA, S GUSTAFSSON, K PRATT, K SACHS, DH LEGUERN, C TI STRUCTURE AND EXPRESSION OF CLASS-II ALPHA-GENES IN MINIATURE SWINE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MONOCLONAL-ANTIBODIES; HLA-DR; HEAVY-CHAIN; CDNA; ANTIGENS; POLYMORPHISM; HAPLOTYPE; SEQUENCE; CLONING; CELLS AB Two overlapping genomic clones corresponding to the swine DRA class II gene were isolated and characterized. Restriction mapping and partial sequence data of the exon-containing fragments allowed identification and orientation of the five exons encoding the alpha-chain. Two full length cDNA clones corresponding to the transcribed DRA gene from two different haplotypes of the swine MHC were sequenced. Nucleotide sequence alignments revealed that the two swine DRA cDNA were very similar and closely related to the human DRA equivalent. An additional glycosylation site, compared with those of human DRA, was found in the second external domain of the protein. Northern analyses showed that porcine DRA and DQA genes were the only two class II alpha-genes expressed in the spleen, despite the presence of DPA and DZA genes in the genome. In addition to transfected cells expressing homologous pairs of alpha and beta-chains from SLA-DR, stable transfectants expressing nonhomologous pairs of alpha and beta-chains from DR and DQ loci were obtained, suggesting that such associations may contribute to the functional heterogeneity of class II products. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. NR 36 TC 46 Z9 52 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 AUG 1 PY 1992 VL 149 IS 3 BP 841 EP 846 PG 6 WC Immunology SC Immunology GA JF474 UT WOS:A1992JF47400014 PM 1634772 ER PT J AU ROSENGARD, BR OJIKUTU, CA FISHBEIN, J KORTZ, EO SACHS, DH AF ROSENGARD, BR OJIKUTU, CA FISHBEIN, J KORTZ, EO SACHS, DH TI SELECTIVE BREEDING OF MINIATURE SWINE LEADS TO AN INCREASED RATE OF ACCEPTANCE OF MHC-IDENTICAL, BUT NOT OF CLASS-I-DISPARATE, RENAL-ALLOGRAFTS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; TRANSPLANTATION; ANTIGEN; RECOGNIZE; SURVIVAL AB Previous work from this laboratory demonstrated that tolerance to MHC-identical or class I-disparate renal allografts develops in approximately one third of miniature swine without exogenous immunosuppression. A back-cross study indicated that rejection of MHC-identical transplants due to minor Ag was controlled by one or possibly two non-MHC-linked, autosomal dominant Ir genes. According to this hypothesis, and assuming complete penetrance, graft acceptors would be homozygous recessive at the relevant Ir loci, as would their offspring. Alternatively, if the gene(s) were incompletely penetrant, then two acceptors could give rise to a rejector. However, a high rate of MHC-identical graft acceptance would still be expected in the offspring of acceptors even if the Ir gene(s) were incompletely penetrant. To test this hypothesis and to obtain a higher frequency of acceptor animals for studies of tolerance, a program of selective breeding of renal allograft acceptors was begun. In the present paper, we assess the effect of selective breeding on renal graft acceptance. The analysis indicates a marked increase in the rate of MHC-identical graft acceptance, from 27.3% (n = 24) for the earliest of the four chronologic subgroups assessed to 64.5% (n = 33) for the most recent subgroup (p < 0.0001). Calculations of kinship revealed that the increased acceptance of MHC-identical grafts was not the result of differences between acceptors and rejectors in donor/recipient consanguinity. Class I-disparate grafts (n = 128) were similarly stratified chronologically and compared. Unlike MHC-identical grafts, the rate of acceptance of class I-disparate grafts has not changed over time. We conclude that rejector/acceptor status with respect to class I MHC incompatibility is determined by genetic factors in addition to those that control responses to minor antigen incompatibilities only. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. FU NIAID NIH HHS [1 R01 AI 31046-01] NR 16 TC 19 Z9 19 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 AUG 1 PY 1992 VL 149 IS 3 BP 1099 EP 1103 PG 5 WC Immunology SC Immunology GA JF474 UT WOS:A1992JF47400048 PM 1634765 ER PT J AU GRABBE, S BRUVERS, S LINDGREN, AM HOSOI, J TAN, KC GRANSTEIN, RD AF GRABBE, S BRUVERS, S LINDGREN, AM HOSOI, J TAN, KC GRANSTEIN, RD TI TUMOR-ANTIGEN PRESENTATION BY EPIDERMAL ANTIGEN-PRESENTING CELLS IN THE MOUSE - MODULATION BY GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR, TUMOR-NECROSIS-FACTOR-ALPHA, AND ULTRAVIOLET-RADIATION SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE TUMOR IMMUNITY; SKIN CANCER; CYTOKINES; LANGERHANS CELLS ID IMMUNOSTIMULATORY DENDRITIC CELLS; ACTIVATING FACTOR INTERLEUKIN-1; RENAL-TRANSPLANT RECIPIENTS; LANGERHANS CELLS; CONTACT HYPERSENSITIVITY; PROTEIN ANTIGENS; IMMUNE-RESPONSE; LIGHT; KERATINOCYTES; INVITRO AB I-A+ epidermal antigen-presenting cells (APCs, Langerhans cells) have been shown to present tumor-associated antigens (TAAs) and to induce tumor immunity in vivo. This study examined the effects of ultraviolet radiation (UVR) and the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha) on the ability of epidermal cells (ECs) to induce or to elicit immunity against the murine spindle cell tumor S1509a. Naive syngeneic mice were immunized three times at weekly intervals with ECs that had been cultured in GM-CSF for 18 h and then pulsed with TAA derived from S1509a. This resulted in protective immunity against subsequent tumor challenge, providing a model to study the conditions required for sensitization against TAAs by epidermal APCs. Culture of ECs in GM-CSF was required for induction of significant protective tumor immunity, and UV irradiation or incubation in TNF-alpha for 2 h after GM-CSF incubation abrogated the immunostimulatory effect of GM-CSF. However, unlike UVR, TNF-alpha did not significantly inhibit the induction of immunity when ECs were exposed to TNF-alpha before overnight incubation in GM-CSF, together with GM-CSF, or after pulsing with TAA, and anti-TNF-alpha antibody treatment did not abrogate the effects of UVR on this system. Furthermore, TNF-alpha incubation of ECs augmented their ability to elicit delayed-type hypersensitivity (DTH) and also enhanced elicitation of DTH by GM-CSF-cultured ECs, whereas UV-irradiation reduced it in a dose-dependent fashion. Taken together, these results demonstrate that GM-CSF, TNF-alpha, and UVR arc significant regulators of tumor antigen presentation by epidermal APCs and that the effects of the cytokines examined differ with regard to induction or elicitation of immunity. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,DEPT PERMATOL,BOSTON,MA 02114. UNIV MUNSTER,DEPT DERMATOL,W-4400 MUNSTER,GERMANY. FU NEI NIH HHS [EY07782]; NIAMS NIH HHS [AR40667] NR 45 TC 60 Z9 62 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD AUG PY 1992 VL 52 IS 2 BP 209 EP 217 PG 9 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA JQ370 UT WOS:A1992JQ37000012 PM 1506778 ER PT J AU GRABAREK, Z TAO, T GERGELY, J AF GRABAREK, Z TAO, T GERGELY, J TI MOLECULAR MECHANISM OF TROPONIN-C FUNCTION SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Review ID SKELETAL-MUSCLE TROPONIN; PROTON-MAGNETIC-RESONANCE; CALCIUM-BINDING SITES; AMINO-ACID-SEQUENCE; MYOFIBRILLAR ADENOSINE-TRIPHOSPHATASE; INDUCED CONFORMATIONAL-CHANGES; CENTRAL HELIX MUTANTS; N-TERMINAL DOMAIN; X-RAY-DIFFRACTION; CARDIAC TROPONIN C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP GRABAREK, Z (reprint author), BOSTON BIOMED RES INST,DEPT MUSCLE RES,20 STANIFORD ST,BOSTON,MA 02114, USA. OI Grabarek, Zenon/0000-0002-3636-5701 FU NHLBI NIH HHS [R37-HL-05949]; NIAMS NIH HHS [AR 21673] NR 118 TC 135 Z9 136 U1 1 U2 2 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 AUG PY 1992 VL 13 IS 4 BP 383 EP 393 DI 10.1007/BF01738034 PG 11 WC Cell Biology SC Cell Biology GA JG764 UT WOS:A1992JG76400001 PM 1401036 ER PT J AU FROSCH, MP LIPTON, SA DICHTER, MA AF FROSCH, MP LIPTON, SA DICHTER, MA TI DESENSITIZATION OF GABA-ACTIVATED CURRENTS AND CHANNELS IN CULTURED CORTICAL-NEURONS SO JOURNAL OF NEUROSCIENCE LA English DT Article ID GAMMA-AMINOBUTYRIC ACID; NICOTINIC ACETYLCHOLINE-RECEPTOR; RETINAL GANGLION-CELLS; HIPPOCAMPAL-NEURONS; VOLTAGE-CLAMP; NEUROMUSCULAR-JUNCTION; CHOLINERGIC RECEPTORS; KINETIC-PROPERTIES; MEMBRANE PATCHES; PYRAMIDAL CELLS AB Application of GABA to rat neocortical neurons maintained in cell culture produced a response that declined over several seconds, even in the continued presence of agonist. The decrement could be attributed to both a redistribution of Cl- and a true decline in GABA-induced membrane conductance, or desensitization. The extent and rate of desensitization were dose dependent in a manner similar to the dose dependence of the GABA-induced current, but were not related to the absolute magnitude of the current or to the charge transfer. Bicuculline slowed desensitization while diazepam enhanced the rate of desensitization, consistent with a localization of desensitization to the agonist-receptor binding site. When measured in the whole-cell recording mode, desensitization was voltage dependent, becoming much slower as the membrane was depolarized. Changes in extracellular or intracellular [Ca2+] did not appear to grossly affect the desensitization process or its voltage dependence. GABA-activated single channels, recorded in the out-side-out configuration, also desensitized in the continued presence of agonist. However, desensitization differed from that seen in the same neurons in the whole-cell mode. Desensitization was considerably more rapid and did not show any voltage sensitivity. Moreover, single-channel responses often failed to recover after only a few exposures to agonist. Desensitization of GABA responses may play a role in the regulation of cortical inhibition, especially under conditions of intense excitatory and inhibitory synaptic activation. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. GRAD HOSP PHILADELPHIA,DEPT NEUROL,PHILADELPHIA,PA 19146. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. RP FROSCH, MP (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY05477]; NINDS NIH HHS [NS00879, NS24927] NR 53 TC 59 Z9 59 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD AUG PY 1992 VL 12 IS 8 BP 3042 EP 3053 PG 12 WC Neurosciences SC Neurosciences & Neurology GA JH370 UT WOS:A1992JH37000013 PM 1379634 ER PT J AU SNYDER, GL GIRAULT, JA CHEN, JYC CZERNIK, AJ KEBABIAN, JW NATHANSON, JA GREENGARD, P AF SNYDER, GL GIRAULT, JA CHEN, JYC CZERNIK, AJ KEBABIAN, JW NATHANSON, JA GREENGARD, P TI PHOSPHORYLATION OF DARPP-32 AND PROTEIN PHOSPHATASE INHIBITOR-1 IN RAT CHOROID-PLEXUS - REGULATION BY FACTORS OTHER THAN DOPAMINE SO JOURNAL OF NEUROSCIENCE LA English DT Article ID ADENOSINE 3'-5'-MONOPHOSPHATE-REGULATED PHOSPHOPROTEIN; CEREBROSPINAL-FLUID PRODUCTION; INNERVATED BRAIN-REGIONS; RABBIT SKELETAL-MUSCLE; VASOACTIVE INTESTINAL POLYPEPTIDE; LOWERS INTRAOCULAR-PRESSURE; SENSITIVE ADENYLATE-CYCLASE; ATRIAL NATRIURETIC FACTOR; CYCLIC-AMP METABOLISM; RENAL TUBULE CELLS AB The molecular mechanisms underlying regulation of fluid production by secretory epithelia such as the choroid plexus are poorly understood. Two cAMP-regulated inhibitors of protein phosphatase-1, inhibitor-1 (I1) and a dopamine- and cAMP-regulated phosphoprotein, M(r) = 32,000 (DARPP-32), are enriched in the choroid plexus. We show here that these two phosphoproteins are colocalized in choroid plexus epithelial cells. We have developed a novel method for studying the phosphorylation state of DARPP-32 and I1 in intact cells, using a phosphorylation state-specific monoclonal antibody. Several drugs and hormones that are known to alter fluid secretion and that increase cAMP levels (forskolin, isoproterenol, vasoactive intestinal peptide) or cGMP levels (atrial natriuretic peptide) or that may use additional second messenger pathways (5-HT), increase the phosphorylation of I1 and DARPP-32 in rat choroid plexus. In contrast, dopamine does not alter cAMP and cGMP levels, or I1 and DARPP-32 phosphorylation. Our results indicate that DARPP-32, known to be regulated by dopamine in a number of tissues, can be phosphorylated in response to non-dopaminergic factors, including hormones acting through non-cAMP-dependent pathways. Our results also raise the possibility that inhibition of phosphatase-1, as a result of I1 and DARPP-32 phosphorylation, might be part of a final common pathway in the action of several factors that are known or thought to alter cerebrospinal fluid production. C1 ABBOTT LABS,ABBOTT PK,IL 60064. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02114. RP SNYDER, GL (reprint author), ROCKEFELLER UNIV,DEPT MOLEC & CELLULAR NEUROSCI,MOLEC & CELLULAR NEUROSCI LAB,NEW YORK,NY 10021, USA. RI Girault, Jean-Antoine/F-7518-2013 OI Girault, Jean-Antoine/0000-0002-7900-1705 FU NEI NIH HHS [EY05077]; NIMH NIH HHS [MH40899] NR 80 TC 127 Z9 129 U1 1 U2 1 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD AUG PY 1992 VL 12 IS 8 BP 3071 EP 3083 PG 13 WC Neurosciences SC Neurosciences & Neurology GA JH370 UT WOS:A1992JH37000015 PM 1494946 ER PT J AU VONDEIMLING, A LOUIS, DN VONAMMON, K PETERSEN, I HOELL, T CHUNG, RY MARTUZA, RL SCHOENFELD, DA YASARGIL, MG WIESTLER, OD SEIZINGER, BR AF VONDEIMLING, A LOUIS, DN VONAMMON, K PETERSEN, I HOELL, T CHUNG, RY MARTUZA, RL SCHOENFELD, DA YASARGIL, MG WIESTLER, OD SEIZINGER, BR TI ASSOCIATION OF EPIDERMAL GROWTH-FACTOR RECEPTOR GENE AMPLIFICATION WITH LOSS OF CHROMOSOME-10 IN HUMAN GLIOBLASTOMA-MULTIFORME SO JOURNAL OF NEUROSURGERY LA English DT Article DE TUMOR SUPPRESSOR GENE; CHROMOSOME-10; ONCOGENE; EPIDERMAL GROWTH FACTOR; BRAIN NEOPLASM; GENE AMPLIFICATION; GLIOBLASTOMA ID MALIGNANT HUMAN GLIOMAS; HUMAN-BRAIN-TUMORS; HUMAN ASTROCYTOMAS; SHORT ARM; HETEROZYGOSITY; EXPRESSION; ABNORMALITIES; MUTATIONS; TUMORIGENESIS; FEATURES AB Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted to the glioblastomas. Of the 58 glioblastoma patients, 72% showed loss of chromosome 10 and 38% showed EGFR gene amplification. The remaining 28% had neither loss of chromosome 10 nor EGFR gene amplification. Without exception, the glioblastomas that exhibited EGFR gene amplification had also lost genetic material on chromosome 10 (p < 0.00 1). This invariable association suggests a relationship between the two genetic events. Moreover, the presence of 15 cases of glioblastoma with loss of chromosome 10 but without EGFR gene amplification may further imply that the loss of a tumor suppressor gene (or genes) on chromosome 10 precedes EGFR gene amplification in glioblastoma tumorigenesis. C1 MASSACHUSETTS GEN HOSP,CTR BIOSTAT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV ZURICH,DEPT NEUROSURG,CH-8006 ZURICH,SWITZERLAND. UNIV ZURICH,DEPT PATHOL,CH-8006 ZURICH,SWITZERLAND. RP SEIZINGER, BR (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,MOLEC NEUROONCOL LAB,NEUROSURG SERV,149 13TH ST,BOSTON,MA 02129, USA. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [1 F32 CA 09144]; NIGMS NIH HHS [2 T32 GMO 7753-12, T32 GM007753] NR 36 TC 197 Z9 198 U1 0 U2 1 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 AUG PY 1992 VL 77 IS 2 BP 295 EP 301 DI 10.3171/jns.1992.77.2.0295 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA JE705 UT WOS:A1992JE70500018 PM 1320666 ER PT J AU YASUDA, T MOLINAMURPHY, IL VANDERVOORT, PM SOUTHERN, JF AF YASUDA, T MOLINAMURPHY, IL VANDERVOORT, PM SOUTHERN, JF TI ACUTE ONSET OF CARDIOGENIC-SHOCK ASSOCIATED WITH NORMAL CORONARY-ARTERIES, DIFFUSE MYOCARDIAL NECROSIS, AND RAPID CLINICAL RECOVERY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID HYPERTROPHIC CARDIOMYOPATHY; ENDOMYOCARDIAL BIOPSY; INFARCTION SECONDARY; MAGNETIC-RESONANCE; UNSTABLE ANGINA; ANTIMYOSIN FAB; HEART-DISEASE; THROMBOSIS; OCCLUSION; DIAGNOSIS C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 76 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD AUG PY 1992 VL 33 IS 8 BP 1558 EP 1565 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JF501 UT WOS:A1992JF50100027 ER PT J AU FISCHMAN, AJ STRAUSS, HW AF FISCHMAN, AJ STRAUSS, HW TI CLINICAL PET - THE DEBATE CONTINUES - REPLY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Letter RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD AUG PY 1992 VL 33 IS 8 BP 1587 EP 1588 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JF501 UT WOS:A1992JF50100035 ER PT J AU AMBROSINO, DM LEE, MYC CHEN, DH SHAMBERGER, RC WESSON, D PRIEBE, CJ AF AMBROSINO, DM LEE, MYC CHEN, DH SHAMBERGER, RC WESSON, D PRIEBE, CJ TI RESPONSE TO HAEMOPHILUS-INFLUENZAE TYPE-B CONJUGATE VACCINE IN CHILDREN UNDERGOING SPLENECTOMY SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article; Proceedings Paper CT 43RD ANNUAL MEETING OF THE SURGICAL SECTION OF THE AMERICAN ACADEMY OF PEDIATRICS CY OCT 26-27, 1991 CL NEW ORLEANS, LA SP AMER ACAD PEDIAT, SURG SECT DE SPLENECTOMY; IMMUNIZATION ID CAPSULAR POLYSACCHARIDE; HEMOPHILUS-INFLUENZAE; POSTSPLENECTOMY SEPSIS; PNEUMOCOCCAL VACCINE; ANTIBODY-RESPONSE; DISEASE; IMMUNIZATION; PREVENTION C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02115. RP AMBROSINO, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI 29263] NR 21 TC 11 Z9 11 U1 0 U2 0 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 AUG PY 1992 VL 27 IS 8 BP 1045 EP 1048 PG 4 WC Pediatrics; Surgery SC Pediatrics; Surgery GA JF865 UT WOS:A1992JF86500021 PM 1403533 ER PT J AU RYAN, DP DOODY, DP AF RYAN, DP DOODY, DP TI TREATMENT OF ACUTE PULMONARY FAILURE WITH EXTRACORPOREAL SUPPORT - 100-PERCENT SURVIVAL IN A PEDIATRIC POPULATION SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article; Proceedings Paper CT 43RD ANNUAL MEETING OF THE SURGICAL SECTION OF THE AMERICAN ACADEMY OF PEDIATRICS CY OCT 26-27, 1991 CL NEW ORLEANS, LA SP AMER ACAD PEDIAT, SURG SECT DE EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO); PEDIATRIC RESPIRATORY FAILURE; ADULT RESPIRATORY DISTRESS SYNDROME ID RESPIRATORY-DISTRESS SYNDROME; POSITIVE-PRESSURE VENTILATION; MEMBRANE-OXYGENATION; MORTALITY; CHILDREN; REMOVAL; INJURY; ECMO; ARDS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RYAN, DP (reprint author), MASSACHUSETTS GEN HOSP,DEPT PEDIAT SURG,FRUIT ST,BOSTON,MA 02114, USA. NR 22 TC 14 Z9 14 U1 0 U2 0 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 AUG PY 1992 VL 27 IS 8 BP 1111 EP 1117 DI 10.1016/0022-3468(92)90570-W PG 7 WC Pediatrics; Surgery SC Pediatrics; Surgery GA JF865 UT WOS:A1992JF86500035 PM 1328587 ER PT J AU STRACK, S AF STRACK, S TI PROFILE CLUSTERS FOR MEN AND WOMEN ON THE PERSONALITY ADJECTIVE CHECK LIST SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article ID MCMI-II; SCALES; INVENTORY AB This study examined the major personality profiles found for men and women on the Personality Adjective Check List (Strack, 1991b). Subjects were 1,058 men and 1,194 women from a number of samples of normal adults (Strack, 1991b). Ward's (1963) agglomerative hierarchical procedure yielded five clusters for men and four for women that were replicated in subsequent K-means nonhierarchical analyses. Correlates of cluster membership obtained from subgroups of subjects on four personality measures provided strong evidence for the classification. RP STRACK, S (reprint author), US DEPT VET AFFAIRS,OUTPATIENT CLIN,PSYCHOL SERV 116B,425 S HILL ST,LOS ANGELES,CA 90013, USA. NR 31 TC 4 Z9 4 U1 0 U2 0 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 AUG PY 1992 VL 59 IS 1 BP 204 EP 217 DI 10.1207/s15327752jpa5901_17 PG 14 WC Psychology, Clinical; Psychology, Social SC Psychology GA JG141 UT WOS:A1992JG14100017 PM 16370856 ER PT J AU CARDOZO, C EDELMAN, J LESSER, M AF CARDOZO, C EDELMAN, J LESSER, M TI LIPOPOLYSACCHARIDE-INDUCED STIMULATION OF ALVEOLAR MACROPHAGE OPSONIN-INDEPENDENT PHAGOCYTOSIS SO JOURNAL OF SURGICAL RESEARCH LA English DT Article ID RESPIRATORY-DISTRESS SYNDROME; INDUCED LUNG INJURY; CANINE MODEL; ENDOTOXIN; COMPLEMENT; SHOCK; RATS; INFECTIONS; LEUKOCYTES; INVITRO C1 BRONX VET AFFAIRS MED CTR,PULM SECT,130 W KINGSBRIDGE RD,BRONX,NY 10468. MT SINAI MED CTR,DEPT MED,NEW YORK,NY 10029. NR 27 TC 9 Z9 9 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD AUG PY 1992 VL 53 IS 2 BP 170 EP 174 DI 10.1016/0022-4804(92)90030-4 PG 5 WC Surgery SC Surgery GA JN949 UT WOS:A1992JN94900010 PM 1405605 ER PT J AU GONZALEZ, E GANGE, RW MOMTAZ, KT AF GONZALEZ, E GANGE, RW MOMTAZ, KT TI TREATMENT OF TELANGIECTASES AND OTHER BENIGN VASCULAR-LESIONS WITH THE 577 NM PULSED DYE-LASER SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID ARGON-LASER; TUNABLE DYE; THERAPY; STAINS AB Background: This study was undertaken to evaluate the effectiveness and safety of the 577 nm pulsed dye laser in the treatment of various vascular lesions of the face. Objective: Our purpose was to make observations on the effects of different variables that could affect response. Methods. Ninety-two adults with telangiectases of the face were sequentially selected for treatment according to a protocol previously established. Evaluation consisted of visual inspection by two investigators, and before and after photographs at 2-month intervals. A few patients with other vascular lesions were also treated and reported. Results: Ninety-one percent of the patients (84 of 92) showed good to excellent response after a single treatment. Recurrence occurred in 2%. Atrophy of the skin occurred in 2%. Venous lakes, pyogenic granulomas, and mucosal vascular malformations showed significant improvement. Conclusion: The 5 77 nm pulsed dye laser is effective and safe for vascular lesions of the face. RP GONZALEZ, E (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,PROF OFF BLDG,SUITE 503,BOSTON,MA 02114, USA. NR 20 TC 32 Z9 32 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD AUG PY 1992 VL 27 IS 2 BP 220 EP 226 DI 10.1016/0190-9622(92)70174-E PN 1 PG 7 WC Dermatology SC Dermatology GA JG537 UT WOS:A1992JG53700011 PM 1430360 ER PT J AU HUTTER, AM AF HUTTER, AM TI ACC COMMITTEES - STRUCTURE AND APPOINTMENTS 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 AUG PY 1992 VL 20 IS 2 BP 509 EP 511 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JG375 UT WOS:A1992JG37500039 ER PT J AU LONDON, MJ FRANKS, M VERRIER, ED MERRICK, SH LEVIN, J MANGANO, DT AF LONDON, MJ FRANKS, M VERRIER, ED MERRICK, SH LEVIN, J MANGANO, DT TI THE SAFETY AND EFFICACY OF 10 PERCENT PENTASTARCH AS A CARDIOPULMONARY BYPASS PRIMING SOLUTION - A RANDOMIZED CLINICAL-TRIAL SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID WEIGHT HYDROXYETHYL STARCH; LACTATED RINGERS SOLUTION; OXYGEN-TRANSPORT; PULMONARY-EDEMA; ALBUMIN; HEMODILUTION; HEMODYNAMICS; COAGULATION; INCREASES; PRESSURE AB Ten percent pentastarch is a low-molecular-weight hydroxyethyl starch with greater oncotic pressure and shorter intravascular persistence than 6 % hetastarch. To evaluate its safety and efficacy as a component of cardiopulmonary bypass priming solution, we prospectively studied 90 patients undergoing coronary artery bypass grafting or valve replacement necessitating cardiopulmonary bypass (bubble oxygenator and moderate systemic hypothermia). Sixty patients were randomized to receive 75 gm of either 10 % pentastarch (group P) or 25 % albumin (group A), and 30 patients received lactated Ringer's solution alone (group C). Intravascular colloid osmotic pressure during cardiopulmonary bypass was highest with either of the colloid primes (15-minute measurement: group P, 15.7 +/- 2.2 mm Hg (mean +/- standard deviation); group A, 15.2 +/- 2.0 mm Hg; group C, 11.3 +/- 1.7 mm Hg, p < 0.05, groups P and A compared with group C). This was associated with a lower volume requirement during cardiopulmonary bypass to maintain the venous reservoir (group P, 333 +/- 318 ml; group A, 483 +/- 472 ml; group C, 1332 +/- 1013 ml; p < 0.05, groups P and A compared with group C). Urine output during cardiopulmonary bypass was similar in each group. Net intraoperative fluid balance was lowest in the colloid groups (groups P and A, 5.7 +/- 1.4 L; group C, 6.9 +/-1.3 L; p < 0.05, groups P and A compared with group C). Cardiac index shortly after weaning from cardiopulmonary bypass was greatest in group P (group P, 3.2 +/- 0.9; group A, 2.8 +/- 0.8; group C, 2.7 +/- 0.6 dyne . sec . cm-5; p < 0.05, group P compared with group C). Changes in alveolar-arterial oxygen gradients, shunt fraction, and effective compliance were similar in all groups. During cardiopulmonary bypass, pentastarch appeared to cause the greatest degree of hemodilution, as suggested by the lowest hemoglobin, factor VII and IX levels and platelet count. The activated partial thromboplastin time was significantly prolonged during and immediately after cardiopulmonary bypass in group P relative to groups A and C (p < 0.05), although there were no significant differences in the activated clotting time before cardiopulmonary bypass, during cardiopulmonary bypass, or after heparin neutralization. As well, clinical indices of hemostasis, including mediastinal drainage, red cell, platelet, and fresh frozen plasma requirements, and reoperation for excessive postoperative bleeding, were similar. We conclude that pentastarch, when used in cardiopulmonary bypass prime, is as safe as either albumin or Ringer's solution alone. Its greater oncotic pressure and intravascular persistence appear to confer at least short-term physiologic benefits, especially when compared with Ringer's solution alone. C1 UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT CARDIAC SURG,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. RP LONDON, MJ (reprint author), SAN FRANCISCO VET AFFAIRS MED CTR,ANESTHESIA 112A,1055 CLERMONT,DENVER,CO 80220, USA. NR 32 TC 49 Z9 49 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 AUG PY 1992 VL 104 IS 2 BP 284 EP 296 PG 13 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA JH475 UT WOS:A1992JH47500009 PM 1379660 ER PT J AU MCDOUGAL, WS AF MCDOUGAL, WS TI STEPLADDER INCISION TECHNIQUE FOR LENGTHENING OF BOWEL MESENTERY - COMMENT SO JOURNAL OF UROLOGY LA English DT Editorial Material RP MCDOUGAL, WS (reprint author), MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD AUG PY 1992 VL 148 IS 2 BP 352 EP 352 PN 1 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA JF960 UT WOS:A1992JF96000034 ER PT J AU HALL, MC KOCH, MO MCDOUGAL, WS AF HALL, MC KOCH, MO MCDOUGAL, WS TI MECHANISM OF AMMONIUM TRANSPORT BY INTESTINAL SEGMENTS FOLLOWING URINARY-DIVERSION - EVIDENCE FOR IONIZED NH4+ TRANSPORT VIA K+-PATHWAYS SO JOURNAL OF UROLOGY LA English DT Article DE URINARY DIVERSION; AMMONIA; POTASSIUM ID THICK ASCENDING LIMB; ABSORPTION; KIDNEY; COLON AB Using a previously reported in vivo intestinal perfusion model in the rat, we have shown that net total ammonium absorption accounts for the majority of the acid load resulting from urinary intestinal diversion. In the present study, by varying perfusate pH and therefore NH3 concentrations, we demonstrated that the net flux of total ammonium did not correlate with non-ionized NH3 concentrations (r = .039). This indicates that the basic mechanism of total ammonium flux is via ionized NH4+ movement. To more precisely define the transport processes involved, we manipulated this system with the following chemical and pharmacologic probes of electrolyte transport: amiloride (0.5 mM/l.), furosemide (1 mM/l.), 2,4,6-triaminopyrimidine (TAP) (15 mM/l.), methylprednisilone (3 mg./100gm./B.W.) S.Q. x 3 days followed by perfusion, and barium (Ba2+) (15 mM/l.). Net solute flux was not significantly altered by the mucosal addition of amiloride or TAP. Methylprednisilone treated rats exhibited significantly diminished Na+ secretion (p < .01) and increased Cl- absorption (p <.05) without affecting net total ammonium flux providing evidence for the inducibility of Na+ conductance channels and against significant NH4+ movement via this pathway. The mucosal addition of furosemide resulted in significantly decreased net absorption of both total ammonium (p <.001) and K+ (p <.05). The addition of Ba2+ resulted in a three-fold reduction of ammonium absorption (p <.001) and a greater than ten-fold reduction in K+ absorption (p <.001). The observation of significant inhibition of ammonium absorption by furosemide and barium suggests that K+ transport pathways play a significant role in the intestinal transport of NH4+. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT UROL,MED CTR N,NASHVILLE,TN 37232. MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114. NR 18 TC 19 Z9 19 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD AUG PY 1992 VL 148 IS 2 BP 453 EP 457 PN 1 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA JF960 UT WOS:A1992JF96000072 PM 1635156 ER PT J AU YAO, XJ GOTTLINGER, H HASELTINE, WA COHEN, EA AF YAO, XJ GOTTLINGER, H HASELTINE, WA COHEN, EA TI ENVELOPE GLYCOPROTEIN AND CD4 INDEPENDENCE OF VPU-FACILITATED HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 CAPSID EXPORT SO JOURNAL OF VIROLOGY LA English DT Note ID HTLV-III/LAV; ASSAY; HIV-1; CELLS; GENE; INFECTIVITY; EFFICIENT; PROTEIN; RNAS; DNA AB The effect of vpu on the release of human immunodeficiency type 1 capsid proteins was examined in the presence or absence of virus-encoded envelope glycoproteins as well as in cells which constitutively express either the CD4 or CD8 protein. The results show that vpu-mediated facilitated export of capsid proteins from HeLa cells does not require expression of the envelope glycoprotein. The experiments also show that export of virus capsid proteins from HeLa cells facilitated by vpu is not affected by coexpression of either the CD4 or CD8 protein. The vpu protein acts in trans to facilitate export of virus capsid proteins from HeLa cells. C1 UNIV MONTREAL,FAC MED,DEPT MICROBIOL & IMMUNOL,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]; NIAID NIH HHS [AI 24845, AI 29873] NR 24 TC 86 Z9 86 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 AUG PY 1992 VL 66 IS 8 BP 5119 EP 5126 PG 8 WC Virology SC Virology GA JF098 UT WOS:A1992JF09800062 PM 1629967 ER PT J AU BRUNNER, HR COHEN, JJ PIRSON, Y VANES, LA REMUZZI, G MADIAS, NE ZUSMAN, RM KOCH, KM BAGGIO, B WINEARLS, CG JAEGER, P VANYPERSELE, C AF BRUNNER, HR COHEN, JJ PIRSON, Y VANES, LA REMUZZI, G MADIAS, NE ZUSMAN, RM KOCH, KM BAGGIO, B WINEARLS, CG JAEGER, P VANYPERSELE, C TI ACE INHIBITORS IN RENAL-DISEASE SO KIDNEY INTERNATIONAL LA English DT Discussion ID ANGIOTENSIN-CONVERTING-ENZYME; 2-KIDNEY GOLDBLATT HYPERTENSION; MICRO-CIRCULATORY DYNAMICS; GLOMERULAR-FILTRATION RATE; BLOOD-PRESSURE CONTROL; II-BINDING-SITES; RENOVASCULAR HYPERTENSION; ARTERY STENOSIS; DIABETIC NEPHROPATHY; ANTIHYPERTENSIVE THERAPY C1 SUNY STONY BROOK,MED,STONY BROOK,NY 11794. CLIN UNIV ST LUC,RENAL UNIT,SERV ASSOCIE,B-1200 BRUSSELS,BELGIUM. LEIDEN UNIV HOSP,DEPT NEPHROL,2333 AA LEIDEN,NETHERLANDS. MARIO NEGRI INST PHARMACOL RES,KIDNEY DIS LAB,I-20157 MILAN,ITALY. NEW ENGLAND MED CTR,DIV NEPHROL,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DIV HYPERTENS & VASC MED,BOSTON,MA 02114. HANNOVER MED SCH,MED,W-3000 HANNOVER 61,GERMANY. INST INTERNAL MED,DIV NEPHROL,PADUA,ITALY. RP BRUNNER, HR (reprint author), CHU VAUDOIS,CH-1011 LAUSANNE,SWITZERLAND. NR 192 TC 72 Z9 72 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD AUG PY 1992 VL 42 IS 2 BP 463 EP 479 DI 10.1038/ki.1992.311 PG 17 WC Urology & Nephrology SC Urology & Nephrology GA JE812 UT WOS:A1992JE81200028 PM 1405331 ER PT J AU AMREIN, PC FABIAN, RL AF AMREIN, PC FABIAN, RL TI TREATMENT OF RECURRENT HEAD AND NECK-CANCER WITH CISPLATIN AND 5-FLUOROURACIL VS THE SAME PLUS BLEOMYCIN AND METHOTREXATE SO LARYNGOSCOPE LA English DT Article ID SQUAMOUS-CELL CARCINOMA; INFUSION; CHEMOTHERAPY; THERAPY AB A prospective randomized trial of 62 patients with recurrent squamous cell carcinoma of the head and neck was conducted to compare the effectiveness of our standard chemotherapy program with that of our test regimen. The standard chemotherapy regimen consisted of cisplatin 80 mg/M2 on day 1 followed by 5-fluorouracil 800 mg/M2 days 2 through 6. Our test regimen consisted of the same two drugs plus 15 U bleomycin on day 1 and methotrexate 100 mg/M2 on day 16 followed in 24 hours with 15 mg leucovorin every 6 hours for six doses. One patient in each arm of the study was not evaluated. Among 29 patients receiving the two-drug regimen, there was 1 complete response and 10 partial responses (38% response rate). Among 31 patients receiving the four-drug regimen, there were 3 complete responses and 16 partial responses (61% response rate; two vs. four-drug regimen, P = .06). The failure-free survival in the four-drug group was better than the two-drug group, median 4.5 vs. 2.3 months (P = .02). The overall survival for both groups was the same (median of 7.8 months). A detailed analysis of toxicity did not reveal any important differences between the two regimens. The addition of bleomycin and methotrexate to our cisplatin and 5-fluorouracil regimen resulted in an increase in effectiveness without adding toxicity. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 18 TC 5 Z9 5 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD AUG PY 1992 VL 102 IS 8 BP 901 EP 907 DI 10.1288/00005537-199208000-00010 PG 7 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA JH387 UT WOS:A1992JH38700010 PM 1379664 ER PT J AU DUTCHER, JP EUDEY, L WIERNIK, PH PAIETTA, E BENNETT, JM ARLIN, Z KELLERMEYER, R ROWE, J OCONNELL, M OKEN, M CASSILETH, PA AF DUTCHER, JP EUDEY, L WIERNIK, PH PAIETTA, E BENNETT, JM ARLIN, Z KELLERMEYER, R ROWE, J OCONNELL, M OKEN, M CASSILETH, PA TI PHASE-II STUDY OF MITOXANTRONE AND 5-AZACYTIDINE FOR ACCELERATED AND BLAST CRISIS OF CHRONIC MYELOGENOUS LEUKEMIA - A STUDY OF THE EASTERN-COOPERATIVE-ONCOLOGY-GROUP SO LEUKEMIA LA English DT Article ID DOSE CYTOSINE-ARABINOSIDE AB A total of 40 evaluable patients were treated for blastic crisis of chronic myelogenous leukemia with mitoxantrone, 12 mg/m2 per day for three days and 5-azacytidine 150 mg/m2 per day for 5 days. Toxicity was primarily hematologic and was manageable. The overall response rate was 23%, including five complete responders, two partial responders, and two with hematologic improvement. Cytogenetic and immunophenotypic characterization of the leukemia was performed on all patients with aspirable bone marrow, and these results were correlated with response and survival, but did not have predictive value once the patient was in blastic crisis. Only initial platelet count (p = 0.02), hemoglobin (p = 0.03), and lower white blood cell count (p = 0.09) were somewhat predictive of response. Lack of hepatic involvement (p = 0.05), lower white blood cell count (0.05), and higher platelet count (p = 0.02) were predictive of prolonged survival. Although response did not strongly correlate with survival, one third of responders were alive at one year. This regimen produces results similar to those of other recently published regimens in this disease. Earlier intervention and more effective therapy is necessary in these patients. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104. RP DUTCHER, JP (reprint author), ALBERT EINSTEIN CANC CTR,1825 EASTCHESTER RD,BRONX,NY 10461, USA. FU NCI NIH HHS [CA 23318, CA 14958, CA 11083] NR 19 TC 27 Z9 28 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD AUG PY 1992 VL 6 IS 8 BP 770 EP 775 PG 6 WC Oncology; Hematology SC Oncology; Hematology GA JJ507 UT WOS:A1992JJ50700005 PM 1379312 ER PT J AU HUNNINGHAKE, GW MONKS, BG GEIST, LJ MONICK, MM MONROY, MA STINSKI, MF WEBB, AC DAYER, JM AURON, PE FENTON, MJ AF HUNNINGHAKE, GW MONKS, BG GEIST, LJ MONICK, MM MONROY, MA STINSKI, MF WEBB, AC DAYER, JM AURON, PE FENTON, MJ TI THE FUNCTIONAL IMPORTANCE OF A CAP SITE-PROXIMAL REGION OF THE HUMAN PROINTERLEUKIN-1-BETA GENE IS DEFINED BY VIRAL PROTEIN TRANSACTIVATION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN CYTOMEGALO-VIRUS; IMMEDIATE-EARLY GENE; TRANSCRIPTION FACTOR ATF; ELEMENT-BINDING PROTEIN; PREINITIATION COMPLEX; IMMUNOGLOBULIN GENES; NUCLEOTIDE-SEQUENCE; MAMMALIAN-CELLS; INTERLEUKIN-1; EXPRESSION AB Prointerleukin 1-beta (IL-1-beta) is a cytokine that mediates a broad range of biological activities. Genomic sequences that regulate IL-1-beta transcription include both inducible regulatory elements located more than 2,700 bp upstream of the transcriptional start site (cap site) and proximal elements located near the TATA box of this gene. In this study, we focused on the identification and characterization of trans-acting nuclear regulatory proteins that bind to the cap site-proximal region of the human IL-1-beta gene. We identified a protein, termed NFIL-1-beta-A (NF-beta-A), that binds to a highly conserved 12-bp DNA sequence (-49 to -38) located upstream of the TATA box motif in both the human and murine IL-1-beta genes. The IL-1-alpha gene, which lacks a TATA motif, does not possess an NF-beta-A-binding sequence within the promoter region, suggesting that NF-beta-A may selectively regulate IL-1-beta expression. Using electrophoretic mobility shift assays, we identified several distinct DNA-protein complexes that are expressed in a cell-type-specific manner. In monocytic cell lines, the relative abundance of these complexes varies rapidly following stimulation of the cells with phorbol esters or lipopolysaccharide. UV cross-linking analysis identified two distinct DNA-binding polypeptides that comprise distinct complexes. The functional role of NF-beta-A was assessed in transient transfection assays. These data indicate that NF-beta-A is required for both basal and inducible promoter activity in monocytic cells. Furthermore, the human cytomegalovirus immediate-early 1 gene product requires the presence of NF-beta-A in order to trans-activate the proximal IL-1-beta promoter in a monocytic cell line. We propose that NF-beta-A is a factor that mediates either direct or indirect activation by the immediate-early 1 gene product. The proximity of this essential factor to the TATA motif suggests a possible role in transcriptional initiation. C1 BOSTON UNIV,MED CTR,DEPT MED,BOSTON,MA 02118. UNIV IOWA,COLL MED,DEPT MED,IOWA CITY,IA 52242. BOSTON UNIV,MED CTR,EVANS DEPT CLIN RES,BOSTON,MA 02118. WELLESLEY COLL,DEPT BIOL SCI,WELLESLEY,MA 02181. HOP CANTONAL LAUSANNE,DEPT MED,DIV IMMUNOL & ALLERGY,CH-1011 LAUSANNE,SWITZERLAND. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02129. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RI Monks, Brian/B-8362-2015 OI Monks, Brian/0000-0003-4008-3093 FU NHLBI NIH HHS [HL-37121, HL-07638]; NIAID NIH HHS [AI-29088] NR 55 TC 67 Z9 68 U1 0 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 AUG PY 1992 VL 12 IS 8 BP 3439 EP 3448 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JE748 UT WOS:A1992JE74800015 PM 1630455 ER PT J AU WENTWORTH, BM RHODES, C SCHNETZLER, B GROSS, DJ HALBAN, PA VILLAKOMAROFF, L AF WENTWORTH, BM RHODES, C SCHNETZLER, B GROSS, DJ HALBAN, PA VILLAKOMAROFF, L TI THE RATIO OF MOUSE INSULIN-I - INSULIN-II DOES NOT REFLECT THAT OF THE CORRESPONDING PREPROINSULIN MESSENGER-RNAS SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE PREPROINSULIN MESSENGER RNAS; S1 NUCLEASE; HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY ID ENDOPLASMIC-RETICULUM MEMBRANE; SIGNAL-RECOGNITION-PARTICLE; ISOLATED PANCREATIC-ISLETS; CELL-SPECIFIC EXPRESSION; DNA-DNA HYBRIDIZATION; TRANSLATIONAL CONTROL; TRANSGENIC MICE; GENE-EXPRESSION; INTRACELLULAR DEGRADATION; EUKARYOTIC RIBOSOMES AB Rats and mice both express two, non-allelic, insulin genes. In the rat the ratio of the two preproinsulin mRNAs closely matches that of the mature insulin peptides. The experiments reported here demonstrate that this is not the case in the mouse. The relative amounts of the two murine proinsulin RNAs were measured by an S1 nuclease assay. The ratio of preproinsulin I mRNA to preproinsulin II mRNA was 4:1 in RNA extracted from the pancreas of mice fed ad libitum or fasted for 72 h. A similar value was found in mouse islets of Langerhans after maintenance in tissue culture for 48 h at either 2.8 or 16.7 mM glucose. The ratio of insulin I : insulin II peptides, assessed by separating the two insulins using reversed phase high-performance liquid chromatography, was approximately 1:3 in both pancreas and islets. Thus in the mouse, unlike the rat, the ratio of the two insulin peptides does not reflect that of the two preproinsulin mRNAs. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,NEUROL RES ENDERS 260,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,JOSLIN RES LAB,BOSTON,MA 02215. UNIV GENEVA,SCH MED,LABS RECH LOUIS JEANTET,CH-1211 GENEVA 4,SWITZERLAND. HADASSAM UNIV HOSP,DEPT ENDOCRINOL & METAB,JERUSALEM,ISRAEL. FU NICHD NIH HHS [HD18655]; NIDDK NIH HHS [DK35292] NR 53 TC 17 Z9 17 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 AUG PY 1992 VL 86 IS 3 BP 177 EP 186 DI 10.1016/0303-7207(92)90142-S PG 10 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA JH394 UT WOS:A1992JH39400006 PM 1511787 ER PT J AU BACHWICH, D MERCHANT, J BRAND, SJ AF BACHWICH, D MERCHANT, J BRAND, SJ TI IDENTIFICATION OF A CIS-REGULATORY ELEMENT MEDIATING SOMATOSTATIN INHIBITION OF EPIDERMAL GROWTH FACTOR-STIMULATED GASTRIN GENE-TRANSCRIPTION SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID AMP-INDEPENDENT ACTIONS; VASOACTIVE INTESTINAL PEPTIDE; INTRACELLULAR FREE CALCIUM; PERTUSSIS TOXIN BLOCKS; RIBONUCLEIC-ACID; GH3 CELLS; IMMUNOGLOBULIN ENHANCERS; POTASSIUM CONDUCTANCE; PROLACTIN SECRETION; RESPONSE ELEMENT AB Antral gastrin secretion and gene expression is inhibited by the paracrine release of somatostatin from antral D cells. Transforming growth factor-alpha and epidermal growth factor (EGF) stimulate gastrin reporter gene constructs when transfected into pituitary GH4 cells. Somatostatin inhibits EGF stimulation of gastrin gene expression, which is in part mediated at the level of transcriptional regulation as somatostatin inhibits EGF stimulation of gastrin reporter gene constructs. Somatostatin inhibition was abolished by pertussis toxin, indicating somatostatin inhibits transcription through the inhibitory G protein G(i). Somatostatin inhibition was unaffected by vanadate and okadaic acid, implying this inhibitory pathway is mediated neither through phosphotyrosine phosphatases nor serine/threonine phosphatases, respectively. Gastrin reporter genes containing 82 base pairs of the 5'-flanking DNA were sufficient to confer both EGF responsiveness and inhibition by somatostatin in GH4 cells. However, transcription of a gastrin reporter gene construct containing only the EGF response element (GGGGCGGGGTGGGGGG), located at -68 to -53, was stimulated by EGF but was not inhibited by somatostatin. Thus, somatostatin inhibits EGF-stimulated gastrin gene transcription by a mechanism other than by interfering with cell signals elicited by the EGF receptor. Since the 82 GASCAT is inhibited by somatostatin, this result also implies that sequences adjacent to the EGF response element contain a cis-regulatory element mediating transcriptional inhibition by somatostatin. This cis-element was located using gastrin reporter genes comprising sequential segments of the human gastrin promoter sequence from the transcriptional start site to -82 in the 5'-flanking DNA. Gastrin oligonucleotide constructs lacking the D oligonucleotide (gatcCATATGGCAGGGTA), located at -82 to -69 in the 5'-flanking DNA, were not inhibited by somatostatin, indicating that a somatostatin inhibitory cis-element is located between -82 and -69 in the 5'-flanking DNA of the human gastrin promoter. C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, JACKSON 7, FRUIT ST, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [F32 DK-08405, R29 DK-40543, R01 DK-42147] NR 40 TC 27 Z9 28 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD AUG PY 1992 VL 6 IS 8 BP 1175 EP 1184 DI 10.1210/me.6.8.1175 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL963 UT WOS:A1992JL96300001 PM 1357547 ER PT J AU GOLDBERG, MB BOYKO, SA BUTTERTON, JR STOEBNER, JA PAYNE, SM CALDERWOOD, SB AF GOLDBERG, MB BOYKO, SA BUTTERTON, JR STOEBNER, JA PAYNE, SM CALDERWOOD, SB TI CHARACTERIZATION OF A VIBRIO-CHOLERAE VIRULENCE FACTOR HOMOLOGOUS TO THE FAMILY OF TONB-DEPENDENT PROTEINS SO MOLECULAR MICROBIOLOGY LA English DT Article ID OUTER-MEMBRANE PROTEIN; ESCHERICHIA-COLI K-12; MEDIATED IRON-TRANSPORT; MOLECULAR CHARACTERIZATION; HEMOLYSIN PRODUCTION; NUCLEOTIDE-SEQUENCE; CIR GENE; RECEPTOR; TOXIN; SYSTEM AB IrgA is an iron-regulated virulence factor for infection in an animal model with classical Vibrio cholerae strain 0395. We detected gene sequences hybridizing to irgA at high stringency in clinical isolates in addition to 0395, including another classical strain of V. cholerae, three V. cholerae strains of the El Tor biotype, three non-O1 isolates of V. cholerae, and individual isolates of Vibrio parahaemolyticus, Vibrio fluvialis, and Vibrio alginolyticus. No hybridization to irgA was seen with chromosomal DNA from Vibrio vulnificus or Aeromonas hydrophila. To verify that irgA is the structural gene for the major iron-regulated outer membrane protein of V. cholerae, we determined the amino-terminal sequence of this protein recovered after gel electrophoresis and demonstrated that it corresponds to the amino acid sequence of IrgA deduced from the nucleotide sequence. Gel electrophoresis showed that two El Tor strains of V. cholerae had a major iron-regulated outer membrane protein identical in size and appearance to IrgA in strain 0395, consistent with the findings of DNA hybridization. We have previously suggested that IrgA might be the outer membrane receptor for the V. cholerae siderophore, vibriobactin. Biological data presented here, however, show that a mutation in irgA had no effect on the transport of vibriobactin and produced no defect in the utilization of iron from ferrichrome, ferric citrate, haemin or haemoglobin. The complete deduced amino acid sequence of IrgA demonstrated homology to the entire class of Escherichia coli TonB-dependent proteins, particularly Cir. Unlike the situation with Cir, however, we were unable to demonstrate a role for IrgA as a receptor for catechol-substituted cephalosporins. The role of IrgA in the pathogenesis of V. cholerae infection, its function as an outer membrane receptor, and its potential interaction with a TonB-like protein in V. cholerae remain to be determined. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. UNIV TEXAS,DEPT MICROBIOL,AUSTIN,TX 78712. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NIAID NIH HHS [AI27329] NR 53 TC 44 Z9 46 U1 0 U2 3 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD AUG PY 1992 VL 6 IS 16 BP 2407 EP 2418 DI 10.1111/j.1365-2958.1992.tb01415.x PG 12 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA JJ447 UT WOS:A1992JJ44700019 PM 1406279 ER PT J AU MACDONELL, RAL CROS, D SHAHANI, BT AF MACDONELL, RAL CROS, D SHAHANI, BT TI LUMBOSACRAL NERVE ROOT STIMULATION COMPARING ELECTRICAL WITH SURFACE MAGNETIC COIL TECHNIQUES SO MUSCLE & NERVE LA English DT Article DE LUMBOSACRAL NERVE ROOT; MAGNETIC STIMULATION AB Stimulation of lumbosacral nerve roots using a monopolar needle electrode was compared with magnetic stimulation using a 7-cm diameter surface coil. Compound muscle action potentials were recorded from the tibialis anterior (TA) and flexor hallucis brevis (FHB) muscles. Although the mean latency of CMAPs did not differ using the two techniques, amplitudes were considerably larger using a needle. Mean amplitudes were 66% (TA) and 64% (FHB) of the direct M response obtained by distal, supramaximal stimulation compared with mean values using maximal magnetic coil stimulation of 36% (TA) and 25% (FHB). Minimum F-wave latencies from FHB were used to estimate the site of nerve root stimulation using both techniques. Although there was a large amount of variability in the data from individual subjects, the results suggested that, on the average, both forms of stimulation act proximal to the intervertebral foramen. We conclude that a needle electrode is a more suitable technique for stimulating lumbosacral nerve roots. C1 MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LAB,BOSTON,MA 02114. SPAULDING REHABIL HOSP,BOSTON,MA 02114. NR 17 TC 40 Z9 40 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD AUG PY 1992 VL 15 IS 8 BP 885 EP 890 DI 10.1002/mus.880150804 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA JF812 UT WOS:A1992JF81200003 PM 1495504 ER PT J AU BURGLIN, TR RUVKUN, G AF BURGLIN, TR RUVKUN, G TI NEW MOTIF IN PBX GENES SO NATURE GENETICS LA English DT Letter ID HOMEODOMAIN-DNA INTERACTIONS; CRYSTAL-STRUCTURE; BINDING DOMAIN; POU DOMAIN; PROTEIN; CONSERVATION; COMPLEX C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT GENET,BOSTON,MA 02114. RP BURGLIN, TR (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,WELLMAN 8,BOSTON,MA 02114, USA. NR 15 TC 67 Z9 70 U1 0 U2 2 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 AUG PY 1992 VL 1 IS 5 BP 319 EP 320 DI 10.1038/ng0892-319 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA JJ121 UT WOS:A1992JJ12100004 PM 1363814 ER PT J AU MCCOMBIE, WR MARTINGALLARDO, A GOCAYNE, JD FITZGERALD, M DUBNICK, M KELLEY, JM CASTILLA, L LIU, LI WALLACE, S TRAPP, S TAGLE, D WHALEY, WL CHENG, S GUSELLA, J FRISCHAUF, AM POUSTKA, A LEHRACH, H COLLINS, FS KERLAVAGE, AR FIELDS, C VENTER, JC AF MCCOMBIE, WR MARTINGALLARDO, A GOCAYNE, JD FITZGERALD, M DUBNICK, M KELLEY, JM CASTILLA, L LIU, LI WALLACE, S TRAPP, S TAGLE, D WHALEY, WL CHENG, S GUSELLA, J FRISCHAUF, AM POUSTKA, A LEHRACH, H COLLINS, FS KERLAVAGE, AR FIELDS, C VENTER, JC TI EXPRESSED GENES, ALU REPEATS AND POLYMORPHISMS IN COSMIDS SEQUENCED FROM CHROMOSOME-4P16.3 SO NATURE GENETICS LA English DT Article ID HUNTINGTON DISEASE GENE; PROTEIN-CODING REGIONS; HUMAN GENOME; DNA-SEQUENCES; NEUROFIBROMATOSIS TYPE-1; RETINOBLASTOMA; SUBFAMILY; DELETION; CLUSTER; FAMILY AB The sequences of three cosmids (90 kilobases) from the Huntington's disease region in chromosome 4p16.3 have been determined. A 30,837 base overlap of DNA sequenced from two individuals was found to contain 72 DNA sequence polymorphisms, an average of 2.3 polymorphisms per kilobase (kb). The assembled 58 kb contig contains 62 Alu repeats, and eleven predicted exons representing at least three expressed genes that encode previously unidentified proteins. Each of these genes is associated with a CpG island. The structure of one of the new genes, hda1-1, has been determined by characterizing cDNAs from a placental library. This gene is expressed in a variety of tissues and may encode a novel housekeeping gene. C1 NINCDS,RECEPTOR BIOCHEM & MOLEC BIOL SECT,BETHESDA,MD 20892. IMPERIAL CANC RES FUND,DEPT GENOME ANAL,LONDON WC2A 3PX,ENGLAND. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. HARVARD UNIV,DEPT GENET,BOSTON,MA 02129. DEUTSCH KREBSFORSCHUNGSZENTRUM,W-6900 HEIDELBERG,GERMANY. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. OI Fields, Chris/0000-0002-4812-0744; McCombie, W. Richard/0000-0003-1899-0682 NR 72 TC 45 Z9 46 U1 0 U2 1 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 AUG PY 1992 VL 1 IS 5 BP 348 EP 353 DI 10.1038/ng0892-348 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA JJ121 UT WOS:A1992JJ12100013 PM 1338771 ER PT J AU DAVIS, AE AULAK, K PARAD, RB STECKLEIN, HP ELDERING, E HACK, CE KRAMER, J STRUNK, RC BISSLER, J ROSEN, FS AF DAVIS, AE AULAK, K PARAD, RB STECKLEIN, HP ELDERING, E HACK, CE KRAMER, J STRUNK, RC BISSLER, J ROSEN, FS TI C1 INHIBITOR HINGE REGION MUTATIONS PRODUCE DYSFUNCTION BY DIFFERENT MECHANISMS SO NATURE GENETICS LA English DT Article ID HEREDITARY ANGIONEUROTIC-EDEMA; POLYMERASE CHAIN-REACTION; HUMAN C1BAR INHIBITOR; STRUCTURAL CHARACTERIZATION; C1-INHIBITOR PROTEINS; PLASMA KALLIKREIN; CRYSTAL-STRUCTURE; ANTITHROMBIN; COMPLEMENT; MODEL AB Heterozygosity for a mutant dysfunctional C1 inhibitor protein, a member of the serine proteinase inhibitor (serpin) superfamily, results in type II hereditary angioneurotic oedema. We identified a "hinge" region mutation in C1 inhibitor with a Val to Glu replacement at P14 Val-432. Recombinant C1 inhibitors P10 Ala --> Thr and P14 Val --> Glu did not form stable complexes with fluid phase C1s or kallikrein. The P14 Val --> Glu mutant, however, was cleaved to a 96K form by C1s, while the P10 Ala --> Thr mutant was not. The recombinant P10 mutant also did not complex with C1s, kallikrein or beta-factor XIIa-Sepharose. The two mutations, therefore, result in dysfunction by different mechanisms: in one (P14 Val --> Glu), the inhibitor is converted to a substrate, while in the other (P10 Ala --> Thr), interaction with target protease is blocked. C1 UNIV CINCINNATI,COLL MED,DEPT PEDIAT,CINCINNATI,OH 45229. CHILDRENS HOSP MED CTR,JOINT PROGRAM NEONATOL,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,DEPT PEDIAT,ST LOUIS,MO 63110. CTR BLOOD RES,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV NEPHROL,BOSTON,MA 02115. NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,AMSTERDAM,NETHERLANDS. UNIV AMSTERDAM,EXPTL & CLIN IMMUNOL LAB,AMSTERDAM,NETHERLANDS. RP DAVIS, AE (reprint author), CHILDRENS HOSP RES FDN,DIV NEPHROL,CINCINNATI,OH 45229, USA. RI Parad, Richard/E-8559-2010 NR 44 TC 63 Z9 65 U1 0 U2 2 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 AUG PY 1992 VL 1 IS 5 BP 354 EP 358 DI 10.1038/ng0892-354 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA JJ121 UT WOS:A1992JJ12100014 PM 1363816 ER PT J AU KARLINSKY, H VAULA, G HAINES, JL RIDGLEY, J BERGERON, C MORTILLA, M TUPLER, RG PERCY, ME ROBITAILLE, Y NOLDY, NE YIP, TCK TANZI, RE GUSELLA, JF BECKER, R BERG, JM MCLACHLAN, DRC STGEORGEHYSLOP, PH AF KARLINSKY, H VAULA, G HAINES, JL RIDGLEY, J BERGERON, C MORTILLA, M TUPLER, RG PERCY, ME ROBITAILLE, Y NOLDY, NE YIP, TCK TANZI, RE GUSELLA, JF BECKER, R BERG, JM MCLACHLAN, DRC STGEORGEHYSLOP, PH TI MOLECULAR AND PROSPECTIVE PHENOTYPIC CHARACTERIZATION OF A PEDIGREE WITH FAMILIAL ALZHEIMERS-DISEASE AND A MISSENSE MUTATION IN CODON 717 OF THE BETA-AMYLOID PRECURSOR PROTEIN GENE SO NEUROLOGY LA English DT Article ID HETEROGENEITY AB We present prospective clinical and neuropathologic details of a pedigree segregating familial Alzheimer's disease (FAD) associated with a mutation (G-->A substitution) at nucleotide 2149 in exon 17 of the amyloid precursor protein (APP) gene. This mutation, which is predicted to cause the missense substitution of isoleucine for valine at codon 717 of APP, cosegregated perfectly with the FAD trait (lod score = 3.49 at theta = 0.00). The earliest clinical manifestations of the disease relate to deficits in memory function, cognitive processing speed, and attention to complex cognitive sets. These changes occurred in the absence of changes in nonmemory language and visuospatial functions. The neuropathologic features of FAD associated with the APP717 mutation in this family include severe neuronal loss, abundant neurofibrillary tangles, amyloid plaques, and amyloid angiopathy. These results provide independent confirmation that mutations in the APP gene are linked to the FAD trait in some families. C1 UNIV TORONTO,CTR RES NEURODEGENERAT DIS,ROOM 120,TANZ NEUROSCI BLDG,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,DEPT PSYCHIAT,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,DEPT MED,DIV NEUROL,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,DEPT PSYCHOL,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,DEPT PATHOL,DIV NEUROPATHOL,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,DEPT OBSTET & GYNECOL,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,DEPT RADIOL,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,ADDICT RES FDN,INST CLIN RES & TREATMENT,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,QUEEN ELIZABETH HOSP,TORONTO HOSP,CONJOINT GERIATR PSYCHIAT SERV,TORONTO M5S 1A8,ONTARIO,CANADA. UNIV TORONTO,SURREY PL CTR,TORONTO M5S 1A8,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MONTREAL NEUROL HOSP & INST,DEPT NEUROPATHOL,MONTREAL H3A 2B4,QUEBEC,CANADA. MCGILL UNIV,JEWISH REHABIL HOSP,DEPT MED,MONTREAL H3A 2T5,QUEBEC,CANADA. RI Haines, Jonathan/C-3374-2012; Tupler, Rossella/C-9500-2015 OI Tupler, Rossella/0000-0002-3797-1789 NR 37 TC 131 Z9 131 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD AUG PY 1992 VL 42 IS 8 BP 1445 EP 1453 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA JH221 UT WOS:A1992JH22100002 PM 1520398 ER PT J AU NOZAKI, K BOCCALINI, P MOSKOWITZ, MA AF NOZAKI, K BOCCALINI, P MOSKOWITZ, MA TI EXPRESSION OF C-FOS-LIKE IMMUNOREACTIVITY IN BRAIN-STEM AFTER MENINGEAL IRRITATION BY BLOOD IN THE SUBARACHNOID SPACE SO NEUROSCIENCE LA English DT Article ID LATERAL RETICULAR NUCLEUS; GENE-RELATED PEPTIDE; CEREBROVASCULAR NERVE-FIBERS; CAROTID-SINUS NERVE; RAT SPINAL-CORD; HORSERADISH-PEROXIDASE; AREA POSTREMA; PARABRACHIAL NUCLEUS; SOLITARY TRACT; CENTRAL PROJECTIONS AB The expression of c-fos protein was examined by immunohistochemistry in serial sections of brainstem following the instillation of either autologous arterial blood (0.3 ml) or mock cerebrospinal fluid (0.3ml) through a catheter placed in the cisterna magna, or following catheter placement alone in pentobarbital-anesthetized Sprague Dawley rats. After injection. blood was distributed within the subarachnoid space surrounding the brainstem and in the region of the circle of Willis. c-fos protein-like immunoreactivity was present at 1 h, peaked at 2 h and decreased by 8 h. At 2 h, immunoreactivity was strongly expressed within trigeminal nucleus caudalis (lamina I, IIo), as well as within nucleus of the solitary tract, area postrema, ependyma, pia mater and arachnoid in every animal. Moderate labeling was found in parabrachial nucleus, medullary lateral reticular nucleus and central gray. Sparse labeling was present in trigeminal nucleus caudalis (lamina III-V) and trigeminal nucleus interpolaris; few or no labeled cells were detected in other parts of the trigeminal nuclear complex, thalamus, cerebral cortex, cerebellar cortex or trigeminal ganglion. The Dumber of positive cells was not related to the volume of injectate but was related to the amount of injected blood. The density of cell labeling evoked by injecting mock cerebrospinal fluid or after catheter placement was markedly lower than after blood in all brainstem areas. The number of labeled cells was greatly reduced within trigeminal nuclear complex, parabrachial nucleus and medullary lateral reticular nucleus, but not within the nucleus of the solitary tract, area postrema or ependyma when blood was injected into adult animals in which unmyelinated C-fibers were destroyed by neonatal capsaicin treatment. Similar results were obtained after blood was instilled into the cisterna magna of rats in which meningeal afferents were chronically sectioned at the ethmoidal foramen bilaterally. We conclude that blood in the subarachnoid space is an effective stimulus for activating c-fos expression within subpopulations of brainstem neurons. Activation within trigeminal nucleus caudalis is mediated in large part by excitation of small-caliber meningeal afferents (trigeminovascular fibers), whereas c-fos expression within nucleus of the solitary tract and area postrema may reflect direct stimulation of blood or blood products, or possibly the response to autonomic activation from noxious stimulation. We suggest that c-fos expression in this rodent model may reflect tonic activation of those brainstem regions which are associated with the processing of information relating to the features of headache, nausea, vomiting, as well as hyper- and hypotension and autonomic instability after noxious chemicals enter the subarachnoid space in man. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,32 FRUIT ST,BOSTON,MA 02114. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS 21558] NR 93 TC 103 Z9 104 U1 2 U2 7 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD AUG PY 1992 VL 49 IS 3 BP 669 EP 680 DI 10.1016/0306-4522(92)90235-T PG 12 WC Neurosciences SC Neurosciences & Neurology GA JE546 UT WOS:A1992JE54600014 PM 1501769 ER PT J AU OGILVY, CS LOUIS, DN OJEMANN, RG AF OGILVY, CS LOUIS, DN OJEMANN, RG TI INTRAMEDULLARY CAVERNOUS ANGIOMAS OF THE SPINAL-CORD - CLINICAL PRESENTATION, PATHOLOGICAL FEATURES, AND SURGICAL-MANAGEMENT SO NEUROSURGERY LA English DT Article DE CAVERNOUS ANGIOMA; CLINICAL PRESENTATION; SPINAL CORD; VASCULAR MALFORMATION ID VASCULAR MALFORMATIONS; CAUDA-EQUINA; BRAIN-STEM; HEMANGIOMA; HEMORRHAGE; DIAGNOSIS; SPECTRUM AB CAVERNOUS ANGIOMAS OF the spinal cord are rare lesions that can cause severe neurological symptoms. We add a series of 6 patients with intramedullary cavernous angiomas of the spinal cord to 30 patients with 31 histologically verified lesions already described in the literature. Four types of clinical presentation were seen in the 36 patients: 1) discrete episodes of neurological deterioration with varying degrees of recovery between episodes (13 patients); 2) slow progression of neurological decline (1 2 patients); 3) acute onset of symptoms with rapid decline (8 patients); and 4) acute onset of mild symptoms with subsequent gradual decline lasting weeks to months (3 patients). Of the 36 patients, 25 (69%) were women and 11 (31%) were men. The peak age of presentation was in the fourth decade. The thoracic spinal cord was affected in more than half the patients, with the cervical cord being the next most common location. Histological examination demonstrated the closely apposed vascular channels characteristic of cavernous angiomas. While most vascular channels were thickened and hyalinized, three angiomas had foci of small vessels resembling a capillary angioma. The available data suggest that surgical management of intramedullary angiomas should attempt complete extirpation. The lesions are often well circumscribed with a glial plane between the lesion and normal cord. However, spinal cord angiomas, unlike cranial lesions, have little room for enlargement before devastating symptoms occur. We achieved complete excision in all of our patients, who are all ambulatory and have improved symptoms. Little, if any, increase in neurological deficit was caused by myelotomy and lesion excision. These spinal lesions should be considered for surgery early, before repeated hemorrhage or enlargement can occur. C1 MASSACHUSETTS GEN HOSP,NEUROPATHOL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP OGILVY, CS (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 36 TC 118 Z9 120 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD AUG PY 1992 VL 31 IS 2 BP 219 EP 230 PG 12 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA JJ520 UT WOS:A1992JJ52000007 PM 1513428 ER PT J AU KWONG, YY HUSAIN, Z BISWAS, DK AF KWONG, YY HUSAIN, Z BISWAS, DK TI C-HA-RAS GENE MUTATION AND ACTIVATION PRECEDE PATHOLOGICAL-CHANGES IN DMBA-INDUCED INVIVO CARCINOGENESIS SO ONCOGENE LA English DT Article ID MULTISTEP CARCINOGENESIS; CELLULAR ONCOGENES; COLORECTAL CANCERS; CARCINOMA; NEOPLASIA; MODEL; DNA AB We have previously reported a stage-specific and sequential overexpression of the c-Ha-ras and c-erhB genes in 7, 12-dimethylbenzanthracene (DMBA)-induced in vivo carcinogenesis in hamster buccal pouch epithelium (HBPE). In this investigation, the immunoreactive protein product of the c-Ha-ras gene (p21 protein) was identified in HBPE cells, specifically in treated tissues and cultured cells established after 3 weeks of DMBA treatment. Microscopic examination did not show any histopathological changes in these tissues. The p21 protein was detected in a few selective cells, which were dispersed away from the more densely populated basal layer. The overexpression of the c-Ha-ras gene was accompanied by a point mutation of A --> T in codon 61 (CAA), inducing an amino acid substitution from the wild-type glutamine to leucine in the- peptide. The concurrent molecular modifications preceded any detectable histopathological changes. The cellular morphology and orientation in treated HBPE at this early stage was indistinguishable from the control tissue. Yet the genetic alterations, such as the point mutation and overexpression of the gene, were evident at the predysplastic stage. Amplification and overexpression of the second proto-oncogene, c-erbB, and its product, epidermal growth factor receptor (EGFR), were detected in HBPE cells at the later stages of extensive cell proliferation and invasion. By using double antibodies and two immunoreporter systems, we demonstrated overexpression of both c-Ha-ras and c-erbB genes in the same HBPE cells during this chemically induced in vivo carcinogenesis. C1 HARVARD UNIV,SCH DENT MED,MOLEC BIOL LAB,188 LONGWOOD AVE,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,BOSTON,MA 02115. NR 31 TC 22 Z9 22 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD AUG PY 1992 VL 7 IS 8 BP 1481 EP 1489 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA JE813 UT WOS:A1992JE81300003 PM 1630811 ER PT J AU RUBIN, PAD SHORE, JW JAKOBIEC, FA TO, K AF RUBIN, PAD SHORE, JW JAKOBIEC, FA TO, K TI HEMANGIOPERICYTOMA OF THE LACRIMAL SAC SO OPHTHALMIC SURGERY AND LASERS LA English DT Note AB Hemangiopericytoma is a rare soft-tissue neoplasm composed histologically of pericytes. Hemangiopericytoma of the lacrimal sac is exceedingly rare. This case provided the first known computed tomographic image of a hemangiopericytoma of the lacrimal sac prior to surgical intervention. RP RUBIN, PAD (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114, USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD AUG PY 1992 VL 23 IS 8 BP 562 EP 563 PG 2 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA JF869 UT WOS:A1992JF86900013 PM 1508491 ER PT J AU TOPPING, TM AF TOPPING, TM TI RETAINED INTRAVITREAL LENS FRAGMENTS AFTER CATARACT-SURGERY - DISCUSSION SO OPHTHALMOLOGY LA English DT Discussion C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP TOPPING, TM (reprint author), MASSACHUSETTS EYE & EAR INFIRM,CTR EYE RES,BOSTON,MA 02114, USA. NR 6 TC 4 Z9 4 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 AUG PY 1992 VL 99 IS 8 BP 1268 EP 1269 PG 2 WC Ophthalmology SC Ophthalmology GA JJ122 UT WOS:A1992JJ12200023 ER PT J AU GUYER, DR MUKAI, S EGAN, KM SEDDON, JM WALSH, SM GRAGOUDAS, ES AF GUYER, DR MUKAI, S EGAN, KM SEDDON, JM WALSH, SM GRAGOUDAS, ES TI RADIATION MACULOPATHY AFTER PROTON-BEAM IRRADIATION FOR CHOROIDAL MELANOMA SO OPHTHALMOLOGY LA English DT Article ID CILIARY BODY; OCULAR COMPLICATIONS; COBALT PLAQUE; RETINOPATHY; THERAPY; EYE AB Purpose: Radiation maculopathy is a microangiopathy of the retina, which is often observed after irradiation of the eye. To quantitatively determine the frequency of anatomic and functional features of this condition, the authors reviewed a large series of patients with choroidal melanomas who were treated by proton beam irradiation. Methods: Color photographs and/or fluorescein angiograms of 218 patients with paramacular choroidal melanomas were graded by two independent masked readers to determine the frequency of the various lesions of radiation maculopathy. Results: Overall, 194 (89%) of the 218 patients in this study developed some degree of radiation maculopathy. The earliest and most common finding was macular edema, which was observed in 87% of patients, overall, by the end of year 3. Microvascular changes (microaneurysms and/or telangiectasia), intraretinal hemorrhages, and capillary nonperfusion were noted in 76%, 70%, and 64% of eyes, respectively, by the end of postirradiation year 3. Visual acuity was retained at 20/200 or better in 90% of eyes 1 year after irradiation and in 67% of eyes 3 years after treatment. Conclusion: Radiation maculopathy is common after proton beam irradiation of paramacular choroidal melanomas. However, ambulatory vision is preserved in many eyes. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02115. NR 41 TC 61 Z9 64 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD AUG PY 1992 VL 99 IS 8 BP 1278 EP 1285 PG 8 WC Ophthalmology SC Ophthalmology GA JJ122 UT WOS:A1992JJ12200025 PM 1325044 ER PT J AU RIZZO, JF GITTINGER, JW AF RIZZO, JF GITTINGER, JW TI SELECTIVE IMMUNOHISTOCHEMICAL STAINING IN THE PARANEOPLASTIC RETINOPATHY SYNDROME SO OPHTHALMOLOGY LA English DT Article ID CANCER-ASSOCIATED RETINOPATHY; PARA-NEOPLASTIC SYNDROME; CALCIUM-BINDING PROTEIN; SMALL CELL-CARCINOMA; PHOTORECEPTOR DEGENERATION; CEREBELLAR DEGENERATION; MYASTHENIA-GRAVIS; AUTOIMMUNE BASIS; LUNG-CARCINOMA; ANTIBODIES AB Background. The mechanism leading to visual loss in paraneoplastic retinopathy is not known. An autoimmune process has been imputed based on immunologic investigations of several patients and by analogy to certain other paraneoplastic syndromes. Methods: Two patients with documented small cell carcinoma of the lung who had clinical evidence of paraneoplastic retinopathy are described. Histopathologic examination of the retina from one patient and immunohistochemical staining of human retina with serum from control subjects and both patients were performed. Results: Electroretinograms demonstrated dysfunction of photoreceptors in both patients, with predominant loss of rod function in one patient. Post mortem examination showed patchy loss of photoreceptors of the extramacular retina and relative sparing of cones, findings consistent with the clinical and electrophysiologic test results. Serum from both patients stained the retina in an identical manner, with restriction of the stain to the outer retina. Stain was present over the outer plexiform layer, the outer nuclear layer, and the inner and outer segments of most photoreceptors. A sharp demarcation was present between those areas that did and did not stain. All rod inner and outer segments appeared to stain, and many cone inner segments were not stained. Immunologic tests obtained elsewhere did not show serum antibody to the 23 kD protein. Conclusion: These findings support the concept of an autoimmune pathogenesis by showing selectivity of the immune response and correlation between the apparent target of the immune response and the clinical and pathologic findings. The mechanism by which cell loss occurs in the retina is not answered by this study. The absence of antibody to the 23 kD protein does not exclude the diagnosis of paraneoplastic retinopathy. C1 UNIV MASSACHUSETTS,SCH MED,DEPT OPHTHALMOL,WORCESTER,MA 01605. MASSACHUSETTS EYE & EAR INFIRM,NEUROOPHTHALMOL SERV,243 CHARLES ST,BOSTON,MA 02114. RP RIZZO, JF (reprint author), HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115, USA. NR 34 TC 51 Z9 53 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 AUG PY 1992 VL 99 IS 8 BP 1286 EP 1295 PG 10 WC Ophthalmology SC Ophthalmology GA JJ122 UT WOS:A1992JJ12200026 PM 1325045 ER PT J AU BOND, JB HAIK, BG TAVERAS, JL FRANCIS, BA NUMAGUCHI, Y MIHARA, F GUPTA, KL AF BOND, JB HAIK, BG TAVERAS, JL FRANCIS, BA NUMAGUCHI, Y MIHARA, F GUPTA, KL TI MAGNETIC-RESONANCE-IMAGING OF ORBITAL LYMPHANGIOMA WITH AND WITHOUT GADOLINIUM CONTRAST ENHANCEMENT SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY OCT, 1991 CL ANAHEIM, CA SP AMER ACAD OPHTHALMOL ID OPTIC-NERVE; DTPA; AGENT AB Background. Lymphangioma is a vascular tumor of the orbit with a propensity for recurrent hemorrhage. These tumors may be difficult to diagnose in young patients who present with sudden proptosis due to hemorrhage into a previously unrecognized lesion. Magnetic resonance imaging (MRI) should be ideally suited for evaluating lymphangioma due to the unique ability of MRI to characterize hemorrhage because of the paramagnetic qualities of hemoglobin. Methods: The authors performed T1-, T2-, and proton density-weighted MRI on 12 patients with orbital lymphangioma. Six patients underwent MRI with gadolinium-DTPA contrast enhancement. The MRI studies were performed using a 1.5 Tesla super-conducting magnetic resonance unit, except for 3 early studies performed with a 0.5 Tesla unit. All studies were performed with orbital surface coil imaging. Computed tomography (CT) was performed in 10 patients. Results: Tumor was visible on MRI in all 12 patients. Magnetic resonance imaging delineated clearly the internal structure of subacute and chronic hemorrhagic cysts, and differentiated between these tumors because of the different paramagnetic qualities of subacute hemorrhage compared to chronic hemorrhage. In two patients, MRI detected large tumor feeding vessels by the flow void phenomenon unique to MRI. Computed tomography did not detect these vessels. Gadolinium-contrasted T1-weighted MRI did not further delineate or characterize the tumor. Conclusion: Magnetic resonance imaging is the modality of choice for imaging orbital lymphangioma because of its unequalled differentiation of hemorrhagic cysts, and its unique ability to detect tumor feeding vessels by the flow void phenomenon. C1 TULANE UNIV,MED CTR,DEPT OPHTHALMOL,1430 TULANE AVE,NEW ORLEANS,LA 70112. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. UNIV MARYLAND,SCH MED,DEPT DIAGNOST RADIOL,BALTIMORE,MD 21201. TULANE UNIV,MED CTR,DEPT RADIOL,NEW ORLEANS,LA 70118. NR 14 TC 27 Z9 29 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD AUG PY 1992 VL 99 IS 8 BP 1318 EP 1324 PG 7 WC Ophthalmology SC Ophthalmology GA JJ122 UT WOS:A1992JJ12200031 PM 1513586 ER PT J AU STRIEDER, DJ AF STRIEDER, DJ TI OF PNEUMOGRAMS AND POLYSOMNOGRAPHY SO PEDIATRIC PULMONOLOGY LA English DT Editorial Material ID INFANTS; APNEA RP STRIEDER, DJ (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,PULM LAB,BOSTON,MA 02114, USA. NR 6 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 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD AUG PY 1992 VL 13 IS 4 BP 200 EP 201 DI 10.1002/ppul.1950130404 PG 2 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA JH255 UT WOS:A1992JH25500003 PM 1523027 ER PT J AU LYNFIELD, R HERRIN, JT RUBIN, RH AF LYNFIELD, R HERRIN, JT RUBIN, RH TI VARICELLA IN PEDIATRIC RENAL-TRANSPLANT RECIPIENTS SO PEDIATRICS LA English DT Article DE VARICELLA; PEDIATRIC RENAL TRANSPLANT ID CYTOMEGALO-VIRUS INFECTION; EPSTEIN-BARR VIRUS; ZOSTER VIRUS; IMMUNOCOMPROMISED CHILDREN; IMMUNOSUPPRESSED CHILDREN; ALLOGRAFT RECIPIENTS; ACYCLOVIR THERAPY; IMPACT; VACCINE; CYCLOSPORIN AB As of November 1991, 8 of 83 children who had received renal transplants at Massachusetts General Hospital since January 1979 required admission for primary varicella. All 8 had cutaneous manifestations of disease, and 4 had evidence of visceral disease. Three of these 8 children received varicella zoster immune globulin (VZIG) after exposure to varicella; in the remaining children, exposure was not revealed until symptoms were present. All 8 children were treated with high-dose intravenous acyclovir. Two children died of complications of varicella infection, including 1 child who received VZIG on the day of exposure to varicella. Neither VZIG prophylaxis nor treatment with intravenous acyclovir offers complete protection against severe varicella infection to immunosuppressed children who have received organ transplants. A high priority should be given to the evaluation of alternative treatments, such as vaccination to the varicella virus, which could be administered to susceptible transplant candidates, preferably prior to transplantation. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RP LYNFIELD, R (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,INFECT DIS UNIT,149 13TH ST,BOSTON,MA 02129, USA. NR 35 TC 76 Z9 79 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 AUG PY 1992 VL 90 IS 2 BP 216 EP 220 PN 1 PG 5 WC Pediatrics SC Pediatrics GA JG577 UT WOS:A1992JG57700010 PM 1322522 ER PT J AU KOLLIAS, N BAQER, A SADIQ, I SAYRE, RM AF KOLLIAS, N BAQER, A SADIQ, I SAYRE, RM TI INVITRO AND INVIVO ULTRAVIOLET-INDUCED ALTERATIONS OF OXYHEMOGLOBIN AND DEOXYHEMOGLOBIN SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID FREE-RADICALS AB Ultraviolet (UV) radiation was found to convert oxyhemoglobin and deoxyhemoglobin stoichiometrically into methemoglobin and a met-like product, respectively. The peak conversion efficiency for oxyhemoglobin occurred at 285 nm and decreased by a factor of 100 by 315 nm. The peak conversion efficiency for deoxyhemoglobin occurred at 290 nm and decreased by a factor of 30 by 320 nm. The transformation of oxyhemoglobin to methemoglobin was also documented in intact erythrocytes using UV-B radiation. Finally, similar transformations were found to occur in human skin with UV-B exposure but not on all volunteers tested. These results imply that methemoglobin will be formed in vivo on solar exposure and provide evidence that UV-B photons reach the blood vessels. C1 MINIST PUBL HLTH KUWAIT,AL SABAH HOSP,DEPT DERMATOL,KUWAIT,KUWAIT. MEMPHIS STATE UNIV,DEPT PHYS,MEMPHIS,TN 38152. RP KOLLIAS, N (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 12 TC 21 Z9 21 U1 0 U2 1 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD AUG PY 1992 VL 56 IS 2 BP 223 EP 227 DI 10.1111/j.1751-1097.1992.tb02150.x PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JC905 UT WOS:A1992JC90500011 PM 1502266 ER PT J AU AFZALI, L KUWABARA, F ZACHAZEWSKI, J BROWNE, P ROBINSON, B AF AFZALI, L KUWABARA, F ZACHAZEWSKI, J BROWNE, P ROBINSON, B TI A NEW METHOD FOR THE DETERMINATION OF THE CHARACTERISTIC SHAPE OF AN ISOKINETIC QUADRICEPS FEMORIS MUSCLE TORQUE CURVE SO PHYSICAL THERAPY LA English DT Article DE MUSCLE PERFORMANCE; MEASUREMENT; TESTS AND MEASUREMENTS; FUNCTIONAL AB It has been suggested that visual analysis of isokinetic quadriceps femoris muscle torque curve (TC) shapes may have potential use in the diagnosis and prognosis of knee pathologies The primary purpose of this pilot study was to develop a method for analyzing the shape of an isokinetic TC. Our method normalizes and averages the TC, and then uses curvilinear analysis of the TC shape to aid in diagnosis and prognosis For demonstration, the method was applied to isokinetic quadriceps femoris muscle TC data collected using a LIDO(R) digital dynamometer from 25 healthy volunteer subjects and retrospectively acquired from the uninvolved limbs of 37 patients with unilateral knee pathologies. The preliminary results revealed (1) that a common quadriceps femoris muscle TC shape existed for the volunteer group at 60-degrees and 180-degrees/s; (2) that the uninvolved limbs of the patient group exhibited the same shape at 60-degrees/s, but not at 180-degrees/s; and (3) that the quadriceps femoris muscle TC shape demonstrated no significant differences with respect to limb dominance or gender for either group. Further testing of this quantitative method on a larger sample is needed to determine its usefulness in the analysis and implications of TC shape concerning pathology and diagnosis. C1 UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,TORRANCE,CA 90509. MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,POST PROFESS PHYS THERAPY PROGRAM,BOSTON,MA 02114. CHAPMAN UNIV,CHILDRENS HOSP LOS ANGELES,SCH PHYS THERAPY,LOS ANGELES,CA 90027. RP AFZALI, L (reprint author), UNIV CALIF LOS ANGELES,MED CTR,DEPT PHYS THERAPY,A2-226 CHS,10833 LECONTE AVE,LOS ANGELES,CA 90024, USA. NR 24 TC 10 Z9 11 U1 0 U2 2 PU AMER PHYS THER ASSN PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD AUG PY 1992 VL 72 IS 8 BP 585 EP 592 PG 8 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA JH066 UT WOS:A1992JH06600007 PM 1635943 ER PT J AU AFZALI, L KUWABARA, F ZACHAZEWSKI, J BROWNE, P ROBINSON, B AF AFZALI, L KUWABARA, F ZACHAZEWSKI, J BROWNE, P ROBINSON, B TI A NEW METHOD FOR THE DETERMINATION OF THE CHARACTERISTIC SHAPE OF AN ISOKINETIC QUADRICEPS FEMORIS MUSCLE TORQUE CURVE - RESPONSE SO PHYSICAL THERAPY LA English DT Letter C1 UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,TORRANCE,CA 90509. MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,POST PROFESS PHYS THERAPY PROGRAM,BOSTON,MA 02114. CHAPMAN UNIV,CHILDRENS HOSP LOS ANGELES,SCH PHYS THERAPY,LOS ANGELES,CA 90027. RP AFZALI, L (reprint author), UNIV CALIF LOS ANGELES,MED CTR,DEPT PHYS THERAPY,A2-226 CHS,10833 LEGONTE AVE,LOS ANGELES,CA 90024, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER PHYS THER ASSN PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD AUG PY 1992 VL 72 IS 8 BP 594 EP 595 PG 2 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA JH066 UT WOS:A1992JH06600009 ER PT J AU ONEIL, MB WOODARD, M SOSA, V HUNTER, L MULROW, CD GERETY, MB TULEY, M AF ONEIL, MB WOODARD, M SOSA, V HUNTER, L MULROW, CD GERETY, MB TULEY, M TI PHYSICAL THERAPY ASSESSMENT AND TREATMENT PROTOCOL FOR NURSING-HOME RESIDENTS SO PHYSICAL THERAPY LA English DT Article DE ELDERLY; NURSING HOMES; PHYSICAL THERAPY ID AGREEMENT; SCALE; INDEX AB This article describes a standard protocol for assessing physical function in elderly nursing home residents. Major physical dimensions that are measured with the protocol include range of motion, muscle force, muscle reflex activity, sensation, soft tissue status, balance/coordination, and posture. A practical, functionally prioritized treatment model based on the assessment is also presented The standardized assessment and treatment plan may be useful to the physical therapist in (1) planning and prioritizing treatment, (2) identifying when goals have been met, (3) recognizing when there is a need for treatment plan modification, and (4) educating physical therapy students in applying problem-solving skills in their treatment sessions. C1 AUDIE L MURPHY MEM VET ADM MED CTR,QUAL LIFE PROJECTS,AMBULATORY CARE 11C,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DIV GERIATR,SAN ANTONIO,TX 78284. FU NIA NIH HHS [UOIAG09117-01] NR 31 TC 12 Z9 12 U1 3 U2 4 PU AMER PHYS THER ASSN PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD AUG PY 1992 VL 72 IS 8 BP 596 EP 604 PG 9 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA JH066 UT WOS:A1992JH06600010 PM 1635944 ER PT J AU CHIODO, LK GERETY, MB MULROW, CD RHODES, MC TULEY, MR AF CHIODO, LK GERETY, MB MULROW, CD RHODES, MC TULEY, MR TI PHYSICAL THERAPY EVALUATION IS CRUCIAL - RESPONSE SO PHYSICAL THERAPY LA English DT Letter C1 AUDIE L MURPHY MEM VET ADM MED CTR,EDUC & CLIN CTR,SAN ANTONIO,TX 78284. RP CHIODO, LK (reprint author), UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER PHYS THER ASSN PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD AUG PY 1992 VL 72 IS 8 BP 610 EP 611 PG 2 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA JH066 UT WOS:A1992JH06600018 ER PT J AU ZALESKE, DJ AF ZALESKE, DJ TI FETAL FRACTURE-HEALING IN A LAMB MODEL - DISCUSSION SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Discussion ID EARLY REVASCULARIZATION; MEMBRANOUS BONE RP ZALESKE, DJ (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT ORTHOPAED UNIT,BOSTON,MA 02114, USA. NR 10 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD AUG PY 1992 VL 90 IS 2 BP 172 EP 173 PG 2 WC Surgery SC Surgery GA JG694 UT WOS:A1992JG69400002 ER PT J AU TATE, B ABOODYGUTERMAN, KS MORRIS, AM WALCOTT, EC MAJOCHA, RE MAROTTA, CA AF TATE, B ABOODYGUTERMAN, KS MORRIS, AM WALCOTT, EC MAJOCHA, RE MAROTTA, CA TI DISRUPTION OF CIRCADIAN REGULATION BY BRAIN GRAFTS THAT OVEREXPRESS ALZHEIMER-BETA/A4 AMYLOID SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ALZHEIMER DEMENTIA; CIRCADIAN RHYTHMS; GENETIC TRANSFECTION; SUPRACHIASMATIC NUCLEI ID GENETICALLY TRANSFORMED-CELLS; LOCOMOTOR-ACTIVITY RHYTHMS; BETA-PROTEIN; SUPRACHIASMATIC NUCLEUS; SENILE DEMENTIA; DISEASE; CORTEX; RAT; ANTIBODIES; NEURONS AB Alzheimer disease patients exhibit irregularities in the patterns of normally circadian (daily) rhythms. Alzheimer-type pathology has been reported in the hypothalamus and in the suprachiasmatic nuclei, the putative site of the circadian oscillator. We examined the relationship between the neuropathology of Alzheimer disease, as modeled by an animal system, and circadian dysregulation by grafting genetically transformed cells that overexpress beta/A4 amyloid into the suprachiasmatic nuclei of adult rats. Grafts of beta/A4-positive cells, but not of control cells, significantly altered the pattern of activity of implanted rats. Although experimental conditions included light-dark cycles that normally tend to drive rats to 24-h rhythms, animals with grafts of beta/A4-positive cells showed abnormally high levels of activity during the light phase in addition to a disrupted circadian pattern. Periodogram analysis demonstrated significant rhythms outside of a circadian range. The body temperature rhythm of these animals was also weak 6 weeks after grafting; however, unlike activity patterns, body temperature regained a circadian period by 8 weeks after cell implantation. These data indicate that disruption of circadian activity is a behavioral measure of the consequences of beta/A4 accumulation in brain implants. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MCLEAN HOSP,MAILMAN RES CTR,BELMONT,MA 02178. RP TATE, B (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,NEUROBIOL LAB,BULFINCH 4,BOSTON,MA 02114, USA. FU NIA NIH HHS [P01 AG 02126] NR 35 TC 42 Z9 43 U1 0 U2 1 PU NATL ACAD PRESS 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 AUG 1 PY 1992 VL 89 IS 15 BP 7090 EP 7094 DI 10.1073/pnas.89.15.7090 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JF856 UT WOS:A1992JF85600089 PM 1496005 ER PT J AU VOYTAS, DF CUMMINGS, MP KONIECZNY, A AUSUBEL, FM RODERMEL, SR AF VOYTAS, DF CUMMINGS, MP KONIECZNY, A AUSUBEL, FM RODERMEL, SR TI COPIA-LIKE RETROTRANSPOSONS ARE UBIQUITOUS AMONG PLANTS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TRANSPOSABLE ELEMENT; REVERSE TRANSCRIPTASE; MOLECULAR EVOLUTION ID COMPLETE NUCLEOTIDE-SEQUENCE; TRANSPOSABLE ELEMENT; ARABIDOPSIS-THALIANA; EVOLUTION; FAMILY; TRANSCRIPTION; GENOME; NUMBER AB Transposable genetic elements are assumed to be a feature of all eukaryotic genomes. Their identification, however, has largely been haphazard, limited principally to organisms subjected to molecular or genetic scrutiny. We assessed the phylogenetic distribution of copia-like retrotransposons, a class of transposable element that proliferates by reverse transcription, using a polymerase chain reaction assay designed to detect copia-like element reverse transcriptase sequences. copia-like retrotransposons were identified in 64 plant species as well as the photosynthetic protist Volvox carteri. The plant species included representatives from 9 of 10 plant divisions, including bryophytes, lycopods, ferns, gymnosperms, and angiosperms. DNA sequence analysis of 29 cloned PCR products and of a maize retrotransposon cDNA confirmed the identity of these sequences as copia-like reverse transcriptase sequences, thereby demonstrating that this class of retrotransposons is a ubiquitous component of plant genomes. C1 HARVARD UNIV,MUSEUM COOPERAT ZOOL,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP VOYTAS, DF (reprint author), IOWA STATE UNIV,DEPT BOT,AMES,IA 50010, USA. NR 33 TC 279 Z9 312 U1 1 U2 7 PU NATL ACAD PRESS 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 AUG 1 PY 1992 VL 89 IS 15 BP 7124 EP 7128 DI 10.1073/pnas.89.15.7124 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JF856 UT WOS:A1992JF85600096 PM 1379734 ER PT J AU HAHN, WC ROSENSTEIN, Y CALVO, V BURAKOFF, SJ BIERER, BE AF HAHN, WC ROSENSTEIN, Y CALVO, V BURAKOFF, SJ BIERER, BE TI A DISTINCT CYTOPLASMIC DOMAIN OF CD2 REGULATES LIGAND AVIDITY AND T-CELL RESPONSIVENESS TO ANTIGEN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-CELL ADHESION; ANTIGEN RESPONSIVENESS; CD58 ID ERYTHROCYTE RECEPTOR; ALTERNATIVE PATHWAY; SIGNAL TRANSDUCTION; ADHESION PATHWAYS; MOLECULAR-CLONING; LYMPHOCYTES-T; ACTIVATION; EXPRESSION; BINDING; LFA-1 AB The T-cell glycoprotein CD2 not only contributes to intercellular adhesion but also plays a direct role in T-cell activation. Here we demonstrate that the interaction of CD2 with its ligand lymphocyte function-associated antigen 3 (CD58) is regulated by T-cell receptor-CD3 signaling. T-cell receptor-CD3 crosslinking by specific antigen or monoclonal antibodies rapidly increases the avidity with which cell-surface CD2 binds immunoaffinity-purified CD58. Mutational analysis of the CD2 cytoplasmic domain demonstrates that the carboxyl-terminal asparagine is essential for T-cell receptor-induced changes in CD2 avidity but is not essential for CD2-mediated signaling, establishing that the cytoplasmic portion of CD2 consists of distinct functional domains. Furthermore, cell lines expressing CD2 molecules incapable of avidity regulation exhibit a marked deficiency in an antigen-specific response. Thus, the regulation of CD2 adhesiveness has a profound effect on the ability of CD2 to enhance antigen responsiveness. These observations demonstrate that adhesion strengthening resulting from increased CD2 avidity contributes directly to T-cell responsiveness independently of CD2-mediated signal transduction. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RI Calvo, Victor/L-5024-2014 OI Calvo, Victor/0000-0002-5913-7058 FU NIAID NIH HHS [AI28554, AI31868] NR 28 TC 53 Z9 53 U1 0 U2 0 PU NATL ACAD PRESS 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 AUG 1 PY 1992 VL 89 IS 15 BP 7179 EP 7183 DI 10.1073/pnas.89.15.7179 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JF856 UT WOS:A1992JF85600107 PM 1353888 ER PT J AU PETEET, JR ROSS, DM MEDEIROS, C WALSHBURKE, K RIEKER, P AF PETEET, JR ROSS, DM MEDEIROS, C WALSHBURKE, K RIEKER, P TI RELATIONSHIPS WITH PATIENTS IN ONCOLOGY - CAN A CLINICIAN BE A FRIEND SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article AB ENCOUNTERS with patients who are experiencing a life crisis such as cancer can be profoundly meaningful to both patients and those caring for them. Intense emotional involvement with patients can also lead to difficulties including "burnout" (Davitz and Davitz 1975), interstaff conflict (Burnham 1966; Pollack and Battle 1963; Robinson 1984; Weintraub 1964), and violation of professional boundaries (Applebaum 1990; Gartrell et al. 1986; Gutheil 1989a, 1989b). Nicholi (1988) has reviewed the challenges that psychotherapists face in maintaining relationships with patients that are both close and therapeutic. However, there has been little research into the relationships that clinicians in other medical disciplines have with their patients. This report describes both the stresses and rewards of relationships with oncology patients in a comprehensive sample of 192 staff members at a regional cancer center, interviewed about factors affecting their job satisfaction. C1 HARVARD UNIV,SCH MED,SCH DIVIN & EXTENS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC CONTROL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 16 TC 2 Z9 2 U1 0 U2 2 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD AUG PY 1992 VL 55 IS 3 BP 223 EP 229 PG 7 WC Psychiatry SC Psychiatry GA JH236 UT WOS:A1992JH23600002 PM 1509010 ER PT J AU TALAL, N AF TALAL, N TI SJOGRENS-SYNDROME - HISTORICAL OVERVIEW AND CLINICAL SPECTRUM OF DISEASE SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID LUPUS-ERYTHEMATOSUS C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. FU NIDCR NIH HHS [DEO9311-01] NR 14 TC 69 Z9 71 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-857X J9 RHEUM DIS CLIN N AM JI Rheum. Dis. Clin. North Am. PD AUG PY 1992 VL 18 IS 3 BP 507 EP 515 PG 9 WC Rheumatology SC Rheumatology GA LA278 UT WOS:A1992LA27800002 PM 1496158 ER PT J AU WANDS, JR LIANG, TJ BLUM, HE SHAFRITZ, DA AF WANDS, JR LIANG, TJ BLUM, HE SHAFRITZ, DA TI MOLECULAR PATHOGENESIS OF LIVER-DISEASE DURING PERSISTENT HEPATITIS-B VIRUS-INFECTION SO SEMINARS IN LIVER DISEASE LA English DT Review ID POLYMERASE CHAIN-REACTION; SURFACE-ANTIGEN; HEPATOCELLULAR-CARCINOMA; HBSAG-CARRIERS; MONOCLONAL-ANTIBODIES; ESCHERICHIA-COLI; PRECORE REGION; HBV INFECTION; VIRAL GENOME; PRE-C C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. YESHIVA UNIV ALBERT EINSTEIN COLL MED,MARION BESSIN LIVER RES CTR,BRONX,NY 10461. FU NCI NIH HHS [CA-35711, CA 32605]; NIAAA NIH HHS [AA-08169] NR 64 TC 17 Z9 22 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0272-8087 J9 SEMIN LIVER DIS JI Semin. Liver Dis. PD AUG PY 1992 VL 12 IS 3 BP 252 EP 264 DI 10.1055/s-2007-1007397 PG 13 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JU162 UT WOS:A1992JU16200004 PM 1439878 ER PT J AU WEICHSELBAUM, RR BECKETT, MA HALLAHAN, DE KUFE, DW VOKES, EE AF WEICHSELBAUM, RR BECKETT, MA HALLAHAN, DE KUFE, DW VOKES, EE TI MOLECULAR TARGETS TO OVERCOME RADIORESISTANCE SO SEMINARS IN ONCOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; FACTOR GENE-EXPRESSION; X-RAY-SENSITIVITY; PROTEIN-KINASE-C; IONIZING-RADIATION; IRRADIATION REPAIR; ENDOTHELIAL-CELLS; PHORBOL ESTER; GROWTH-FACTOR; RADIOTHERAPY C1 UNIV CHICAGO HOSP & CLIN,DEPT MED,HEMATOL ONCOL SECT,CHICAGO,IL 60637. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. RP WEICHSELBAUM, RR (reprint author), UNIV CHICAGO HOSP & CLIN,DEPT RADIAT & CELLULAR ONCOL,5841 S MARYLAND,MC 0085,CHICAGO,IL 60637, USA. FU PHS HHS [41068, 42596] NR 43 TC 12 Z9 12 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD AUG PY 1992 VL 19 IS 4 SU 11 BP 14 EP 20 PG 7 WC Oncology SC Oncology GA JK970 UT WOS:A1992JK97000004 PM 1509276 ER PT J AU GARNICK, MB AF GARNICK, MB TI INTRODUCTION - HEMATOPOIETIC GROWTH-FACTORS SO SEMINARS IN ONCOLOGY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP GARNICK, MB (reprint author), GENET INST,CLIN DEV,CAMBRIDGE,MA, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD AUG PY 1992 VL 19 IS 4 BP 347 EP 348 PG 2 WC Oncology SC Oncology GA JK493 UT WOS:A1992JK49300001 ER PT J AU DEMETRI, GD ANTMAN, KHS AF DEMETRI, GD ANTMAN, KHS TI GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR (GM-CSF) - PRECLINICAL AND CLINICAL INVESTIGATIONS SO SEMINARS IN ONCOLOGY LA English DT Review ID BONE-MARROW TRANSPLANTATION; ACUTE MYELOBLASTIC-LEUKEMIA; HUMAN RECOMBINANT GRANULOCYTE; HUMAN-IMMUNODEFICIENCY-VIRUS; HEMATOPOIETIC STEM-CELLS; HIGH-DOSE CYCLOPHOSPHAMIDE; TUMOR NECROSIS FACTOR; NON-HODGKINS-LYMPHOMA; NON-LYMPHOBLASTIC LEUKEMIA; MYELOID PROGENITOR CELLS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DEMETRI, GD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01CA-38493] NR 212 TC 41 Z9 42 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD AUG PY 1992 VL 19 IS 4 BP 362 EP 385 PG 24 WC Oncology SC Oncology GA JK493 UT WOS:A1992JK49300003 PM 1509275 ER PT J AU BERNSTEIN, SH KUFE, DW AF BERNSTEIN, SH KUFE, DW TI FUTURE OF BASIC CLINICAL HEMATOPOIESIS RESEARCH IN THE ERA OF HEMATOPOIETIC GROWTH-FACTOR AVAILABILITY SO SEMINARS IN ONCOLOGY LA English DT Article ID LEUKEMIA-INHIBITORY FACTOR; COLONY-STIMULATING FACTOR; STEM-CELL FACTOR; TYROSINE KINASE RECEPTOR; TUMOR NECROSIS FACTOR; C-KIT PROTOONCOGENE; PROGENITOR CELLS; MYELOID-LEUKEMIA; BONE-MARROW; W-LOCUS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115. ROSWELL PK CANC INST,DEPT HEMATOL ONCOL,BUFFALO,NY. ROSWELL PK CANC INST,BONE MARROW TRANSPLANT UNIT,BUFFALO,NY. NR 65 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 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD AUG PY 1992 VL 19 IS 4 BP 441 EP 448 PG 8 WC Oncology SC Oncology GA JK493 UT WOS:A1992JK49300010 PM 1380734 ER PT J AU YUCEL, EK GIFT, DA AF YUCEL, EK GIFT, DA TI MAGNETIC-RESONANCE ANGIOGRAPHY OF THE LOWER-EXTREMITY AND RENAL-ARTERIES SO SEMINARS IN ULTRASOUND CT AND MRI LA English DT Article RP YUCEL, EK (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 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 0887-2171 J9 SEMIN ULTRASOUND CT JI Semin. Ultrasound CT MRI PD AUG PY 1992 VL 13 IS 4 BP 291 EP 302 PG 12 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JG726 UT WOS:A1992JG72600006 PM 1503796 ER PT J AU EHARA, S KATTAPURAM, SV ROSENBERG, AE AF EHARA, S KATTAPURAM, SV ROSENBERG, AE TI FIBROUS DYSPLASIA OF THE SPINE SO SPINE LA English DT Note C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 0 TC 14 Z9 14 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-2436 J9 SPINE JI SPINE PD AUG PY 1992 VL 17 IS 8 BP 977 EP 979 DI 10.1097/00007632-199208000-00020 PG 3 WC Clinical Neurology; Orthopedics SC Neurosciences & Neurology; Orthopedics GA JK254 UT WOS:A1992JK25400020 PM 1523499 ER PT J AU KIM, K AF KIM, K TI STUDY DURATION FOR GROUP SEQUENTIAL CLINICAL-TRIALS WITH CENSORED SURVIVAL-DATA ADJUSTING FOR STRATIFICATION SO STATISTICS IN MEDICINE LA English DT Article ID LOGRANK TESTS; BOUNDARIES; DESIGN AB The study duration in a clinical trial with censored survival data is the sum of the accrual duration, which determines the sample size in a traditional sense, and the follow-up duration, which more or less controls the number of events to be observed. We propose a design procedure for determining the study duration or for calculating the power in a group sequential clinical trial with censored survival data and possibly unequal patient allocation between treatments, adjusting for stratified randomization. The group sequential method is based on the use function approach. We describe a clinical trial recently activated by the Eastern Cooperative Oncology Group for an illustration of the proposed procedure. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP KIM, K (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,44 BINNEY ST,MAYER 4,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-52733] NR 26 TC 6 Z9 6 U1 0 U2 3 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD AUG PY 1992 VL 11 IS 11 BP 1477 EP 1488 DI 10.1002/sim.4780111106 PG 12 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA JN614 UT WOS:A1992JN61400005 PM 1329172 ER PT J AU BRUNSWICK, DJ BENMANSOUR, S TEJANIBUTT, SM HAUPTMANN, M AF BRUNSWICK, DJ BENMANSOUR, S TEJANIBUTT, SM HAUPTMANN, M TI EFFECTS OF HIGH-DOSE METHAMPHETAMINE ON MONOAMINE UPTAKE SITES IN RAT-BRAIN MEASURED BY QUANTITATIVE AUTORADIOGRAPHY SO SYNAPSE LA English DT Article DE NEUROTOXICITY; SEROTONIN; DOPAMINE; NOREPINEPHRINE ID TYROSINE-HYDROXYLASE ACTIVITY; SEROTONERGIC NERVE-TERMINALS; NOREPINEPHRINE UPTAKE SITES; TRYPTOPHAN-HYDROXYLASE; -LABELED DESIPRAMINE; FILM AUTORADIOGRAPHY; H-3 CYANOIMIPRAMINE; METHYLAMPHETAMINE; DOPAMINE; BINDING AB The neurotoxicity of methamphetamine to monoaminergic neurons was examined. Neurotoxicity was assessed by quantitative autoradiography using radioligands specific for binding to norepinephrine, dopamine, and serotonin uptake sites. High-dose administration of methamphetamine led to decreases in binding to uptake sites for the three monoamines. Norepinephrine binding sites were decreased in certain amygdaloid nuclei and in the dorsomedial hypothalamic nucleus. Serotonin binding sites were reduced in widespread brain areas, while dopamine binding sites were reduced in the caudate putamen, olfactory tubercle, and nucleus accumbens. The decreases in binding site density for the three monoamines are limited to terminal field areas; cell body areas are not affected. Our results indicate that methamphetamine is neurotoxic to serotonin, dopamine, and norepinephrine neurons. The neurotoxicity to norepinephrine neurons is in selected brain areas. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. RP BRUNSWICK, DJ (reprint author), DEPT VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [DA05137]; NIMH NIH HHS [MH 45472] NR 39 TC 70 Z9 70 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-4476 J9 SYNAPSE JI Synapse PD AUG PY 1992 VL 11 IS 4 BP 287 EP 293 DI 10.1002/syn.890110404 PG 7 WC Neurosciences SC Neurosciences & Neurology GA JF141 UT WOS:A1992JF14100003 PM 1502685 ER PT J AU HASENKRUG, KJ STIMPFLING, JH WINN, HJ NATHENSON, SG AF HASENKRUG, KJ STIMPFLING, JH WINN, HJ NATHENSON, SG TI TRANSPLANTATION EFFECTS OF A UNIQUE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I MUTATION SO TRANSPLANTATION LA English DT Article ID TOXIC LYMPHOCYTES-T; MONOCLONAL-ANTIBODIES; MHC MOLECULES; CELL RECEPTOR; PEPTIDES; ANTIGEN; HLA-A2; IDENTIFICATION; MUTAGENESIS; SELECTION AB This study describes a novel MHC class I mouse mutant that was discovered because of loss of reactivity of its cells to monoclonal antibodies. The mutation occurred in the H-2K(s) molecule and is the first in vivo mutation described that has a single altered amino acid residue (amino acid 107) distant from the regions considered to be peptide or TCR contacts. Nevertheless, skin grafts from the mutant to the parent are rejected by CD8+ T-cells. In the reciprocal direction, the mutant shows partial tolerance to parental skin grafts, suggesting that the mutant is inefficient in selecting alloreactive T-cells specific for the wild-type K(s) molecule. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT CELL BIOL,BRONX,NY 10461. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MICROBIOL & IMMUNOL,BRONX,NY 10461. MCLAUGHLIN RES INST,GREAT FALLS,MT 59401. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. FU NCI NIH HHS [5T32CA09173, 2P30CA133330]; NIAID NIH HHS [5R37AI07289] NR 25 TC 2 Z9 2 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 AUG PY 1992 VL 54 IS 2 BP 368 EP 371 DI 10.1097/00007890-199208000-00031 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA JJ753 UT WOS:A1992JJ75300032 PM 1496547 ER PT J AU MOSKOWITZ, MA AF MOSKOWITZ, MA TI NEUROGENIC VERSUS VASCULAR MECHANISMS OF SUMATRIPTAN AND ERGOT ALKALOIDS IN MIGRAINE SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Editorial Material ID RAT DURA-MATER; PLASMA EXTRAVASATION; BLOOD-VESSELS; ELECTRICAL-STIMULATION; TRANSCRANIAL DOPPLER; TRIGEMINAL GANGLION; SPINAL-CORD; PROTEIN; BRAIN; CIRCULATION AB Sumatriptan and the ergot alkaloids are useful tools for deciphering drug mechanisms in migraine and related headaches. Both neuronal and vascular mechanisms have been proposed on the basis of actions of 5-HT at receptors resembling the 5-HT1D subtype. In this Viewpoint article, Michael A. Moskowitz argues that blockade of neural transmission and the neurogenic inflammatory response provides a mechanism by which sumatriptan and ergot alkaloids alleviate vascular headaches. He postulates, with similar arguments, that sumatriptan and ergot alkaloids may block headaches that develop from meningovascular inflammatory disorders such as from viral and bacterial meningitis and from the sequelae of head injury. C1 MASSACHUSETTS GEN HOSP,NEUROSURG & NEUROL SERV,STROKE RES LAB,BOSTON,MA 02114. RP MOSKOWITZ, MA (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 35 TC 364 Z9 374 U1 0 U2 17 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD AUG PY 1992 VL 13 IS 8 BP 307 EP 311 DI 10.1016/0165-6147(92)90097-P PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JG052 UT WOS:A1992JG05200004 PM 1329294 ER PT J AU HENEY, NM AF HENEY, NM TI NATURAL-HISTORY OF SUPERFICIAL BLADDER-CANCER - PROGNOSTIC FEATURES AND LONG-TERM DISEASE COURSE SO UROLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID TRANSITIONAL-CELL-CARCINOMA; LASER PHOTODYNAMIC THERAPY; BACILLUS CALMETTE-GUERIN; URINARY-BLADDER; PROGRESSION; TUMORS; RECURRENCE; INSITU; RESECTION; SURVIVAL C1 MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 30 TC 137 Z9 139 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0094-0143 J9 UROL CLIN N AM JI Urol. Clin. N. Am. PD AUG PY 1992 VL 19 IS 3 BP 429 EP 433 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA LA256 UT WOS:A1992LA25600003 PM 1636228 ER PT J AU GOTTLINGER, HG DORFMAN, T COHEN, EA HASELTINE, WA AF GOTTLINGER, HG DORFMAN, T COHEN, EA HASELTINE, WA TI THE ROLE OF THE TNV PROTEIN AND TNV RNA SPLICING SIGNALS IN REPLICATION OF HIV-1 IIIB-ISOLATES SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; OPEN READING FRAME; SITE-SPECIFIC MUTAGENESIS; TRANS-ACTIVATOR GENE; MESSENGER-RNA; FUNCTIONAL-ANALYSIS; MAMMALIAN INTRONS; FUSION PROTEIN; HTLV-III/LAV; TYPE-1 RP GOTTLINGER, HG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,HUMAN RETROVIROL LAB,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 44460]; NIAID NIH HHS [AI 28785, P30 AI 28691] NR 39 TC 21 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD AUG PY 1992 VL 189 IS 2 BP 618 EP 628 DI 10.1016/0042-6822(92)90585-D PG 11 WC Virology SC Virology GA JF684 UT WOS:A1992JF68400022 PM 1641982 ER PT J AU WEISSBACH, L TREADWELL, BV AF WEISSBACH, L TREADWELL, BV TI A PLASMINOGEN-RELATED GENE IS EXPRESSED IN CANCER-CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ACTIVATION; MATRIX; FIBRINOLYSIS; ANGIOGENESIS; INHIBITOR; KINETICS; LIVER; ACID RP WEISSBACH, L (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED RES LABS,BOSTON,MA 02114, USA. FU NIADDK NIH HHS [AM16265-17] NR 20 TC 29 Z9 30 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JUL 31 PY 1992 VL 186 IS 2 BP 1108 EP 1114 DI 10.1016/0006-291X(92)90861-E PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JF844 UT WOS:A1992JF84400073 PM 1379800 ER PT J AU YOKOTA, M PETERSON, JW KAOUTZANIS, M KOWALL, NW AF YOKOTA, M PETERSON, JW KAOUTZANIS, M KOWALL, NW TI IMMUNOHISTOCHEMICAL DISTRIBUTION OF PROTEIN-KINASE-C ISOZYMES IS DIFFERENTIALLY ALTERED IN ISCHEMIC GERBIL HIPPOCAMPUS SO BRAIN RESEARCH LA English DT Article DE PROTEIN KINASE-C; ISOZYME; GLOBAL ISCHEMIA; GERBIL; IMMUNOHISTOCHEMISTRY ID TRANSIENT CEREBRAL-ISCHEMIA; RAT-BRAIN; FOREBRAIN ISCHEMIA; DOWN-REGULATION; NEURONAL DEATH; AMINO-ACIDS; ADULT-RAT; GLUTAMATE; CALCIUM; ACCUMULATION AB We used monoclonal antibodies to examine the immunohistochemical distribution of the three major Ca2+-dependent protein kinase C (PKC) isozymes (I, II, and III) in ischemic gerbil hippocampus. Groups of four animals were sacrificed at 15 min, 4 h, 1 day, 2 days, 3 days, and 7 days after a 10-min episode of global forebrain ischemia. In control animals, PKC-I immunoreactivity was greater in CA1 neurons than in CA3-4. Terminal-like staining was not evident. PKC-II immunoreactivity was observed in all CA fields and in the outer molecular layer of the dentate gyrus. PKC-III staining was present in the CA fields, the inner molecular layer of the dentate gyrus and the subiculum. Dentate granule cells and mossy fibers were not stained with any of the PKC antibodies. Fifteen minutes and 4 h after ischemia, PCK-I, -II and -III immunoreactivity were all increased in CA1 neurons and PKC-III immunoreactivity alone was visualized in granule cells and mossy fibers. Staining patterns returned to baseline one day after ischemia. PKC-II and -III terminal-like staining were preserved in the stratum lacunosum-moleculare for 3 days and 2 days after ischemia respectively and then disappeared. The altered patterns of PKC staining in the hippocampus may reflect activation and/or down-regulation of PKC isozymes. Ca2+-dependent PKC isozymes may, therefore, potentially play a role in the pathogenesis of delayed ischemic neuronal death. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,EXPTL NEUROPATHOL LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,CEREBROVASC BIOPHYS LAB,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NHLBI NIH HHS [HL44554-01]; NIA NIH HHS [AG05134] NR 34 TC 17 Z9 17 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 JUL 31 PY 1992 VL 587 IS 1 BP 123 EP 129 DI 10.1016/0006-8993(92)91436-I PG 7 WC Neurosciences SC Neurosciences & Neurology GA JK140 UT WOS:A1992JK14000014 PM 1525642 ER PT J AU KYRIAKIS, JM APP, H ZHANG, XF BANERJEE, P BRAUTIGAN, DL RAPP, UR AVRUCH, J AF KYRIAKIS, JM APP, H ZHANG, XF BANERJEE, P BRAUTIGAN, DL RAPP, UR AVRUCH, J TI RAF-1 ACTIVATES MAP KINASE-KINASE SO NATURE LA English DT Article ID THREONINE PROTEIN-KINASE; EPIDERMAL GROWTH-FACTOR; T-CELL ACTIVATION; TYROSINE PHOSPHORYLATION; SIGNAL-TRANSDUCTION; INSULIN; PATHWAYS; CASCADE AB THE normal cellular homologue of the acutely transforming oncogene v-raf is c-raf-1, which encodes a serine/threonine protein kinase that is activated by many extracellular stimuli1. The physiological substrates of the protein c-Raf-1 are unknown. The mitogen-activated protein (MAP) kinases Erk1 and 2 are also activated by mitogens through phosphorylation of Erk tyrosine and threonine residues catalysed by a protein kinase of relative molecular mass 50,000, MAP kinase-kinase (MAPK-K)2-7. Here we report that MAPK-K as well as Erk1 and 2 are constitutively active in v-raf-transformed cells. MAPK-K partially purified from v-raf-transformed cells or from mitogen-treated cells3 can be deactivated by phosphatase 2A. c-Raf-1 purified after mitogen stimulation can reactivate the phosphatase 2A-inactivated MAPK-K over 30-fold in vitro. c-Raf-1 reactivation of MAPK-K coincides with the selective phosphorylation at serine/threonine residues of a polypeptide with M(r) 50,000 which coelutes precisely on cation-exchange chromatography with the MAPK-K activatable by c-Raf-1. These results indicate that c-Raf-1 is an immediate upstream activator of MAPK-K in vivo. To our knowledge, MAPK-K is the first physiological substrate of the c-raf-1 protooncogene product to be identified. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. BROWN UNIV,DIV BIOL & MED,PROVIDENCE,RI 02912. RP KYRIAKIS, JM (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,DIABET UNIT,149 13TH ST,BOSTON,MA 02129, USA. NR 26 TC 1122 Z9 1131 U1 2 U2 30 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JUL 30 PY 1992 VL 358 IS 6385 BP 417 EP 421 DI 10.1038/358417a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JF853 UT WOS:A1992JF85300057 PM 1322500 ER PT J AU HARRIS, JR LIPPMAN, ME VERONESI, U WILLETT, W AF HARRIS, JR LIPPMAN, ME VERONESI, U WILLETT, W TI MEDICAL PROGRESS .1. BREAST-CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID ORAL-CONTRACEPTIVE USE; PREMENOPAUSAL WOMEN; UNITED-STATES; DIETARY-FAT; SCREENING TRIAL; AMERICAN-WOMEN; RISK-FACTORS; PAST DECADE; BODY SIZE; AGE C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RADIAT ONCOL,BOSTON,MA 02115. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PHARMACOL,WASHINGTON,DC 20007. IST NAZL STUDIO & CURA TUMORI,I-20133 MILAN,ITALY. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,CHANNING LAB,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. RP HARRIS, JR (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT ONCOL,50 BINNEY ST,BOSTON,MA 02115, USA. NR 102 TC 551 Z9 559 U1 0 U2 11 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 JUL 30 PY 1992 VL 327 IS 5 BP 319 EP 328 DI 10.1056/NEJM199207303270505 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA JF655 UT WOS:A1992JF65500005 PM 1620171 ER PT J AU EAGLE, KA FALLON, JT DINSMORE, RE SCULLY, RE WU, VHT AF EAGLE, KA FALLON, JT DINSMORE, RE SCULLY, RE WU, VHT TI A 68-YEAR-OLD MAN WITH ACUTE MITRAL REGURGITATION - CORONARY-ARTERY DISEASE, WITH THROMBOSIS OF RIGHT CORONARY-ARTERY AND ACUTE MYOCARDIAL-INFARCTION - RUPTURE OF POSTEROMEDIAL PAPILLARY-MUSCLE, WITH MITRAL REGURGITATION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID VALVE-REPLACEMENT; ANGIOPLASTY; DYSFUNCTION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP EAGLE, KA (reprint author), MASSACHUSETTS GEN HOSP,CLIN CARDIOL,BOSTON,MA 02114, USA. NR 26 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 JUL 30 PY 1992 VL 327 IS 5 BP 338 EP 345 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA JF655 UT WOS:A1992JF65500007 ER PT J AU AURON, PE QUIGLEY, GJ ROSENWASSER, LJ GEHRKE, L AF AURON, PE QUIGLEY, GJ ROSENWASSER, LJ GEHRKE, L TI MULTIPLE AMINO-ACID SUBSTITUTIONS SUGGEST A STRUCTURAL BASIS FOR THE SEPARATION OF BIOLOGICAL-ACTIVITY AND RECEPTOR-BINDING IN A MUTANT INTERLEUKIN-1-BETA PROTEIN SO BIOCHEMISTRY LA English DT Article ID CRYSTAL-STRUCTURE; IL-1 RECEPTOR; NMR-SPECTROSCOPY; T-CELLS; ANTAGONIST; EXPRESSION; IDENTIFICATION; RESOLUTION; INHIBITOR; 1-ALPHA AB Receptor binding and biological activity properties of human interleukin-1-beta can be dissociated by mutating a single amino acid, arginine 127, to glycine (IL-1-beta(R-->G) [Gehrke et al. (1990) J. Biol. Chem. 265, 5922-5925]. The mechanism underlying the reduced biological activity has been examined by replacing arginine 127 with several other amino acids, followed by determination of biological activity using a T-helper cell proliferation assay. Mutant IL-1-beta proteins containing lysine, glutamic acid, tryptophan, or alanine in place of arginine 127 maintain biological activity. These data strongly suggest that IL-1-beta biological activity is not directly dependent upon the specific properties of charge, hydrophobicity/hydrophilicity, or side-chain group presented by the residue at position 127. Molecular modeling analyses indicate that the structural integrity of the antiparallel beta-strand 1/12 pair is disturbed in the glycine 127 mutant protein. Collapse of beta-strand 1 into a hydrated space between strands 1, 2, and 4 could structurally alter a cleft in IL-1-beta that contains a cluster of highly conserved amino acids, including a key aspartic acid residue [Ju et al. (1991) Proc. Natl. Acad. Sci. U.S.A. 88, 2658-2662]. Mutagenesis data and the differential activities of the IL-1-beta(R-->G) and IL-1 receptor antagonist proteins in stimulating early and late gene expression [Conca et al. (1991) J. Biol. Chem. 266, 16265-16268] suggest that multiple receptor-ligand contacts, exclusive of those required for receptor binding, are required for the stimulation of full IL-1 biological activity. C1 NATL JEWISH CTR IMMUNOL & RESP MED,DEPT MED,DENVER,CO 80206. CTR BLOOD RES,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,LE MARTIN LABS,BOSTON,MA 02129. CUNY HUNTER COLL,DEPT CHEM,NEW YORK,NY 10021. MIT,HARVARD MIT DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. RP AURON, PE (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI 27850]; NIGMS NIH HHS [GM 41359, GM 42504, R01 GM042504] NR 39 TC 25 Z9 25 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUL 28 PY 1992 VL 31 IS 29 BP 6632 EP 6638 DI 10.1021/bi00144a002 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JF654 UT WOS:A1992JF65400002 PM 1386253 ER PT J AU JANSSENS, SP SHIMOUCHI, A QUERTERMOUS, T BLOCH, DB BLOCH, KD AF JANSSENS, SP SHIMOUCHI, A QUERTERMOUS, T BLOCH, DB BLOCH, KD TI CLONING AND EXPRESSION OF A CDNA-ENCODING HUMAN ENDOTHELIUM-DERIVED RELAXING FACTOR NITRIC-OXIDE SYNTHASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID NEURONAL NADPH DIAPHORASE; VASCULAR ENDOTHELIUM; SMOOTH-MUSCLE; CELLS; RELEASE AB Nitric oxide, which accounts for the biological activity of endothelium-derived relaxing factor (EDRF), is synthesized in endothelial cells from L-arginine by nitric oxide synthase (NOS). We report here the cloning and functional expression of a cDNA encoding human endothelial NOS. Oligonucleotides corresponding to amino acid sequences shared by cytochrome P450 reductase and the recently identified brain NOS were synthesized to amplify a partial cDNA encoding a bovine endothelial cell NOS-related protein. This partial cDNA was used to isolate a cDNA encoding a human vascular endothelial NOS. The translated human protein is 1294 amino acids long and shares 52% of its amino acid sequence with brain NOS. Using RNA blot hybridization, abundant endothelial NOS mRNA was detected in unstimulated human umbilical vein endothelial cells. To determine the functional activity of the endothelial protein, we ligated the cDNA into an expression vector and transfected it into NIH3T3 cells. Cells expressing this cDNA contained abundant NADPH diaphorase activity, a histochemical marker for NOS. In co-culture assays, nitric oxide production by transfected cells increased guanylate cyclase activity in reporter rat fetal lung fibroblasts. In addition, NOS-catalyzed conversion of arginine to citrulline in transfected cells was significantly increased by A23187, a calcium ionophore. Isolation of a cDNA encoding a calcium-regulated, constitutively expressed human endothelial NOS, capable of producing EDRF in blood vessels, will accelerate the characterization of the role of this enzyme in normal and abnormal endothelial regulation of vascular tone. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. FU NHLBI NIH HHS [HL42397, HL45895]; NIAMS NIH HHS [AR01866] NR 28 TC 550 Z9 558 U1 0 U2 5 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 JUL 25 PY 1992 VL 267 IS 21 BP 14519 EP 14522 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JF088 UT WOS:A1992JF08800002 PM 1378832 ER PT J AU HELIN, K LEES, JA VIDAL, M DYSON, N HARLOW, E FATTAEY, A AF HELIN, K LEES, JA VIDAL, M DYSON, N HARLOW, E FATTAEY, A TI A CDNA-ENCODING A PRB-BINDING PROTEIN WITH PROPERTIES OF THE TRANSCRIPTION FACTOR E2F SO CELL LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; LARGE T-ANTIGEN; ADENOVIRUS E1A PROTEINS; REGION 1A PROTEINS; SV40 LARGE-T; CELL-CYCLE; DNA-BINDING; RB GENE; REGULATORY SEQUENCES; TRANS-ACTIVATION AB The retinoblastoma protein (PRB) plays an important role in the control of cell proliferation, apparently by binding to and regulating cellular transcription factors such as E2F. Here we describe the characterization of a cDNA clone that encodes a protein with properties of E2F. This clone, RBP3, was identified by the ability of its gene product to interact with pRB. RBP3 bound to pRB both in vitro and in vivo, and this binding was competed by viral proteins known to disrupt pRB-E2F association. RBP3 bound to E2F recognition sequences in a sequence-specific manner. Furthermore, transient expression of RBP3 caused a 10-fold transactivation of the adenovirus E2 promoter, and this transactivation was dependent on the E2F recognition sequences. These properties suggest that RBP3 encodes E2F, or an E2F-like protein. RP HELIN, K (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02129, USA. NR 79 TC 629 Z9 636 U1 1 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JUL 24 PY 1992 VL 70 IS 2 BP 337 EP 350 DI 10.1016/0092-8674(92)90107-N PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JE757 UT WOS:A1992JE75700016 PM 1638634 ER PT J AU KAELIN, WG KREK, W SELLERS, WR DECAPRIO, JA AJCHENBAUM, F FUCHS, CS CHITTENDEN, T LI, Y FARNHAM, PJ BLANAR, MA LIVINGSTON, DM FLEMINGTON, EK AF KAELIN, WG KREK, W SELLERS, WR DECAPRIO, JA AJCHENBAUM, F FUCHS, CS CHITTENDEN, T LI, Y FARNHAM, PJ BLANAR, MA LIVINGSTON, DM FLEMINGTON, EK TI EXPRESSION CLONING OF A CDNA-ENCODING A RETINOBLASTOMA-BINDING PROTEIN WITH E2F-LIKE PROPERTIES SO CELL LA English DT Article ID LARGE T-ANTIGEN; SUSCEPTIBILITY GENE-PRODUCT; E2F TRANSCRIPTION FACTOR; SV40 LARGE-T; DNA-BINDING; REGULATORY ELEMENT; IMMUNE INTERFERON; MESSENGER-RNA; RB GENE; CELLS AB An expression vector was modified to permit the rapid synthesis of purified, P-32-labeled, glutathione S-transferase (GST)-retinoblastoma (RB) fusion proteins. The products were used to screen lambda-gt11 expression libraries, from which we cloned a cDNA encoding a polypeptide (RBAP-1) capable of binding directly to a putative functional domain (the pocket) of the retinoblastoma gene product (RB). The RB "pocket" is known to bind, directly or indirectly, to the cellular transcription factor, E2F, implicated in cell growth control. We have found that RBAP-1 copurifies with E2F, interacts specifically with the adenovirus E4 ORF 6/7 protein, binds specifically and directly to a known E2F DNA recognition sequence, and contains a functional transactivation domain. Therefore, RBAP-1 is a species of E2F and can bind specifically to the RB pocket. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706. UNIV CALIF SAN FRANCISCO,SCH MED,HORMONE RES INST,SAN FRANCISCO,CA 94143. RP KAELIN, WG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 73 TC 819 Z9 825 U1 1 U2 15 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JUL 24 PY 1992 VL 70 IS 2 BP 351 EP 364 DI 10.1016/0092-8674(92)90108-O PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JE757 UT WOS:A1992JE75700017 PM 1638635 ER PT J AU BEAL, MF SWARTZ, KJ ISACSON, O AF BEAL, MF SWARTZ, KJ ISACSON, O TI DEVELOPMENTAL-CHANGES IN BRAIN KYNURENIC ACID CONCENTRATIONS SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Note DE EXCITATORY AMINO ACID; KYNURENIC ACID; KYNURENINE; N-METHYL-D-ASPARTATE ID CENTRAL-NERVOUS-SYSTEM; D-ASPARTATE RECEPTOR; GLYCINE MODULATORY SITE; QUINOLINIC ACID; RAT HIPPOCAMPUS; MAMMALIAN BRAIN; NMDA RECEPTORS; AMINO-ACIDS; IDENTIFICATION; ANTAGONISTS AB The cerebral distribution and regulation of excitatory amino acid levels may play a crucial role in neuronal development. In the present study we examined concentrations of the endogenous excitatory amino acid antagonist kynurenic acid and related substances during development in fetal and neonatal rat brain and fetal non-human primate cerebral cortex. Kynurenic acid concentrations in rat fetal whole brain were significantly increased 4-5 fold prenatally, then declined rapidly at 1 day after birth, and reached adult concentrations at 7 days after birth. L-Kynurenine concentrations were also markedly increased prior to birth and then declined to adult concentrations at 1 day after birth. L-Tryptophan was increased 3 fold before birth, and decreased to adult concentrations 1 day after birth. In contrast concentrations of dopamine, norepinephrine, 3,4-dihydroxyphenylacetic acid and homovanillic acid increased 1 day prior to birth and continued to increase following birth. Fetal baboon cerebral cortex showed significant increases in kynurenic acid concentrations both pre-term and near-term as compared with adult concentrations. These results show that marked changes in kynurenic acid concentrations occur prior to and following birth. It is possible that high levels of kynurenic acid prior to birth inhibit neurite branching and development of excitatory synapses, which then develop rapidly in parallel with the decrease in kynurenic acid levels. C1 HARVARD UNIV,SCH MED,NEUROREGENERAT LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MCLEAN HOSP,MRC,BELMONT,MA 02178. RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,NEUROL RES 4,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS10828, NS16367, NS29178] NR 30 TC 36 Z9 36 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD JUL 24 PY 1992 VL 68 IS 1 BP 136 EP 139 PG 4 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA JK050 UT WOS:A1992JK05000016 PM 1521320 ER PT J AU TEPPER, RI COFFMAN, RL LEDER, P AF TEPPER, RI COFFMAN, RL LEDER, P TI AN EOSINOPHIL-DEPENDENT MECHANISM FOR THE ANTITUMOR EFFECT OF INTERLEUKIN-4 SO SCIENCE LA English DT Article ID LYMPHOCYTES AB Murine interleukin-4 (IL-4) exhibits potent antitumor activity when present at the site of tumor cell challenge. Associated with tumor cell death is the appearance of an inflammatory infiltrate comprised predominantly of eosinophils and macrophages, but with few lymphocytes. Antibodies that specifically block the accumulation of granulocytes at the site of inflammation were injected in vivo to define the cell type responsible for the antitumor action of IL-4. These studies implicate eosinophils in IL-4-mediated tumor cytotoxicity. The lymphoid-independent nature of IL-4 action is supported by the analysis of mutant mouse strains with defined lymphocyte immunodeficiencies. The observed regression of established tumor masses by localized IL-4 action provides a rationale for exploring IL-4-mediated tumor killing as a potential therapy for human malignant disorders. C1 DNAX RES INST MOLEC & CELLULAR BIOL INC,PALO ALTO,CA 94304. HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP TEPPER, RI (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114, USA. NR 8 TC 450 Z9 454 U1 1 U2 5 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD JUL 24 PY 1992 VL 257 IS 5069 BP 548 EP 551 DI 10.1126/science.1636093 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JE755 UT WOS:A1992JE75500035 PM 1636093 ER PT J AU SIBER, GR AF SIBER, GR TI IMMUNE GLOBULIN TO PREVENT NOSOCOMIAL INFECTIONS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP SIBER, GR (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 10 TC 19 Z9 19 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 JUL 23 PY 1992 VL 327 IS 4 BP 269 EP 271 DI 10.1056/NEJM199207233270409 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JE381 UT WOS:A1992JE38100009 PM 1614468 ER PT J AU AXELROD, L AF AXELROD, L TI GLUCOCORTICOID THERAPY AND PITUITARY-ADRENAL RESPONSES TO CORTICOTROPIN-RELEASING HORMONE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP AXELROD, L (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUL 23 PY 1992 VL 327 IS 4 BP 282 EP 283 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JE381 UT WOS:A1992JE38100023 PM 1614480 ER PT J AU NEER, RM AF NEER, RM TI CALCITRIOL OR CALCIUM FOR POSTMENOPAUSAL OSTEOPOROSIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP NEER, RM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUL 23 PY 1992 VL 327 IS 4 BP 284 EP 284 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JE381 UT WOS:A1992JE38100026 PM 1614483 ER PT J AU WANG, TC BONNERWEIR, S OATES, PS CHULAK, M MERLINO, G SCHMIDT, EV BRAND, SJ AF WANG, TC BONNERWEIR, S OATES, PS CHULAK, M MERLINO, G SCHMIDT, EV BRAND, SJ TI GASTRIN PROMOTES ISLET CELL-GROWTH THROUGH INTERACTIONS WITH TRANSFORMING GROWTH FACTOR-ALPHA SO REGULATORY PEPTIDES LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. JOSLIN DIABET CTR,BOSTON,MA. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD JUL 23 PY 1992 VL 40 IS 2 BP 275 EP 275 PG 1 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA JG987 UT WOS:A1992JG98700344 ER PT J AU WANG, TC OATES, PS BABYATSKY, M CHULAK, M SCHMIDT, EV BRAND, SJ AF WANG, TC OATES, PS BABYATSKY, M CHULAK, M SCHMIDT, EV BRAND, SJ TI TISSUE SPECIFIC REGULATION OF HUMAN AND RAT GASTRIN PROMOTERS IN TRANSGENIC MICE SO REGULATORY PEPTIDES LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD JUL 23 PY 1992 VL 40 IS 2 BP 275 EP 275 PG 1 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA JG987 UT WOS:A1992JG98700345 ER PT J AU SCHMALBACH, TK DATTA, R KUFE, DW SHERMAN, ML AF SCHMALBACH, TK DATTA, R KUFE, DW SHERMAN, ML TI TRANSCRIPTIONAL REGULATION OF CYTOKINE EXPRESSION BY DIETHYLDITHIOCARBAMATE IN HUMAN HL-60 PROMYELOCYTIC LEUKEMIA-CELLS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; COLONY-STIMULATING FACTOR; HUMAN-IMMUNODEFICIENCY-VIRUS; FACTOR GENE-EXPRESSION; BONE-MARROW TOXICITY; NF-KAPPA-B; MOLECULAR-CLONING; COMPLEMENTARY-DNA; POSTTRANSCRIPTIONAL REGULATION; MESSENGER-RNA AB Diethyldithiocarbamate (DDTC) is an investigational agent used to ameliorate chemotherapy- or radiotherapy-induced myelosuppression. We studied the effects of DDTC on the regulation of hematopoietic cytokine production in human myeloid cells. The results demonstrated that DDTC decreases proliferation of human HL-60 promyelocytic leukemia cells in a concentration-dependent manner. DDTC treatment also increased interleukin-alpha (IL-1-alpha), IL-1-beta, and tumor necrosis factor (TNF) expression in these cells. Similar findings were obtained in normal human peripheral blood monocytes. Peak induction of these cytokines occurred 6-12 hr after exposure to DDTC; levels returned to those in control cells by 24-48 hr in HL-60 cells. This effect was specific for IL-1 and TNF in that there was no detectable increase in IL-3, macrophage colony-stimulating factor or granulocyte/macrophage colony-stimulating factor RNA expression. Transcriptional run-on analysis demonstrated that exposure to DDTC increased the rate of TNF gene transcription in HL-60 cells. These data suggest that the myeloprotective effects of DDTC may be mediated, at least in part, by the induction of TNF, IL-1-alpha, and IL-1-beta. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [K08CA01092] NR 39 TC 11 Z9 11 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 JUL 22 PY 1992 VL 44 IS 2 BP 365 EP 371 DI 10.1016/0006-2952(92)90021-A PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JG230 UT WOS:A1992JG23000021 PM 1322666 ER PT J AU FREDETTE, BJ ADAMS, JC MUGNAINI, E AF FREDETTE, BJ ADAMS, JC MUGNAINI, E TI GABAERGIC NEURONS IN THE MAMMALIAN INFERIOR OLIVE AND VENTRAL MEDULLA DETECTED BY GLUTAMATE-DECARBOXYLASE IMMUNOCYTOCHEMISTRY SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE GAD, INHIBITION; LOCAL CIRCUIT NEURONS; HUMAN INFERIOR OLIVE ID GABA-CONTAINING NEURONS; ACID-DECARBOXYLASE; RAT-BRAIN; CAT; NUCLEUS; COMPLEX; LOCALIZATION; LIGHT; IMMUNOREACTIVITY; SYNAPTOLOGY AB Neurons containing glutamic acid decarboxylase (GAD) (presumed GABAergic neurons) were mapped by immunocytochemistry in the ventral medulla of rat, rabbit, cat, rhesus monkey, and human, with emphasis on the inferior olive. In all species, three categories of GABAergic neurons were identified: periolivary neurons in the gray matter and the white matter surrounding the inferior olive, internuclear neurons located in the white matter between the subnuclei of the inferior olive, and intranuclear neurons located within the olivary gray matter. The intranuclear GABAergic neurons of the inferior olive had a characteristic morphology which differed from non-GABAergic olivary neurons; they were usually smaller, and, wherever their processes were stained, they had radiating, sparsely branching dendrites. They were also usually distinguished from the other GABAergic neurons by their smaller size. The intraolivary GABAergic neurons constituted only a minor proportion of the total olivary neuronal population, but they were concentrated in regions of the olive that varied by species. In the rat, they were situated in the rostral tip of the medial accessory olive and in the caudal subdivision of the dorsal accessory olive, while in the rabbit, they were located in the caudal two-thirds of the medial accessory olive, in the dorsal cap, and in the ventral lateral outgrowth. Such neurons were extremely rare in the cat; only a few were found in the rostral parts of the principal olive, the medial accessory olive, and the dorsal accessory olive. In the rhesus monkey, the principal olive and the lateral region of the rostral medial accessory olive contained most of the intranuclear GABAergic neurons, but some were also present in the dorsal accessory olive. In the human, such neurons occurred in the principal olive, the dorsal accessory olive and the rostral medial accessory olive, but as in the rhesus monkey, most were observed in the principal olive. C1 UNIV CONNECTICUT,NEUROMORPHOL LAB,BOX U-154,STORRS,CT 06269. MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,BOSTON,MA 02114. FU NINDS NIH HHS [NS09904, NS21307] NR 58 TC 22 Z9 22 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JUL 22 PY 1992 VL 321 IS 4 BP 501 EP 514 DI 10.1002/cne.903210402 PG 14 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA JG114 UT WOS:A1992JG11400001 PM 1506483 ER PT J AU BROWN, MC BENSON, TE AF BROWN, MC BENSON, TE TI TRANSNEURONAL LABELING OF COCHLEAR NUCLEUS NEURONS BY HRP-LABELED AUDITORY-NERVE FIBERS AND OLIVOCOCHLEAR BRANCHES IN MICE SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE ENDBULB OF HELD; TRANSSYNAPTIC LABELING; BUSHY CELL ID WHEAT-GERM-AGGLUTININ; SPHERICAL BUSHY CELLS; HORSERADISH-PEROXIDASE; BRAIN-STEM; INTRACELLULAR INJECTION; INTERNEURONAL TRANSFER; ELECTRON-MICROSCOPY; CENTRAL PROJECTIONS; TETANUS TOXIN; VISUAL-SYSTEM AB Auditory nerve fibers were labeled by extracellular injections of horseradish into the spiral ganglion in mice. The labeled fibers were traced in an anterograde direction through the auditory nerve into the cochlear nucleus. In almost half of the injections, the labeled endings of auditory nerve fibers contacted cochlear nucleus neurons that were also labeled with horseradish peroxidase and were presumably transneuronally labeled. Only darkly labeled endings were associated with transneuronally labeled neurons, but not all darkly labeled endings had targets that were transneuronally labeled. Transneuronal labeling occurred almost exclusively in the ventral cochlear nucleus, often between endbulbs and bushy cells. Both "modified" endbulbs and the larger endbulbs of Held transneuronally labeled the bushy cells that they contacted. At the ultrastructural level, transneuronal labeling was evident as a darkening of ribosomes and the membrane surfaces of mitochondria, endoplasmic reticulum, and the nucleus. Transneuronal labeling occurred rarely in octopus, small, and stellate cells, and in neurons of the dorsal cochlear nucleus. Spiral ganglion injections also label olivocochlear fibers, efferent fibers that pass through the ganglion en route to the hair cells. These fibers give off branches to the cochlear nucleus that were rarely associated with transneuronal labeling. In eight instances, the targets of olivocochlear branches were stellate cells or small cells. We suggest that in our mouse preparation, horseradish peroxidase is effective as a transneuronal marker because the short distance from injection site to the cochlear nucleus results in a high concentration of horseradish peroxidase in the endings of the auditory nerve fibers. C1 HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT LARYNGOL,BOSTON,MA 02114. BOSTON UNIV,DEPT BIOMED ENGN,BOSTON,MA 02215. RP BROWN, MC (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC00119, DC00310, DC01089] NR 58 TC 27 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 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JUL 22 PY 1992 VL 321 IS 4 BP 645 EP 665 DI 10.1002/cne.903210411 PG 21 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA JG114 UT WOS:A1992JG11400010 PM 1380524 ER PT J AU RICHTER, JM GRAEMECOOK, F FERRUCCI, JT SCULLY, RE BAKER, GP KELSEY, PB AF RICHTER, JM GRAEMECOOK, F FERRUCCI, JT SCULLY, RE BAKER, GP KELSEY, PB TI A 76-YEAR-OLD WOMAN WITH RECURRENT DIARRHEA SEVERAL MONTHS AFTER TREATMENT FOR TROPICAL-SPRUE - CROHNS-DISEASE OF ILEUM - EXACERBATED BY INFECTIOUS GASTROENTERITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID INFLAMMATORY BOWEL-DISEASE; CELIAC-DISEASE; INTESTINAL TUBERCULOSIS; PYODERMA GANGRENOSUM; RECTAL BIOPSY; LYMPHOMA; ENTERITIS; FEATURES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RICHTER, JM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 49 TC 1 Z9 1 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUL 16 PY 1992 VL 327 IS 3 BP 182 EP 191 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA JD319 UT WOS:A1992JD31900009 ER PT J AU CHESEBRO, JH FUSTER, V AF CHESEBRO, JH FUSTER, V TI THROMBOSIS IN UNSTABLE ANGINA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID HEPARIN; HIRUDIN C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP CHESEBRO, JH (reprint author), MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 16 TC 60 Z9 62 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUL 16 PY 1992 VL 327 IS 3 BP 192 EP 194 DI 10.1056/NEJM199207163270310 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JD319 UT WOS:A1992JD31900010 PM 1608410 ER PT J AU JANG, IK GOLD, HK AF JANG, IK GOLD, HK TI ANGIOSCOPIC EVALUATION OF CORONARY-ARTERY THROMBI IN ACUTE CORONARY SYNDROMES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP JANG, IK (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUL 16 PY 1992 VL 327 IS 3 BP 206 EP 207 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JD319 UT WOS:A1992JD31900031 PM 1608426 ER PT J AU WEISS, HS SHINGLETON, BJ GOODE, SM BELLOWS, AR RICHTER, CU AF WEISS, HS SHINGLETON, BJ GOODE, SM BELLOWS, AR RICHTER, CU TI ARGON-LASER GONIOPLASTY IN THE TREATMENT OF ANGLE-CLOSURE GLAUCOMA SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID TRABECULOPLASTY AB We used argon laser gonioplasty to treat angle-closure glaucoma unrelieved by patent iridectomy. Laser energy (mean; 30 spots, 723 mW, and 0.2 second) was applied to the peripheral iris stroma to open the anterior chamber angle. Twenty of 32 eyes were successfully treated. After a median follow-up period of 18 months, 17 of these 20 successfully treated eyes (85%) had an intraocular pressure less than or equal to 19 mm Hg, and 19 of these 20 successfully treated eyes (95%) had an intraocular pressure less than or equal to 21 mm Hg. The 20 successfully treated eyes had a median duration of angle closure of 12 days. Twelve unsuccessfully treated eyes had a median duration of angle closure of 90 days. All successfully treated eyes had more than 50% of-the treated angle opened by argon laser gonioplasty and all but three successfully treated eyes had more than three clock hours opened by argon laser gonioplasty. Argon laser gonioplasty may be successful in treating angle-closure glaucoma unrelieved by iridectomy, especially in cases that are recognized and treated soon after onset. C1 OPHTHALM CONSULTANTS BOSTON INC,BOSTON,MA. CTR EYE RES,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA CONSULTAT SERV,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. UNIV TEXAS SW,DEPT OPHTHALMOL,GLAUCOMA SERV,DALLAS,TX. NR 17 TC 12 Z9 13 U1 1 U2 1 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JUL 15 PY 1992 VL 114 IS 1 BP 14 EP 18 PG 5 WC Ophthalmology SC Ophthalmology GA JC195 UT WOS:A1992JC19500003 PM 1621781 ER PT J AU HEMADY, R DELAMAZA, MS RAIZMAN, MB FOSTER, CS AF HEMADY, R DELAMAZA, MS RAIZMAN, MB FOSTER, CS TI 6 CASES OF SCLERITIS ASSOCIATED WITH SYSTEMIC INFECTION SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID NECROTIZING SCLERITIS; COMPLICATIONS; EPISCLERITIS AB Isolated scleritis (without keratitis) associated with infections is uncommon, and correct diagnosis and appropriate therapy for it are often delayed. Six patients with infection-associated scleritis were seen at our institution between May 1983 and May 1990 (these patients represented 4.6% of all patients with scleritis [six of 130 patients] in that period). Three of these cases were associated with systemic infections. One was associated with syphilis, one was associated with tuberculosis, and one was associated with toxocariasis. Three cases resulted from local infections. One was associated with infection with Proteus mirabilis, one was associated with infection with herpes zoster virus, and one was associated with infection with Aspergillus. The Aspergillus infection developed after trauma and the P. mirabilis-induced infection developed after strabismus surgical procedures. Four of the six cases were initially misdiagnosed and inappropriately managed. Correct diagnosis was made seven days to four years after onset of symptoms. Review of systems, scleral biopsy, culture, and laboratory investigation were used to make the diagnosis. Differential diagnosis of scleritis must include infective agents. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,BOSTON,MA 02114. NR 31 TC 25 Z9 25 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JUL 15 PY 1992 VL 114 IS 1 BP 55 EP 62 PG 8 WC Ophthalmology SC Ophthalmology GA JC195 UT WOS:A1992JC19500010 PM 1621786 ER PT J AU LANE, TA ANDERSON, KC GOODNOUGH, LT KURTZ, S MOROFF, G PISCIOTTO, PT SAYERS, M SILBERSTEIN, LE AF LANE, TA ANDERSON, KC GOODNOUGH, LT KURTZ, S MOROFF, G PISCIOTTO, PT SAYERS, M SILBERSTEIN, LE TI LEUKOCYTE REDUCTION IN BLOOD COMPONENT THERAPY SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE LEUKOCYTES; BLOOD COMPONENT TRANSFUSION; HLA ANTIGENS; ALLOIMMUNIZATION ID CYTOMEGALO-VIRUS INFECTION; VERSUS-HOST DISEASE; DONOR PLATELET TRANSFUSIONS; POOR BLOOD; RED-CELLS; LYMPHOCYTOTOXIC ANTIBODY; MULTITRANSFUSED PATIENTS; ULTRAVIOLET-IRRADIATION; DEPLETED BLOOD; HLA ANTIGENS AB Purpose: To review methods of preventing or minimizing the adverse effects associated with the transfusion of passenger leukocytes present in cellular blood components and to define groups of patients who are at risk for adverse effects. Data Sources: English-language articles on transfusion medicine. Study Selection: Original reports describing the pathogenesis of leukocyte-induced adverse effects in transfusion recipients and the influence of leukocyte-reduced blood components on these effects. Data Extraction: Evaluation of the diagnosis, transfusion history, and treatment of the study patients; the methods and results of leukocyte reduction; and specific outcomes, including development of alloimmunization to leukocytes, febrile reactions to transfusion, and platelet refractoriness. Data Synthesis: Passenger leukocytes are the chief cause of alloimmunization to human leukocyte antigen (HLA) and leukocyte-specific antigens in transfusion recipients. Alloimmunization may result in febrile transfusion reactions, platelet refractoriness, and acute lung injury. Leukocytes are also the vector for transfusion-associated cytomegalovirus infection. Technologic advances in the leukocyte reduction of cellular blood components have made it possible to reduce the number of leukocytes to fewer than 10(7) per transfusion. Findings suggest that the use of leukocyte-reduced cellular blood components may minimize or prevent recurrent febrile reactions and alloimmunization to leukocyte antigens. Cytomegalovirus may not be transmitted by blood components containing fewer than 10(7) leukocytes. Conclusions: Leukocyte reduction in red blood cell and platelet transfusions using third-generation filters is indicated for selected patients who are likely to receive long-term transfusion support, to prevent recurrent febrile reactions and to prevent or delay alloimmunization to leukocyte antigens. Leukocyte-depleted transfusions may also be indicated to delay or prevent refractoriness to platelet transfusion. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV HOSP CLEVELAND,DEPT MED,CLEVELAND,OH 44106. LAHEY CLIN FDN,BURLINGTON,MA 01805. AMER RED CROSS,JEROME HOLLAND LAB,ROCKVILLE,MD 20855. UNIV CONNECTICUT,CTR HLTH,DEPT LAB MED,FARMINGTON,CT 06030. PUGET SOUND BLOOD CTR & PROGRAM,SEATTLE,WA 98104. HOSP UNIV PENN,BLOOD BANK,PHILADELPHIA,PA 19104. RP LANE, TA (reprint author), UNIV CALIF SAN DIEGO,SCH MED,DEPT PATHOL 0612,9500 GILMAN DR,LA JOLLA,CA 92093, USA. NR 95 TC 94 Z9 95 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JUL 15 PY 1992 VL 117 IS 2 BP 151 EP 162 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA JD123 UT WOS:A1992JD12300010 PM 1605430 ER PT J AU PAK, PH RYAN, ET DESANCTIS, RW AF PAK, PH RYAN, ET DESANCTIS, RW TI GALLBLADDER-DISEASE AND ANGINA-PECTORIS - RESPONSE SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP PAK, PH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JUL 15 PY 1992 VL 117 IS 2 BP 172 EP 172 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JD123 UT WOS:A1992JD12300026 ER PT J AU LUSKEY, BD ROSENBLATT, M ZSEBO, K WILLIAMS, DA AF LUSKEY, BD ROSENBLATT, M ZSEBO, K WILLIAMS, DA TI STEM-CELL FACTOR, INTERLEUKIN-3, AND INTERLEUKIN-6 PROMOTE RETROVIRAL-MEDIATED GENE-TRANSFER INTO MURINE HEMATOPOIETIC STEM-CELLS SO BLOOD LA English DT Article ID HUMAN ADENOSINE-DEAMINASE; GROWTH-FACTOR; EXPRESSION; MICE; CULTURE; SYSTEM; LIGAND; MOUSE; SAFE; LINE C1 INDIANA UNIV,SCH MED,HERMAN B WELLS CTR PEDIAT RES,HOWARD HUGHES MED INST,INDIANAPOLIS,IN 46202. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. AMGEN INC,THOUSAND OAKS,CA. FU NHLBI NIH HHS [I PO1 HL45168-01A1] NR 38 TC 132 Z9 133 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JUL 15 PY 1992 VL 80 IS 2 BP 396 EP 402 PG 7 WC Hematology SC Hematology GA JD588 UT WOS:A1992JD58800013 PM 1378319 ER PT J AU WEREMOWICZ, S KUPSKY, WJ MORTON, CC FLETCHER, JA AF WEREMOWICZ, S KUPSKY, WJ MORTON, CC FLETCHER, JA TI CYTOGENETIC EVIDENCE FOR A CHROMOSOME-22 TUMOR SUPPRESSOR GENE IN EPENDYMOMA SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID ABNORMALITIES; MENINGIOMA; GLIOMAS; BRAIN AB Although ependymomas comprise 5-10% of pediatric brain tumors, consistent cytogenetic aberrations have not been identified in these neoplasms. We report karyotypes for two ependymomas. A predominantly well-differentiated ependymoma contained several numerical chromosome aberrations, including monosomy 22. In contrast, an anaplastic ependymoma had a more complex karyotype that included loss of one chromosome 22 homologue and a balanced translocation at q13.3 in the remaining 22 homologue. These findings suggest the location of an ependymoma tumor suppressor gene on the long arm of chromosome 22. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [1-K11-CA-01498-02] NR 17 TC 56 Z9 56 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD JUL 15 PY 1992 VL 61 IS 2 BP 193 EP 196 DI 10.1016/0165-4608(92)90085-M PG 4 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA JG990 UT WOS:A1992JG99000015 PM 1638502 ER PT J AU MARCILLAC, I TROALEN, F BIDART, JM GHILLANI, P RIBRAG, V ESCUDIER, B MALASSAGNE, B DROZ, JP LHOMME, C ROUGIER, P DUVILLARD, P PRADE, M LUGAGNE, PM RICHARD, F POYNARD, T BOHUON, C WANDS, J BELLET, D AF MARCILLAC, I TROALEN, F BIDART, JM GHILLANI, P RIBRAG, V ESCUDIER, B MALASSAGNE, B DROZ, JP LHOMME, C ROUGIER, P DUVILLARD, P PRADE, M LUGAGNE, PM RICHARD, F POYNARD, T BOHUON, C WANDS, J BELLET, D TI FREE HUMAN CHORIONIC-GONADOTROPIN BETA-SUBUNIT IN GONADAL AND NONGONADAL NEOPLASMS SO CANCER RESEARCH LA English DT Article ID ECTOPIC PRODUCTION; GLYCOPROTEIN HORMONES; CARCINOEMBRYONIC ANTIGEN; TROPHOBLASTIC DISEASE; MONOCLONAL-ANTIBODIES; LUTEINIZING-HORMONE; PLACENTAL-LACTOGEN; URINARY-BLADDER; HUMAN PITUITARY; TUMOR-MARKERS AB The diagnostic value of elevated human chorionic gonadotropin (hCG) and its free-alpha (hCG-alpha) and beta (hCG-beta) subunit serum levels as specific tumor markers for nongonadal malignancies is controversial. In the present report, different monoclonal based immunoradiometric assays specific for hCG and its free hCG-alpha and hCG-beta subunits have been used to reevaluate the presence of these molecules in the serum of patients with a wide variety of tumors. Serum samples from patients with newly diagnosed, persistent, or recurrent malignancies of either known (n = 717) or unknown (n = 32) primary site, healthy blood donors (n = 309), and nonmalignant disease controls (n = 86) were studied using four highly specific and sensitive monoclonal based immunoradiometric assays to hCG and its free subunits. Low level hCG elevations (<1000 pg/ml) were found to be common in cancer patients, normal subjects, and disease controls. However, serum levels >1000 pg/ml were highly diagnostic of gonadal tumors and specifically identified nonseminomatous testicular tumors. Significant serum elevations of free hCG-alpha subunit (as high as 3000 pg/ml) were found in approximately 96% of cancer patients, normal individuals, and disease controls. In contrast, free hCG-beta subunit levels (greater-than-or-equal-to 100 pg/ml) were detected in 70 and 50% of patients with nonseminomatous and seminomatous testicular cancers, respectively, and in 47% of bladder, 32% of pancreatic, and 30% of cervical carcinomas. All normal subjects and disease controls had free hCG-beta levels <100 pg/ml. Thus, the detection of the free hCG-beta subunit in serum of nonpregnant subjects was highly diagnostic of malignancy in general and specifically defines a subgroup of aggressive nongonadal malignancies. C1 INST GUSTAVE ROUSSY,DEPT MOLEC IMMUNOL,38 RUE CAMILLE DESMOULINS,F-94805 VILLEJUIF,FRANCE. INST GUSTAVE ROUSSY,DEPT MED,F-94805 VILLEJUIF,FRANCE. INST GUSTAVE ROUSSY,DEPT PATHOL,F-94805 VILLEJUIF,FRANCE. INST GUSTAVE ROUSSY,INTENS CARE UNIT,F-94805 VILLEJUIF,FRANCE. HOP PITIE,F-75013 PARIS,FRANCE. HOP ANTOINE BECLERE,F-92140 CLAMART,FRANCE. FAC PHARM PARIS,DEPT IMMUNOL,CNRS,URA 1484,F-75270 PARIS 06,FRANCE. MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02129. OI Poynard, Thierry/0000-0002-2050-640X FU NCI NIH HHS [CA-35711]; NICHD NIH HHS [HD-20469] NR 62 TC 172 Z9 176 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 JUL 15 PY 1992 VL 52 IS 14 BP 3901 EP 3907 PG 7 WC Oncology SC Oncology GA JC586 UT WOS:A1992JC58600012 PM 1377600 ER PT J AU CALORINI, L MAROZZI, A BYERS, HR WANECK, GL LEE, KW ISSELBACHER, KJ GATTONICELLI, S AF CALORINI, L MAROZZI, A BYERS, HR WANECK, GL LEE, KW ISSELBACHER, KJ GATTONICELLI, S TI EXPRESSION OF A TRANSFECTED H-2KB GENE IN B16 CELLS CORRELATES WITH SUPPRESSION OF LIVER METASTASES IN TRIPLE IMMUNODEFICIENT MICE SO CANCER RESEARCH LA English DT Article ID CLASS-I GENE; TUMOR-CELLS; HISTOCOMPATIBILITY ANTIGENS; CHOROIDAL MELANOMA; INSULIN-RECEPTOR; GROWTH; PHENOTYPE; INVITRO; LINE; DNA AB In vivo experiments performed with NIH (nu/nu, bg/bg, xid/xid) triple immunodeficient (TD) mice revealed the striking ability of i.v. injected B16-F1 and B16-F10 murine melanoma cells to colonize not only the lungs but also the liver of TD mice. Subsequently, B16 melanoma cell cultures, which express very low levels of H-2K(b) antigen, were cotransfected with plasmids pRSVneo, containing the neomycin resistance gene, and 6-2B1pMT, expressing the H-2K(b) complentary DNA under the control of the metallothionein enhancer-promoter. Several neomycin-resistant clones were analyzed for H-2K(b) and H-2D(b) expression by RNase protection and flow cytometry assays. All parental lines and transfected clones expressed normal levels of H-2D(b) mRNA, while only some of the transfected clones expressed easily detectable levels of H-2K(b) mRNA. Moreover, in these clones H-2K(b) expression could be enhanced in the presence of Zn2+, indicating that the metallothionein enhancer was functioning properly. Parental cells and transfected clones were injected i.v. in TD mice to assess the possible involvement of H-2K(b) antigen in regulating the metastatic potential of B16 melanoma cells. We observed a remarkable correlation between expression of H-2K(b) antigen and suppression of liver-specific metastases in TD mice. Identical results were obtained when we gave TD mice injections of mixed populations of transfectants expressing H-2K(b) antigen, obtained by fluorescence-activated cell sorting. These experiments allowed us to rule out the possibility that the observed changes in metastatic potential were due to clonal variability among individual transfected clones. Taken together, the results of our in vivo studies with immunodeficient mice support the notion that specific major histocompatibility complex Class I molecules modulate the metastatic potential of malignant cells also by mechanisms which are independent of their well-established role in antigen presentation. C1 NEW ENGLAND MED CTR HOSP,DEPT RADIAT ONCOL,DIV RADIAT & CANC BIOL,BOX 824,750 WASHINGTON ST,BOSTON,MA 02111. UNIV MILAN,DEPT BIOL & GENET,I-20122 MILAN,ITALY. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. NR 29 TC 13 Z9 13 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUL 15 PY 1992 VL 52 IS 14 BP 4036 EP 4041 PG 6 WC Oncology SC Oncology GA JC586 UT WOS:A1992JC58600032 PM 1617680 ER PT J AU STOECKLE, JD GOODSON, JG AF STOECKLE, JD GOODSON, JG TI GENERAL INTERNAL-MEDICINE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 23 TC 0 Z9 0 U1 1 U2 1 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 JUL 15 PY 1992 VL 268 IS 3 BP 358 EP 360 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JC352 UT WOS:A1992JC35200030 PM 1613919 ER PT J AU HASHIMOTO, N FEENER, EP ZHANG, WR GOLDSTEIN, BJ AF HASHIMOTO, N FEENER, EP ZHANG, WR GOLDSTEIN, BJ TI INSULIN-RECEPTOR PROTEIN-TYROSINE PHOSPHATASES - LEUKOCYTE COMMON ANTIGEN-RELATED PHOSPHATASE RAPIDLY DEACTIVATES THE INSULIN-RECEPTOR KINASE BY PREFERENTIAL DEPHOSPHORYLATION OF THE RECEPTOR REGULATORY DOMAIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID HUMAN-PLACENTA; BETA-SUBUNIT; CLONING; AUTOPHOSPHORYLATION; FAMILY; PHOSPHORYLATION; IDENTIFICATION; EXPRESSION; MEMBER; SITES AB A number of protein-tyrosine phosphatase(s) (PTPases) have been shown to dephosphorylate the insulin receptor in vitro; however, it is not known whether any individual PTPase has specificity for certain phosphotyrosine residues of the receptor that regulate its intrinsic tyrosine kinase activity. We evaluated the deactivation of the insulin receptor kinase by three candidate enzymes that are expressed in insulin-sensitive rat tissues, including the receptor-like PTPases LAR and LRP, and the intracellular enzyme, PTPase1B. Purified insulin receptors were activated by insulin and receptor dephosphorylation, and kinase activity was quantitated after incubation with recombinant PTPases from an Escherichia coli expression system. When related to the level of overall receptor dephosphorylation, LAR deactivated the receptor kinase 3.1 and 2.1 times more rapidly than either PTPase1B or LRP, respectively (p < 0.03). To assess whether these effects were associated with preferential dephosphorylation of the regulatory (Tyr-1150) domain of the receptor beta-subunit, we performed tryptic mapping of the insulin receptor beta-subunit after dephosphorylation by PTPases. Relative to the rate of initial loss of P-32 from receptor C-terminal sites, LAR dephosphorylated the Tris-phosphorylated Tyr-1150 domain 3.5 and 3.7 times more rapidly than either PTPase1B or LRP, respectively (p < 0.01). The accelerated deactivation of the insulin receptor kinase by LAR and its relative preference for regulatory phosphotyrosine residues further support a potential role for this transmembrane PTPase in the physiological regulation of insulin receptors in intact cells. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK36836, DK43396, P30 DK036836] NR 42 TC 96 Z9 96 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 JUL 15 PY 1992 VL 267 IS 20 BP 13811 EP 13814 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JD325 UT WOS:A1992JD32500006 PM 1321126 ER PT J AU HOLLANDER, GA LUSKEY, BD WILLIAMS, DA BURAKOFF, SJ AF HOLLANDER, GA LUSKEY, BD WILLIAMS, DA BURAKOFF, SJ TI FUNCTIONAL EXPRESSION OF HUMAN CD8 IN FULLY RECONSTITUTED MICE AFTER RETROVIRAL-MEDIATED GENE-TRANSFER OF HEMATOPOIETIC STEM-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN ADENOSINE-DEAMINASE; LONG-TERM EXPRESSION; TYROSINE-PROTEIN-KINASE; MOUSE LYMPHOCYTES-T; CLASS-I MOLECULES; ALPHA-3 DOMAIN; PHYSICAL ASSOCIATION; CYTOPLASMIC DOMAINS; ANTIGEN RECEPTOR; ACTIVATION AB Retroviral-mediated gene transfer has been used in an attempt to efficiently and stably express functional cell-surface molecules in lymphoid and myeloid cells. The human CD8 molecule is a T cell-specific surface receptor that is intimately involved in class I MHC-restricted Ag recognition and subsequent T cell activation. After infection with a recombinant, replication-defective retrovirus containing the human CD8-alpha cDNA, bone marrow cells were transplanted into lethally irradiated recipients. The majority of lymphoid and myeloid cells of reconstituted animals expressed high levels of human CD8 for at least 8 months after transplantation. Transfer of bone marrow and spleen cells from these recipients 100 days after transplantation into secondary recipients also resulted in long term expression of CD8 in lymphoid and myeloid cells. CD8 expressed in splenic T cells associated with the lymphoid-specific tyrosine protein kinase p56lck, participated in T cell activation and conferred an increased xenogeneic response to human MHC class I Ag. Thus, retroviral-mediated gene transfer allows the long term, functional expression of cell-surface molecules in normal murine lymphoid and myeloid cells. C1 BRIGHAM & WOMENS HOSP,DEPT PEDIAT,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV PEDIAT HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP HOLLANDER, GA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU PHS HHS [17258] NR 46 TC 14 Z9 14 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 JUL 15 PY 1992 VL 149 IS 2 BP 438 EP 444 PG 7 WC Immunology SC Immunology GA JD122 UT WOS:A1992JD12200010 PM 1624791 ER PT J AU TANAKA, T CAMERINI, D SEED, B TORIMOTO, Y DANG, NH KAMEOKA, J DAHLBERG, HN SCHLOSSMAN, SF MORIMOTO, C AF TANAKA, T CAMERINI, D SEED, B TORIMOTO, Y DANG, NH KAMEOKA, J DAHLBERG, HN SCHLOSSMAN, SF MORIMOTO, C TI CLONING AND FUNCTIONAL EXPRESSION OF THE T-CELL ACTIVATION ANTIGEN CD26 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID DIPEPTIDYL PEPTIDASE-IV; HUMAN LYMPHOCYTE-T; MEMBRANE GLYCOPROTEIN; MOLECULAR-CLONING; SIGNAL SEQUENCE; PLASMA-MEMBRANE; AMINOPEPTIDASE; RECEPTOR; DOMAIN; CDNA AB A cDNA encoding the T cell activation Ag CD26 was isolated from human PHA-activated T cells by using an expression cloning method. The nucleotide sequence obtained predicts a protein of 766 amino acids of type II membrane topology, with six amino acids in the cytoplasmic region. The predicted amino acid sequence of the Ag was 85% homologous to that of the dipeptidyl peptidase IV enzyme isolated from rat liver. Derivatives of the human leukemic T cell line Jurkat transfected with a CD26 expression plasmid were established. Characterization of the CD26 Ag expressed by the transfected Jurkat cells revealed that the Ag could be immunoprecipitated as a 110-kDa molecule similar to that found on peripheral blood T cells and that the Ag had dipeptidyl peptidase IV activity. Functional analysis of these Jurkat transfectants showed that cross-linking of the CD26 and CD3 Ag with their respective antibodies resulted in enhanced intracellular calcium mobilization and IL-2 production. These results provide direct evidence that the CD26 Ag plays a role in T cell activation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. FU NIAID NIH HHS [AI29530, AI12069]; NIAMS NIH HHS [AR33713] NR 45 TC 189 Z9 190 U1 0 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUL 15 PY 1992 VL 149 IS 2 BP 481 EP 486 PG 6 WC Immunology SC Immunology GA JD122 UT WOS:A1992JD12200015 PM 1352530 ER PT J AU VIDARD, L ROCK, KL BENACERRAF, B AF VIDARD, L ROCK, KL BENACERRAF, B TI DIVERSITY IN MHC CLASS-II OVALBUMIN T-CELL EPITOPES GENERATED BY DISTINCT PROTEASES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTIGEN PRESENTATION; INFLUENZA HEMAGGLUTININ; SYNTHETIC PEPTIDES; LYMPHOCYTES-T; HA1 SUBUNIT; RECOGNITION; MOLECULES; DETERMINANT; RESIDUES; BINDING AB It is generally accepted that a limited number of T cell epitopes are generated by APC from an immunogenic protein. To ascertain the number of determinants on OVA recognized in the context of the H-2s haplotype, we generated 19 T-T hybridomas against OVA and H-2s and we synthesized 46 overlapping peptides spanning the entire protein. Eighteen T-T hybrids were stimulated by eight different peptides. The peptide recognized by one T cell hybrid was not identified. The effect of four protease inhibitors on the processing and presentation of OVA by the LS.102.9 B cell hybridoma seemed to implicate several groups of proteases in the processing of this Ag. Alkylation of cysteine residues with iodoacetic acid showed in a few cases a dramatic decrease in the capacity of OVA to stimulate T-T hybrids recognizing cysteine-free peptides. In contrast, two T-T hybrids recognizing cysteine containing peptides were not affected by the alkylation, suggesting that alkylation inhibited the processing of OVA without affecting peptide interaction with class II MHC molecules. These data demonstrate that the repertoire of peptides generated by APC from OVA is not limited to one or few immunodominant peptides, and results from the activity of several endopeptidases and/or exopeptidases. In addition, the structure of the Ag (native or denatured) was shown to affect the efficiency with which different epitopes are generated. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. INST CURIE,CNRS,UNITE IMMUNOGENET 1413,F-75231 PARIS 05,FRANCE. RP VIDARD, L (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 46967]; NIAID NIH HHS [AI 20248] NR 46 TC 65 Z9 66 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 JUL 15 PY 1992 VL 149 IS 2 BP 498 EP 504 PG 7 WC Immunology SC Immunology GA JD122 UT WOS:A1992JD12200018 PM 1378066 ER PT J AU ZHOU, LJ SCHWARTING, R SMITH, HM TEDDER, TF AF ZHOU, LJ SCHWARTING, R SMITH, HM TEDDER, TF TI A NOVEL CELL-SURFACE MOLECULE EXPRESSED BY HUMAN INTERDIGITATING RETICULUM CELLS, LANGERHANS CELLS, AND ACTIVATED LYMPHOCYTES IS A NEW MEMBER OF THE IG SUPERFAMILY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMUNOGLOBULIN SUPERFAMILY; PERIPHERAL MYELIN; ADHESION MOLECULE; B-CELLS; ANTIGEN; RECEPTOR; GENE; CDNA; SEQUENCE; CD28 AB cDNA isolated from a human lymphocyte library were analyzed and shown to encode a novel cell-surface glycoprotein, termed HB15, expressed by dendritic cell subsets and activated lymphocytes. The predicted mature 186 amino acid protein was composed of a single extracellular V-type Ig-like domain, a transmembrane region, and a 39-amino acid cytoplasmic domain. In contrast to most Ig-like domains, analysis of a partial genomic DNA clone revealed that the extracellular Ig-like domain of HB15 was encoded by at least two exons. Northern blot analysis revealed that HB15 derived from three mRNA transcripts of approximately 1.7, 2.0, and 2.5 kb expressed by lymphoblastoid cell lines. Two mAb reactive with HB15 were produced and used to show that HB15 is expressed as a single chain cell-surface glycoprotein of M(r) 45,000. HB15 expression was specific for lymphoblastoid cell lines and mitogen-activated lymphocytes, and HB15 was not expressed at detectable levels by circulating leukocytes. Immunohistologic analysis revealed that HB15 had a unique pattern of expression, being found predominantly in hemopoietic tissues with strong expression by scattered interfollicular interdigitating reticulum cells and weak expression by germinal center cells. HB15 was also expressed by Langerhans cells within the skin. HB15 therefore serves as a unique marker for the subset of dendritic cells represented by Langerhans cells and interdigitating reticulum cells. Thus, the HB15 glycoprotein represents a newly identified member of the Ig superfamily that may play a significant role in Ag presentation or the cellular interactions that follow lymphocyte activation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR BIOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. THOMAS JEFFERSON UNIV,DEPT PATHOL,PHILADELPHIA,PA 16802. FU NCI NIH HHS [CA-34183]; NIAID NIH HHS [AI-26872] NR 51 TC 260 Z9 272 U1 1 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUL 15 PY 1992 VL 149 IS 2 BP 735 EP 742 PG 8 WC Immunology SC Immunology GA JD122 UT WOS:A1992JD12200052 PM 1378080 ER PT J AU ETTINGER, DS FINKELSTEIN, DM ABELOFF, MD SKEEL, RT STOTT, PB FRONTIERA, MS BONOMI, PD AF ETTINGER, DS FINKELSTEIN, DM ABELOFF, MD SKEEL, RT STOTT, PB FRONTIERA, MS BONOMI, PD TI JUSTIFICATION FOR EVALUATING NEW ANTICANCER DRUGS IN SELECTED UNTREATED PATIENTS WITH EXTENSIVE-STAGE SMALL-CELL LUNG-CANCER - AN EASTERN-COOPERATIVE-ONCOLOGY-GROUP RANDOMIZED STUDY SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID PHASE-II TRIAL; TENIPOSIDE; CARCINOMA; 7-CON-O-METHYLNOGAROL; IDENTIFICATION; CHEMOTHERAPY; ETOPOSIDE; THERAPY; AGENT AB Background: Studies have shown that response to a given chemotherapy in previously untreated patients with extensive-stage small-cell lung cancer is superior to that in patients previously treated with other regimens. This finding raises the question of whether it is necessary and ethical to study the effects of new anticancer agents in untreated patients. Such studies appear to be the best test for drug development, but there has been no evaluation of whether survival of untreated patients, whose cancer is sensitive to established drugs, is adversely affected in trials of new drugs. Purpose: This randomized study of untreated patients with extensive-stage small-cell lung cancer was designed (a) to compare the survival of patients treated with either effective standard chemotherapy or an investigational anticancer drug as initial therapy and (b) to evaluate response rates and toxic effects of such therapies. Methods: Eighty-six patients were randomly assigned to receive, as initial therapy, either the standard CAV regimen-cyclophosphamide (1000 mg/m2), doxorubicin (50 mg/m2), and vincristine (1.4 mg/m2) every 3 weeks-or the phase II drug menogaril (200 Mg/M2) every 4 weeks. Treatment after induction therapy varied, depending on patient response, but nonresponders and those with disease progression received salvage chemotherapy-etoposide (120 mg/m2 on days 1, 2, and 3) and cisplatin (60 mg/m2 on day 1), repeated every 3 weeks. Results: Of the 43 patients on CAV, 42% responded (eight complete responses and 10 partial responses); 5% of the 43 on menogaril responded (two partial responses) (P = .0001). Twelve (22%) of 54 patients responded to salvage chemotherapy (five complete responses and seven partial responses). Within 3 months from start of treatment, twelve patients died-3 patients in the CAV group and nine patients in the menogaril group (P = .12). The estimated median survival was 37 weeks with menogaril and 45 weeks with CAV (P = .28). At 6 months, survival was 76.7% for the CAV group and 67.4% for the menogaril group. At 12 months, survival rates were 24.4% and 27.9%, respectively. Confidence intervals (95%) for the differences between the proportions surviving in the two groups were -9%-28% at 6 months and -25%-14% at 12 months. Use of CAV resulted in significantly higher occurrence of severe and life-threatening treatment-related complications (P = .002). Conclusion: The confidence intervals for the differences in survival are too wide to conclude that evaluation of a new drug in untreated patients with extensive-stage small-cell lung cancer is or is not harmful. The data do suggest, however, that use of this study design may have no adverse effect on survival. C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. MED COLL OHIO,TOLEDO,OH 43699. BORGESS BRONSON HOSP,KALAMAZOO COMMUNITY CLIN ONCOL PROGRAM,KALAMAZOO,MI. UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53706. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. RP ETTINGER, DS (reprint author), JOHNS HOPKINS UNIV HOSP,CTR ONCOL,600 N WOLFE ST,BALTIMORE,MD 21205, USA. FU NCI NIH HHS [CA-14958, CA-21115, CA-06594] NR 26 TC 41 Z9 42 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUL 15 PY 1992 VL 84 IS 14 BP 1077 EP 1084 DI 10.1093/jnci/84.14.1077 PG 8 WC Oncology SC Oncology GA JC869 UT WOS:A1992JC86900012 PM 1320131 ER PT J AU LINNEKIN, D EVANS, GA DANDREA, A FARRAR, WL AF LINNEKIN, D EVANS, GA DANDREA, A FARRAR, WL TI ASSOCIATION OF THE ERYTHROPOIETIN RECEPTOR WITH PROTEIN TYROSINE KINASE-ACTIVITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SIGNAL TRANSDUCTION; PROTEIN PHOSPHORYLATION ID COLONY-STIMULATING FACTOR; SIGNAL TRANSDUCTION; EXPRESSION CLONING; MOLECULAR-CLONING; CELL-LINES; PHOSPHORYLATION; INTERLEUKIN-3; GLYCOPROTEIN; GROWTH; SUPERFAMILY AB We have examined the signal transduction mechanism of the hematopoietic growth factor erythropoietin (Epo). Epo stimulation of Ba/F3 cells transfected with the Epo receptor resulted in increases in tyrosine phosphorylation of proteins of 97, 75, and 55 kDa. Epo-induced increases in tyrosine phosphorylation of a 97-kDa protein were also detected within the Epo receptor complex, suggesting that a protein tyrosine kinase is associated with the Epo receptor. Protein tyrosine kinase activity was found within the Epo receptor complex and modulation of this activity was observed after treatment of cells with Epo. Furthermore, constitutively high amounts of protein kinase activity were observed in Epo receptor complexes isolated from autonomously growing cells coexpressing the Epo receptor and the leukemogenic glycoprotein gp55. The dominant phosphotyrosylprotein found associated with the Epo receptor was 97 kDa. An Epo receptor-associated protein of identical molecular mass was also found to bind ATP, a characteristic critical for protein kinases. Collectively, these data demonstrate that the Epo receptor is associated with protein tyrosine kinase activity and further suggest that a 97-kDa phosphotyrosylprotein associated with the Epo receptor is a protein tyrosine kinase involved in Epo-mediated signal transduction. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. NCI,FREDERICK CANC RES & DEV CTR,DYN CORP,PROGRAM RESOURCES INC,FREDERICK,MD 21701. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DIV HEMATOL ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [N01-CO-74102] NR 33 TC 61 Z9 61 U1 0 U2 0 PU NATL ACAD PRESS 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 JUL 15 PY 1992 VL 89 IS 14 BP 6237 EP 6241 DI 10.1073/pnas.89.14.6237 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JD675 UT WOS:A1992JD67500003 PM 1378622 ER PT J AU SPOSI, NM ZON, LI CARE, A VALTIERI, M TESTA, U GABBIANELLI, M MARIANI, G BOTTERO, L MATHER, C ORKIN, SH PESCHLE, C AF SPOSI, NM ZON, LI CARE, A VALTIERI, M TESTA, U GABBIANELLI, M MARIANI, G BOTTERO, L MATHER, C ORKIN, SH PESCHLE, C TI CELL CYCLE-DEPENDENT INITIATION AND LINEAGE-DEPENDENT ABROGATION OF GATA-1 EXPRESSION IN PURE DIFFERENTIATING HEMATOPOIETIC PROGENITORS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HEMATOPOIETIC GROWTH FACTORS; ERYTHROID AND MYELOID DEVELOPMENT; TRANSCRIPTION FACTORS ID COLONY-STIMULATING FACTOR; ERYTHROID TRANSCRIPTION FACTOR; SERUM-FREE CULTURE; MOLECULAR-CLONING; COMPLEMENTARY-DNA; GROWTH-FACTOR; BFU-E; IDENTIFICATION; ERYTHROPOIETIN; MARROW AB The programmed activation/repression of transcription factors in early hematopoietic differentiation has not yet been explored. The DNA-binding protein GATA-1 is required for normal erythroid development and regulates erythroid-expressed genes in maturing erythroblasts. We analyzed GATA-1 expression in early human adult hematopoiesis by using an in vitro system in which "pure" early hematopoietic progenitors are induced to gradual and synchronized differentiation selectively along the erythroid or granulocyte-macrophage pathway by differential treatment with hematopoietic growth factors. The GATA-1 gene, though virtually silent in quiescent progenitors, is activated after entrance into the cell cycle upon stimulation with hematopoietic growth factors. Subsequently, increasing expression along the erythroid pathway contrasts with an abrupt downregulation in the granulocyte-macrophage lineage. These results suggest a microenvironment-directed, two-step model for GATA-1 expression in differentiating hematopoietic progenitors that involves (i) cycle-dependent initiation and (ii) lineage-dependent maintenance or suppression. Hypothetically, on/off switches of lineage-restricted transactivators may underlie the binary fate decisions of hematopoietic progenitors. C1 IST SUPER SANITA,DEPT HEMATOL ONCOL,VIALE REGINA ELENA 299,I-00161 ROME,ITALY. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115. RI valtieri, mauro/H-1044-2016; CARE', Alessandra/H-5090-2016; Testa, ugo/J-6472-2016 OI valtieri, mauro/0000-0002-9139-6754; CARE', Alessandra/0000-0003-4106-3342; Testa, ugo/0000-0001-7900-8942 FU NHLBI NIH HHS [HL02347, HL32259, HL32262] NR 31 TC 146 Z9 149 U1 0 U2 6 PU NATL ACAD PRESS 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 JUL 15 PY 1992 VL 89 IS 14 BP 6353 EP 6357 DI 10.1073/pnas.89.14.6353 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JD675 UT WOS:A1992JD67500027 PM 1631130 ER PT J AU FREBOURG, T KASSEL, J LAM, KT GRYKA, MA BARBIER, N ANDERSEN, TI BORRESEN, AL FRIEND, SH AF FREBOURG, T KASSEL, J LAM, KT GRYKA, MA BARBIER, N ANDERSEN, TI BORRESEN, AL FRIEND, SH TI GERM-LINE MUTATIONS OF THE P53 TUMOR SUPPRESSOR GENE IN PATIENTS WITH HIGH-RISK FOR CANCER INACTIVATE THE P53 PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID WILD-TYPE; CELLS; TRANSFORMATION; GROWTH AB Germ-line mutations in the p53 tumor suppressor gene have been observed in patients with Li-Fraumeni syndrome, brain tumors, second malignancies, and breast cancers. It is unclear whether all of these mutations have inactivated p53 and thereby provide an increased risk for cancer. Therefore, it is necessary to establish the biological significance of these germ-line mutations by the functional and structural analysis of the resulting mutant p53 proteins. We analyzed the ability of seven germ-line mutant proteins observed in patients with Li-Fraumeni syndrome, second primary neoplasms, or familial breast cancer to block the growth of malignant cells and compared the structural properties of the mutant proteins to that of the wild-type protein. Six of seven missense mutations disrupted the growth inhibitory properties and structure of the wild-type protein. One germ-line mutation retained the features of the wild-type p53. Genetic analysis of the breast cancer family in which this mutation was observed indicated that this germ-line mutation was not associated with the development of cancer. These results demonstrate that germ-line p53 mutations observed in patients with Li-Fraumeni syndrome and with second malignancies have inactivated the p53 tumor suppressor gene. The inability of the germ-line p53 mutants to block the growth of malignant cells can explain why patients with these germ-line mutations have an increased risk for cancer. The observation of a functionally silent germ-line mutation indicates that, before associating a germ-line tumor suppressor gene mutation with cancer risk, it is prudent to consider its functional significance. C1 MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,MGH E,BOSTON,MA 02129. NORWEGIAN RADIUM HOSP,INST CANC RES,DEPT GENET,N-0310 OSLO 3,NORWAY. CHILDRENS HOSP MED CTR,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 31 TC 93 Z9 93 U1 0 U2 2 PU NATL ACAD PRESS 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 JUL 15 PY 1992 VL 89 IS 14 BP 6413 EP 6417 DI 10.1073/pnas.89.14.6413 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JD675 UT WOS:A1992JD67500039 PM 1631137 ER PT J AU NOELLE, RJ ROY, M SHEPHERD, DM STAMENKOVIC, I LEDBETTER, JA ARUFFO, A AF NOELLE, RJ ROY, M SHEPHERD, DM STAMENKOVIC, I LEDBETTER, JA ARUFFO, A TI A 39-KDA PROTEIN ON ACTIVATED HELPER T-CELLS BINDS CD40 AND TRANSDUCES THE SIGNAL FOR COGNATE ACTIVATION OF B-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MONOCLONAL-ANTIBODY; LYMPHOCYTES-T; PROLIFERATION; LYMPHOKINES; MOLECULES; INDUCTION; RECEPTOR AB CD40 is a B-cell surface molecule that has been shown to induce B-cell growth upon ligation with monoclonal antibodies. This report shows that triggering via CD40 is essential for the activation of resting B cells by helper T cells (T(h)). A soluble fusion protein of CD40 and human immunoglobulin, CD40-Ig, inhibited the induction of B-cell cycle entry, proliferation, and differentiation by activated T(h)1 and T(h)2. The ligand for CD40 was identified as a 39-kDa membrane protein that was selectively expressed on activated T(h). A monoclonal antibody specific for the 39-kDa protein inhibited CD40-Ig binding and also inhibited the activation of B cells by T(h). These data indicate that the 39-kDa membrane protein expressed on activated T(h) is a binding protein for CD40 and functions to transduce the signal for T(h)-dependent B-cell activation. C1 BRISTOL MYERS SQUIBB PHARMACEUT,RES INST,SEATTLE,WA 98121. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP NOELLE, RJ (reprint author), DARTMOUTH COLL,SCH MED,DEPT MICROBIOL,1 MED CTR DR,LEBANON,NH 03756, USA. FU NIAID NIH HHS [AI26296]; NIGMS NIH HHS [GM37767, GM43257] NR 28 TC 739 Z9 741 U1 0 U2 5 PU NATL ACAD PRESS 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 JUL 15 PY 1992 VL 89 IS 14 BP 6550 EP 6554 DI 10.1073/pnas.89.14.6550 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JD675 UT WOS:A1992JD67500067 PM 1378631 ER PT J AU ZAZOPOULOS, E HASELTINE, WA AF ZAZOPOULOS, E HASELTINE, WA TI MUTATIONAL ANALYSIS OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ELI NEF FUNCTION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID LONG TERMINAL REPEAT; III HTLV-III/LAV; PROTEIN; REPLICATION; EXPRESSION; GENE; EFFICIENT; PRODUCT; REGION; HIV-1 AB The studies presented here define an internally consistent experimental system that permits systematic analysis of the effect of nef on the rate of the human immunodeficiency virus type 1 (HIV-1) replication in a CD4+ tumor T-cell line and in primary peripheral blood mononuclear cells. The parental full-length Nef protein, derived from the Eli strain of HIV-1, accelerates virus replication in both cell types. Mutations that destabilize or alter the intracellular location of the protein affect the ability of the Nef protein to accelerate virus replication. A set of mutants was made in amino acids proposed to be required for Nef function, including threonine and serine residues proposed to be targets for phosphorylation, and in sequences thought to resemble the G-1, G-3, and G-4 sites of the family of G proteins. In most cases alterations of the critical amino acids yield stable Nef proteins of parental phenotype. These results challenge the existing theories for the mechanism of Nef function. The results also identify two residues in the carboxyl half of the protein that are important for Nef function. 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 32 TC 55 Z9 55 U1 0 U2 1 PU NATL ACAD PRESS 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 JUL 15 PY 1992 VL 89 IS 14 BP 6634 EP 6638 DI 10.1073/pnas.89.14.6634 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JD675 UT WOS:A1992JD67500084 PM 1631166 ER PT J AU PRENTICE, HL KINGSTON, RE AF PRENTICE, HL KINGSTON, RE TI MAMMALIAN PROMOTER ELEMENT FUNCTION IN THE FISSION YEAST SCHIZOSACCHAROMYCES-POMBE SO NUCLEIC ACIDS RESEARCH LA English DT Article ID HUMAN HSP70 PROMOTER; HEAT-SHOCK FACTOR; TRANSCRIPTION INITIATION SITES; SACCHAROMYCES-CEREVISIAE; BINDING-PROTEIN; TATA ELEMENT; GENE; EXPRESSION; ACTIVATION; PURIFICATION AB We have analyzed the function of several mammalian promoter elements in the fission yeast, Schizosaccharomyces pombe. Mutants of the human HSP70 promoter were introduced into S. pombe as single copy integrants at a specific location. Transcription initiation sites utilized in S. pombe with the HSP70 TATA element were similar to those used in mammalian cells. Of three mammalian TATA elements tested, only the HSP70 TATA element functioned in S. pombe. The adenovirus Ella TATA element had little or no activity in S. pombe, indicating that S. pombe is deficient in the factor(s) necessary for recognition of this element. Of upstream promoter elements tested, the CCAAT, Sp1 binding, ATF binding and heat shock elements were functional in S. pombe. Strains containing mutant promoters fused to the ble gene were used to demonstrate that phleomycin can be used as a graded selection in S. pombe. These data demonstrate that S. pombe should provide a useful system in which to characterize and isolate mammalian factors involved in initiation site determination and transcriptional regulation. C1 MASSACHUSETTS GEN HOSP, DEPT MOLEC BIOL, WELLMAN 10, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT GENET, BOSTON, MA 02115 USA. NR 44 TC 15 Z9 15 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 EI 1362-4962 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUL 11 PY 1992 VL 20 IS 13 BP 3383 EP 3390 DI 10.1093/nar/20.13.3383 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JE818 UT WOS:A1992JE81800016 PM 1321414 ER PT J AU ROSOWSKY, A FORSCH, RA MORAN, RG AF ROSOWSKY, A FORSCH, RA MORAN, RG TI N-[4-[[(3,4-DIHYDRO-4-OXO-1,2,3-BENZOTRIAZIN-6-YL)METHYL]AMINO]BENZOYL]- L-GLUTAMIC ACID, A NOVEL A-RING ANALOG OF 2-DESAMINO-5,8-DIDEAZAFOLIC ACID SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID INHIBITING THYMIDYLATE SYNTHASE; ANTIFOLATE N-10-PROPARGYL-5,8-DIDEAZAFOLIC ACID; MAMMALIAN FOLYLPOLYGLUTAMATE SYNTHETASE; HUMAN DIHYDROFOLATE-REDUCTASE; FOLIC-ACID; 5,8-DIDEAZA ANALOGS; ESCHERICHIA-COLI; FOLATE ANALOGS; QUINAZOLINE; L1210 AB N-[4-[[(3,4-Dihydro-4-oxo-1,2,3-benzotriazin-6-yl)methyl]amino]benzoyl]-L-glutamic acid (''2-aza-2-desamino-5,8-dideazafolic acid'', ADDF) was synthesized from 2-amino-5-methylbenzamide via a four-step sequence consisting of diazotization, benzylic bromination, condensation with dimethyl N-(4-aminobenzoyl)-L-glutamate, and ester hydrolysis. ADDF was an inhibitor of recombinant mouse thymidylate synthase; inhibition was competitive with 5,10-methylenetetrahydrofolate as variable substrate (K(i) = 2.3-mu-M). It was a substrate for murine folylpolyglutamate synthetase with kinetic characteristics (K(m) = 28-mu-M) comparable to those of aminopterin, and it inhibited the growth of L1210 cells in culture (IC50 = 0.52-mu-M). The structural modification of the A-ring embodied in ADDF appears to offer a novel, heretofore unexplored approach to the design of TS inhibitors. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. UNIV SO CALIF,COMPREHENS CANC CTR,LOS ANGELES,CA 90033. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA39867] NR 40 TC 4 Z9 4 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD JUL 10 PY 1992 VL 35 IS 14 BP 2626 EP 2630 DI 10.1021/jm00092a013 PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA JD597 UT WOS:A1992JD59700013 PM 1635061 ER PT J AU GRUBER, ML DAVIS, KR SOBEL, RA AF GRUBER, ML DAVIS, KR SOBEL, RA TI A 45-YEAR-OLD MAN WITH CONFUSION, SEIZURES, AND FEW FOCAL FINDINGS - METASTATIC MALIGNANT-MELANOMA, ENCEPHALITIC FORM, IN LEPTOMENINGES AND CEREBRAL-CORTEX SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID CENTRAL-NERVOUS-SYSTEM; HERPES-SIMPLEX ENCEPHALITIS; INTERCELLULAR-ADHESION MOLECULE-1; CHRONIC MENINGITIS; NEUROLOGIC MANIFESTATIONS; MONOCLONAL-ANTIBODIES; ISOLATED ANGIITIS; BRAIN BIOPSY; DIAGNOSIS; INFECTIONS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GRUBER, ML (reprint author), MASSACHUSETTS GEN HOSP,NEUROL,BOSTON,MA 02114, USA. NR 53 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 JUL 9 PY 1992 VL 327 IS 2 BP 107 EP 116 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA JC214 UT WOS:A1992JC21400008 ER PT J AU ANAND, KJS HICKEY, PR AF ANAND, KJS HICKEY, PR TI ANESTHESIA IN NEONATAL CARDIAC-SURGERY - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID SUFENTANIL; RESPONSES; FENTANYL; INFANTS; TRIAL C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. RP ANAND, KJS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 11 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 JUL 9 PY 1992 VL 327 IS 2 BP 126 EP 127 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JC214 UT WOS:A1992JC21400019 ER PT J AU ARYSTARKHOVA, E GASPARIAN, M MODYANOV, NN SWEADNER, KJ AF ARYSTARKHOVA, E GASPARIAN, M MODYANOV, NN SWEADNER, KJ TI NA,K-ATPASE EXTRACELLULAR SURFACE PROBED WITH A MONOCLONAL-ANTIBODY THAT ENHANCES OUABAIN BINDING SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SITE-DIRECTED MUTAGENESIS; SODIUM DODECYL-SULFATE; ALPHA-SUBUNIT; CATALYTIC SUBUNIT; GEL-ELECTROPHORESIS; NA+/K+-ATPASE; NA+,K+-ATPASE; PROTEINS; RAT; IDENTIFICATION AB The Na,K-stimulated ATPase is inhibited by extracellular cardiac glycosides, which bind to the enzyme's alpha-subunit. We used a monoclonal antibody, VG4, as a probe of the extracellular surface. The antibody was specific for Na,K-ATPase and bound to intact cells. The epitope was mapped to the first extracellular loop (H1-H2) of alpha, using a combination of techniques including trypsinolysis, N-terminal sequence of a fragment containing the determinant, and analysis of the effects of species-specific sequence differences. The antibody inhibited Na,K-ATPase activity under certain circumstances, indicating that the H1-H2 loop participates in conformational changes that are transmitted to the active site. Mutations in the H1-H2 loop have been shown by others to affect ouabain affinity. Ouabain and the antibody acted synergistically to inhibit the enzyme, which seemingly supported the hypothesis that the H1-H2 loop is an essential part of the cardiac glycoside binding site. Direct measurements of the binding of [H-3]ouabain, however, indicated that VG, enhanced rather than inhibited binding, presumably by promoting favorable conformation changes. The data suggest the possibility that the cardiac glycoside binding site may be intramembrane rather than extracellular. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSURG RES,WELLMAN 4,FRUIT ST,BOSTON,MA 02114. MM SHEMYAKIN BIOORGAN CHEM INST,MOSCOW 117871,USSR. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. RI Chernyak, Boris/D-9917-2012 FU NHLBI NIH HHS [HL 36271] NR 41 TC 63 Z9 63 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 JUL 5 PY 1992 VL 267 IS 19 BP 13694 EP 13701 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JB746 UT WOS:A1992JB74600094 PM 1377691 ER PT J AU WILDEN, PA SIDDLE, K HARING, E BACKER, JM WHITE, MF KAHN, CR AF WILDEN, PA SIDDLE, K HARING, E BACKER, JM WHITE, MF KAHN, CR TI THE ROLE OF INSULIN-RECEPTOR KINASE DOMAIN AUTOPHOSPHORYLATION IN RECEPTOR-MEDIATED ACTIVITIES - ANALYSIS WITH INSULIN AND ANTIRECEPTOR ANTIBODIES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSINE KINASE; MONOCLONAL-ANTIBODIES; BETA-SUBUNIT; PHOSPHORYLATION SITES; INTACT-CELLS; PROTEIN; ACTIVATION; REPLACEMENT; BINDING; HORMONE AB The role of specific tyrosine autophosphorylation sites in the human insulin receptor kinase domain (Tyr1158, Tyr1162, and Tyr1163) was analyzed using in vitro mutagenesis to replace tyrosine residues individually or in combination. Each of the three single-Phe, the three possible double-Phe a triple-Phe and a triple-Ser mutant receptors, stably expressed in Chinese hamster ovary cells, were compared with the wild-type receptor in their ability to mediate stimulation of receptor kinase activity, glycogen synthesis, and DNA synthesis by insulin or the human-specific anti-receptor monoclonal antibody 83-14. At a concentration of 0.1 nM insulin which produced approximately half-maximal responses with wild-type receptor, DNA synthesis and glycogen synthesis mediated by the three single-Phe mutants ranged from 52 to 88% and from 32 to 79% of the wild-type receptor, respectively. The corresponding figures for the double-Phe mutants averaged 15 and 6%, whereas the triple-mutants were unresponsive in both assays. The level of biological function approximately paralleled the insulin-stimulated tyrosine kinase activity in the intact cell as estimated by tyrosine phosphorylation of the insulin receptor and its endogenous substrate pp185/IRS-1. Interestingly, all mutants showed a marked decrease in insulin-stimulated receptor internalization. Anti-receptor antibody stimulated receptor kinase activity and mimicked insulin action in these cells. In general, the impairment of the metabolic response was greater and impairment of the growth response was less when antibody was the stimulus. These experiments show that the level and specific sites of autophosphorylation are critical determinants of receptor function. The data are consistent with a requirement for the receptor tyrosine kinase either as an obligatory step or a modulator, in both metabolic and growth responses, and demonstrate the important role of the level of insulin receptor kinase domain autophosphorylation in regulating insulin sensitivity. C1 BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 31036, DK 33201, DK 38712] NR 56 TC 123 Z9 123 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 JUL 5 PY 1992 VL 267 IS 19 BP 13719 EP 13727 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JB746 UT WOS:A1992JB74600098 PM 1320027 ER PT J AU GUIGO, R KNUDSEN, S DRAKE, N SMITH, T AF GUIGO, R KNUDSEN, S DRAKE, N SMITH, T TI PREDICTION OF GENE STRUCTURE SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE GENE IDENTIFICATION; EXON STRUCTURE; INTRON SPLICING; CODING SEQUENCE; ARTIFICIAL INTELLIGENCE ID PROTEIN CODING REGIONS; NUCLEIC-ACID SEQUENCES; DNA-SEQUENCES; TOOL C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC BIOL COMP RES RESOURCE,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RI Guigo, Roderic/D-1303-2010 OI Guigo, Roderic/0000-0002-5738-4477 FU NLM NIH HHS [LM05205] NR 21 TC 192 Z9 199 U1 1 U2 3 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD JUL 5 PY 1992 VL 226 IS 1 BP 141 EP 157 DI 10.1016/0022-2836(92)90130-C PG 17 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JC809 UT WOS:A1992JC80900014 PM 1619647 ER PT J AU FERGUSON, CM SAINI, S STEPHENS, G SCULLY, RE GAZ, RD LEWANDROWSKI, K CARTER, P AF FERGUSON, CM SAINI, S STEPHENS, G SCULLY, RE GAZ, RD LEWANDROWSKI, K CARTER, P TI A 20-YEAR-OLD MAN WITH RECENT INTERMITTENT ABDOMINAL-PAIN, CONSTIPATION, AND DIARRHEA - DIVERTICULITIS, WITH PERIDIVERTICULAR ABSCESS AND PERITONITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID DISEASE C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FERGUSON, CM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 14 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 JUL 2 PY 1992 VL 327 IS 1 BP 40 EP 44 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JA761 UT WOS:A1992JA76100008 ER PT J AU LEE, KS KIMURA, RS AF LEE, KS KIMURA, RS TI ISCHEMIA OF THE ENDOLYMPHATIC SAC SO ACTA OTO-LARYNGOLOGICA LA English DT Article DE SIGMOID SINUS; VASCULAR LESION; PATHOGENESIS; ENDOLYMPHATIC HYDROPS ID MENIERES-DISEASE; MOUSE AB A decrease in vascular density in the endolymphatic sac was suspected as a factor in the pathogenesis of endolymphatic hydrops in Meniere's disease. The present study was undertaken to explore this possibility by cutting the posterior meningeal artery and the sigmoid sinus above and below the external aperture of the vestibular aqueduct or by incision of the dura adjacent to the sinus in 18 guinea pigs. The lesions in the sac were greater in the segmental ablation of the artery and sinus and were consistently associated with the development of endolymphatic hydrops. Among the lesions shown in the sac epithelia, the intermediate portion was most often and most severely affected with a decrease in rugose formation and a flattening of the tall epithelial cells or replacement of epithelial cells by squamous type cells. A high correlation between the lesions in the intermediate portion and occurrence of hydrops suggests that the intermediate portion plays a greater role in the pathogenesis of endolymphatic hydrops. The sac luminal precipitates known to be increased in human Meniere's cases were decreased or absent in this study, which suggests that the increased amount is unlikely to be the cause of endolymphatic hydrops. The evidence supports the hypothesis that these substances are secreted by the endolymphatic sac. The limited sensory cell lesions seen in the cochleae and saccules are likely to be due to a temporary vascular ischemia and endolymphatic hydrops. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114. UNIV KOREA,GURO HOSP,DEPT OTOLARYNGOL,SEOUL,SOUTH KOREA. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [2 RO1 DC00073] NR 21 TC 24 Z9 25 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 JUL PY 1992 VL 112 IS 4 BP 658 EP 666 DI 10.3109/00016489209137456 PG 9 WC Otorhinolaryngology SC Otorhinolaryngology GA JF446 UT WOS:A1992JF44600013 PM 1442012 ER PT J AU FAVA, M ROSENBAUM, JF BIRNBAUM, R KELLY, K OTTO, MW MACLAUGHLIN, R AF FAVA, M ROSENBAUM, JF BIRNBAUM, R KELLY, K OTTO, MW MACLAUGHLIN, R TI THE THYROTROPIN RESPONSE TO THYROTROPIN-RELEASING-HORMONE AS A PREDICTOR OF RESPONSE TO TREATMENT IN DEPRESSED OUTPATIENTS SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE THYROTROPIN; TRH; DEPRESSION ID ADENOSYL-L-METHIONINE; ANTIDEPRESSANT; TRH AB We evaluated the predictive value of the thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) in 32 depressed outpatients completing a double-blind placebo-controlled trial of s-adenosyl-1-methionine (SAMe), which failed to show any significant difference between SAMe and placebo. Treatment response was defined as the change in Hamilton Rating Scale for Depression (HRSD-24) score between baseline and the end of the six-week trial. Subjects with TSH response outside the normal range (7-25 uU/ml) had a significantly greater response than patients with a normal response. There was also a significant correlation between absolute deviations from the mean TSH response (16 uU/ml) and changes in HRSD-24 scores. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 12 TC 23 Z9 23 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PD JUL PY 1992 VL 86 IS 1 BP 42 EP 45 DI 10.1111/j.1600-0447.1992.tb03223.x PG 4 WC Psychiatry SC Psychiatry GA JE563 UT WOS:A1992JE56300007 PM 1414398 ER PT J AU HALE, RL RANDALL, CL BECKER, HC MIDDAUGH, LD AF HALE, RL RANDALL, CL BECKER, HC MIDDAUGH, LD TI THE EFFECT OF PRENATAL ETHANOL EXPOSURE ON SCENTMARKING IN THE C57BL/6J AND C3H/HE MOUSE STRAINS SO ALCOHOL LA English DT Article DE PRENATAL ETHANOL; SEXUAL DIMORPHISM; SCENTMARKING; MICE STRAINS ID SEXUALLY DIMORPHIC NUCLEUS; PITUITARY-ADRENAL ACTIVITY; ALCOHOL EXPOSURE; PREOPTIC AREA; MALE-RATS; SACCHARIN PREFERENCE; AROMATASE-ACTIVITY; FEMALE RATS; ADULT; TESTOSTERONE AB In utero exposure to ethanol has been shown to alter sexually dimorphic behaviors in rats. However, it is not clear whether this phenomenon is robust in other species, such as the mouse, which is sensitive to ethanol-induced birth defects. Further, it is not known whether significant differences exist across murine strains. If similar to the classic teratogenic effects of ethanol, it would be expected that strain differences in sensitivity should be evident, with some strains demonstrating an alteration in sexually dimorphic behavior and other strains demonstrating little or no effect. As a first attempt to address these issues, we have examined two mouse strains widely used in prenatal alcohol research, the inbred C3H/He and C57BL/6J strains. Scentmarking was selected as the behavior of interest. It is robustly sexually dimorphic in the rat and mouse, with males marking more than females and preliminary reports have demonstrated that in utero ethanol exposure reduces this behavior in the male rat. In the mouse strains selected for study, pregnant females were provided with either a liquid diet consisting of 25% ethanol-derived calories or pair-fed an isocaloric liquid diet from gestation days 6-18. An additional control group was included which was fed laboratory chow ad lib throughout gestation. Male and female offspring of each strain were tested for scentmarking at 65-75 days of age. As expected, results showed that the effect of prenatal ethanol exposure on scentmarking varied with both strain and sex. In the C3H/He strain, scentmarking was reduced significantly in male ethanol-exposed offspring (i.e., the males were feminized). In contrast, prenatally exposed C57BL/6J males did not differ significantly from their control. No changes in scentmarking due to prenatal treatment were detected in females of either strain. These findings suggest that the demasculinization of behavior noted in rats also can be found in mice but that not all murine strains are equally susceptible. Thus, mice may prove to be valuable murine complements to other rodent models in the investigation of the mechanism(s) underlying changes in sexually dimorphic behaviors due to prenatal ethanol exposure. C1 MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC 29425. RP HALE, RL (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,RES SERV 151,109 BEE ST,CHARLESTON,SC 29403, USA. FU NIAAA NIH HHS [AA06611, AA07474] NR 34 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0741-8329 J9 ALCOHOL JI Alcohol PD JUL-AUG PY 1992 VL 9 IS 4 BP 287 EP 292 DI 10.1016/0741-8329(92)90068-L PG 6 WC Substance Abuse; Pharmacology & Pharmacy; Toxicology SC Substance Abuse; Pharmacology & Pharmacy; Toxicology GA JD742 UT WOS:A1992JD74200002 PM 1637494 ER PT J AU XIN, Y ROSMAN, AS LASKER, JM LIEBER, CS AF XIN, Y ROSMAN, AS LASKER, JM LIEBER, CS TI MEASUREMENT OF CARBOHYDRATE-DEFICIENT TRANSFERRIN BY ISOELECTRIC-FOCUSING WESTERN BLOTTING AND BY MICRO ANION-EXCHANGE CHROMATOGRAPHY RADIOIMMUNOASSAY - COMPARISON OF DIAGNOSTIC-ACCURACY SO ALCOHOL AND ALCOHOLISM LA English DT Article ID ALCOHOL-CONSUMPTION; MARKERS; CURVES AB At present, the most reliable marker of recent and heavy alcohol intake is carbohydrate-deficient transferrin (CDT). While most CDT quantitation methods (including immunofixation and micro anion-exchange chromatography [MAEC] combined with radioimmunoassay [RIA]) either lack the precision required for diagnostic usage or are not commercially available, we recently described an isoelectric focusing/Western blotting (IEF/WB) procedure that provides sensitive and specific assessment of serum CDT content. However, a modified MAEC/RIA kit, supposedly more reliable than the original, is also being advanced as suitable for widespread clinical application. Therefore, we compared this modified MAEC/RIA procedure to the IEF/WB method of CDT quantitation in the following 108 subjects; 53 alcoholics undergoing detoxification without clinical or histological evidence of liver disease, 24 recently drinking alcoholics with biopsy-proven liver disease, eight alcoholics abstinent for more than 30 days with biopsy-proven liver disease, seven non-drinking patients with non-alcoholic liver disease, and 16 healthy controls. Although CDT measurements by the two methods were correlated (r = 0.60, P <0.01), serum CDT values obtained with IEF/WB were nearly five-fold higher than those obtained with MAEC/RIA (e.g. 140.0 +/- 58 versus 28.5 +/- 16 mg/l among the active drinkers). Of the two methods, IEF/WB exhibited significantly greater sensitivity than MAEC/RIA for detecting recent, heavy drinking (75% versus 61 %, P < 0.05) and generated no false positives whereas MAEC/RIA gave falsely elevated CDT levels in 37% of the abstinent alcoholics. Receiver operating characteristic (ROC) analysis, which was used to assess the accuracy of the two methods for discriminating alcoholics admitted for detoxification from healthy controls, suggested an increase in area under the ROC curve for IEF/WB compared to MAEC/RIA (0.92 versus 0.86, P = 0.09). For discriminating recent drinkers with liver disease from non-drinking patients with liver disease (including abstinent alcoholics), the area under the ROC curve was significantly greater for IEF/WB compared to MAEC/RIA (0.97 versus 0.68, P < 0.001). Serum CDT/total transferrin ratios, the latter of which was measured by ELISA, offered no advantage over serum CDT alone as determined by either method for distinguishing heavy drinking. Our results indicate that for detecting recent and heavy alcohol misuse, the IEF/WB method of serum CDT measurement has a greater degree of diagnostic accuracy than the modified MAEC/RIA method, particularly in the presence of liver disease. C1 ALCOHOL RES & TREATMENT CTR,130 W KINGSBRIDGE RD,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. FU NIAAA NIH HHS [AA-07802, AA-03508] NR 15 TC 46 Z9 47 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0735-0414 J9 ALCOHOL ALCOHOLISM JI Alcohol Alcohol. PD JUL PY 1992 VL 27 IS 4 BP 425 EP 433 PG 9 WC Substance Abuse SC Substance Abuse GA JZ243 UT WOS:A1992JZ24300014 PM 1418115 ER PT J AU PICARD, MH WILKINS, GT RAY, PA WEYMAN, AE AF PICARD, MH WILKINS, GT RAY, PA WEYMAN, AE TI PROGRESSIVE CHANGES IN VENTRICULAR STRUCTURE AND FUNCTION DURING THE YEAR AFTER ACUTE MYOCARDIAL-INFARCTION SO AMERICAN HEART JOURNAL LA English DT Article ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY; CROSS-SECTIONAL ECHOCARDIOGRAPHY; ANEURYSM FORMATION; NATURAL-HISTORY; 2-DIMENSIONAL ECHOCARDIOGRAPHY; HIBERNATING MYOCARDIUM; WALL MOTION; SIZE; ASYNERGY; EXTENT AB To investigate the long-term changes in left ventricular structure and function after myocardial infarction, 51 patients with a first myocardial infarction (17 anterior, 23 inferior, and 11 non-Q wave) were studied by two-dimensional echocardiography at the time of entry into the hospital, at 3 months, and 1 year after infarction. The left ventricular endocardial surface was reconstructed from these echocardiograms, and the endocardial surface area (ESA) index (in cm2/m2) and area of abnormal wall motion (AWM in cm2) were quantitated. Despite different trends in the ESA index between entry and 3-month values in those with and without early infarct expansion, a decrease in the ESA index from 3 months to 1 year was noted in anterior and non-Q wave infarctions (anterior with early expansion: 96.3 +/- 8.6 to 81.5 +/- 4.2 cm2/m2, p < 0.05; anterior without early expansion: 59.7 +/- 2.0 to 54.7 +/- 2.0 cm2/m2, p < 0.01; non-Q wave: 64.1 +/- 3.5 to 57.9 +/- 4.4 cm2/m2, p < 0.01). The mean decline in ESA from 3 months to 1 year of 8.9 +/- 2.5 cm2 was independent of initial infarct size. Regional function, as represented by the area of AWM, was also improved but the timing of the improvement was related to the location and size of the infarction. Although decreases in AWM were noted in both the inferior and non-Q wave groups from entry to 3 months (inferior: 27.1 +/- 3.3 to 21.8 +/- 3.4 cm2, p < 0.5; non-Q wave: 18.9 +/- 4.5 to 12.1 +/- 5.5 cm2, p < 0.05), decreases in AWM in anterior infarctions were not present until the 3-month to 1-year time period (anterior with expansion: 79.1 + 18.6 to 59.8 +/- 14.9 cm2, p < 0.05; anterior without expansion: 27.7 +/- 6.2 to 16.5 +/- 4.9 cm 2, p < 0.05). Even in the absence of intervention, global left ventricular size decreases and regional wall motion improves in both Q wave and non-Q wave infarctions when quantitated 1 year after infarction. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PICARD, MH (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC NONINVAS LAB,CARDIAC UNIT,FOUNDERS HOUSE 8,FRUIT ST,BOSTON,MA 02114, USA. OI Picard, Michael/0000-0002-9264-3243 FU NHLBI NIH HHS [HL-07535, HL-26215] NR 42 TC 20 Z9 20 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 JUL PY 1992 VL 124 IS 1 BP 24 EP 31 DI 10.1016/0002-8703(92)90916-J PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JC387 UT WOS:A1992JC38700005 PM 1535474 ER PT J AU COLES, NA LAUER, MS FIELD, TS CONNOLLY, M EAGLE, KA AF COLES, NA LAUER, MS FIELD, TS CONNOLLY, M EAGLE, KA TI CARDIAC EMERGENCIES AT A MAJOR INTERNATIONAL AIRPORT - A PROSPECTIVE OBSERVATIONAL STUDY SO AMERICAN HEART JOURNAL LA English DT Editorial Material ID MEDICAL EMERGENCIES; COMMERCIAL AIRLINES; EQUIPMENT C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,32 FRUIT ST,BOSTON,MA 02114. LOGAN INT AIRPORT,FIRE HOUSE,BOSTON,MA. MASSACHUSETTS GEN HOSP,GEN MED UNIT,BOSTON,MA 02114. RI Lauer, Michael/L-9656-2013 OI Lauer, Michael/0000-0002-9217-8177 NR 9 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD JUL PY 1992 VL 124 IS 1 BP 257 EP 260 DI 10.1016/0002-8703(92)90959-Y PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JC387 UT WOS:A1992JC38700048 PM 1615824 ER PT J AU MURPHY, JM MONSON, RR OLIVIER, DC ZAHNER, GEP SOBOL, AM LEIGHTON, AH AF MURPHY, JM MONSON, RR OLIVIER, DC ZAHNER, GEP SOBOL, AM LEIGHTON, AH TI RELATIONS OVER TIME BETWEEN PSYCHIATRIC AND SOMATIC DISORDERS - THE STIRLING COUNTY STUDY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ANXIETY; COMORBIDITY; DEPRESSION; HOLISTIC HEALTH; PSYCHIATRY ID GENERAL-POPULATION; PHYSICAL ILLNESS; DEPRESSION; ANXIETY; DIAGNOSIS; COMMUNITY; PREVALENCE; MORBIDITY; MORTALITY; SURVIVAL AB A longitudinal study of a general population in Atlantic Canada provided information on associations between two broad categories of illness: somatic disorders and disorders involving depression and/or anxiety. Prevalence was investigated in a sample of 1,003 adults selected in 1952 and another sample of 1,094 adults selected in 1970. Using a cohort of 618 survivors from the 1952 sample who were followed up in 1968, the authors studied prevalence at the beginning and end of the 16-year period. Incidence was also investigated so that the strength of associations between prior illness of one type and subsequent illness of the other type could be assessed. Data were obtained by interviewing subjects with the same structured schedule at each time of investigation. In prevalence enumerations, psychiatric disorders were found to be significantly associated with somatic disorders. Prior somatic disorder was significantly associated with subsequent incidence of depression and/or anxiety and vice versa. The results did not, however, show one direction of influence ("psyche-to-soma" or "soma-to-psyche") to be markedly stronger than the other. The results mainly support the concept of "generalized vulnerability" and draw attention to the importance of recognizing comorbidity in diagnosis and clinical practice. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,INSTRUCT COMP FACIL,BOSTON,MA 02115. DALHOUSIE UNIV,FAC MED,DEPT PSYCHIAT,HALIFAX B3H 4H2,NS,CANADA. DALHOUSIE UNIV,FAC MED,DEPT COMMUNITY HLTH & EPIDEMIOL,HALIFAX B3H 4H2,NS,CANADA. RP MURPHY, JM (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,EPIDEMIOL UNIT,705 WARREN BLDG,FRUIT ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH39576] NR 42 TC 19 Z9 19 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUL 1 PY 1992 VL 136 IS 1 BP 95 EP 105 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JN538 UT WOS:A1992JN53800011 PM 1415135 ER PT J AU WIENS, A MARLES, S SAFNECK, J KWIATKOWSKI, DJ MAURY, CPJ ZELINSKI, T PHILIPPS, S EKINS, MB GREENBERG, CR AF WIENS, A MARLES, S SAFNECK, J KWIATKOWSKI, DJ MAURY, CPJ ZELINSKI, T PHILIPPS, S EKINS, MB GREENBERG, CR TI EXCLUSION OF THE GELSOLIN GENE ON 9Q32-34 AS THE CAUSE OF FAMILIAL LATTICE CORNEAL-DYSTROPHY TYPE-I SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID CRANIAL NEUROPATHY; PROTEIN-AA; AMYLOIDOSIS; FINNISH; DNA AB Familial lattice corneal dystrophy type I (LCD1) is a localized form of inherited amyloidosis limited to the corneal stroma. Recently the Finnish form of hereditary amyloidosis with lattice corneal dystrophy has been shown to be due to a mutation in the gelsolin gene (G654-->A; Asp187-->Asn). In this paper we exclude the gelsolin gene as the cause of the autosomal dominant form of isolated LCD1. C1 UNIV MANITOBA,DEPT PEDIAT & CHILD HLTH,WINNIPEG R3T 2N2,MANITOBA,CANADA. UNIV MANITOBA,DEPT HUMAN GENET,WINNIPEG R3T 2N2,MANITOBA,CANADA. UNIV MANITOBA,DEPT PATHOL,WINNIPEG R3T 2N2,MANITOBA,CANADA. UNIV MANITOBA,DEPT OPHTHALMOL,WINNIPEG R3T 2N2,MANITOBA,CANADA. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. UNIV HELSINKI,DEPT MED 4,SF-00100 HELSINKI 10,FINLAND. NR 24 TC 8 Z9 8 U1 0 U2 2 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 JUL PY 1992 VL 51 IS 1 BP 156 EP 160 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA JA467 UT WOS:A1992JA46700016 PM 1319113 ER PT J AU DOLL, R NATOWICZ, MR SCHIFFMANN, R SMITH, FI AF DOLL, R NATOWICZ, MR SCHIFFMANN, R SMITH, FI TI MOLECULAR DIAGNOSTICS FOR MYELIN PROTEOLIPID PROTEIN GENE-MUTATIONS IN PELIZAEUS-MERZBACHER DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MEMBRANE; DISORDER AB Pelizaeus-Merzbacher disease (PMD) is a clinically heterogeneous, slowly progressive leukodystrophy. The recent detection of mutations in the myelin proteolipid protein (PLP) gene in several PMD patients offers the opportunity both to design DNA-based tests that would be useful in diagnosing a proportion of PMD cases and, in particular, to evaluate the diagnostic utility of single-strand conformation polymorphism (SSCP) analysis for this disease. A combination of SSCP analysis and direct sequencing of PCR-amplified DNA was used to screen for PLP mutations in 24 patients affected with leukodystrophies of unknown etiology. Two heretofore undescribed mutations in the PLP gene were identified, Asp202His in exon 4 and Gly73Arg in exon 3. The ease and efficiency of SSCP analysis in detecting new mutations support the utilization of this technique in screening for PLP mutations in patients with unexplained leukodystrophies. C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV BIOCHEM & MOLEC BIOL,200 TRAPELO RD,WALTHAM,MA 02254. EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HADASSAH UNIV,MED CTR,PEDIAT NEUROL UNIT,JERUSALEM,ISRAEL. FU NIDDK NIH HHS [DK38381] NR 23 TC 44 Z9 45 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 JUL PY 1992 VL 51 IS 1 BP 161 EP 169 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA JA467 UT WOS:A1992JA46700017 PM 1376966 ER PT J AU STRIKER, GE HIRSCHMAN, GH ANDERSON, A EDINGTON, B NORWOOD, E KLAHR, S LEVEY, AS STEINMAN, T ROSA, R JOHNSON, A UNDERHILL, M PEARLSTEIN, G CHOLAKOS, B BRENNER, BM MITCH, WE SEIFTER, J LAZARUS, JM HESTER, N WETSTEIN, L DESMOND, M KOPPLE, JD ADLER, S DICHIRO, J MCKAY, SM WALSER, M WALKER, WG WARD, L BARNES, C BLAHA, C DREW, H COGGINS, CH GRONICH, J CORNELL, B MENGERT, T HUGGINS, N LEVEY, AS DWYER, J PERRONE, RD SHAH, BV LAWLOR, M STOLLAR, C RAIZMAN, D MARTIN, A FURLONG, D HUNSICKER, LG FREEMAN, RM BERTOLATUS, JA SNETSELAAR, L BROOKS, L KURTZMAN, D EASTIN, S CAMPBELL, C MASSRY, SG FEINSTEIN, E KAPTEIN, EM MATSUMOTO, J KIEFER, S TESCHAN, PE DIRAIMONDO, C HAKIM, R POWERS, S JONES, H BUSH, A ROGERS, NL WILLIAMS, GW BECK, GJ GASSMAN, JJ BERG, RL LEATHERMAN, JR MCPHERSON, JA FATICA, KJ DRABIK, MJ SKIBINSKI, CI KOVACS, MM HOUSER, HB PETOT, GJ HULL, AL MATHEWS, R NELSON, S HALL, PM ROLIN, HA PEXA, DS NAITO, HK DAVID, JA ERDEI, LM SOUTH, CA PROUDFIT, WL UNDERWOOD, DA JONES, EH UNGAR, JA LAIDLAW, S BLAGG, CR DENNIS, V GRIZZLE, JE HAWKINS, CM HOLLIDAY, MA MYERS, BD RUDMAN, D YOUNG, DS YOUNG, V DIRKS, JH GRANTHAM, J HARPER, AE PETERS, K STEIN, JH PELLEGRINO, ED VANYPERSELE, C BAROFSKY, I HELD, PJ AF STRIKER, GE HIRSCHMAN, GH ANDERSON, A EDINGTON, B NORWOOD, E KLAHR, S LEVEY, AS STEINMAN, T ROSA, R JOHNSON, A UNDERHILL, M PEARLSTEIN, G CHOLAKOS, B BRENNER, BM MITCH, WE SEIFTER, J LAZARUS, JM HESTER, N WETSTEIN, L DESMOND, M KOPPLE, JD ADLER, S DICHIRO, J MCKAY, SM WALSER, M WALKER, WG WARD, L BARNES, C BLAHA, C DREW, H COGGINS, CH GRONICH, J CORNELL, B MENGERT, T HUGGINS, N LEVEY, AS DWYER, J PERRONE, RD SHAH, BV LAWLOR, M STOLLAR, C RAIZMAN, D MARTIN, A FURLONG, D HUNSICKER, LG FREEMAN, RM BERTOLATUS, JA SNETSELAAR, L BROOKS, L KURTZMAN, D EASTIN, S CAMPBELL, C MASSRY, SG FEINSTEIN, E KAPTEIN, EM MATSUMOTO, J KIEFER, S TESCHAN, PE DIRAIMONDO, C HAKIM, R POWERS, S JONES, H BUSH, A ROGERS, NL WILLIAMS, GW BECK, GJ GASSMAN, JJ BERG, RL LEATHERMAN, JR MCPHERSON, JA FATICA, KJ DRABIK, MJ SKIBINSKI, CI KOVACS, MM HOUSER, HB PETOT, GJ HULL, AL MATHEWS, R NELSON, S HALL, PM ROLIN, HA PEXA, DS NAITO, HK DAVID, JA ERDEI, LM SOUTH, CA PROUDFIT, WL UNDERWOOD, DA JONES, EH UNGAR, JA LAIDLAW, S BLAGG, CR DENNIS, V GRIZZLE, JE HAWKINS, CM HOLLIDAY, MA MYERS, BD RUDMAN, D YOUNG, DS YOUNG, V DIRKS, JH GRANTHAM, J HARPER, AE PETERS, K STEIN, JH PELLEGRINO, ED VANYPERSELE, C BAROFSKY, I HELD, PJ TI THE MODIFICATION OF DIET IN RENAL-DISEASE STUDY - DESIGN, METHODS, AND RESULTS FROM THE FEASIBILITY STUDY SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE CHRONIC RENAL DISEASE; PROGRESSION OF RENAL DISEASE; CONTROLLED CLINICAL TRIAL; RENAL FUNCTION; DIET; BLOOD PRESSURE ID GLOMERULAR-FILTRATION-RATE; AMINO-ACID SUPPLEMENT; LOW-PROTEIN-DIET; DIABETIC NEPHROPATHY; SUBCUTANEOUS INJECTION; NUTRITIONAL-STATUS; KIDNEY-DISEASE; KETO ACID; FAILURE; PROGRESSION C1 CLEVELAND CLIN EDUC FDN,CENT ELECTROCARDIOG LAB,CLEVELAND,OH 44106. CLEVELAND CLIN EDUC FDN,CTR DRUG DISTRIBUT,CLEVELAND,OH 44106. UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,CENT AMINO ACID LAB,TORRANCE,CA 90509. NEW ENGLAND MED CTR,CTR CLIN,BOSTON,MA 02111. UNIV IOWA HOSP & CLIN,CTR CLIN,IOWA CITY,IA 52242. UNIV SO CALIF,CTR CLIN,LOS ANGELES,CA 90089. NIDDKD,ADM HLTH CARE FINANCING,BETHESDA,MD. NIDDKD,COMM STEERING,BETHESDA,MD. UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,CTR CLIN,TORRANCE,CA 90509. JOHNS HOPKINS UNIV HOSP,CTR CLIN,BALTIMORE,MD 21205. BETH ISRAEL HOSP,CTR CLIN,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,CTR CLIN,BOSTON,MA 02115. VANDERBILT UNIV,MED CTR,CTR CLIN,NASHVILLE,TN 37240. MASSACHUSETTS GEN HOSP,CTR CLIN,BOSTON,MA 02114. CASE WESTERN RESERVE UNIV,CTR NUTR COORDINATING,CLEVELAND,OH 44106. RP STRIKER, GE (reprint author), CLEVELAND CLIN EDUC FDN,DEPT BIOSTAT & EPIDEMIOL,CTR STUDY DATA COORDINATING,9500 EUCLID AVE,CLEVELAND,OH 44106, USA. NR 59 TC 24 Z9 24 U1 1 U2 3 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 JUL PY 1992 VL 20 IS 1 BP 18 EP 33 PG 16 WC Urology & Nephrology SC Urology & Nephrology GA JD485 UT WOS:A1992JD48500002 ER PT J AU WEINRAUCH, LA DELIA, JA MONACO, AP GLEASON, RE WELTY, F NISHAN, PC NESTO, RW AF WEINRAUCH, LA DELIA, JA MONACO, AP GLEASON, RE WELTY, F NISHAN, PC NESTO, RW TI PREOPERATIVE EVALUATION FOR DIABETIC RENAL-TRANSPLANTATION - IMPACT OF CLINICAL, LABORATORY, AND ECHOCARDIOGRAPHIC PARAMETERS ON PATIENT AND ALLOGRAFT SURVIVAL SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID RECOMBINANT-HUMAN-ERYTHROPOIETIN; CORONARY-ARTERY DISEASE; AWAITING KIDNEY-TRANSPLANTATION; FAILURE; ANGIOGRAPHY; THERAPY; CARDIOMYOPATHY; SENSITIZATION; DYSFUNCTION; NEPHROPATHY AB OBJECTIVE: To assess the impact on renal transplant patients and graft survival of clinical, laboratory, and echocardiographic parameters commonly measured prior to surgery. PATIENTS: Forty-seven consecutive diabetics with preoperative echocardiograms at the time of transplantation. METHODs: Clinical history, standard chest roentgenogram, electrocardiogram blood tests, echocardiograms, and HLA testing at baseline, follow-up from 2 to 7 years with periodic reassessment of graft function. RESULTS: Patient survival did not appear to be influenced by age, sex, or type of allograft. A history of either myocardial infarction, congestive heart failure, or angina was present in 15 patients with 3-year survival of 50% (72% if not present, p <0.05). Histocompatibility testing did not impact on survival Serum sodium, potassium, calcium, phosphate, and calcium-phosphate product did not discern different survival groups. A hematocrit greater than 30% was present in 15 patients with 3-year survival of 43% (73% if not present, p <0.05). Greater than 10% antibody sensitization of the recipient resulted in a 3-year survival of 38% in eight patients (68% if not present, p <0.05). Radiologic evidence of cardiomegaly or congestive heart failure and standard electrocardiographic evidence for left ventricular hypertrophy or strain did not impact on survival. Echocardiographic measurements of left ventricular end-diastolic diameter, posterior wall thickness, or ejection fraction were also not predictive. Increased end-systolic diameter (10 patients, 30% 3-year survival versus 69%, p <0.05) and decreased velocity of circumferential fiber shortening (11 patients, 45% 3-year survival versus 71%, p <0.05) both appeared to be related to survival. Increased accuracy of prediction could be obtained by adding risk factors so that a history of coronary artery disease and increased end-systolic diameter predicted 3-year survival of 42% versus 82% if neither was present. In terms of graft survival, no clinical, radiographic, or electrocardiographic result yielded predictive information. Among the laboratory tests, only highly antibody-sensitized patients (eight patients, 0% 3-year survival versus 66% 3-year survival, p <0.001) showed different survival patterns. Echocardiographic elevated end-systolic diameter predicted a significantly (p <0.001) decreased graft survival (3-year survival 33% versus 63%). CONCLUSION: Preoperative prediction of patient and graft survival in diabetic renal transplantation may be enhanced by echocardiographic assessment of systolic load and function. For patients with normal systolic function, whose hematocrit is below 30%, with preformed antibodies less than 10%, renal transplantation has an excellent prognosis; invasive cardiac procedures are not likely required. Since these risk factors are likely additive, a high-risk group may be identified. These latter patients should undergo coronary angiography. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,JOHN COOK RENAL UNIT,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV CARDIOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV NEPHROL & TRANSPLANTAT,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,INST PREVENT CARDIOVASC DIS,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV ENDOCRINE HYPERTENS,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. MT AUBURN HOSP,DEPT MED,CAMBRIDGE,MA 02138. OI Weinrauch, Larry/0000-0003-1357-9528 NR 43 TC 19 Z9 19 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 JUL PY 1992 VL 93 IS 1 BP 19 EP 28 DI 10.1016/0002-9343(92)90675-2 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA JC655 UT WOS:A1992JC65500005 PM 1626568 ER PT J AU GEFFNER, DL HERSHMAN, JM AF GEFFNER, DL HERSHMAN, JM TI BETA-ADRENERGIC-BLOCKADE FOR THE TREATMENT OF HYPERTHYROIDISM SO AMERICAN JOURNAL OF MEDICINE LA English DT Review ID ADRENOCEPTOR BLOCKING-AGENTS; SERUM THYROID-HORMONES; HYPER-THYROIDISM; PARATHYROID-HORMONE; GRAVES-DISEASE; CLINICAL PHARMACOKINETICS; PREOPERATIVE TREATMENT; CALCIUM CONCENTRATION; THYROTOXIC PATIENTS; SURGICAL-TREATMENT AB PURPOSE: To review the clinical and biochemical effects of beta-adrenergic blocking drugs on hyperthyroidism. MATERIALs AND METHODS: Studies published since 1972 were identified through a computerized search of MEDLINE and extensive searching of the bibliographies of the articles identified. Based on an understanding of the differences in beta-blocker metabolism in euthyroid and hyperthyroid patients, we reviewed the differences in pharmacokinetics and metabolic and clinical outcomes during their use in hyperthyroidism, as reported in the articles reviewed. RESULTS: beta-Blockers have been used to modify the severity of the hyperadrenergic symptoms of hyperthyroidism for the past 20 years. The clinical efficacy of these agents is affected by hyperthyroid-induced alterations in their gastrointestinal absorption, hepatic metabolism, and renal excretion. The mechanisms whereby these clinical changes are effected is unknown. The agents differ in their beta-1 cardioselectivity, membrane-stabilizing activity, intrinsic sympathomimetic activity, and lipid solubility. They do not appear to alter synthesis or secretion of thyroid hormone by the thyroid gland. Their effects on thyroxine metabolism are contradictory. Decreased thyroxine to triiodothyronine conversion is caused by some, but not all, beta-blockers, and this appears to correlate with membrane-stabilizing activity. There does not appear to be any alteration in catecholamine sensitivity during beta-adrenergic blockade. CONCLUSIONS: The principal mechanism of action of beta-blockers in hyperthyroidism is to antagonize beta-receptor-mediated effects of catecholamines. beta-Blockers are effective in treating hypermetabolic symptoms in a variety of hyperthyroid states. Used alone, they offer significant symptomatic relief. They are also useful adjuvants to antithyroid medications, surgery, and radioactive iodide treatment in patients with Graves' disease and toxic nodular goiters. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,DIV ENDOCRINOL & METAB,LOS ANGELES,CA 90024. RP GEFFNER, DL (reprint author), CIGNA HLTH PLANS CALIF,DIV ENDOCRINOL & METAB,1711 W TEMPLE ST,LOS ANGELES,CA 90026, USA. NR 136 TC 48 Z9 48 U1 3 U2 4 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 JUL PY 1992 VL 93 IS 1 BP 61 EP 68 DI 10.1016/0002-9343(92)90681-Z PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA JC655 UT WOS:A1992JC65500011 PM 1352658 ER PT J AU CHIEN, D KWONG, KK GRESS, DR BUONANNO, FS BUXTON, RB ROSEN, BR AF CHIEN, D KWONG, KK GRESS, DR BUONANNO, FS BUXTON, RB ROSEN, BR TI MR DIFFUSION IMAGING OF CEREBRAL INFARCTION IN HUMANS SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE BRAIN, INFARCTION; MAGNETIC RESONANCE, DIFFUSION WEIGHTED SCANNING ID WATER; BRAIN; PERFUSION; MUSCLE; NMR AB Purpose: MR diffusion imaging was performed to investigate changes in water diffusion in patients with cerebral infarction. Methods: Diffusion maps of the apparent diffusion coefficient (ADC) were created to show local water mobility in the brain tissue in 15 patients. These ADC maps were compared with conventional T2-weighted images. Results: Distinct subregions with different water diffusions were detected, even when the infarcted area appeared homogeneous on a T2-weighted image. The results also show that stroke lesions of the same age can have very different water diffusions. A trend towards an increasing diffusion coefficient in a lesion during the first several days following an acute event was observed in a group of patients imaged at multiple timepoints. Conclusion: The measurement of diffusion coefficients in vivo now offers an opportunity for greater understanding of the biophysical changes that occur during the evolution of infarction in humans. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94121. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92037. VET ADM MED CTR,SAN FRANCISCO,CA 94121. FU NCI NIH HHS [R01-CA40303, T32-CA90362]; NHLBI NIH HHS [R01-HL39810] NR 24 TC 229 Z9 232 U1 0 U2 4 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD JUL-AUG PY 1992 VL 13 IS 4 BP 1097 EP 1102 PG 6 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA JD502 UT WOS:A1992JD50200009 PM 1636519 ER PT J AU LAWRENCE, WD WHITAKER, D SUGIMURA, H CUNHA, GR DICKERSIN, GR ROBBOY, SJ AF LAWRENCE, WD WHITAKER, D SUGIMURA, H CUNHA, GR DICKERSIN, GR ROBBOY, SJ TI AN ULTRASTRUCTURAL-STUDY OF THE DEVELOPING UROGENITAL TRACT IN EARLY HUMAN FETUSES SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE ULTRASTRUCTURE; FETUS; UROGENITAL; PARAMESONEPHRIC; MULLERIAN; MESONEPHRIC; WOLFFIAN ID REPRODUCTIVE-TRACT; MULLERIAN DUCT; MORPHOGENESIS AB OBJECTIVES: This study examines the gonoducts during the ambisexual stage of human fetal development to define their ultrastructural characteristics, including the origin and anatomic relationship of the mesonephric and paramesonephric ducts during gonoductal development. STUDY DESIGN: The reproductive tracts from five fetuses ranging in gestational age from 35 to 45 days were processed for ultrastructural examination. The developing mesonephric ducts, paramesonephric ducts, and their surrounding mesenchyme were studied with a Phillips 300 transmission electron microscope. RESULTS: The mesonephric ducts and paramesonephric ducts have distinctive cytoplasmic and cell surface ultrastructural characteristics, as well as different morphologic patterns of epithelial-mesenchymal interaction. Cephalad portions of mesonephric ducts and paramesonephric ducts are separated by mesenchyme, but more caudal aspects move progressively closer until they are juxtaposed but separate. CONCLUSIONS: Early mesonephric ducts and paramesonephric ducts may be distinguished because of their distinctive ultrastructural features; epithelial-mesenchymal interaction may be important in their differentiation and maintenance; both gonoducts retain their morphologic identity throughout, supporting their separate origins. C1 MIE UNIV,SCH MED,DEPT UROL,TSU,MIE 514,JAPAN. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,NEWARK,NJ 07103. WAYNE STATE UNIV,DETROIT MED CTR,DEPT PATHOL,DETROIT,MI 48201. HOSP UNIV PENN,PHILADELPHIA,PA 19104. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV CALIF SAN FRANCISCO,DEPT ANAT,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP LAWRENCE, WD (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,SCH MED,DEPT PATHOL,DIV ANAT PATHOL,DETROIT,MI 48201, USA. FU NCRR NIH HHS [SO-7RR05486-22]; NICHD NIH HHS [HD-17491] NR 9 TC 8 Z9 8 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD JUL PY 1992 VL 167 IS 1 BP 185 EP 193 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA JE313 UT WOS:A1992JE31300043 PM 1442924 ER PT J AU ZEIDEL, ML HAMMOND, T BOTELHO, B HARRIS, HW AF ZEIDEL, ML HAMMOND, T BOTELHO, B HARRIS, HW TI FUNCTIONAL AND STRUCTURAL CHARACTERIZATION OF ENDOSOMES FROM TOAD BLADDER EPITHELIAL-CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE VASOPRESSIN; WATER PERMEABILITY; KIDNEY; COLLECTING DUCT; ENDOCYTOSIS; TOAD URINARY BLADDER ID WATER PERMEABILITY RESPONSE; URINARY-BLADDER; ANTIDIURETIC-HORMONE; ENDOCYTIC VESICLES; MEMBRANE-VESICLES; TRANSPORT; CHANNELS; PROTON; FLOW; MARKERS AB Previous functional studies of toad bladder endosomes have been complicated by the presence of multiple endosome subpopulations each possessing different permeability characteristics. To identify and characterize both water channel-containing vesicles (WCV) and other endosome sub-populations, we combined flow cytometry, electron microscopy, stop-flow fluorometry, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Flow cytometry of endosomes identified distinct populations of fluorescein-labeled endosomes in bladders after removal of antidiuretic hormone (ADH) stimulation (ADH withdrawal). Centrifugation separated the larger fluorescein-labeled vesicles, sedimenting at lower speed (intermediate pellet, IP), from the smaller fluorescein-labeled vesicles, sedimenting at high speed (high-speed pellet, HSP). Permeability and structural studies of these subpopulations revealed the following. 1) IP endosomes labeled 10 min after ADH withdrawal (ADH IP) represented a highly purified population of WCV with high water permeability (P(f)) that exhibited a low-activation energy and sensitivity to organic mercurials. 2) IP endosomes from unstimulated bladders did not contain functional water channels. 3) HSP from either ADH withdrawal or unstimulated bladders exhibited low P(f) and acidified after addition of extravesicular ATP; moreover, protein compositions of purified HSP were distinct from those of purified IP. These results suggest that HSPs represent constitutive and not ADH-sensitive endosomes. 4) High permeability to protons (P(H+)) was seen in ADH IP endosomes but not the other fractions, providing strong evidence that the ADH water channel conducts protons. 5) Multivesicular bodies (MVB) exhibited low P(f) and P(H+), indicating that they do not possess functional water channels. 6) Because protein compositions of ADH IP and MVB were strikingly similar, it is possible that water channel proteins are transferred from the 10-min IP fraction to MVB and inactivated. C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. VET ADM MED CTR W ROXBURY,RES SERV,BOSTON,MA 02132. RP ZEIDEL, ML (reprint author), VET ADM MED CTR W ROXBURY,MED SERV,RENAL SECT,1400 VFW PKWY,BOSTON,MA 02132, USA. FU NIDDK NIH HHS [DK-38744, R01-DK-43955] NR 33 TC 22 Z9 22 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUL PY 1992 VL 263 IS 1 BP F62 EP F76 PN 2 PG 15 WC Physiology SC Physiology GA JF321 UT WOS:A1992JF32100082 PM 1636745 ER PT J AU SORENSEN, G GOLDBERG, R OCKENE, J KLAR, J TANNENBAUM, T LEMESHOW, S AF SORENSEN, G GOLDBERG, R OCKENE, J KLAR, J TANNENBAUM, T LEMESHOW, S TI HEAVY SMOKING AMONG A SAMPLE OF EMPLOYED WOMEN SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Article AB Understanding the phenomenon of heavy smoking among women and factors related to it is of considerable public health importance. Whereas lighter smokers have been more successful in their cessation attempts, the percentage of smokers who smoke more than 25 cigarettes per day has increased in recent years. This article examines the hypothesis that, compared to lighter smokers, female heavy smokers will report more responsiveness to internal cues to smoke, less interest in quitting, more difficulty with previous cessation attempts, more uncertainty about cessation strategies, and more concern about weight gain as a result of quitting. We collected data in 1984 through a self-administered survey completed by 874 women employed as nurses in acute care, chronic care, and home care nursing in Worcester, Massachusetts; we base our analyses on data collected from 158 light and moderate smokers and 67 heavy smokers. Our findings suggest that, compared to lighter smokers, heavy smokers may depend more on nicotine and are likely to respond to a broader array of cues to smoke, factors that appear to contribute to heavy smokers' greater difficulties with quitting. These female heavy smokers are just as likely as lighter smokers to have made previous attempts to quit and want to quit just as much. Major barriers to quitting for female heavy smokers include a lack of confidence in their ability to quit, insufficient tools to succeed with cessation attempts, and fear that weight gain will accompany quitting. RP SORENSEN, G (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 26 Z9 26 U1 1 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0749-3797 J9 AM J PREV MED JI Am. J. Prev. Med. PD JUL-AUG PY 1992 VL 8 IS 4 BP 207 EP 214 PG 8 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA JJ970 UT WOS:A1992JJ97000002 PM 1524856 ER PT J AU GREENE, R AF GREENE, R TI IMAGING THE RESPIRATORY SYSTEM IN THE 1ST FEW YEARS AFTER DISCOVERY OF THE X-RAY - CONTRIBUTIONS OF WILLIAMS,FRANCIS,H. SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article AB Imaging of the respiratory system developed with exceptional rapidity in North America during the spring of 1896, after Roentgen's discovery of X-rays in November 1895, largely because of the efforts of a unique physician, Francis H. Williams. With great zeal, this pioneer used fluoroscopy for early detection of tuberculosis and other life-threatening chest disorders. By the summer of 1896, he had accumulated more than 100 volumes containing tracings of clinical chest fluoroscopy. As a result of his extensive clinical experience, his dedication to patients' welfare, and his sense of scientific inquiry, several inventions and many landmark clinical observations were made in the first few years after the discovery of the X-ray. These included (1) the invention of a "densitometer" for standardized measurements of relative X-ray attenuation of the lung, (2) the invention of a "seehear" device to correlate auscultative findings and fluoroscopic observations, (3) the recognition that fluoroscopy was more accurate than percussion for estimating mediastinal displacement, (4) the discovery that clinically occult tuberculosis and congestive heart failure could be detected with fluoroscopy, (5) the documentation that unilateral chest disease caused decreased ipsilateral ventilatory compliance and increased contralateral ventilation, (6) the identification of the classical imaging characteristics of tuberculosis, pneumonia, pneumothorax, tension pneumothorax, pleural effusion, hydropneumothorax, emphysema, congestive heart failure, and air trapping. In April 1896, Dr. Williams described the "air bronchogram" in a radiograph of a patient with pneumonia. RP GREENE, R (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 23 TC 2 Z9 2 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 JUL PY 1992 VL 159 IS 1 BP 1 EP 7 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JA200 UT WOS:A1992JA20000001 PM 1609679 ER PT J AU DISLER, DG CHEW, FS AF DISLER, DG CHEW, FS TI GASTRIC LEIOMYOSARCOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 4 TC 4 Z9 5 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD JUL PY 1992 VL 159 IS 1 BP 58 EP 58 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JA200 UT WOS:A1992JA20000014 PM 1609721 ER PT J AU KADEL, NJ TEITZ, CC KRONMAL, RA AF KADEL, NJ TEITZ, CC KRONMAL, RA TI STRESS-FRACTURES IN BALLET DANCERS SO AMERICAN JOURNAL OF SPORTS MEDICINE LA English DT Article AB We surveyed 54 female dancers in two professional ballet companies. A total of 27 fractures were reported in 17 dancers. Metatarsal fractures were the most common (63%), followed by fractures of the tibia (22%) and spine (7%). Dancers who danced >5 hours per day were significantly more likely to have a stress fracture than those dancing <5 hours per day. Dancers in the stress fracture group also had a significantly longer duration of amenorrhea than those in the group with no stress fractures. No significant difference was found between the dancers who had stress fractures and those who did not with regard to any of the other variables examined. These data suggest that prolonged amenorrheic intervals and heavy training schedules may predispose ballet dancers to stress fractures. Of the 17 dancers with stress fractures, only 1 had neither of these risk factors. RP KADEL, NJ (reprint author), CARE OF LEWIS S,MASSACHUSETTS GEN HOSP,ORTHOPAED TEACHING OFF,GRAY 6,BOSTON,MA 02114, USA. NR 0 TC 78 Z9 79 U1 1 U2 10 PU AMER ORTHOPAEDIC SOC SPORT MED PI WALTHAM PA 230 CALVARY STREET, WALTHAM, MA 02154 SN 0363-5465 J9 AM J SPORT MED JI Am. J. Sports Med. PD JUL-AUG PY 1992 VL 20 IS 4 BP 445 EP 449 DI 10.1177/036354659202000414 PG 5 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA JE569 UT WOS:A1992JE56900014 PM 1357994 ER PT J AU BANKS, PM CHAN, J CLEARY, ML DELSOL, G DEWOLFPEETERS, C GATTER, K GROGAN, TM HARRIS, NL ISAACSON, PG JAFFE, ES MASON, D PILERI, S RALFKIAER, E STEIN, H WARNKE, RA AF BANKS, PM CHAN, J CLEARY, ML DELSOL, G DEWOLFPEETERS, C GATTER, K GROGAN, TM HARRIS, NL ISAACSON, PG JAFFE, ES MASON, D PILERI, S RALFKIAER, E STEIN, H WARNKE, RA TI MANTLE CELL LYMPHOMA - A PROPOSAL FOR UNIFICATION OF MORPHOLOGICAL, IMMUNOLOGICAL, AND MOLECULAR-DATA SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article ID INTERMEDIATE LYMPHOCYTIC LYMPHOMA; MALIGNANT-LYMPHOMAS; ZONE LYMPHOMA; MONOCLONAL-ANTIBODIES; CENTROCYTIC LYMPHOMA; GERMINAL CENTER; B-CELLS; DIFFERENTIATION; LEUKEMIA; MARKERS C1 NCI,HEMAPATHOL SECT,PATHOL LAB,BLDG 10,ROOM 2N 202,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. QUEEN ELIZABETH HOSP,INST PATHOL,KOWLOON,HONG KONG. STANFORD UNIV,MED CTR,SCH MED,DEPT PATHOL,EXPTL ONCOL LAB,STANFORD,CA 94305. CHU PURPAN,HOP TOULOUSE,CENT ANAT PATHOL,PURPAN,FRANCE. UNIV HOSP ST RAPHAEL,PATHOL ONTLEEDKUNDE 2,LOUVAIN,BELGIUM. UNIV OXFORD,JOHN RADCLIFFE HOSP,NUFFIELD DEPT PATHOL,OXFORD OX3 9DU,ENGLAND. UNIV ARIZONA,DEPT PATHOL,TUCSON,AZ 85721. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LAB,BOSTON,MA 02114. UNIV COLL & MIDDLESEX SCH MED,MIDDLESEX HOSP,DEPT HISTOPATHOL,LONDON,ENGLAND. UNIV OXFORD,JOHN RADCLIFFE HOSP,DEPT HISTOPATHOL,OXFORD OX3 9DU,ENGLAND. UNIV BOLOGNA,POLICLIN S ORSOLA,IST ANAT & ISTOL PATOL,I-40126 BOLOGNA,ITALY. UNIV HOSP HELLERUP,KAS GENTOFTE,INST PATHOL,HELLERUP,DENMARK. FREE UNIV BERLIN,KLINIKUM STEGLITZ,INST PATHOL,W-1000 BERLIN 45,GERMANY. STANFORD UNIV,MED CTR,SURG PATHOL LAB,STANFORD,CA 94305. NR 44 TC 395 Z9 401 U1 1 U2 12 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 JUL PY 1992 VL 16 IS 7 BP 637 EP 640 DI 10.1097/00000478-199207000-00001 PG 4 WC Pathology; Surgery SC Pathology; Surgery GA JA445 UT WOS:A1992JA44500001 PM 1530105 ER PT J AU HARRIS, NL AF HARRIS, NL TI CLONAL TERMINOLOGY - REPLY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter RP HARRIS, NL (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD JUL PY 1992 VL 16 IS 7 BP 730 EP 730 PG 1 WC Pathology; Surgery SC Pathology; Surgery GA JA445 UT WOS:A1992JA44500014 ER PT J AU SPIRO, MJ SPIRO, RG AF SPIRO, MJ SPIRO, RG TI MONOSACCHARIDE DETERMINATION OF GLYCOCONJUGATES BY REVERSE-PHASE HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY OF THEIR PHENYLTHIOCARBAMYL DERIVATIVES SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID AMINO-ACID-ANALYSIS; CARBOHYDRATE UNITS; SUGARS; PHENYLISOTHIOCYANATE; DERIVATIZATION; HYDRAZONES C1 JOSLIN DIABET CTR,ELLIOT P JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 36836, DK 17325] NR 22 TC 20 Z9 20 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD JUL PY 1992 VL 204 IS 1 BP 152 EP 157 DI 10.1016/0003-2697(92)90155-Z PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA JB524 UT WOS:A1992JB52400025 PM 1514682 ER PT J AU POLANER, DM KIMBALL, WR FRATACCI, MD WAIN, JC TORRES, A KACMAREK, RM ZAPOL, WM AF POLANER, DM KIMBALL, WR FRATACCI, MD WAIN, JC TORRES, A KACMAREK, RM ZAPOL, WM TI EFFECTS OF AMINOPHYLLINE ON REGIONAL DIAPHRAGMATIC SHORTENING AFTER THORACOTOMY IN THE AWAKE LAMB SO ANESTHESIOLOGY LA English DT Article DE PHARMACOLOGY, AMINOPHYLLINE; THEOPHYLLINE; MUSCLE, SKELETAL, DIAPHRAGM; SURGERY, THORACOTOMY, POSTOPERATIVE RESPIRATORY FUNCTION; VENTILATION ID UPPER ABDOMINAL-SURGERY; CONTRACTILITY; THEOPHYLLINE; STRENGTH; RAT AB Aminophylline has been reported to augment diaphragmatic contraction, although this remains a controversial finding. We studied the effect of aminophylline on regional diaphragmatic shortening, changes in transdiaphragmatic pressure (DELTA-P(di)), and integrated regional electromyographic (EMG) activity of the diaphragm (E(di)) after a right thoracotomy in nine lambs using sonomicrometry, esophageal and gastric balloons, and EMG. Sonomicrometer crystals and EMG leads were implanted into the costal and crural regions of the diaphragm through a right thoracotomy, and a tracheostomy was performed. The animals were studied while awake within 4 days after surgery. Fractional costal and crural diaphragmatic shortening was measured using the sonomicrometer; DELTA-P(di) was calculated from esophageal and gastric pressures. Respiratory variables were measured through the tracheostomy. Data were collected during quiet breathing and during CO2 rebreathing. After control measurements, aminophylline (10 mg/kg) was administered intravenously, producing a serum concentration of 17.7 +/- 1.5-mu-g/ml. Aminophylline did not augment shortening, increase DELTA-P(di), or overcome postoperative diaphragmatic inhibition acutely in the awake sheep after a right lateral thoracotomy. A small decrease of end-tidal CO2, from 5.2% to 4.9%, was measured at rest during aminophylline infusion, but E(di) was unchanged. Although during CO2 rebreathing diaphragmatic shortening increased, the addition of aminophylline did not further augment shortening. Our data in awake lambs suggest that aminophylline does not improve diaphragmatic contraction in the acute postoperative period. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. RP POLANER, DM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114, USA. OI Polaner, David/0000-0001-8716-6289 NR 26 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD JUL PY 1992 VL 77 IS 1 BP 93 EP 100 DI 10.1097/00000542-199207000-00014 PG 8 WC Anesthesiology SC Anesthesiology GA JB534 UT WOS:A1992JB53400014 PM 1610014 ER PT J AU HALLEK, M WANDERS, L STROHMEYER, S EMMERICH, B AF HALLEK, M WANDERS, L STROHMEYER, S EMMERICH, B TI THYMIDINE KINASE - A TUMOR-MARKER WITH PROGNOSTIC VALUE FOR NON-HODGKINS-LYMPHOMA AND A BROAD RANGE OF POTENTIAL CLINICAL-APPLICATIONS SO ANNALS OF HEMATOLOGY LA English DT Review DE THYMIDINE KINASE; TUMOR MARKER; PROGNOSIS; NON-HODGKINS LYMPHOMA; VIRAL INFECTION ID SERUM DEOXYTHYMIDINE KINASE; CHRONIC LYMPHOCYTIC-LEUKEMIA; CELL LUNG-CANCER; MULTIVARIATE-ANALYSIS; BIOCHEMICAL MARKERS; MULTIPLE-MYELOMA; VIRUS-INFECTION; BREAST-CANCER; BRAIN-TUMORS; STAGE AB Thymidine kinase (TK) is a cellular enzyme which is involved in a "salvage pathway" of DNA synthesis. It is activated in the G1/S phase of the cell cycle, and its activity has been shown to correlate with the proliferative activity of tumor cells. Additionally, certain viruses are able to induce cellular TK production and activity. Clinical studies have reported elevated serum TK levels in a variety of neoplasias. The majority of these studies concerned hematologic malignancies. TK seems to be a useful marker in non-Hodgkin's lymphoma, where it correlates with clinical staging and provides significant prognostic information on (progression-free) survival. Preliminary results in acute myeloid leukemia indicate that pretreatment serum TK values may predict the response to the first induction chemotherapy. Moreover, serum TK appears to have some clinical value in such solid tumors as prostate cancer, breast cancer, and small-cell lung cancer, whereas it is not a reliable marker of non-small-cell lung cancer and brain tumors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP HALLEK, M (reprint author), UNIV MUNICH,MED KLIN,KLINIKUM INNENSTADT,ZIEMSSENSTR 1,W-8000 MUNICH 2,GERMANY. NR 55 TC 81 Z9 81 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0939-5555 J9 ANN HEMATOL JI Ann. Hematol. PD JUL PY 1992 VL 65 IS 1 BP 1 EP 5 DI 10.1007/BF01715117 PG 5 WC Hematology SC Hematology GA JH110 UT WOS:A1992JH11000001 PM 1643153 ER PT J AU DELZOPPO, GJ POECK, K PESSIN, MS WOLPERT, SM FURLAN, AJ FERBERT, A ALBERTS, MJ ZIVIN, JA WECHSLER, L BUSSE, O GREENLEE, R BRASS, L MOHR, JP FELDMANN, E HACKE, W KASE, CS BILLER, J GRESS, D OTIS, SM AF DELZOPPO, GJ POECK, K PESSIN, MS WOLPERT, SM FURLAN, AJ FERBERT, A ALBERTS, MJ ZIVIN, JA WECHSLER, L BUSSE, O GREENLEE, R BRASS, L MOHR, JP FELDMANN, E HACKE, W KASE, CS BILLER, J GRESS, D OTIS, SM TI RECOMBINANT TISSUE PLASMINOGEN-ACTIVATOR IN ACUTE THROMBOTIC AND EMBOLIC STROKE SO ANNALS OF NEUROLOGY LA English DT Article ID HEMORRHAGIC INFARCTION; THROMBOLYTIC THERAPY; CEREBRAL INFARCTION; OCCLUSION; CT; ARTERIES AB An open angiography-based, dose rate escalation study on the effect of intravenous infusion of recombinant tissue plasminogen activator (rt-PA) on cerebral arterial recanalization in patients with acute focal cerebral ischemia was performed at 16 centers. Arterial occlusions consistent with acute ischemia in the carotid or vertebrobasilar territory in the absence of detectable intracerebral hemorrhage were prerequisites for treatment. After the 60-minute rt-PA infusion, arterial perfusion was assessed by repeat angiography and computed tomography scans were performed at 24 hours to assess hemorrhagic transformation. Of 139 patients with symptoms of focal ischemia, 80.6% (112) had complete occlusion of the primary vessel at a mean of 5.4 +/- 1.7 hours after symptom onset. No dose rate response of cerebral arterial recanalization was observed in 93 patients who completed the rt-PA infusion. Middle cerebral artery division (M2) and branch (M3) occlusions were more likely to undergo recanalization by 60 minutes than were internal carotid artery occlusions. Hemorrhagic infarction occurred in 20.2% and parenchymatous hematoma in 10.6% of patients over all dose rates, while neurological worsening accompanied hemorrhagic transformation (hemorrhagic infarction and parenchymatous hematoma) in 9.6% of patients. All findings were within prospective safety guidelines. No dose rate correlation with hemorrhagic infarction, parenchymatous hematoma, or both was seen. Hemorrhagic transformation occurred significantly more frequently in patients receiving treatment at least 6 hours after symptom onset. No relationship between hemorrhagic transformation and recanalization was observed. This study indicates that site of occlusion, time to recanalization, and time to treatment are important variables in acute stroke intervention with this agent. C1 RWTH KLINIKUM AACHEN, AACHEN, GERMANY. TUFTS UNIV, NEW ENGLAND MED CTR, BOSTON, MA 02111 USA. CLEVELAND CLIN EDUC FDN, CLEVELAND, OH 44106 USA. DUKE UNIV, MED CTR, DURHAM, NC 27710 USA. UNIV CALIF SAN DIEGO, SAN DIEGO, CA 92103 USA. UNIV PITTSBURGH, PITTSBURGH, PA 15260 USA. KLINIKUM I MINDEN, MINDEN, GERMANY. UNIV TEXAS, SW MED CTR, DALLAS, TX 75230 USA. YALE UNIV, SCH MED, NEW HAVEN, CT 06510 USA. COLUMBIA UNIV, INST NEUROL, NEW YORK, NY 10027 USA. RHODE ISL HOSP, PROVIDENCE, RI 02902 USA. UNIV HEIDELBERG, W-6900 HEIDELBERG, GERMANY. BOSTON UNIV, MED CTR, BOSTON, MA 02215 USA. UNIV IOWA, COLL MED, IOWA CITY, IA 52242 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. RP DELZOPPO, GJ (reprint author), SCRIPPS RES INST, DEPT MOLEC & EXPTL MED, 10666 N TORREY PINES RD, LA JOLLA, CA 92037 USA. NR 32 TC 646 Z9 648 U1 1 U2 8 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JUL PY 1992 VL 32 IS 1 BP 78 EP 86 DI 10.1002/ana.410320113 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA JK416 UT WOS:A1992JK41600011 PM 1642475 ER PT J AU CLARY, RA CUNNINGHAM, MJ EAVEY, RD AF CLARY, RA CUNNINGHAM, MJ EAVEY, RD TI ORBITAL COMPLICATIONS OF ACUTE SINUSITIS - COMPARISON OF COMPUTED-TOMOGRAPHY SCAN AND SURGICAL FINDINGS SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE COMPUTED TOMOGRAPHY; ORBITAL ABSCESS; ORBITAL CELLULITIS; PARANASAL SINUSITIS ID MANAGEMENT; CELLULITIS; ABSCESS AB The accuracy of computed tomography (CT) in distinguishing an abscess from cellulitis in children who present with orbital manifestations of paranasal sinus infection remains in question. In this 10-year retrospective study, CT results are compared with surgical findings in 19 patients with orbital complications who underwent surgical exploration within 24 hours of their CT scans. Fifteen of the 19 CT scan interpretations indicated abscesses that were verified intraoperatively. Two patients had negative surgical explorations despite CT interpretations predicting abscesses. An abscess was also surgically documented in 1 of 2 patients whose preoperative scans indicated cellulitis alone. We conclude that the correlation between radiologic and operative findings in 16 of these 19 cases, although not absolute, does substantiate the use of CT scanning as a therapeutic guide in children presenting with orbital disease secondary to paranasal sinusitis. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. NR 11 TC 25 Z9 31 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 JUL PY 1992 VL 101 IS 7 BP 598 EP 600 PG 3 WC Otorhinolaryngology SC Otorhinolaryngology GA JD339 UT WOS:A1992JD33900010 PM 1626907 ER PT J AU GRILLO, HC SUEN, HC MATHISEN, DJ WAIN, JC PAIROLERO, PC AF GRILLO, HC SUEN, HC MATHISEN, DJ WAIN, JC PAIROLERO, PC TI RESECTIONAL MANAGEMENT OF THYROID-CARCINOMA INVADING THE AIRWAY SO ANNALS OF THORACIC SURGERY LA English DT Article ID TRACHEA AB Fifty-two patients had thyroid carcinoma invading the airway. Thirty-four underwent resection; 18 were male and 16 female. Age ranged from 17 to 79 years. Twenty-seven had resection with airway reconstruction (1 wedge excision, 10 sleeve tracheal resections, 6 tracheal resections with a portion of the cricoid cartilage, and 10 complex laryngotracheoplastic resections). Seven required cervicomediastinal exenteration with mediastinal tracheostomy; 3 of these had esophagectomy with colon interposition. Nineteen tumors were papillary, 6 follicular, 4 mixed papillary and follicular, 1 squamous, 2 undifferentiated giant cell, 1 anaplastic spindle cell carcinoma, and 1 carcinosarcoma. Three postoperative deaths occurred. Thirteen of the 31 survivors died of cancer from 1/4 to 10 1/4 years postoperatively (average, 4.4 years). Four died of other diseases. Fourteen are alive from 1/12 to 14 1/3 years postoperatively (average, 5.3 years). Only 2 patients had airway recurrence. Resection of the airway invaded by thyroid malignancy in the absence of extensive metastases offers prolonged palliation, avoids suffocation due to bleeding or obstruction, and may produce cure. Airway reconstruction should be performed whenever technically feasible. C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP GRILLO, HC (reprint author), MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,BOSTON,MA 02114, USA. NR 20 TC 72 Z9 75 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 JUL PY 1992 VL 54 IS 1 BP 3 EP 10 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA JA809 UT WOS:A1992JA80900002 PM 1610250 ER PT J AU ERON, JJ JOHNSON, VA MERRILL, DP CHOU, TC HIRSCH, MS AF ERON, JJ JOHNSON, VA MERRILL, DP CHOU, TC HIRSCH, MS TI SYNERGISTIC INHIBITION OF REPLICATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1, INCLUDING THAT OF A ZIDOVUDINE-RESISTANT ISOLATE, BY ZIDOVUDINE AND 2',3'-DIDEOXYCYTIDINE INVITRO SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; PHASE-I TRIAL; 2',3'-DIDEOXYINOSINE DDI; DOUBLE-BLIND; AZT; 2',3'-DIDEOXYNUCLEOSIDES; AZIDOTHYMIDINE; INFECTION; THERAPY AB The combination of zidovudine (AZT) and 2',3'-dideoxycytidine synergistically inhibits human immunodeficiency virus type 1 (HIV-1) replication in vitro with AZT-sensitive and AZT-resistant clinical isolates and HIV-1IIIB. Synergy was,determined by the median-effect principle and isobologram techniques. Cytotoxicity of the agents was not observed. Clinical trials are ongoing to define the combination's role in HIV-1 therapy. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MEM SLOAN KETTERING CANC CTR,BIOCHEM PHARMACOL LAB,NEW YORK,NY 10021. RI Chou, Ting-Chao/B-4111-2009 OI Chou, Ting-Chao/0000-0002-3340-1594 FU NCI NIH HHS [CA12464, CA35020]; NIAID NIH HHS [T32AIO7061] NR 36 TC 61 Z9 61 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 JUL PY 1992 VL 36 IS 7 BP 1559 EP 1562 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA JC894 UT WOS:A1992JC89400036 PM 1324648 ER PT J AU ROBINSON, JK SALASCHE, SJ AF ROBINSON, JK SALASCHE, SJ TI ISOTRETINOIN DOES NOT PREVENT BASAL-CELL CARCINOMA SO ARCHIVES OF DERMATOLOGY LA English DT Editorial Material ID VITAMIN-A; SUBSEQUENT RISK; BETA-CAROTENE; CANCER; TUMORS; ACID C1 MASSACHUSETTS GEN HOSP,MED CLIN,BOSTON,MA 02114. RP ROBINSON, JK (reprint author), NORTHWESTERN UNIV,SCH MED,DEPT DERMATOL,303 E CHICAGO AVE,TARRY 4-767,CHICAGO,IL 60611, USA. NR 13 TC 11 Z9 11 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD JUL PY 1992 VL 128 IS 7 BP 975 EP 976 DI 10.1001/archderm.128.7.975 PG 2 WC Dermatology SC Dermatology GA JD499 UT WOS:A1992JD49900016 PM 1626967 ER PT J AU WIRSHING, WC VANPUTTEN, T ROSENBERG, J MARDER, S AMES, D HICKSGRAY, T AF WIRSHING, WC VANPUTTEN, T ROSENBERG, J MARDER, S AMES, D HICKSGRAY, T TI FLUOXETINE, AKATHISIA, AND SUICIDALITY - IS THERE A CAUSAL CONNECTION SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter ID DRUGS RP WIRSHING, WC (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 7 TC 73 Z9 73 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUL PY 1992 VL 49 IS 7 BP 580 EP 581 PG 2 WC Psychiatry SC Psychiatry GA JC527 UT WOS:A1992JC52700010 PM 1627050 ER PT J AU JENIKE, MA BAER, L AF JENIKE, MA BAER, L TI PSYCHOSURGICAL TREATMENT OF OBSESSIVE-COMPULSIVE DISORDER - REPLY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter ID GLUCOSE METABOLIC RATES RP JENIKE, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,FRUIT ST,BOSTON,MA 02114, USA. NR 6 TC 1 Z9 1 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUL PY 1992 VL 49 IS 7 BP 583 EP 584 PG 2 WC Psychiatry SC Psychiatry GA JC527 UT WOS:A1992JC52700013 ER PT J AU HELLER, H FROMOWITZ, F FUHRER, J AF HELLER, H FROMOWITZ, F FUHRER, J TI LUETIC CERVICAL ADENITIS IN PATIENTS WITH HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Note ID SECONDARY SYPHILIS; HIV INFECTION AB The clinical course of syphilis may be altered in some patients with human immunodeficiency virus type 1 infection. We report two cases of syphilis in patients with human immunodeficiency virus type 1 infection who presented with marked unilateral anterior cervical adenopathy after engaging in oral-genital sex. Neither of the patients had evidence of oropharyngeal chancres. one patient developed a cutaneous rash of secondary syphilis soon after the cervical adenopathy developed. Both patients responded well to antibiotic therapy. C1 SUNY STONY BROOK,DEPT PATHOL,STONY BROOK,NY 11794. SUNY STONY BROOK,DEPT MED,DIV INFECT DIS,STONY BROOK,NY 11794. RP HELLER, H (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,GRAY 5,FRUIT ST,BOSTON,MA 02114, USA. NR 18 TC 9 Z9 9 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0886-4470 J9 ARCH OTOLARYNGOL JI Arch. Otolaryngol. Head Neck Surg. PD JUL PY 1992 VL 118 IS 7 BP 757 EP 758 PG 2 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA JC547 UT WOS:A1992JC54700016 PM 1627299 ER PT J AU GINSBURG, KS WRIGHT, EA LARSON, MG FOSSEL, AH ALBERT, M SCHUR, PH LIANG, MH AF GINSBURG, KS WRIGHT, EA LARSON, MG FOSSEL, AH ALBERT, M SCHUR, PH LIANG, MH TI A CONTROLLED-STUDY OF THE PREVALENCE OF COGNITIVE DYSFUNCTION IN RANDOMLY SELECTED PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS SO ARTHRITIS AND RHEUMATISM LA English DT Article ID NEUROPSYCHIATRIC MANIFESTATIONS; CLASSIFICATION; IMPAIRMENT; CRITERIA; EXPOSURE; DISEASE AB Objective. To investigate the prevalence of cognitive dysfunction in randomly selected patients with systemic lupus erythematosus (SLE). Methods. Randomly selected, ambulatory patients with SLE (n = 49) or with rheumatoid arthritis (RA) (n = 40) completed neuropsychological tests. These included Associate Learning, Switching Attention, Continuous Performance, Associate Recall, Hand-Eye Coordination, Pattern Comparison, Pattern Memory, the Stroop Color and Word Test, and the Symptoms Checklist-90R. Results were evaluated by multiple linear regression analysis. Results. SLE patients had poorer performance than RA patients on the test of attention (P = 0.002) and tests of visuospatial ability (P = 0.03 and P = 0.04), independent of age, education, or steroid use. The conservative level of statistical significance, adjusting for multiple comparisons, was 0.005. SLE patients reported more symptoms of cognitive difficulty. Conclusion. Cognitive dysfunction is common in ambulatory SLE patients as measured by standardized tests and is a cause of distress and impaired functioning. Self-reported cognitive difficulty appears to correlate with objective performance. C1 ROBERT B BRIGHAM MULTIPURPOSE ARTHRIT CTR,75 FRANCIS ST,PBB-B2,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL IMMUNOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NCRR NIH HHS [RR-05951]; NIAMS NIH HHS [AR-07530, AR-36308] NR 24 TC 110 Z9 110 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD JUL PY 1992 VL 35 IS 7 BP 776 EP 782 DI 10.1002/art.1780350711 PG 7 WC Rheumatology SC Rheumatology GA JC545 UT WOS:A1992JC54500010 PM 1622416 ER PT J AU SEIDEN, MV ELIAS, A AYASH, L HUNT, M EDER, JP SCHNIPPER, LE FREI, E ANTMAN, KH AF SEIDEN, MV ELIAS, A AYASH, L HUNT, M EDER, JP SCHNIPPER, LE FREI, E ANTMAN, KH TI PULMONARY TOXICITY ASSOCIATED WITH HIGH-DOSE CHEMOTHERAPY IN THE TREATMENT OF SOLID TUMORS WITH AUTOLOGOUS MARROW TRANSPLANT - AN ANALYSIS OF 4 CHEMOTHERAPY REGIMENS SO BONE MARROW TRANSPLANTATION LA English DT Article ID COLONY-STIMULATING FACTOR; PHASE-I-II; TOTAL-BODY IRRADIATION; NON-HODGKINS-LYMPHOMA; BREAST-CANCER; CYCLOPHOSPHAMIDE; SUPPORT; COMPLICATIONS; LEUKEMIA; THIOTEPA AB We retrospectively reviewed the pulmonary toxicity of six high dose chemotherapy protocols using four chemotherapy regimens in the treatment of solid tumors. All protocols used either high dose cyclophosphamide or ifosfamide in combination with one to three additional chemotherapeutic agents. In each protocol autologous bone marrow was reinfused post chemotherapy to shorten the period of severe myelosuppression. Of 178 patients there were 20 cases of fatal or life-threatening pulmonary toxicity including nine cases of pneumonia, nine cases of interstitial pneumonitis and two cases of pulmonary hemorrhage. Pulmonary function tests revealed modest changes in FEV1 and DLCO in the majority of patients, although 24 patients had more dramatic changes in DLCO suggesting interstitial damage. Significant decrements in FEV1 were seen in the BCNU containing regimen. Statistically significant or nearly significant decreases in DLCO were seen after all cyclophosphamide containing regimens. A regimen containing ifosfamide, carboplatin, and etoposide had minimal associated pulmonary toxicity. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT STAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CANC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. FU NCI NIH HHS [P01CA-38493] NR 34 TC 37 Z9 37 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD JUL PY 1992 VL 10 IS 1 BP 57 EP 63 PG 7 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA JJ602 UT WOS:A1992JJ60200009 PM 1515880 ER PT J AU MALT, RA AF MALT, RA TI REBOUND TENDERNESS TEST SO BRITISH JOURNAL OF SURGERY LA English DT Letter RP MALT, RA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1323 J9 BRIT J SURG JI Br. J. Surg. PD JUL PY 1992 VL 79 IS 7 BP 712 EP 713 DI 10.1002/bjs.1800790749 PG 2 WC Surgery SC Surgery GA JD860 UT WOS:A1992JD86000042 ER PT J AU AOBA, T SHIMODA, S SHIMOKAWA, H INAGE, T AF AOBA, T SHIMODA, S SHIMOKAWA, H INAGE, T TI COMMON EPITOPES OF MAMMALIAN AMELOGENINS AT THE C-TERMINUS AND POSSIBLE FUNCTIONAL ROLES OF THE CORRESPONDING DOMAIN IN ENAMEL MINERALIZATION SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE AMELOGENESIS; PIG, COW, RAT, RABBIT AMELOGENINS; EPITOPES AT THE C-TERMINUS; ADSORPTION; ENAMEL MINERALIZATION ID AMINO-ACID-SEQUENCE; MATRIX PROTEINS; BIOCHEMICAL-CHARACTERIZATION; PORCINE-AMELOGENINS; SECRETORY ENAMEL; COMPONENTS; ANTIBODIES AB The present studies were undertaken to investigate the presence of common epitopes of mammalian amelogenins at the C-terminus and the possible functional importance of the conserved C-terminal domain in enamel mineralization during mammalian amelogenesis. Enamel proteins, including the intact amelogenins and their degraded polypeptides, were isolated from the secretory enamel of pig, cow, rat, and rabbit incisors. Rabbit and rat antipeptide sera, as well as rat anti-25 kD and 20 kD pig amelogenin sera, were used to identify the amelogenins among the isolated matrix proteins of each of the animal species. The antipeptide sera were developed previously (Aoba et al. [19]) using as immunogens the two synthetic peptides, C13 and C25, which correspond to the last 12 (plus Cys for KLH-conjugation) and 25 amino acid residues of pig intact amelogenin, respectively. Reactivity of the enamel proteins with each antiserum was examined by Western blot analysis. The results of immunoblotting showed that a few enamel matrix proteins in each of the mammalian species were recognized by the anti-C13 serum, specifically, pig amelogenin at 25 kD (and trace components at 27, 22, and 18 kD), cow amelogenin at 28 kD (trace components at 26, 22, 19, and 14 kD), rat amelogenins at 28 and 26 kD (and a trace component at 20 kD), and rabbit amelogenins at 24 and 21 kD (and a trace at 13 kD). The anti-C25 serum reacted additionally with pig amelogenin at 23 kD, cow amelogenin at 27 kD (a major matrix constituent), and rabbit protein at 19 kD. The anti-pig 20 kD amelogenin (lacking the last 25 amino acid residues at the C-terminus) serum reacted with a large number of pig, cow, and rat amelogenins but, interestingly, with none of the rabbit enamel proteins. Probing of rat enamel proteins with Maclura pomifera lectin showed the heterogeneity of glycosylation of rat amelogenins, particularly between the 28 and 26 kD intact amelogenins. In parallel adsorption studies, part of the enamel protein samples isolated from each of the species was used as adsorbates to investigate the selective adsorption of amelogenins onto hydroxyapatite. Immunoblot analysis of the proteins adsorbed onto the crystals revealed that the mammalian amelogenins having the common epitopes at the C-terminus, in general, adsorb preferentially onto hydroxyapatite. The adsorption affinity of the degraded amelogenins decreased significantly with the loss of reactivity toward the anti-C13 serum. The overall results support the contention that the intact mammalian amelogenins, including rat and rabbit amelogenins, share common epitopes at the C-terminus and that the conserved C-terminal domain plays an important role in setting the molecular structures of the intact amelogenins so as to facilitate the protein-enamel mineral interaction. C1 TSURUMI UNIV,SCH DENT,YOKOHAMA 230,JAPAN. TOKYO MED & DENT UNIV,SCH DENT,TOKYO 113,JAPAN. NIHON UNIV,SCH DENT,TOKYO 101,JAPAN. RP AOBA, T (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE07623, DE08670] NR 36 TC 20 Z9 20 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD JUL PY 1992 VL 51 IS 1 BP 85 EP 91 DI 10.1007/BF00296224 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ626 UT WOS:A1992HZ62600019 PM 1382821 ER PT J AU BILLETT, AL CARLS, A GELBER, RD SALLAN, SE AF BILLETT, AL CARLS, A GELBER, RD SALLAN, SE TI ALLERGIC REACTIONS TO ERWINIA ASPARAGINASE IN CHILDREN WITH ACUTE LYMPHOBLASTIC-LEUKEMIA WHO HAD PREVIOUS ALLERGIC REACTIONS TO ESCHERICHIA-COLI ASPARAGINASE SO CANCER LA English DT Article DE CHILDHOOD ACUTE LYMPHOBLASTIC LEUKEMIA; ASPARAGINASE; ALLERGIC REACTION; TOXIC EFFECTS ID INTENSIVE ASPARAGINASE; INDUCTION; TOXICITY AB Background. Escherichia coli asparaginase is an active antileukemia agent in the treatment of childhood acute lymphoblastic leukemia. Allergic reactions occurred in 31 of 125 patients (24.8%) treated with weekly high-dose (25,000 IU/m2) intramuscular E. coli asparaginase and necessitated discontinuation of the drug. Methods. The authors evaluated the toxic effects of Erwinia asparaginase in the 31 children who had allergic reactions to the E. coli preparation. Results. Subsequent allergic reactions to Erwinia asparaginase occurred in 7 of the 31 children (22.6%). In contrast to previous reports with intravenous administration, most allergic reactions to both asparaginase preparations were characterized by mild urticaria that responded to use of diphenhydramine; none of the reactions was life-threatening. Conclusions. In summary, the authors found Erwinia asparaginase to be an acceptable substitute for E. coli asparaginase for most children who had allergic reactions. Through the use of both E. coli and Erwinia asparaginase, 94% of children could receive their intended asparaginase. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP BILLETT, AL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 34183] NR 26 TC 52 Z9 53 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 JUL 1 PY 1992 VL 70 IS 1 BP 201 EP 206 DI 10.1002/1097-0142(19920701)70:1<201::AID-CNCR2820700131>3.0.CO;2-M PG 6 WC Oncology SC Oncology GA HZ758 UT WOS:A1992HZ75800030 PM 1606543 ER PT J AU COCKETT, ATK BARRY, MJ HOLTGREWE, HL SIHELNICK, S WILLIAMS, R MCCONNELL, J AF COCKETT, ATK BARRY, MJ HOLTGREWE, HL SIHELNICK, S WILLIAMS, R MCCONNELL, J TI INDICATIONS FOR TREATMENT OF BENIGN PROSTATIC HYPERPLASIA - THE AMERICAN UROLOGICAL ASSOCIATION STUDY SO CANCER LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON PROSTATIC CANCER AND HYPERPLASIA CY OCT 26-29, 1991 CL SEA ISLAND, GA SP AMER CANC SOC, AMER UROL ASSOC DE PROSTATE ENLARGEMENT; BENIGN PROSTATIC HYPERPLASIA ID PROSTATECTOMY; MORTALITY AB Background. In 1990, a pilot study was begun that evaluated benign prostatic hyperplasia [BPH] at five clinical institutions. Data management and coordination of this study was performed at the Medical Practices Evaluation Center at Massachusetts General Hospital. Because of decreased patient enrollment, one institution was dropped. This was a randomized, prospective, clinical study that provided an initial overview of the trial and a rationale for the project. Methods. Patients with clinically significant signs and symptoms of BPH were enrolled in this study. A symptom index consisting of seven items was used to document patient complaints of prostatic enlargement. Prostate size was determined using ultrasonography. Uroflowmetry [peak flow and mean flow] and residual urine volumes were documented. Abdominal ultrasonography was performed to rule out the presence of a dilated upper urinary tract. Cystoscopy was completed to determine the extent of prostatic and bladder neck obstruction. Trabeculations or cellules in the bladder, if present, were also documented. Conclusions. Preliminary results were obtained. The operative and nonoperative options depending on prostate size are shown in the figures of this article. The use of an interactive video disc has been beneficial in explaining the risks and benefits of each treatment option applicable to the patient in this randomized, controlled study. C1 UNIV IOWA,DEPT UROL,IOWA CITY,IA 52242. UNIV ROCHESTER,ROCHESTER,NY 14627. AMER UROL ASSOC,BALTIMORE,MD. WALTER REED ARMY HOSP & MED CTR,WASHINGTON,DC. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV TEXAS,SW UNIV,DIV UROL,DALLAS,TX 75230. NR 6 TC 25 Z9 25 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JUL 1 PY 1992 VL 70 IS 1 SU S BP 280 EP 283 DI 10.1002/1097-0142(19920701)70:1+<280::AID-CNCR2820701315>3.0.CO;2-E PG 4 WC Oncology SC Oncology GA JA174 UT WOS:A1992JA17400013 PM 1376197 ER PT J AU HURWITZ, E ADLER, R SHOUVAL, D TAKAHASHI, H WANDS, JR SELA, M AF HURWITZ, E ADLER, R SHOUVAL, D TAKAHASHI, H WANDS, JR SELA, M TI IMMUNOTARGETING OF DAUNOMYCIN TO LOCALIZED AND METASTATIC HUMAN COLON ADENOCARCINOMA IN ATHYMIC MICE SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Article DE DRUG IMMUNOTARGETING; METASTASES; COLON CARCINOMA; MONOCLONAL ANTIBODY ID MONOCLONAL-ANTIBODY; NUDE-MICE; FREE DRUG; TUMOR; INVIVO; DOXORUBICIN; ADRIAMYCIN; CARCINOMAS; ANTIGEN AB A monoclonal antibody (designated SF25), which recognizes a protein antigen expressed on a large number of human colon carcinomas, was used for drug targeting. Daunomycin-antibody conjugates were prepared by two previously described procedures. In one, the drug was bound to the antibody through a spacer of small molecular mass (cis-aconitic acid), while in the other a dextran bridge served as the link between drug and antibody. High substitution rates of drug to antibody were obtained using the latter binding procedure. Both conjugates were tested in vitro against two human colon carcinoma cell lines, LS180 and KM-12. The efficacy of a daunomycin-dextran-SF25 antibody conjugate was tested against colon carcinoma LS180 tumors transplanted at different sites into athymic mice. The specific conjugate was significantly more inhibitory to a subcutaneous tumor growth than its components or their mixture. SF25 antibody alone showed antitumoral effects against all three forms of transplanted tumor tested, namely, local, metastatic or intrahepatic, whereas daunomycin, on its own, was effective only against the subcutaneous tumor. Binding of daunomycin to dextran partially improved its inhibitory activity against the metastatic tumor. The conjugate, daunomycin-dextran-SF25 antibody reduced the number of metastatic foci, increased the survival rate and delayed death. Yet against lymph node metastases it was not significantly better than a mixture of both constituents. However, results obtained with an intrahepatic tumor, a model that mimics the natural progression of the disease, resembled those described with the subcutaneous tumor. Daunomycin-dextran-SF25 antibody was significantly more effective than all components separately and than a mixture of drug and antibody, provided a highly drug-substituted conjugate was used. C1 HADASSAH UNIV HOSP,DEPT MED,LIVER UNIT,IL-91120 JERUSALEM,ISRAEL. MASSACHUSETTS GEN HOSP,CTR MOLEC HEPATOL,BOSTON,MA 02114. RP HURWITZ, E (reprint author), WEIZMANN INST SCI,DEPT CHEM IMMUNOL,IL-76100 REHOVOT,ISRAEL. NR 29 TC 13 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD JUL PY 1992 VL 35 IS 3 BP 186 EP 192 DI 10.1007/BF01756186 PG 7 WC Oncology; Immunology SC Oncology; Immunology GA JF450 UT WOS:A1992JF45000006 PM 1638555 ER PT J AU SPEEG, KV DELEON, C MCGUIRE, WL AF SPEEG, KV DELEON, C MCGUIRE, WL TI UPTAKE OF THE NONCYTOTOXIC TRANSPORT PROBE PROCAINAMIDE IN THE CHINESE-HAMSTER OVARY MODEL OF MULTIDRUG RESISTANCE SO CANCER RESEARCH LA English DT Article ID MULTIPLE-DRUG RESISTANCE; CELL-LINES; P388 LEUKEMIA; CYTOSOLIC PH; TUMOR-CELLS; VINCRISTINE; ADRIAMYCIN; VERAPAMIL; TISSUES; ACCUMULATION AB Many of the cytotoxic substrates of the multidrug transporter are organic cations. Cimetidine, procainamide, and tetraethylammonium bromide were used in a Chinese hamster ovary model of multidrug resistance, to study handling of noncytotoxic cationic transport probes. Cimetidine and procainamide, but not tetraethylammonium, accumulated to a greater extent (5-fold) in the sensitive CHOAUXB1 (AB) cell line than in the resistant CH(R)C5 (C5) cell line. Accumulation of both cimetidine and procainamide was significantly increased by verapamil in C5 but not AB. Procainamide accumulation in both AB and C5 was temperature dependent and occurred by passive diffusion. Diltiazem, nifedipine, rifampin, tamoxifen, rhodamine, and ethidium also increased procainamide accumulation in C5 but not AB. Azide in glucose-free medium increased procainamide accumulation in C5, and this was reversed when glucose, but not 3-O-methylglucose, was added. Procainamide efflux rates were similar in AB and C5 and not affected by verapamil or azide. The initial rate of procainamide uptake was higher in AB than in C5, and both verapamil and azide increased the initial rate of procainamide uptake in C5. Thus, differences in accumulation of the noncytotoxic transport probe procainamide in the colchicine-sensitive and colchicine-resistant components of the Chinese hamster ovary cell line mimic the accumulation of known cytotoxic substrates for the multidrug transporter, such as colchicine, vinblastine, and doxorubicin. The differential accumulation of procainamide is due to differences in rates of drug influx, rather than efflux. Since procainamide influx is passive and decreased accumulation in the resistant line appears to parallel M(r) 170,000 glycoprotein presence and activity, we would speculate that decreased procainamide accumulation may be due to an indirect effect of the M(r) 170,000 glycoprotein, such as its effect on intracellular pH. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL NUTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV ONCOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NCI NIH HHS [CA30195] NR 34 TC 13 Z9 13 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUL 1 PY 1992 VL 52 IS 13 BP 3539 EP 3546 PG 8 WC Oncology SC Oncology GA JA764 UT WOS:A1992JA76400005 PM 1617623 ER PT J AU PRICE, BD CALDERWOOD, SK AF PRICE, BD CALDERWOOD, SK TI GADD45 AND GADD153 MESSENGER-RNA LEVELS ARE INCREASED DURING HYPOXIA AND AFTER EXPOSURE OF CELLS TO AGENTS WHICH ELEVATE THE LEVELS OF THE GLUCOSE-REGULATED PROTEINS SO CANCER RESEARCH LA English DT Article ID MAMMALIAN-CELLS; GENES; DNA; DAMAGE AB We have investigated overlapping activation pathways for two families of stress genes that are expressed in cells exposed to hypoxia. The growth arrest and DNA damage (gadd) genes are induced by DNA damage and irradiation, and their expression is associated with growth arrest. The glucose-regulated proteins (GRPs) are induced by chemical agents that disrupt protein trafficking in the endoplasmic reticulum such as tunicamycin and A23187 and by hypoxia. Here, we demonstrate that the treatment of NIH-3T3 cells with chemical inducers of GRPs results in increased levels of gadd45 and gadd153 mRNA as well as GRP78 mRNA. In addition, hypoxia was also able to increase gadd45, gadd153, and GRP78 mRNA. Therefore the GRP and gadd genes can be activated by similar stimuli (e.g., hypoxia and chemical inducers). However, the mechanisms leading to increased levels of GRP78 and gadd gene mRNA are different and may involve distinct protein kinases. Increased expression of GRPs after treatment with chemical inducers is sensitive to cycloheximide and the protein kinase inhibitors genistein, 2-aminopurine, and H7, whereas the increase in gadd gene mRNA could be blocked by the protein kinase inhibitors H7 and 2-aminopurine but not by genistein or cycloheximide. GRP78 induction occurs by a pathway that requires protein synthesis and is sensitive to genistein, H7, and 2-aminopurine, whereas gadd gene induction is independent of protein synthesis and is inhibited by H7 and 2-aminopurine only. RP PRICE, BD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,STRESS PROT GRP,BOSTON,MA 02115, USA. FU NCI NIH HHS [R29CA44940]; PHS HHS [R01 47407] NR 19 TC 165 Z9 168 U1 0 U2 3 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 JUL 1 PY 1992 VL 52 IS 13 BP 3814 EP 3817 PG 4 WC Oncology SC Oncology GA JA764 UT WOS:A1992JA76400051 PM 1617653 ER PT J AU KHARBANDA, S DATTA, R RUBIN, E NAKAMURA, T HASS, R KUFE, D AF KHARBANDA, S DATTA, R RUBIN, E NAKAMURA, T HASS, R KUFE, D TI REGULATION OF C-JUN EXPRESSION DURING INDUCTION OF MONOCYTIC DIFFERENTIATION BY OKADAIC ACID SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID TUMOR-NECROSIS-FACTOR; PROTEIN KINASE-C; PROMYELOCYTIC LEUKEMIA-CELLS; GENE-EXPRESSION; GROWTH-FACTOR; POSTTRANSCRIPTIONAL REGULATION; MOLECULAR-CLONING; PHORBOL ESTERS; FOS GENE; ONCOGENE AB The present work has examined the effects of okadaic acid, an inhibitor of type 1 and 2A protein phosphatases, on the regulation of c-jun expression during monocytic differentiation of U-937 leukemia cells. The results demonstrate that okadaic acid treatment is associated with induction of a differentiated monocyte phenotype characterized by: (a) growth arrest; (b) increases in Mac-1 cell surface antigen expression; (c) down-regulation of c-myc transcripts; and (d) induction of tumor necrosis factor gene expression. This induction of monocytic differentiation was associated with transient increases in c-jun mRNA levels, which were maximal at 6 h. Similar effects were obtained for the c-fos gene. Run-on analysis demonstrated detectable levels of c-jun transcription in U-937 cells and that this rate is increased approximately 40-fold following okadaic acid exposure. c-jun mRNA levels were superinduced in cells treated with both okadaic acid and cycloheximide, whereas inhibition of protein synthesis had little, ii any, effect on okadaic acid-induced c-jun transcription. The half-life of c-jun mRNA was similar (45-50 min) in both untreated and okadaic acid-induced cells. In contrast, treatment with both okadaic acid and cycloheximide was associated with stabilization (t1/2 = 90 min) of c-jun transcripts. Taken together, these findings indicate that the induction of c-jun transcription by okadaic acid is controlled primarily by a transcriptional mechanism. Since previous studies have demonstrated that the c-jun gene is autoinduced by Jun/AP-1, we also studied transcription of c-jun promoter (positions -132/+170)-reporter gene constructs with and without a mutated AP-1 element. The results demonstrate that okadaic acid-induced c-jun transcription is mediated at least in part by activation of the AP-1 site. Studies with the protein kinase C inhibitor H7 and after prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate indicate that okadaic acid-induced c-jun expression is mediated by a protein kinase C-independent mechanism. Finally, we demonstrate that okadaic acid also induces c-jun expression and a more differentiated phenotype in human peripheral blood monocytes. These findings support a role for phosphoserine/phosphothreonine protein phosphatases in signaling pathways which control c-jun transcription and induction of monocytic differentiation. RP KHARBANDA, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 FU NCI NIH HHS [CA34183, CA42802] NR 55 TC 31 Z9 31 U1 0 U2 3 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 JUL PY 1992 VL 3 IS 7 BP 391 EP 399 PG 9 WC Cell Biology SC Cell Biology GA JC463 UT WOS:A1992JC46300001 PM 1419903 ER PT J AU MATHISEN, DJ AF MATHISEN, DJ TI DONT GET RUN OVER BY THE BANDWAGON SO CHEST LA English DT Editorial Material RP MATHISEN, DJ (reprint author), MASSACHUSETTS GEN HOSP,GEN THORAC SURG SERV,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD JUL PY 1992 VL 102 IS 1 BP 4 EP 5 DI 10.1378/chest.102.1.4 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA JC254 UT WOS:A1992JC25400004 PM 1623793 ER PT J AU LESSER, BA LEEPER, KV STEIN, PD SALTZMAN, HA CHEN, J THOMPSON, BT HALES, CA POPOVICH, J GREENSPAN, RH WEG, JG AF LESSER, BA LEEPER, KV STEIN, PD SALTZMAN, HA CHEN, J THOMPSON, BT HALES, CA POPOVICH, J GREENSPAN, RH WEG, JG TI THE DIAGNOSIS OF ACUTE PULMONARY-EMBOLISM IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE SO CHEST LA English DT Article AB The clinical features and noninvasive tests, including ventilation perfusion (V/Q) lung scans, were assessed in 108 patients with chronic obstructive pulmonary disease (COPD) suspected of having pulmonary embolism (PE). Twenty-one (19 percent) of 108 patients had PE. In the majority of patients, it was impossible to distinguish between patients with and without PE by clinical assessment alone. However, when a high clinical index of suspicion was present, PE was confirmed by angiography in three of three patients, but the V/Q scan was of intermediate probability. No roentgenographic abnormalities distinguished between PE and no PE. There was no difference between the alveolar-arterial oxygen gradients in either group, nor was there evidence of a reduction in the PaCO2 in patients with PE who had prior hypercapnia. Among the 108 patients with COPD, high, intermediate, low, and normal/near normal probability scans were present in 5 percent, 60 percent, 30 percent, and 5 percent, respectively. The frequency of PE in these V/Q scan categories was five (100 percent) of five, 14 (22 percent) of 65, two (6 percent) of 33, and zero (0 percent) of five, respectively. In conclusion, in the majority of patients, the V/Q scan diagnosis is usually intermediate and such patients require further investigational studies, including angiography. However, among the few patients who demonstrated a high probability lung scan, there was a high positive predictive value for PE effectively avoiding the need for further studies. In those patients with low probability or near normal/normal V/Q scans, the negative predictive value was not lower than the general hospital population. C1 HENRY FORD HOSP,2799 W GRAND,DETROIT,MI 48202. DUKE UNIV,DURHAM,NC 27706. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. YALE UNIV,NEW HAVEN,CT 06520. UNIV MICHIGAN,ANN ARBOR,MI 48109. FU NHLBI NIH HHS [N01-HR-34007, N01-HR-34008, N01-HR-34009] NR 12 TC 94 Z9 101 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD JUL PY 1992 VL 102 IS 1 BP 17 EP 22 DI 10.1378/chest.102.1.17 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA JC254 UT WOS:A1992JC25400008 PM 1623748 ER PT J AU BISHOP, SJ MURPHY, JM JELLINEK, MS QUINN, D POITRAST, FG AF BISHOP, SJ MURPHY, JM JELLINEK, MS QUINN, D POITRAST, FG TI PROTECTING SERIOUSLY MISTREATED CHILDREN - TIME DELAYS IN A COURT SAMPLE SO CHILD ABUSE & NEGLECT LA English DT Article DE CHILD ABUSE AND NEGLECT; ADJUDICATION; TIME DELAYS; CARE AND PROTECTION PETITIONS ID PREVALENCE; PARENTS; ABUSE AB The study examined the progress through the child protective system of a sample of 206 severely abused and/or neglected children brought before the Boston Juvenile Court (BJC) on Care and Protection (C & P) petitions. Overall, children were in the system an average of 5 years from the filing of the first official report of mistreatment to the resolution of their cases. The families had been known to the state child protective service agency for an average of more than 2.5 years before the current court involvement. Once arraigned in juvenile court on the C & P, the average case took almost 1.5 years to reach a disposition. After disposition, children permanently removed from parental custody required. on average, an additional year and a half in Probate Court to reach a permanent placement. Of the more than twenty variables examined, including severity of mistreatment, protective service history, and parental mental illness, no meaningful pattern emerged which could predict delays. Our findings characterize the delays experienced by many abused and neglected children, and highlight the necessity of closer monitoring of the progress of cases through the protective and court systems. C1 MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,BOSTON,MA 02114. BOSTON JUVENILE COURT,BOSTON,MA. NR 21 TC 9 Z9 9 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PD JUL-AUG PY 1992 VL 16 IS 4 BP 465 EP 474 DI 10.1016/0145-2134(92)90063-W PG 10 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA JG973 UT WOS:A1992JG97300002 PM 1393710 ER PT J AU MURPHY, JM BISHOP, SJ JELLINEK, MS QUINN, D POITRAST, FG AF MURPHY, JM BISHOP, SJ JELLINEK, MS QUINN, D POITRAST, FG TI WHAT HAPPENS AFTER THE CARE AND PROTECTION PETITION - REABUSE IN A COURT SAMPLE SO CHILD ABUSE & NEGLECT LA English DT Article DE CHILD ABUSE AND NEGLECT; CARE AND PROTECTION PETITIONS; ADJUDICATION; REABUSE ID PREVALENCE; CHILDREN AB Of 206 cases of serious child mistreatment brought before a metropolitan juvenile court on Care and Protection Petitions (C & P), 63 (31%) were dismissed (returning the child to the parent(s]. During a 2-year follow-up period, 18 (29%) of these dismissed cases had substantiated reports of further mistreatment, and 10 (16%) subsequently returned to court on another C & P. Families that had previously been to court for a C & P, and those in which the parent was diagnosed psychotic or character disordered, were significantly more likely to return to court. In addition, we were surprised to find that 8 (6%) of the 130 children ordered permanently removed from parental custody also returned to court. This study documents the continuing mistreatment of children, even after the state's most serious interventions. The study also highlights the necessity of incorporating clinical research in the form of ongoing follow-up of individual cases into the court process, and suggests that it may be possible to identify cases with a very high probability of reinjury and return to court. C1 BOSTON JUVENILLE COURT,BOSTON,MA. RP MURPHY, JM (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,ACC 725,BOSTON,MA 02114, USA. NR 19 TC 19 Z9 19 U1 0 U2 0 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 JUL-AUG PY 1992 VL 16 IS 4 BP 485 EP 493 DI 10.1016/0145-2134(92)90065-Y PG 9 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA JG973 UT WOS:A1992JG97300004 PM 1393712 ER PT J AU MEYER, GS MCCARTHY, ST AF MEYER, GS MCCARTHY, ST TI CIRCADIAN VARIATION OF ABNORMAL HEART BEATS IN AN ELDERLY POPULATION AND THEIR RELATION TO SUDDEN CARDIAC DEATH SO CHRONOBIOLOGIA LA English DT Article DE ABNORMAL HEART BEATS; AMBULATORY ELECTROCARDIOGRAM; ARRHYTHMIA; CATECHOLAMINE; CHRONIC CONGESTIVE HEART FAILURE; CIRCADIAN VARIATION; ELDERLY; HYPERTENSION; POSTURAL HYPOTENSION; SUDDEN CARDIAC DEATH RP MEYER, GS (reprint author), MASSACHUSETTS GEN HOSP,GIMU,BULFINCH 1,BOSTON,MA 02144, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSOCIATED CHRONOBIOLOGIA RESEARCHERS PI MILAN PA VIA R. DI LAURIA, 12/A, 20149 MILAN, ITALY SN 0390-0037 J9 CHRONOBIOLOGIA PD JUL-DEC PY 1992 VL 19 IS 3-4 BP 175 EP 185 PG 11 WC Biology SC Life Sciences & Biomedicine - Other Topics GA KA828 UT WOS:A1992KA82800007 PM 1478116 ER PT J AU CHEN, CG RODRIGUEZ, L LEVINE, RA WEYMAN, AE THOMAS, JD AF CHEN, CG RODRIGUEZ, L LEVINE, RA WEYMAN, AE THOMAS, JD TI NONINVASIVE MEASUREMENT OF THE TIME CONSTANT OF LEFT-VENTRICULAR RELAXATION USING THE CONTINUOUS-WAVE DOPPLER VELOCITY PROFILE OF MITRAL REGURGITATION SO CIRCULATION LA English DT Article DE DIASTOLIC FUNCTION; DOPPLER ECHOCARDIOGRAPHY; TAU ID CONGESTIVE HEART-FAILURE; CORONARY-ARTERY DISEASE; DIASTOLIC FUNCTION; ISOVOLUMIC RELAXATION; VALVULAR REGURGITATION; MYOCARDIAL-INFARCTION; ECHOCARDIOGRAPHY; FLOW; PRESSURE; INDEXES AB Background. The time constant of isovolumic relaxation (tau) is an important parameter of ventricular diastolic function, but the need for invasive measurement with high-fidelity catheters has limited its use in general clinical cardiology. The Doppler mitral regurgitant velocity spectrum can be used to estimate left ventricular (LV) pressure throughout systole and may provide a new noninvasive method for estimating-tau. Methods and Results. Mitral regurgitation was produced in nine dogs, and ventricular relaxation was adjusted pharmacologically and with hypothermia. High-fidelity ventricular pressures were recorded, and tau was calculated from these hemodynamic data (tau(H)) assuming a zero-pressure asymptote. Continuous-wave mitral regurgitant velocity profiles were obtained, and the ventriculo-atrial (VA) pressure gradient was calculated by the simplified Bernoulli equation; tau was calculated from the Doppler data from the time of maximal negative dP/dt until LV-LA pressure crossover. Three methods were used to correct the Doppler VA gradient to better approximate the LV pressure before calculating-tau: 1) adding actual LA V wave pressure (to yield tau(LA); 2) adding 10 mm Hg (tau-10); and 3) no adjustment at all (actual VA gradient used to calculate tau-0). The agreement between tau(H) and the three Doppler estimates of tau was assessed by linear regression and by the mean and standard deviation of the error between the measurements (DELTA-tau). tau(H) ranged from 29 to 135 msec. Without correction for LA pressure, the Doppler estimate of tau seriously underestimated tau(H): tau-10=0.30-tau(H)+9.4, r=0.79, DELTA-tau=-35+/-18 msec. This error was almost completely eliminated by adding actual LA pressure to the VA pressure gradient: tau(LA)=0.92-tau(H)+7.6, r=0.95, DELTA-tau=2+/-7 msec. Addition of a fixed LA pressure estimate of 10 mm Hg to the VA gradient yielded an estimate that was almost as good: tau-10=0.89-tau(H)+4.9, r=0.88, DELTA-tau=-2+/-12 msec. In general, tau was overestimated when actual LA pressure was below this assumed value, and vice versa. Numerical analysis demonstrated that assuming LA pressure to be 10 mm Hg should yield estimates of tau accurate to +/-15% between true LA pressures of 5 and 20 mm Hg. Conclusions. This study demonstrates that the Doppler mitral regurgitant velocity profile can be used to provide a direct and noninvasive measurement of tau. Because mitral regurgitation is very common in cardiac patients, this method may allow more routine assessment of tau in clinical and research settings, leading to a better understanding of the role of impaired ventricular relaxation in diastolic dysfunction and the effect of therapeutic interventions. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NONINVAS CARDIAC LAB,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-38176] NR 52 TC 44 Z9 50 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JUL PY 1992 VL 86 IS 1 BP 272 EP 278 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA JC457 UT WOS:A1992JC45700031 PM 1617778 ER PT J AU EID, H LARSON, DM SPRINGHORN, JP ATTAWIA, MA NAYAK, RC SMITH, TW KELLY, RA AF EID, H LARSON, DM SPRINGHORN, JP ATTAWIA, MA NAYAK, RC SMITH, TW KELLY, RA TI ROLE OF EPICARDIAL MESOTHELIAL CELLS IN THE MODIFICATION OF PHENOTYPE AND FUNCTION OF ADULT-RAT VENTRICULAR MYOCYTES IN PRIMARY COCULTURE SO CIRCULATION RESEARCH LA English DT Article DE CELL CELL INTERACTION; DIFFERENTIATION; MUSCLE REGENERATION ID CARDIAC-MUSCLE-CELLS; FIBROBLAST GROWTH-FACTOR; FACTOR MESSENGER-RNA; ALPHA-ACTIN; ARACHIDONATE METABOLISM; EXTRACELLULAR-MATRIX; BOVINE PERICARDIUM; ENDOTHELIAL-CELLS; GENE-EXPRESSION; THYROID-HORMONE AB Adult rat ventricular myocytes undergo a well-documented sequence of phenotypic changes during adaptation to primary culture. However, we observed that coculture of myocytes with a specific subset of nonmyocyte cardiac cells could slow and even reverse the process of adaptation. These nonmyocyte cells were isolated and identified by immunohistochemical and ultrastructural criteria as being of epicardial mesothelial origin. When added to long-term primary cultures of adult ventricular myocytes, epicardial mesothelial cells appeared to induce myofibrillar arrays that were more organized than those seen in noncocultured myocytes; these changes that occurred were concurrent with the appearance of large amplitude contractions and multicellular synchronous beating that was facilitated by gap junctions between myocytes and epicardial mesothelial cells. The changes in morphology and function were accompanied by a marked increase in beta-myosin heavy chain isoform transcription in cocultured myocytes, a return to the ratio of cardiac to skeletal alpha-actin expected in adult rat myocardium, and a much reduced expression of smooth muscle alpha-actin. These changes in myocyte phenotype and function appeared to require epicardial cell-myocyte contact, or close apposition, because media conditioned by epicardial mesothelial cells alone or in coculture had no effect. Thus, these rapid and reversible changes in myocyte ultrastructure, function, and gene expression may provide a useful in vitro model with which to study the mechanism responsible for regulating the plasticity of ventricular myocyte phenotype and the role of specific cell-cell interactions. C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DEPT MED,BOSTON,MA 02115. BOSTON UNIV,SCH MED,MALLORY INST PATHOL,BOSTON,MA 02118. RP EID, H (reprint author), UNIV OTTAWA,RES CTR,INST HEART,1053 CARLING AVE,ROOM H-247,OTTAWA K1Y 4E9,ONTARIO,CANADA. FU NHLBI NIH HHS [HL-36141] NR 53 TC 89 Z9 90 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD JUL PY 1992 VL 71 IS 1 BP 40 EP 50 PG 11 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA HZ760 UT WOS:A1992HZ76000007 PM 1606667 ER PT J AU EHARA, S NISHIDA, J ABE, M KAWATA, Y SAITOH, H KATTAPURAM, SV AF EHARA, S NISHIDA, J ABE, M KAWATA, Y SAITOH, H KATTAPURAM, SV TI OSSIFIED SOFT-TISSUE RECURRENCE OF GIANT-CELL TUMOR OF BONE SO CLINICAL IMAGING LA English DT Article DE BONE TUMORS; GIANT CELL TUMOR; SOFT TISSUE RECURRENCE; PLAIN RADIOGRAPHY AB We report 3 cases of soft tissue recurrence of giant cell tumor of bone. A peripheral rim of ossification in the soft tissue mass is pathognomonic of recurrence in the patients after resection of giant cell tumor. C1 AKITA NAKADOHRI HOSP,AKITA,JAPAN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP EHARA, S (reprint author), IWATE MED UNIV,CTR RADIOL SCI,19-1 UCHIMARU,MORIOKA,IWATE 020,JAPAN. NR 3 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0899-7071 J9 CLIN IMAG JI Clin. Imaging PD JUL-SEP PY 1992 VL 16 IS 3 BP 168 EP 171 DI 10.1016/0899-7071(92)90043-9 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JJ146 UT WOS:A1992JJ14600003 PM 1498701 ER PT J AU TALAL, N AF TALAL, N TI PSYCHONEUROIMMUNOLOGY - INTRODUCTION SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Editorial Material ID RESPONSES; HORMONES C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP TALAL, N (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD JUL PY 1992 VL 64 IS 1 BP 5 EP 5 DI 10.1016/0090-1229(92)90050-X PG 1 WC Immunology; Pathology SC Immunology; Pathology GA JA541 UT WOS:A1992JA54100003 ER PT J AU TALAL, N AF TALAL, N TI PSYCHONEUROIMMUNOLOGY - COMMENTARY SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,DEPT MED,HOUSTON,TX 77225. RP TALAL, N (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284, USA. NR 14 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD JUL PY 1992 VL 64 IS 1 BP 28 EP 29 DI 10.1016/0090-1229(92)90055-S PG 2 WC Immunology; Pathology SC Immunology; Pathology GA JA541 UT WOS:A1992JA54100008 PM 1606748 ER PT J AU BAKER, AS OJEMANN, RG BAKER, RA AF BAKER, AS OJEMANN, RG BAKER, RA TI TO DECOMPRESS OR NOT TO DECOMPRESS - SPINAL EPIDURAL ABSCESS - EDITORIAL RESPONSE SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material C1 LAHEY CLIN FDN,DEPT NEURORADIOL,BURLINGTON,MA. MASSACHUSETTS GEN HOSP,NEUROSURG UNIT,BOSTON,MA 02114. RP BAKER, AS (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 6 TC 26 Z9 26 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JUL PY 1992 VL 15 IS 1 BP 28 EP 29 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA JA300 UT WOS:A1992JA30000005 PM 1617071 ER PT J AU RUOFF, KL AF RUOFF, KL TI GROUP-C STREPTOCOCCI - A CURRENT VIEW SO CLINICAL INFECTIOUS DISEASES LA English DT Letter ID CONSTELLATUS; INTERMEDIUS; ANGINOSUS; MILLERI RP RUOFF, KL (reprint author), MASSACHUSETTS GEN HOSP,MICROBIOL LABS,BOSTON,MA 02114, USA. NR 7 TC 9 Z9 9 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JUL PY 1992 VL 15 IS 1 BP 175 EP 176 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA JA300 UT WOS:A1992JA30000031 PM 1445560 ER PT J AU MALONEY, WJ JASTY, M WILLETT, C MULROY, RD HARRIS, WH AF MALONEY, WJ JASTY, M WILLETT, C MULROY, RD HARRIS, WH TI PROPHYLAXIS FOR HETEROTOPIC BONE-FORMATION AFTER TOTAL HIP-ARTHROPLASTY USING LOW-DOSE RADIATION IN HIGH-RISK PATIENTS SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID OSSIFICATION; IRRADIATION; PREVENTION; SURGERY AB Fifteen consecutive total hip arthroplasties (THAs) in 14 patients considered at risk for developing significant heterotopic ossification (HO) were treated postoperatively with 7.5 Gy of external beam radiation in three fractions. Eight hips in eight of the patients (Group I) had developed previous Brooker Class III or IV HO after THA and were radiated after having excision of HO in conjunction with a revision THA. Three additional hips in three patients (Group II) were radiated after primary THA, because they developed significant HO on the contralateral hip after a previous THA. The remaining four hips in three patients (Group III) were radiated after primary THA because they had bilateral hypertrophic arthritis. Precision shielding was employed to minimize the volume of tissue in the radiation field and to protect the bone-implant interface around porous-coated components and the trochanteric osteotomy sites. Of the eight hips in which Class III or IV bone was excised during revision THA (Group I), no new bone formed in five hips and in the other three hips, only Class I bone formed. No heterotopic bone formed in the remaining seven hips of Groups II and III. All six trochanteric osteotomies healed. There were no wound healing problems. There were no significant radiolucencies around any of the components and there was no radiographic evidence of implant instability. This regimen using 7.5 Gy over three fractions minimizes the radiobiologic impact, whereas the use of precision shielding minimizes the total volume of tissue treated. This regimen is an effective means of preventing significant HO after THA in high-risk patients while minimizing radiation exposure. C1 MASSACHUSETTS GEN HOSP,HIP & IMPLANT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT THERAPY,BOSTON,MA 02114. RP MALONEY, WJ (reprint author), PALO ALTO MED CLIN,PALO ALTO,CA 94301, USA. NR 25 TC 16 Z9 16 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JUL PY 1992 IS 280 BP 230 EP 234 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JC246 UT WOS:A1992JC24600030 PM 1611750 ER PT J AU JASTY, M RUBASH, HE PAIEMENT, GD BRAGDON, CR PARR, J HARRIS, WH AF JASTY, M RUBASH, HE PAIEMENT, GD BRAGDON, CR PARR, J HARRIS, WH TI POROUS-COATED UNCEMENTED COMPONENTS IN EXPERIMENTAL TOTAL HIP-ARTHROPLASTY IN DOGS - EFFECT OF PLASMA-SPRAYED CALCIUM-PHOSPHATE COATINGS ON BONE INGROWTH SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article AB The effect of a thin plasma-sprayed, calcium phosphate ceramic coating on bone ingrowth into titanium fiber mesh porous-surfaced prostheses was examined in a controlled canine cementless total hip arthroplasty model. Bone ingrowth was quantified using backscattered scanning electron microscopy of undemineralized sections. When good contact between the bone and porous coating was present, the calcium phosphate-coated prostheses contained significantly higher amounts of bone ingrowth at three weeks postimplantation than the uncoated control prostheses. At six weeks, however, there was no significant difference in the amount of bone ingrowth between the coated prostheses and uncoated prostheses. The ingrown bone seemed to be more intimately associated with the calcium phosphate-coated porous surfaces than the uncoated porous surfaces. When gaps at the bone-porous coating interface occurred, the calcium phosphate coating did not enhance bone ingrowth across those gaps. Plasma-sprayed calcium phosphate coatings may be useful in enhancing the early ingrowth of bone into porous-surfaced joint replacement prostheses, but they may lack long-term effectiveness. The coatings were not effective in enhancing bone ingrowth across gaps between the porous surface and the bone bed prepared at surgery. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV ORTHOPAED PITTSBURGH,PITTSBURGH,PA. ZIMMER INC,WARSAW,IN. MASSACHUSETTS GEN HOSP,HIP & IMPLANT UNIT,BOSTON,MA 02114. RP JASTY, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114, USA. NR 15 TC 24 Z9 24 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JUL PY 1992 IS 280 BP 300 EP 309 PG 10 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JC246 UT WOS:A1992JC24600041 PM 1611761 ER PT J AU DERSHWITZ, M ROSOW, CE DIBIASE, PM JOSLYN, AF SANDERSON, PE AF DERSHWITZ, M ROSOW, CE DIBIASE, PM JOSLYN, AF SANDERSON, PE TI ONDANSETRON IS EFFECTIVE IN DECREASING POSTOPERATIVE NAUSEA AND VOMITING SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Article ID CISPLATIN-INDUCED EMESIS; HIGH-DOSE METOCLOPRAMIDE; ANTAGONIST; DROPERIDOL; SEROTONIN; GR-38032F; ANESTHESIA; PREVENTION; GR38032F AB The efficacy of ondansetron, a selective 5-HT3 receptor antagonist, in preventing postoperative nausea and vomiting in surgical patients was studied. Fifty women were randomized in a double-blind manner to receive either two 8 mg doses of intravenous ondansetron or two doses of placebo vehicle: the first given just before general anesthesia induction and the second 8 hours later. During the first 24 postoperative hours, the number of emetic episodes was recorded and the subjects rated their nausea on a scale from 0 to 10. Ondansetron-treated subjects had fewer emetic episodes (p < 0.001) and lower subjective nausea scores (p < 0.001). The number of complete responders (no emetic episodes and no rescue therapy) was 1 of 24 (4%) and 15 of 26 (58%) in the placebo and ondansetron groups, respectively (p < 0.001). Ondansetron is clearly more effective than placebo in the prophylaxis of postoperative nausea and vomiting. The adverse event profile for ondansetron was similar to that of placebo. C1 GLAXO INC,RES TRIANGLE PK,NC. RP DERSHWITZ, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 20 TC 24 Z9 24 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JUL PY 1992 VL 52 IS 1 BP 96 EP 101 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JE053 UT WOS:A1992JE05300013 PM 1385567 ER PT J AU HEMADY, RK CHU, W FOSTER, CS AF HEMADY, RK CHU, W FOSTER, CS TI INTRAOCULAR PENETRATION OF KETOCONAZOLE IN RABBITS SO CORNEA LA English DT Article DE KETOCONAZOLE; PENETRATION; RABBIT AB We studied penetration of the antifungal agent ketoconazole into the cornea, aqueous humor, and vitreous of rabbits after topical, subconjunctival, and oral administration. The effect of debridement of corneal epithelium on penetration was also investigated. Ketoconazole levels in the cornea and aqueous humor were high after topical or subconjunctival administration, and increased markedly (especially in the cornea) if the corneal epithelium had been debrided before administration of the drug. For example, concentration of ketoconazole in the cornea 1 h after topical drug administration with or without complete corneal epithelial debridement was 44.0 +/- 10.1 and 1,391.5 +/- 130.0-mu-g/g, respectively. Drug levels in the vitreous were not detectable after topical or subconjunctival drug administration, but were improved slightly by prior epithelial debridement (8.3 and 0.12-mu-g/mL after 1 h, respectively). Orally administered ketoconazole resulted in high corneal concentrations (45.0 +/- 7.6-mu-g/g after 1 h) that were still substantial 24 h later (55.0 +/- 7.0-mu-g/g); levels in the aqueous were low. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA & IMMUNOL SERV,243 CHARLES ST,BOSTON,MA 02114. NR 0 TC 18 Z9 20 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 JUL PY 1992 VL 11 IS 4 BP 329 EP 333 DI 10.1097/00003226-199207000-00011 PG 5 WC Ophthalmology SC Ophthalmology GA HZ589 UT WOS:A1992HZ58900011 PM 1424654 ER PT J AU DEMETRI, GD AF DEMETRI, GD TI HEMATOPOIETIC GROWTH-FACTORS - CURRENT KNOWLEDGE, FUTURE-PROSPECTS SO CURRENT PROBLEMS IN CANCER LA English DT Review ID COLONY-STIMULATING FACTOR; STEM-CELL FACTOR; RECOMBINANT HUMAN INTERLEUKIN-3; BONE-MARROW TRANSPLANTATION; LEUKEMIA-INHIBITORY FACTOR; TUMOR NECROSIS FACTOR; ACUTE MYELOID-LEUKEMIA; HIGH-DOSE CHEMOTHERAPY; HUMAN GM-CSF; SERUM IMMUNOREACTIVE ERYTHROPOIETIN AB The introduction of hematopoietic growth factors into clinical medicine represents one of the more exciting developments in oncology in the past several years. The identification, gene cloning, and large-scale production of hematopoietic growth factors represent important examples of the practical benefits that may accrue from application of the sophisticated technology derived from recombinant DNA research. Research, both at the bench and by the bedside, has proceeded at an extraordinarily rapid pace in this field over the past five years, leading to an abundance of new information, novel promising agents, and important clinical controversies related to the biology and appropriate clinical applications of hematopoietic growth factors. With these agents, for the first time in history, the production of human blood cells can be systematically manipulated in vivo in an effort to optimize physiology beyond the endogenous host response. Additionally, investigators utilizing purified hematopoietic growth factors as reagents may provide crucial insights into the mechanisms of blood cell production in health and in various disease states. This review aims to summarize the current state of knowledge regarding the control of blood cell production by specific factors and to put these data in the context of clinical medicine. The emphasis will be on factors that primarily influence myeloid (rather than lymphoid) cell growth, differentiation, and activation, and the clinical focus will be on applications in oncologic therapeutics and in the treatment of primary hematologic disorders. By reviewing what we know and what has already been done, we may be better able to define the important questions that remain and to formulate the means to answer our current uncertainties about the activities and clinical uses of hematopoietic growth factors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV MED ONCOL,BOSTON,MA 02115. RP DEMETRI, GD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. NR 353 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0147-0272 J9 CURR PROB CANCER JI Curr. Probl. Cancer PD JUL-AUG PY 1992 VL 16 IS 4 BP 181 EP 259 DI 10.1016/S0147-0272(06)80011-5 PG 79 WC Oncology SC Oncology GA JF351 UT WOS:A1992JF35100001 ER PT J AU PARK, S ALBERT, DM BOLOGNIA, JL AF PARK, S ALBERT, DM BOLOGNIA, JL TI OCULAR MANIFESTATIONS OF PIGMENTARY DISORDERS SO DERMATOLOGIC CLINICS LA English DT Article C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 18 Z9 18 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8635 J9 DERMATOL CLIN JI Dermatol. Clin. PD JUL PY 1992 VL 10 IS 3 BP 609 EP 622 PG 14 WC Dermatology SC Dermatology GA HY316 UT WOS:A1992HY31600013 PM 1617818 ER PT J AU PUGLIESE, A AWDEH, ZL GALLUZZO, A YUNIS, EJ ALPER, CA EISENBARTH, GS AF PUGLIESE, A AWDEH, ZL GALLUZZO, A YUNIS, EJ ALPER, CA EISENBARTH, GS TI NO INDEPENDENT ASSOCIATION BETWEEN HSP70 GENE POLYMORPHISM AND IDDM SO DIABETES LA English DT Article ID HEAT-SHOCK PROTEINS; DIABETES-MELLITUS; EXPRESSION; MOUSE AB A role for heat shock proteins (HSPs) in autoimmunity has recently been suggested by several authors. Autoantibodies against HSPs have been associated with such autoimmune diseases as systemic lupus erythematosus, polymyositis, and the NOD mouse model of diabetes. Moreover, genes for the major 70,000-M(r) HSP (HSP70) are located within the MHC. To investigate a potential association of an HSP70-2 gene polymorphism with insulin-dependent diabetes mellitus (IDDM), we analyzed restriction-fragment-length polymorphism (RFLP) of this gene in 29 families with one or more member affected by IDDM. With the enzyme Pstl, as reported previously, two HSP70-2 alleles of 8.5- and 9.0-kb were found. The 8.5-kb allele was found more frequently on diabetic haplotypes compared with control haplotypes (41 of 66 [62%] vs. 20 of 46 143%], P = 0.03). This association was due to the conservation of alleles on extended haplotypes we previously reported to be associated with diabetes on initial analysis of families. Twenty-three of 26 diabetic DR3 haplotypes and 3 of 3 normal DR3 haplotypes and all instances of [HLA-B8, SC01, DR3] and [HLA-B18, FlC30, DR3] had the 8.5-kb allele, whereas 0 of 9 normal DR2 haplotypes and 0 of 2 diabetic DR2 haplotypes had the 8.5-kb allele (P = 8 x 10(-7) DR3 vs. DR2 haplotypes). The alleles were equally distributed among DR4 haplotypes. Our studies indicate that the 8.5-kb allele is part of [HLA-B8, SC01, DR3] and [HLA-B18, F1C30, DR3] haplotypes, and the 9.0-kb allele is associated with DR2 but no independent association (greater than DR association) is found between HSP70-2 alleles and diabetes. C1 JOSLIN DIABET CTR,IMMUNOL SECT,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. UNIV PALERMO,MED B CLIN,I-90134 PALERMO,ITALY. FU NIAID NIH HHS [AI-14157]; NIDDK NIH HHS [DK-26844, DK-32083] NR 26 TC 46 Z9 46 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JUL PY 1992 VL 41 IS 7 BP 788 EP 791 DI 10.2337/diabetes.41.7.788 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ793 UT WOS:A1992HZ79300003 PM 1351854 ER PT J AU MARTIN, BC WARRAM, JH ROSNER, B RICH, SS SOELDNER, JS KROLEWSKI, AS AF MARTIN, BC WARRAM, JH ROSNER, B RICH, SS SOELDNER, JS KROLEWSKI, AS TI FAMILIAL CLUSTERING OF INSULIN SENSITIVITY SO DIABETES LA English DT Article ID GLUCOSE-TOLERANCE; PIMA-INDIANS; GENES AB This study's objective was to determine whether there is familial clustering of insulin sensitivity (S(I)) or insulin-independent glucose uptake (S(G)), which would be evidence that they are genetically determined traits. Outpatients had a 3-h intravenous glucose tolerance test. Nondiabetic individuals (n = 183), ranging in age from 16 to 60 yr, were from 105 families that had 2 parents with non-insulin-dependent diabetes mellitus. Of these families, 62 contributed 1 offspring, 21 contributed 2, 13 contributed 3, 6 contributed 4, and 2 and 1 contributed 5 and 6, respectively. The minimal model of glucose disposal and the glucose and insulin values from the intravenous glucose tolerance tests were used to estimate S(I) and S(G). The intraclass correlation coefficient was used to compare the within-family variability of S(I) and S(G) with the respective between-family distributions. The intraclass correlation coefficients were 0.26 (P = 0.008) for S(I) and 0.081 (P = 0.45) for S(G). S(I) and S(G) were uncorrelated (r = -0.059, P = 0.42). The intraclass correlation of S(I) could not be explained by familial clustering of fasting insulin or ideal body weight. Finally, the 10 families with the lowest values of S(I) had a significantly higher within-sibship variability of S(I) than the other 33 families (P < 0.001, F test). S(I) but not S(G) showed familial clustering, which is consistent with a polygenic determinant of S(I). In addition, a large within-family variability of S(I) in some families is compatible with a major gene eff ect with a dominant mode of inheritance. Thus, defects in genes affecting S(I) are plausible candidates for determinants of familial clustering of non-insulin-dependent diabetes mellitus. C1 JOSLIN DIABET CTR,RES DIV,EPIDEMIOL & GENET SECT,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,CAMBRIDGE,MA 02138. NR 15 TC 141 Z9 142 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JUL PY 1992 VL 41 IS 7 BP 850 EP 854 DI 10.2337/diabetes.41.7.850 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ793 UT WOS:A1992HZ79300011 PM 1612199 ER PT J AU SELAM, JL MICOSSI, P DUNN, FL NATHAN, DM FOGEL, H GAZ, R HAGGEN, C MCKITRICK, C LARKIN, M DUNN, F LAVINTOMPLINS, J THOMPSON, M BYRD, P SAKIEWICZ, L GRANT, J SELAM, JL CHARLES, MA WAXMAN, K RACCAH, D JEANDIDIER, N LOZANO, J MICOSSI, P CRISTALLO, M GALIMBERTI, G PETRELLA, G LIBRENTI, MC SCAVINI, M POZZA, G BUCCI, V WINGROVE, T CAFFERTY, M DAY, J SARMIENTO, M BLACKSHEAR, P AF SELAM, JL MICOSSI, P DUNN, FL NATHAN, DM FOGEL, H GAZ, R HAGGEN, C MCKITRICK, C LARKIN, M DUNN, F LAVINTOMPLINS, J THOMPSON, M BYRD, P SAKIEWICZ, L GRANT, J SELAM, JL CHARLES, MA WAXMAN, K RACCAH, D JEANDIDIER, N LOZANO, J MICOSSI, P CRISTALLO, M GALIMBERTI, G PETRELLA, G LIBRENTI, MC SCAVINI, M POZZA, G BUCCI, V WINGROVE, T CAFFERTY, M DAY, J SARMIENTO, M BLACKSHEAR, P TI CLINICAL-TRIAL OF PROGRAMMABLE IMPLANTABLE INSULIN PUMP FOR TYPE-I DIABETES SO DIABETES CARE LA English DT Article ID INTRAPERITONEAL; INFUSION; DELIVERY; THERAPY; SYSTEM AB OBJECTIVE - The first step in the evolution of an artificial pancreas is the development of a reliable implantable pump for insulin delivery. Despite recent advances, significant issues remain, including small size of studies and frequent irreversible catheter obstructions. We report safety, feasibility, and efficacy results from 56 patients, representing 73 patient-yr of pump experience, entered into a multicenter trial with a new implantable programmable pump. RESEARCH DESIGN AND METHODS - All patients had insulin-dependent (type I) diabetes, were 38 +/- 8 yr old, and were not prone to severe hypoglycemia. The pump (Infusaid 1000) has a pulsatile mechanism powered by freon-vapor pressure. Its rate is regulated by battery- powered valves, operated via a hand-held programmer. The pump is refilled transcutaneously with 25 ml U100 insulin (Hoechst 21PH) on a monthly basis and has a second septum (side port) proximal to the catheter, which allows flushing the catheter or lavaging the pump unit. The pumps were implanted after 3 mo intensive subcutaneous insulin therapy and catheters were positioned either in the peritoneum (i.p., n = 38) or the superior vena cava (i.v., n = 18). RESULTS - All implanted pumps have functioned safely with no instance of overdelivery or stoppage. The most frequent complications were flow slow downs, presumably due to insulin precipitation within the pump, which occurred in 86% of pumps and were resolved in all but one case by lavaging the pump in situ with alkaline solution. Flow slow downs due to catheter obstruction occurred in 52% of the intravenous catheters but only 21% of the intraperitoneal catheters (P < 0.05) and were resolved in all but two cases by diluent flushing through the sideport. Incidence of severe hypoglycemia decreased from 0.47 before implant to 0.05 episodes/patient-yr after pump implantation (P < 0.001). Mean HbA1c fell from 7.4 +/- 1.2% after intensive subcutaneous therapy to 7.1 +/- 1.0% 12 mo after implantation. Only 2 patients withdrew from study after recurrent catheter problems, and quality-of-life questionnaires showed improvement in satisfaction with diabetes-specific quality of life when on implantable pump therapy. CONCLUSIONS - Insulin therapy with implantable pumps is effective and safe for periods up to 1.7 yr with a decreased risk of severe hypoglycemia than with intensive subcutaneous insulin therapy. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DIABET UNIT, 32 FRUIT ST, BOSTON, MA 02114 USA. UNIV CALIF IRVINE, DEPT MED, IRVINE, CA 92717 USA. UNIV MILAN, SCH MED, SAN RAFFAELE INST, I-20122 MILAN, ITALY. DUKE UNIV, MED CTR, DURHAM, NC 27710 USA. FU NCRR NIH HHS [M01-RR-30, RR-01066] NR 31 TC 75 Z9 75 U1 0 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 EI 1935-5548 J9 DIABETES CARE JI Diabetes Care PD JUL PY 1992 VL 15 IS 7 BP 877 EP 885 DI 10.2337/diacare.15.7.877 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ646 UT WOS:A1992HZ64600012 PM 1516508 ER PT J AU MACLAUGHLIN, DT HUDSON, PL GRACIANO, AL KENNEALLY, MK RAGIN, RC MANGANARO, TF DONAHOE, PK AF MACLAUGHLIN, DT HUDSON, PL GRACIANO, AL KENNEALLY, MK RAGIN, RC MANGANARO, TF DONAHOE, PK TI MULLERIAN DUCT REGRESSION AND ANTIPROLIFERATIVE BIOACTIVITIES OF MULLERIAN INHIBITING SUBSTANCE RESIDE IN ITS CARBOXY-TERMINAL DOMAIN SO ENDOCRINOLOGY LA English DT Article ID GROWTH FACTOR-BETA; OVARIAN FOLLICULAR-FLUID; AMINO-ACID-SEQUENCE; COLONY GROWTH; TGF-BETA; PROTEIN; HORMONE; FETAL; CELLS; PURIFICATION AB A 25-kilodalton dimeric carboxy-terminal fragment of the recombinant human Mullerian inhibiting substance protein (rhMIS) was produced by proteolytic cleavage with plasmin and purified by size-exclusion chromatography. The identity of the isolated dimer as the carboxy-terminal fragment was confirmed by gel electrophoresis and Western analysis. As was true of every sample of the holo molecule, all preparations of the carboxy-terminal domain of rhMIS (n = 10), when added in the 0.5-5.0-mu-g/ml range, exhibited a dose-dependent partial to complete regression of the 14.5-day fetal rat Mullerian duct in an organ culture assay. The carboxy-terminal dimer also inhibited, in a dose-dependent manner, the growth of A431 cells in monolayer cultures. Daily addition of 5, 10, or 20-mu-g carboxy-terminus for 3 days resulted in 0%, 25%, and 100% inhibition of cell proliferation, respectively. Similar and higher doses of holo rhMIS had no or inconsistent antiproliferative activity (0-34% inhibition), even though the preparations caused Mullerian duct regression. All amino-terminal fragments prepared using this separation protocol were found to be inactive in these assays. These findings suggest that the bioactivity of rhMIS as a regressor of fetal Mullerian ducts and an inhibitor of A431 cell growth resides in its carboxy-terminal domain. These results indicate that the urogenital ridge tissue, but not A431 cells in culture, may be capable of cleaving intact MIS to a biologically active conformation. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP MASSACHUSETTS GEN HOSP, PEDIAT SURG LABS, WARREN 11, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA-17393] NR 43 TC 46 Z9 48 U1 0 U2 0 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JUL PY 1992 VL 131 IS 1 BP 291 EP 296 DI 10.1210/en.131.1.291 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JC258 UT WOS:A1992JC25800043 PM 1612008 ER PT J AU HIRAYAMA, F CLARK, SC OGAWA, M AF HIRAYAMA, F CLARK, SC OGAWA, M TI GROWTH-FACTOR REQUIREMENT OF LYMPHOHEMATOPOIETIC PROGENITORS SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 VET AFFAIRS MED CTR,RALPH H JOHNSON DEPT,CHARLESTON,SC. MED UNIV S CAROLINA,CHARLESTON,SC 29425. GENET INST,CAMBRIDGE,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JUL PY 1992 VL 20 IS 6 BP 734 EP 734 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA JA734 UT WOS:A1992JA73400118 ER PT J AU SHIH, JP OGAWA, M AF SHIH, JP OGAWA, M TI MONOCLONAL-ANTIBODY J11D2 RECOGNIZES THE CELL CYCLE-DORMANT MULTIPOTENTIAL PROGENITORS SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 RALPH H JOHNSON VA MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,CHARLESTON,SC 29425. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JUL PY 1992 VL 20 IS 6 BP 742 EP 742 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA JA734 UT WOS:A1992JA73400150 ER PT J AU ROSS, LO TRECO, D NICOLAS, A SZOSTAK, JW DAWSON, D AF ROSS, LO TRECO, D NICOLAS, A SZOSTAK, JW DAWSON, D TI MEIOTIC RECOMBINATION ON ARTIFICIAL CHROMOSOMES IN YEAST SO GENETICS LA English DT Article ID DOUBLE-STRAND BREAKS; SACCHAROMYCES-CEREVISIAE; GENE CONVERSION; INITIATION SITE; MITOTIC STABILITY; SEGREGATION; DNA; MAP; INTERFERENCE; SYNAPSIS AB We have examined the meiotic recombination characteristics of artificial chromosomes in Saccharomyces cerevisiae. Our experiments were carried out using minichromosome derivatives of yeast chromosome III and yeast artificial chromosomes composed primarily of bacteriophage lambda-DNA. Tetrad analysis revealed that the artificial chromosomes exhibit very low levels of meiotic recombination. However, when a 12.5-kbp fragment from yeast chromosome VIII was inserted into the right arm of the artificial chromosome, recombination within that arm mimicked the recombination characteristics of the fragment in its natural context including the ability of crossovers to ensure meiotic disjunction. Both crossing over and gene conversion (within the ARG4 gene contained within the fragment) were measured in the experiments. Similarly, a 55-kbp region from chromosome III carried on a minichromosome showed crossover behavior indistinguishable from that seen when it is carried on chromosome III. We discuss the notion that, in yeast, meiotic recombination behavior is determined locally by small chromosomal regions that function free of the influence of the chromosome as a whole. C1 UNIV PARIS 11,INST GENET & MICROBIOL,F-91405 ORSAY,FRANCE. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. TKT INC,CAMBRIDGE,MA 02139. RP ROSS, LO (reprint author), TUFTS UNIV,DEPT MOLEC BIOL & MICROBIOL,BOSTON,MA 02111, USA. FU NIGMS NIH HHS [GM40452] NR 41 TC 33 Z9 33 U1 1 U2 2 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD JUL PY 1992 VL 131 IS 3 BP 541 EP 550 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA HZ815 UT WOS:A1992HZ81500004 PM 1385793 ER PT J AU JACOBY, AF YOUNG, RH COLVIN, RB FLOTTE, TJ PREFFER, F SCULLY, RE SWYMER, CM BELL, DA AF JACOBY, AF YOUNG, RH COLVIN, RB FLOTTE, TJ PREFFER, F SCULLY, RE SWYMER, CM BELL, DA TI DNA CONTENT IN JUVENILE GRANULOSA-CELL TUMORS OF THE OVARY - A STUDY OF EARLY-STAGE AND ADVANCED-STAGE DISEASE SO GYNECOLOGIC ONCOLOGY LA English DT Article ID FLOW CYTOMETRIC ANALYSIS; PLOIDY LEVEL; CANCER; CARCINOMA; SURVIVAL C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 18 TC 10 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD JUL PY 1992 VL 46 IS 1 BP 97 EP 103 DI 10.1016/0090-8258(92)90203-U PG 7 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA JH518 UT WOS:A1992JH51800019 PM 1634146 ER PT J AU GRAEMECOOK, F PILCH, BZ AF GRAEMECOOK, F PILCH, BZ TI HAMARTOMAS OF THE NOSE AND NASOPHARYNX SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK LA English DT Article ID RHABDOMYOMA AB Hamartomas are easily diagnosed entities when occurring in the lung and gastrointestinal tract. In the nose and nasopharynx, where such lesions are rare, biopsy of a hamartoma containing epithelial proliferation may lead to a misdiagnosis of cancer, with resultant radical and deforming surgery, particularly if they present in adulthood. We encountered three such lesions over 2 years in the Massachusetts Eye Ear Infirmary, and another was retrieved from the recent files. All presented with nonspecific obstructive symptoms of the nose or nasopharynx, and were treated by resection. Follow-up is short, (4 months to 1 year), but in no case has there been recurrence. The clinical diagnosis was malignancy in 2 cases, inflammatory polyp in one. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP GRAEMECOOK, F (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114, USA. NR 24 TC 25 Z9 30 U1 2 U2 2 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1043-3074 J9 HEAD NECK-J SCI SPEC JI Head Neck-J. Sci. Spec. Head Neck PD JUL-AUG PY 1992 VL 14 IS 4 BP 321 EP 327 DI 10.1002/hed.2880140413 PG 7 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA HY213 UT WOS:A1992HY21300012 PM 1517084 ER PT J AU SCHILLER, JH BITTNER, G OBERLEY, TD KAO, C HARRIS, C MEISNER, LF AF SCHILLER, JH BITTNER, G OBERLEY, TD KAO, C HARRIS, C MEISNER, LF TI ESTABLISHMENT AND CHARACTERIZATION OF A SV40 T-ANTIGEN IMMORTALIZED HUMAN BRONCHIAL EPITHELIAL-CELL LINE SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL LA English DT Letter ID HUMAN UROEPITHELIAL CELLS; TRANSFORMATION; TRANSFECTION; INVITRO; VIRUS C1 UNIV WISCONSIN,CTR CLIN CANC,DEPT MED,MADISON,WI 53792. UNIV WISCONSIN,CTR CLIN CANC,DEPT PATHOL,MADISON,WI 53792. UNIV WISCONSIN,CTR CLIN CANC,DEPT CYTOGENET,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP SCHILLER, JH (reprint author), UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,K4-666 CLIN SCI CTR,MADISON,WI 53792, USA. NR 9 TC 15 Z9 15 U1 1 U2 1 PU SOC IN VITRO BIOLOGY PI COLUMBIA PA 8815 CENTRE PARK DR,STE 210, COLUMBIA, MD 21045 SN 1071-2690 J9 IN VITRO CELL DEV-AN JI In Vitro Cell. Dev. Biol.-Anim. PD JUL-AUG PY 1992 VL 28A IS 7-8 BP 461 EP 464 PG 4 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA JN521 UT WOS:A1992JN52100001 PM 1522038 ER PT J AU ZUCKERMAN, SH QURESHI, N AF ZUCKERMAN, SH QURESHI, N TI INVIVO INHIBITION OF LIPOPOLYSACCHARIDE-INDUCED LETHALITY AND TUMOR-NECROSIS-FACTOR SYNTHESIS BY RHODOBACTER-SPHAEROIDES DIPHOSPHORYL LIPID-A IS DEPENDENT ON CORTICOSTERONE INDUCTION SO INFECTION AND IMMUNITY LA English DT Article ID 17023 BLOCKS INDUCTION; ENDOTOXIN-SHOCK; SEPTIC SHOCK; STRUCTURAL DETERMINATION; SALMONELLA-TYPHIMURIUM; MONOCLONAL-ANTIBODIES; MACROPHAGES; CACHECTIN; MICE; INTERLEUKIN-1 AB Diphosphoryl lipid A from the lipopolysaccharide (LPS) of Rhodobacter sphaeroides (Rs-DPLA) has been demonstrated to block in mice and guinea pigs the increase in the serum tumor necrosis factor (TNF) response induced by highly purified deep rough chemotype LPS from Escherichia coli D31m4 (ReLPS). The present study was designed to determine the role of corticosterone induction by Rs-DPLA and its effect on TNF regulation and survival in lethal endotoxin shock models and to evaluate the ability of Rs-DPLA to induce endotoxin tolerance. Administration of a 100-fold excess of Rs-DPLA 1 h prior to ReLPS administration inhibited the characteristic peak in serum TNF levels induced by LPS. Inhibition was apparent in normal and D-galactosamine (GalN)-sensitized mice and occurred at the pretranslational level, as splenic TNF and interleukin-1-beta-mRNAs were present in lower amounts in LPS-stimulated mice pretreated with Rs-DPLA. Consistent with its effects in reducing serum TNF levels, Rs-DPLA pretreatment protected GalN-sensitized mice from a lethal ReLPS challenge. In contrast, Rs-DPLA did not inhibit the increase in the serum TNF response or protect against a lethal ReLPS challenge in parallel experiments with adrenalectomized (Adrex) mice, for which the 50% lethal dose of ReLPS was comparable to that for GalN-sensitized mice. Furthermore, Rs-DPLA appeared to prime Adrex animals and increase the magnitude of the serum TNF response to a suboptimal LPS stimulus. Priming by Rs-DPLA, however, was not observed in normal or GalN-sensitized mice. Although Rs-DPLA by itself was nontoxic and unable to elevate serum TNF levels in any of the models investigated, it did induce a significant increase in the serum corticosterone response and was capable of inducing endotoxin tolerance in normal mice. The inability of Rs-DPLA to protect Adrex mice from a lethal ReLPS stimulus or to inhibit the increase in the serum TNF response suggests that the protective effect of Rs-DPLA in normal or GalN-sensitized animals occurs through corticosterone induction. These results support the concept that endogenous glucocorticoids can modulate the endotoxic effects of LPS by inhibiting the synthesis of inflammatory cytokines. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. RP ZUCKERMAN, SH (reprint author), ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285, USA. FU NIGMS NIH HHS [GM-36054] NR 49 TC 35 Z9 37 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 1992 VL 60 IS 7 BP 2581 EP 2587 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JB247 UT WOS:A1992JB24700004 PM 1612727 ER PT J AU GALGIANI, JN SUN, SH DUGGER, KO AMPEL, NM GRACE, GG HARRISON, J WIEDEN, MA AF GALGIANI, JN SUN, SH DUGGER, KO AMPEL, NM GRACE, GG HARRISON, J WIEDEN, MA TI AN ARTHROCONIDIAL-SPHERULE ANTIGEN OF COCCIDIOIDES-IMMITIS - DIFFERENTIAL EXPRESSION DURING INVITRO FUNGAL DEVELOPMENT AND EVIDENCE FOR HUMORAL RESPONSE IN HUMANS AFTER INFECTION OR VACCINATION SO INFECTION AND IMMUNITY LA English DT Article ID LINKED IMMUNOSORBENT-ASSAY; TUBE PRECIPITIN ANTIGEN; ANTIBODY; RESISTANCE; EXTRACTION; PROTEIN AB A 33-kDa protein antigen purified from spherules of Coccidioides immitis was analyzed for ultrastructural localization and for binding to serum antibodies from infected or immunized humans. By using colloidal gold detection of affinity-purified anti-33-kDa protein antibodies, electron photomicrographs showed binding to the inner cell wall of arthroconidia and spherules and to the septa and glycocalyx surrounding endospores. Enzyme immunoassay measurements also demonstrated that the antigen was most abundant in mature spherules. Of 37 patients with coccidioidomycosis but without concurrent human immunodeficiency virus infections, all but 2 demonstrated immunoglobulin M (IgM) (usually with early infection) or IgG antibodies for the 33-kDa antigen. In contrast, only one of four HIV-infected patients with active coccidioidal infections demonstrated antibody. On the other hand, 107 of 108 patients without evident coccidioidomycosis and 15 of 16 patients with histoplasmosis did not have similar antibodies, indicating a high degree of specificity. Immunization of humans with a spherule vaccine produced IgM responses to this antigen that were not evident in placebo recipients. C1 VET AFFAIRS MED CTR,RES SERV,SAN ANTONIO,TX 78284. VET AFFAIRS MED CTR,LAB SERV,TUCSON,AZ 85723. UNIV ARIZONA,COLL MED,DEPT MED,TUCSON,AZ 85724. RP GALGIANI, JN (reprint author), VET AFFAIRS MED CTR,MED & RES SERV,TUCSON,AZ 85723, USA. NR 45 TC 26 Z9 26 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 JUL PY 1992 VL 60 IS 7 BP 2627 EP 2635 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JB247 UT WOS:A1992JB24700011 PM 1612732 ER PT J AU BAKER, PJ HRABA, T TAYLOR, CE MYERS, KR TAKAYAMA, K QURESHI, N STUETZ, P KUSUMOTO, S HASEGAWA, A AF BAKER, PJ HRABA, T TAYLOR, CE MYERS, KR TAKAYAMA, K QURESHI, N STUETZ, P KUSUMOTO, S HASEGAWA, A TI STRUCTURAL FEATURES THAT INFLUENCE THE ABILITY OF LIPID-A AND ITS ANALOGS TO ABOLISH EXPRESSION OF SUPPRESSOR T-CELL ACTIVITY SO INFECTION AND IMMUNITY LA English DT Article ID III PNEUMOCOCCAL POLYSACCHARIDE; ANTIBODY-PRODUCING CELLS; RHODOPSEUDOMONAS-SPHAEROIDES; NONTOXIC LIPOPOLYSACCHARIDE; MICE; INACTIVATION; REQUIREMENTS; LYMPHOCYTES; MACROPHAGES; MAGNITUDE AB Lipid A preparations derived from the lipopolysaccharides of several gram-negative bacteria, as well as chemically defined synthetic lipid A's and their analogs (both glucosamine mono- and disaccharides), were used to establish the chemical structures required for (i) abolishing the expression of suppressor T cell (Ts) function and (ii) inducing polyclonal activation of B cells. Salmonella minnesota R595 lipid A (diphosphoryl lipid A) possesses both of these activities. Decreasing the number of phosphate groups in lipid A from two to one (monophosphoryl lipid A) as well as decreasing the fatty acyl content, primarily by removing the residue at the 3 position, resulted in a progressive reduction in toxicity; however, these structural modifications did not influence its ability to abolish the expression of Ts function. Reducing the fatty acyl content from five to four (lipid A precursor IV(A) or I(a)) eliminated the capacity to influence Ts function but not to induce polyclonal activation of B cells. None of the monosaccharide analogs of lipid A examined influenced the expression of Ts activity, although some were able to activate B cells polyclonally. Thus, in order to be able to abolish the expression of Ts function, lipid A (i) must be a glucosamine disaccharide, (ii) may have either one or two phosphate groups, and (iii) must have at least five fatty acyl groups. Also, the chain length of the nonhydroxylated fatty acid, as well as the location of acyloxyacyl groups (2' versus 3' position), may play an important role. These findings indicate that the chemical structures responsible for the toxicity of lipid A differ from those that influence its capacity to abolish the expression of Ts function and to induce polyclonal activation of B cells. C1 RIBI IMMUNOCHEM RES INC,HAMILTON,MT 59840. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. GIFU UNIV,DEPT APPL BIOORGAN CHEM,GIFU 50111,JAPAN. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. OSAKA UNIV,FAC SCI,DEPT CHEM,TOYONAKA,OSAKA 560,JAPAN. RP BAKER, PJ (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK 2 RES FACILITY,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 44 TC 22 Z9 22 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 1992 VL 60 IS 7 BP 2694 EP 2701 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JB247 UT WOS:A1992JB24700021 PM 1535339 ER PT J AU BRUNKHORST, BA KRAUS, E COPPI, M BUDNICK, M NIEDERMAN, R AF BRUNKHORST, BA KRAUS, E COPPI, M BUDNICK, M NIEDERMAN, R TI PROPIONATE INDUCES POLYMORPHONUCLEAR LEUKOCYTE ACTIVATION AND INHIBITS FORMYLMETHIONYL-LEUCYL-PHENYLALANINE-STIMULATED ACTIVATION SO INFECTION AND IMMUNITY LA English DT Article ID HUMAN-NEUTROPHILS; CHEMOTACTIC PEPTIDE; INTRACELLULAR PH; NA+/H+ EXCHANGE; ACTIN POLYMERIZATION; CYTOSKELETAL ACTIN; SUCCINIC ACID; FATTY-ACIDS; BY-PRODUCT; SODIUM AB Short-chain carboxylic acids (SCCA) are metabolic by-products of bacterial pathogens which can alter cytoplasmic pH and inhibit a variety of polymorphonuclear leukocyte (PMN) motile functions. Since cytoskeletal F-actin alterations are central to PMN mobility, in this study we examined the effects of SCCA on cytoskeletal F-actin. Initially, we tested nine SCCA (formate, acetate, propionate, butyrate, valerate, caproate, lactate, succinate, and isobutyrate). We document here that while eight altered cytoplasmic pH, only six altered cytoskeletal F-actin. We then selected one SCCA that altered both F-actin and cytoplasmic pH (propionate) and one SCCA that altered only cytoplasmic pH (lactate) for further study. Propionate, hut not lactate, caused an irregular cell shape and F-actin distribution. Furthermore, propionate, but not lactate, inhibited formylmethionyl-leucyl-phenylalanine (fMLP)-stimulated PMN polarization, F-actin localization, and cytoplasmic pH oscillation. Propionate-induced changes in cytoskeletal F-actin and cytoplasmic acidification were not affected by the fMLP receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine; however, alkalinization was affected. Pertussis toxin treatment completely inhibited propionate-induced changes in F-actin but had no effect on propionate-induced cytoplasmic pH oscillation. These results indicate that propionate (i) bypasses the fMLP receptor and G protein(s) to induce cytoplasmic pH oscillation, (ii) operates through G protein(s) to induce actin oscillation, cell shape changes (to irregular), and F-actin localization, and (iii) inhibits fMLP-stimulated cytoplasmic pH and actin oscillation, PMN polarization, and F-actin localization. C1 FORSYTH RES INST,DEPT CELL BIOL,140 THE FENWAY,BOSTON,MA 02115. FU NIDCR NIH HHS [DE-08415, DE-04881] NR 61 TC 38 Z9 40 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 1992 VL 60 IS 7 BP 2957 EP 2968 PG 12 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JB247 UT WOS:A1992JB24700058 PM 1319407 ER PT J AU KELLER, MB HERZOG, DB LAVORI, PW BRADBURN, IS MAHONEY, EM AF KELLER, MB HERZOG, DB LAVORI, PW BRADBURN, IS MAHONEY, EM TI THE NATURALISTIC HISTORY OF BULIMIA-NERVOSA - EXTRAORDINARILY HIGH-RATES OF CHRONICITY, RELAPSE, RECURRENCE, AND PSYCHOSOCIAL MORBIDITY SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article ID FOLLOW-UP; DEPRESSION; DISORDER; 2-YEAR AB This article extends our previous report on 30 women with bulimia nervosa by increasing the duration of follow-up to 35-42 months. We found surprisingly /ow rates of recovery and very high rates of chronicity, relapse, recurrence, and psychosocial morbidity. Almost one third of the subjects remained in the index episode 3 years after entry into the study. There was a 63% cumulative probability of relapse by 78 weeks after recovery. Fifty percent of subjects who recovered from the first prospective episode relapsed into another episode. Predictors of recovery included having less disturbed eating behaviors and self/body image at intake and having several good friends. C1 MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV CALIF BERKELEY,CLIN PSYCHOL,BERKELEY,CA 94720. RP KELLER, MB (reprint author), BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912, USA. NR 19 TC 71 Z9 71 U1 2 U2 2 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD JUL PY 1992 VL 12 IS 1 BP 1 EP 9 DI 10.1002/1098-108X(199207)12:1<1::AID-EAT2260120102>3.0.CO;2-E PG 9 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA JA329 UT WOS:A1992JA32900001 ER PT J AU CLEMENT, PB SCULLY, RE AF CLEMENT, PB SCULLY, RE TI ENDOMETRIAL STROMAL SARCOMAS OF THE UTERUS WITH EXTENSIVE ENDOMETRIOID GLANDULAR DIFFERENTIATION - A REPORT OF 3 CASES THAT CAUSED PROBLEMS IN DIFFERENTIAL-DIAGNOSIS SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE UTERUS; ENDOMETRIUM; ENDOMETRIAL STROMAL SARCOMA; GLANDULAR DIFFERENTIATION; ADENOSARCOMA; ADENOMYOSIS; ENDOMETRIOSIS; AGGRESSIVE ENDOMETRIOSIS; UTERINE TUMOR RESEMBLING OVARIAN SEX-CORD TUMOR; ENDOMETRIAL ADENOCARCINOMA; MALIGNANT MULLERIAN MIXED TUMOR ID CLINICOPATHOLOGIC ANALYSIS; UTERINE-TUMORS; NEOPLASMS; ELEMENTS AB Three cases of endometrial stromal sarcoma (ESS) with prominent glandular differentiation within the primary or recurrent tumors are described. Each case posed a problem in diagnosis and classification. The patients, who ranged in age from 41 to 47 years, presented with abnormal uterine bleeding, a pelvic mass, or a combination thereof. All the patients underwent hysterectomy with or without bilateral salpingo-oophorectomy. There was no evidence of extrauterine spread of tumor in any case. Polypoid tumors involved the endometrium in two cases, and in one of them, tumor deeply invaded the myometrium. The tumor in the third case was an infiltrative mass that was confined to the myometrium and its vessels. On microscopic examination, the tumors were low-grade ESSs that contained large numbers of endometrioid glands, which were benign appearing in two cases, and in the third varied from atypical to carcinomatous. In one of the cases in the first group, the glandular component was present only in recurrent tumor excised 10 years after hysterectomy; prominent foci of sex-cord-like differentiation were also present in the recurrent tumor. This patient was clinically free of tumor 27 months later; follow-up in the other two patients was uneventful. ESSs with prominent numbers of benign-appearing glands should be distinguished from adenomyosis, endometriosis, ESSs arising in adenomyosis or endometriosis, ESSs with sex-cord-like differentiation, and mullerian adenosarcomas. ESSs with carcinomatous glands should be distinguished from endometrial adenocarcinomas and malignant mullerian mixed tumors (carcinosarcomas). Extrauterine lesions that have been designated "aggressive endometriosis" may be examples of extrauterine ESS with prominent glandular differentiation. C1 UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER V6T 1W5,BC,CANADA. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CLEMENT, PB (reprint author), VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER V5Z 1M9,BC,CANADA. NR 21 TC 73 Z9 74 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD JUL PY 1992 VL 11 IS 3 BP 163 EP 173 PG 11 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA JA559 UT WOS:A1992JA55900001 PM 1399225 ER PT J AU PETERSHEIM, M MOLDOW, RL HALLADAY, HN KASTIN, AJ FISCHMAN, AJ AF PETERSHEIM, M MOLDOW, RL HALLADAY, HN KASTIN, AJ FISCHMAN, AJ TI CONFORMATIONAL STUDIES OF N-TYR-MIF-1 IN AQUEOUS-SOLUTION BY H-1 NUCLEAR-MAGNETIC-RESONANCE SPECTROSCOPY SO INTERNATIONAL JOURNAL OF PEPTIDE AND PROTEIN RESEARCH LA English DT Article DE CONFORMATION; COSY; NOESY; NMR; N-TYR-MIF-1 ID PASSIVE-AVOIDANCE BEHAVIOR; RELEASE-INHIBITING FACTOR; MOTOR-ACTIVITY; BRAIN-TISSUE; RAT-BRAIN; TYR-MIF-1; ANALOGS; NMR; TYR-PRO-LEU-GLY-NH2; MELANOSTATIN AB N-Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) is an endogenous brain peptide with multiple effects on animal behavior. However, there have been no studies on the conformation of this tetrapeptide. In this report, we studied the conformation of N-Tyr-MIF-1 in aqueous solution by conventional one-dimensional and two-dimensional (COSY and NOESY) H-1 nuclear magnetic resonance spectroscopy at 300 MHz. A complete set of assignments for the resolved resonances and approximate assignments for the overlapping resonances were made. The results demonstrate that N-Tyr-MIF-1 is in slow exchange between two conformers, most likely determined by the cis and trans states of the proline residue. The minor conformation represents 30 +/- 3 % of the population over the temperature range from 3-degrees to 73-degrees. In the major conformation, the tyrosine aromatic ring appears to be close enough to interact directly with the proline pyrrolidine ring, as indicated by a strong temperature dependence of the proline C(beta)H, C(delta)H and C(delta)H' chemical shifts. In contrast, this interaction of the tyrosine and proline rings is not present in the minor conformation. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114. SETON HALL UNIV,DEPT CHEM,S ORANGE,NJ 07079. SETON HALL UNIV,DEPT BIOL,S ORANGE,NJ 07079. VET AFFAIRS MED CTR,NEW ORLEANS,LA. TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NR 34 TC 3 Z9 3 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0367-8377 J9 INT J PEPT PROT RES JI Int. J. Pept. Protein Res. PD JUL PY 1992 VL 40 IS 1 BP 41 EP 48 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JP054 UT WOS:A1992JP05400006 PM 1358850 ER PT J AU NITSCHKE, R PRATT, C HARRIS, M KRISCHER, J VIETTI, TJ GRIER, H KAMPS, W TOLEDANO, S AF NITSCHKE, R PRATT, C HARRIS, M KRISCHER, J VIETTI, TJ GRIER, H KAMPS, W TOLEDANO, S TI EVALUATION OF CHIP (IPROPLATIN) IN RECURRENT PEDIATRIC MALIGNANT SOLID TUMORS - A PHASE-II STUDY (PEDIATRIC ONCOLOGY GROUP) SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE CHIP; PEDIATRIC MALIGNANCIES; RECURRENT PEDIATRIC MALIGNANT SOLID TUMORS; PHASE-II STUDY AB CHIP (325 mg/M2), a second generation cisplatin derivative, was administered intravenously every 3 weeks to 85 pediatric patients with recurrent sarcomas (19), osteosarcomas (20), neuroblastoma (23), germ cell tumors (10), and other malignant tumors (7). Thirty-eight of them had been previously exposed to cisplatin. Partial remissions were only observed in 3 of 23 (13% SE = 7%) patients having neuroblastoma. Severe thrombocytopenia (65%) and neutropenia (35%) were the dose limiting factors. C1 OKLAHOMA HLTH SCI CTR, OKLAHOMA CITY, OK USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. HACKENSACK MED CTR, HACKENSACK, NJ USA. UNIV FLORIDA, STAT OFF, PEDIAT ONCOL GRP, GAINESVILLE, FL 32611 USA. WASHINGTON UNIV, SCH MED, ST LOUIS, MO 63110 USA. UNIV GRONINGEN, 9700 AB GRONINGEN, NETHERLANDS. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. UNIV MIAMI, SCH MED, MIAMI, FL 33152 USA. FU NCI NIH HHS [CA-11233, CA-29139, CA-31566] NR 10 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PD JUL PY 1992 VL 10 IS 2 BP 93 EP 96 DI 10.1007/BF00873123 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA JF515 UT WOS:A1992JF51500005 PM 1323551 ER PT J AU ALBERT, DM MARCUS, DM GALLO, JP OBRIEN, JM AF ALBERT, DM MARCUS, DM GALLO, JP OBRIEN, JM TI THE ANTINEOPLASTIC EFFECT OF VITAMIN-D IN TRANSGENIC MICE WITH RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE RETINOBLASTOMA; TRANSGENIC MICE; VITAMIN-D; 1,25 DIHYDROXYCHOLECALCIFEROL; ANGIOGENESIS ID CELL-LINE; MONOCYTIC DIFFERENTIATION; XENOGRAFT MODEL; INHIBITION; CANCER; GROWTH; 1,25-DIHYDROXYVITAMIN-D3; CHEMOTHERAPY; RECEPTORS; PROLIFERATION AB Vitamin D has been shown to inhibit growth of human retinoblastoma in tissue culture and nude mouse heterografts. We have described a heritable transgenic mouse model of retinoblastoma. The in vivo efficacy of 1,25-dihydroxycholecalciferol (vitamin D3) was examined by administering this agent to transgenic mice with retinoblastoma. Forty-six 8-10-week-old transgene-bearing mice were injected intraperitoneally for 5 wk. Experimental animals received 0.05-mu-g (15 animals) or 0.025-mu-g (15 animals) of vitamin D. Sixteen control animals received only a mineral oil vehicle. Eyes were enucleated at 5 mo and were examined histologically by two investigators in a masked fashion. All control animals demonstrated bilateral involvement of retinoblastoma. Four eyes in the low-dose group and six eyes in the high-dose group had no evidence of retinoblastoma. Eyes treated with vitamin D3 showed less extensive involvement of the retina by retinoblastoma. Vitamin D-treated animals demonstrated tumors confined to the retina, whereas control animals demonstrated larger tumors, more often invading the vitreous, anterior chamber, and choroid. Thus, Vitamin D inhibited the growth and local extension in a dose-dependent fashion. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DAVID G COGAN EYE PATHOL LAB,BOSTON,MA 02114. FU NEI NIH HHS [EY01917] NR 47 TC 30 Z9 31 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JUL PY 1992 VL 33 IS 8 BP 2354 EP 2364 PG 11 WC Ophthalmology SC Ophthalmology GA JE509 UT WOS:A1992JE50900002 PM 1634333 ER PT J AU HYLEK, EM AF HYLEK, EM TI HOW THE DOCTOR GOT GAGGED SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP HYLEK, EM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 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 JUL 1 PY 1992 VL 268 IS 1 BP 50 EP 51 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JA165 UT WOS:A1992JA16500010 PM 1472193 ER PT J AU PAPADEMETRIOU, V AF PAPADEMETRIOU, V TI DIURETICS, POTASSIUM, AND VENTRICULAR ARRHYTHMIAS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID SYSTEMIC HYPERTENSION; THERAPY RP PAPADEMETRIOU, V (reprint author), US DEPT VET AFFAIRS,WASHINGTON,DC 20420, USA. OI Papademetriou, Vasilios/0000-0002-2882-2757 NR 6 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 JUL 1 PY 1992 VL 268 IS 1 BP 52 EP 53 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JA165 UT WOS:A1992JA16500014 PM 1608108 ER PT J AU MANSON, JE NATHAN, DM KROLEWSKI, AS STAMPFER, MJ WILLETT, WC HENNEKENS, CH AF MANSON, JE NATHAN, DM KROLEWSKI, AS STAMPFER, MJ WILLETT, WC HENNEKENS, CH TI A PROSPECTIVE-STUDY OF EXERCISE AND INCIDENCE OF DIABETES AMONG UNITED-STATES MALE PHYSICIANS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID GLUCOSE-TOLERANCE; POLYNESIAN POPULATION; PREVALENCE; MELLITUS; PACIFIC; RISK AB Objective.-To examine prospectively the association between regular exercise and the subsequent development of non-insulin-dependent diabetes mellitus (NIDDM). Design.-Prospective cohort study including 5 years of follow-up. Participants.-21 271 US male physicians participating in the Physicians' Health Study, aged 40 to 84 years and free of diagnosed diabetes mellitus, myocardial infarction, cerebrovascular disease, and cancer at baseline. Morbidity follow-up was 99.7% complete. Main Outcome Measure.-Incidence of NIDDM. Results.-At baseline, information was obtained about frequency of vigorous exercise and other risk indicators. During 105 141 person-years of follow-up, 285 new cases of NIDDM were reported. The age-adjusted incidence of NIDDM ranged from 369 cases per 1 00 000 person-years in men who engaged in vigorous exercise less than once weekly to 214 cases per 1 00 000 person-years in those exercising at least five times per week (P, trend, <.001). Men who exercised at least once per week had an age-adjusted relative risk (RR) of NIDDM of 0.64 (95% Cl, 0.51 to 0.82; P=.0003) compared with those who exercised less frequently. The age-adjusted RR of NIDDM decreased with increasing frequency of exercise: 0.77 for once weekly, 0.62 for two to four times per week, and 0.58 for five or more times per week (P, trend, .0002). A significant reduction in risk of NIDDM persisted after adjustment for both age and body-mass index: RR, 0.71 (95% Cl, 0.56 to 0.91; P=.006) for at least once per week compared with less than once weekly, and P, trend, .009, for increasing frequency of exercise. Further control for smoking, hypertension, and other coronary risk factors did not materially alter these associations. The inverse relation of exercise to risk of NIDDM was particularly pronounced among overweight men. Conclusions.-Exercise appears to reduce the development of NIDDM even after adjusting for body-mass index. Increased physical activity may be a promising approach to the primary prevention of NIDDM. C1 HARVARD UNIV,SCH MED,CHANNING LAB,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PREVENT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIABET RES CTR,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. FU NCI NIH HHS [CA 40356]; NIDDK NIH HHS [DK 36798] NR 35 TC 446 Z9 457 U1 2 U2 23 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 JUL 1 PY 1992 VL 268 IS 1 BP 63 EP 67 DI 10.1001/jama.268.1.63 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JA165 UT WOS:A1992JA16500024 PM 1608115 ER PT J AU MCKINSTRY, RC WEISKOFF, RM BELLIVEAU, JW VEVEA, JM MOORE, JB KWONG, KW HALPERN, EF ROSEN, BR AF MCKINSTRY, RC WEISKOFF, RM BELLIVEAU, JW VEVEA, JM MOORE, JB KWONG, KW HALPERN, EF ROSEN, BR TI ULTRAFAST MR IMAGING OF WATER MOBILITY - ANIMAL-MODELS OF ALTERED CEREBRAL PERFUSION SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE BRAIN; BRAIN, PERFUSION; CEREBRAL BLOOD VESSELS, FLOW DYNAMICS; CEREBRAL BLOOD VESSELS; DIFFUSION IMAGING; ECHO-PLANAR IMAGING; RAPID IMAGING AB "Single shot" magnetic resonance (MR) diffusion imaging was used to study the details of signal decay curves in experimental perturbations of cerebral perfusion induced by hypercapnia or death. Despite large perfusion increases observed with dynamic susceptibility-contrast MR imaging, no correlation with these changes was seen in either the diffusion coefficient or any other intravoxel incoherent motion (IVIM) model parameters in dog gray matter as arterial carbon dioxide pressure increased. Non-monoexponential signal decay in cat gray matter was seen both before and after death. In addition, cat gray matter demonstrated a steady decrease in the diffusion coefficient after death. These data are strong evidence that the fast component of the non-monoexponential diffusion-related signal decay is not due solely to perfusion. The authors believe that a second compartment of nonexchanging spins, most likely cerebrospinal fluid, accounts for the non-monoexponential decay. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,CTR MGH NMR,BLDG 149,13TH ST,BOSTON,MA 02129. FU NCI NIH HHS [CA 40303]; NHLBI NIH HHS [R01 HL39810] NR 0 TC 13 Z9 13 U1 0 U2 1 PU SOC MAGNETIC RESONANCE IMAGING PI EASTON PA 1991 NORTHAMPTON ST, EASTON, PA 18042-3189 SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD JUL-AUG PY 1992 VL 2 IS 4 BP 377 EP 384 DI 10.1002/jmri.1880020404 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JD695 UT WOS:A1992JD69500003 PM 1633389 ER PT J AU KREFT, BP TANIMOTO, A BABA, Y ZHAO, LH CHEN, J MIDDLETON, MS COMPTON, CC FINN, JP STARK, DD AF KREFT, BP TANIMOTO, A BABA, Y ZHAO, LH CHEN, J MIDDLETON, MS COMPTON, CC FINN, JP STARK, DD TI DIAGNOSIS OF FATTY LIVER WITH MR IMAGING SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE CONTRAST ENHANCEMENT; GADOLINIUM; IRON; LIVER, DISEASES; LIVER, CIRRHOSIS; LIVER, FATTY; LIVER; MANGANESE AB The diagnosis of fatty liver with magnetic resonance (MR) imaging was evaluated in experimental rat models of simple fatty infiltration and fatty liver with hepatocellular injury. T1 and T2 were measured ex vivo and correlated with the histologic degree of fatty infiltration. Enhancement of fatty liver with four different cell-specific contrast agents was studied with ex vivo relaxometry and in vivo MR imaging. Quantitative analysis of conventional and chemical shift MR images was correlated with biochemically determined fat content of the liver. Diet-induced simple fatty infiltration of the liver caused a decrease in T1 of 15%. whereas the T1 of L-ethionine-induced fatty liver with hepatocellular injury increased by 12%. T2 showed a positive correlation with the degree of fatty infiltration in both models. Cell-specific hepatobiliary contrast agents showed the same liver uptake and relaxation enhancement in fatty livers as in normal livers. Conventional T1-weighted images and chemical shift images showed good correlation (r = .83 and .80, respectively) between signal intensity and the degree of fatty infiltration. However, only chemical shift imaging was reliable in the diagnosis of fatty liver. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. FU NCI NIH HHS [R01 CA50353-01] NR 0 TC 41 Z9 43 U1 3 U2 3 PU SOC MAGNETIC RESONANCE IMAGING PI EASTON PA 1991 NORTHAMPTON ST, EASTON, PA 18042-3189 SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD JUL-AUG PY 1992 VL 2 IS 4 BP 463 EP 471 DI 10.1002/jmri.1880020416 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JD695 UT WOS:A1992JD69500014 PM 1633400 ER PT J AU LI, J LORD, CI HASELTINE, W LETVIN, NL SODROSKI, J AF LI, J LORD, CI HASELTINE, W LETVIN, NL SODROSKI, J TI INFECTION OF CYNOMOLGUS MONKEYS WITH A CHIMERIC HIV-1/SIVMAC VIRUS THAT EXPRESSES THE HIV-1 ENVELOPE GLYCOPROTEINS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE CHIMERIC VIRUS; HIV SIV; CYNOMOLGUS MONKEY ID HUMAN-IMMUNODEFICIENCY-VIRUS; T-LYMPHOTROPIC RETROVIRUS; HTLV-III; PERSISTENT INFECTION; RHESUS-MONKEYS; TYPE-1 VPU; AIDS; CHIMPANZEES; PROTEIN; MACAQUES AB Replication competent chimeric viruses that express the gag and pol proteins of SIV(mac) and the env proteins of HIV-1 were made. One such chimeric virus, SHIV-4, that expresses the vif, vpx, vpr, and nef regulatory genes of SIV and the tat and rev, regulatory genes of HIV-1 replicated efficiently in cynomolgus monkeys. This model system can be used to evaluate the efficacy of anti-HIV-1 vaccines directed at the envelope glycoproteins, anti-HIV-1 envelope glycoprotein antiserum or monoclonal antibodies, and anti-HIV-1 drugs designed to inhibit the tat, rev, or env functions. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,HUMAN RETROVIROL LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,BOSTON,MA 02115. FU NIAID NIH HHS [AI24845] NR 57 TC 274 Z9 279 U1 1 U2 2 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 JUL PY 1992 VL 5 IS 7 BP 639 EP 646 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JB263 UT WOS:A1992JB26300001 PM 1613662 ER PT J AU SCHMALZRIED, TP JASTY, M HARRIS, WH AF SCHMALZRIED, TP JASTY, M HARRIS, WH TI PERIPROSTHETIC BONE LOSS IN TOTAL HIP-ARTHROPLASTY - POLYETHYLENE WEAR DEBRIS AND THE CONCEPT OF THE EFFECTIVE JOINT SPACE SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID AGGRESSIVE GRANULOMATOUS LESIONS; FEMORAL COMPONENTS; REPLACEMENT; RESORPTION; PROSTHESES; LYSIS AB Thirty-four hips in which there had been prosthetic replacement were selected for study because of the presence of linear (diffuse) or lytic (localized) areas of periprosthetic bone loss. In all hips, there was careful documentation of the anatomical location of the material that had been obtained for histological analysis, and the specific purpose of the removal of the tissue was for examination to determine the cause of the resorption of bone. Specimens from twenty-three hips were retrieved during an operation and from eleven hips, at autopsy. The area of bone loss was linear only in sixteen hips, lytic only in thirteen, and both linear and lytic in five. In all thirty-four hips, intracellular particulate debris was found in the macrophages that were present in the area of bone resorption. All thirty-four had intracellular particles of polyethylene, many of which were less than one micrometer in size. Thirty-one hips had extracellular particles of polyethylene as well. Twenty-two of the thirty-four hips had intracellular metallic debris; in ten, metallic debris was found extracellularly as well. Ten of the sixteen cemented specimens had intracellular and extracellular polymethylmethacrylate debris. In the mechanically stable prostheses - cemented and uncemented - polyethylene wear debris was identified in areas of bone resorption far from the articular surfaces. The number of macrophages in a microscopic field was directly related to the amount of particulate polyethylene debris that was visible by light microscopy. Although the gross radiographic appearances of linear bone loss and lytic bone loss were different, the histological appearance of the regions in which there was active bone resorption was similar. Regardless of the radiographic appearance and anatomical origin of the specimen, bone resorption was found to occur in association with macrophages that were laden with polyethylene debris. In general, the number of macrophages present had a direct relationship to the degree of bone resorption that was seen. We believe that these findings indicate that joint fluid penetrates far more extensively than previously thought, even in a well fixed component, along the interface between the prosthesis and bone and in the periprosthetic tissues; it is often more extensive than is shown by arthrography. We therefore suggest the concept of the effective joint space to include all periprosthetic regions that are accessible to joint fluid and thus accessible to particulate debris. We also suggest that the difference between lytic (localized) bone loss and linear (diffuse) bone loss may be related to the local concentration or distribution of particulate wear debris; this may in turn depend on patterns of the flow of joint fluid (preferential flow) within the effective joint space. RP SCHMALZRIED, TP (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114, USA. NR 46 TC 793 Z9 808 U1 3 U2 36 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 JUL PY 1992 VL 74A IS 6 BP 849 EP 863 PG 15 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JH485 UT WOS:A1992JH48500006 PM 1634575 ER PT J AU HODGE, WA CHANDLER, HP AF HODGE, WA CHANDLER, HP TI UNICOMPARTMENTAL KNEE REPLACEMENT - A COMPARISON OF CONSTRAINED AND UNCONSTRAINED DESIGNS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID ARTHROPLASTY AB Seventy-six patients who had eighty-seven unicompartmental knee replacements were followed for an average of fifty-three months (range, two to twelve years). The operation was on the medial side in eighty-two knees and on the lateral side in five. Fifty replacements were unconstrained and thirty-seven were constrained. Of the fifty knees that had an unconstrained replacement, forty-nine (98 per cent) had a good or excellent result, compared with only twenty-six (70 per cent) of the knees that had a constrained replacement; the difference is significant (p = 0.0007). No knee that had an unconstrained replacement had a poor result, compared with nine (24 per cent) of the knees that had a constrained replacement (p = 0.0009). Four (8 per cent) of the fifty knees that had an unconstrained replacement later had a revision total knee arthroplasty, compared with ten (27 per cent) of the thirty-seven knees that had a constrained replacement; the difference is significant (p = 0.04). Noteworthy degenerative changes in the opposite compartment occurred in only one of the eighty-seven knees (a knee in which an unconstrained prosthesis had been inserted). C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 9 TC 24 Z9 24 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 JUL PY 1992 VL 74A IS 6 BP 877 EP 883 PG 7 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JH485 UT WOS:A1992JH48500008 PM 1634577 ER PT J AU BARRACK, RL JASTY, M BRAGDON, C HAIRE, T HARRIS, WH AF BARRACK, RL JASTY, M BRAGDON, C HAIRE, T HARRIS, WH TI THIGH PAIN DESPITE BONE INGROWTH INTO UNCEMENTED FEMORAL STEMS SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article AB Six porous-coated, uncemented femoral components were revised at a mean of 34.5 months for persistent thigh pain. At operation the stems were rigidly stable, difficult to extract, and showed good bony ingrowth. The four men and two women, with an average age of 59 years, all had thigh pain starting within the first year, progressive over time and unresponsive to conservative measures. These cases show that rigid fixation with good bony ingrowth does not guarantee the clinical success of a porous-coated uncemented femoral stem. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,HIP & IMPLANT SURG UNIT,BOSTON,MA 02114. TUFTS UNIV,SCH MED,BOSTON,MA 02111. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 13 TC 49 Z9 51 U1 0 U2 0 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD JUL PY 1992 VL 74 IS 4 BP 507 EP 510 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JC807 UT WOS:A1992JC80700007 PM 1624506 ER PT J AU TEICHER, BA HOLDEN, SA ARA, G HA, CS HERMAN, TS NORTHEY, D AF TEICHER, BA HOLDEN, SA ARA, G HA, CS HERMAN, TS NORTHEY, D TI A NEW CONCENTRATED PERFLUOROCHEMICAL EMULSION AND CARBOGEN BREATHING AS AN ADJUVANT TO TREATMENT WITH ANTITUMOR ALKYLATING-AGENTS SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY LA English DT Article DE PERFLUOROCHEMICAL EMULSION; CARBOGEN BREATHING; ALKYLATING AGENTS ID FLUOSOL-DA; CYTO-TOXICITY; OXYGENATION CONDITIONS; FIBRO-SARCOMA; TUMOR-CELL; MICE; ENHANCEMENT; INVIVO; RADIOSENSITIVITY; CLASSIFICATION AB Many anticancer drugs require oxygen to be cytotoxic or are selectively cytotoxic toward cells under oxygenated conditions. The effects of the dilute perfluorochemical emuolsion Fluosol with a wide variety of chemotherapeutic agents have been explored; however, it has not been possbile to determine the optimal level of circulating perfluorochemical emulsion with anticancer drugs because the volume of Fluosol that may be administered is limiting. Using a new concentrated perfluorochemical emulsion, a wide range of perfluorochemical doses has been examined in combination with melphalan, cyclophosphamide and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in the FSaIIC fibrosarcoma. When the perfluorochemical emulsion was administered by injection i.v. just prior to the injection of melphalan (10 mg/kg), cyclophosphamide (150 mg/kg) or BCNU (50 mg/kg), the greatest tumor growth delays were obtained with dosage levels between 4 g and 12 g of the perfluorochemical perfluorooctyl bromide/kg. With each drug the greatest tumor growth delays were obtained when the drug was prepared in the emulsion and the combination injected i.v. In each case, each dose of drug was followed by 6 h of breathing carbogen. The addition of the perfluorochemical emulsion/carbogen breathing to treatment with melphalan, BCNU or cyclophosphamide resulted in significant increases in the killing of tumor cells by these drugs without a concomitant increase in toxicity to bone marrow granulocyte/macrophage-colony-forming units. In each case, preparing the drug in the perfluorochemical emulsion was most effective. These results indicate that clinical trial of this perfluorochemical emulsion/carbogen breathing in combination with cancer chemotherapy may be warranted. 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 36 TC 11 Z9 11 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-5216 J9 J CANCER RES CLIN JI J. Cancer Res. Clin. Oncol. PD JUL PY 1992 VL 118 IS 7 BP 509 EP 514 DI 10.1007/BF01225265 PG 6 WC Oncology SC Oncology GA JC530 UT WOS:A1992JC53000005 PM 1624542 ER PT J AU GRAVES, RA TONTONOZ, P PLATT, KA ROSS, SR SPIEGELMAN, BM AF GRAVES, RA TONTONOZ, P PLATT, KA ROSS, SR SPIEGELMAN, BM TI IDENTIFICATION OF A FAT-CELL ENHANCER - ANALYSIS OF REQUIREMENTS FOR ADIPOSE TISSUE-SPECIFIC GENE-EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE DIFFERENTIATION; TRANSGENIC; TRANSCRIPTION FACTOR; C/EBP; OBESITY ID DIFFERENTIATION-INDUCED GENE; BINDING-PROTEIN; ADIPOCYTE DIFFERENTIATION; MESSENGER-RNAS; 3T3-ADIPOCYTES; DETERMINANT; COMPLEXES; CAMP; SITE; FOS AB The molecular basis for adipose-specific gene expression is not known. To approach the problem of adipocyte gene expression, we have analyzed in detail the capacity of the 5'-flanking region of the adipocyte P2 (aP2) gene to direct cell-type specific gene expression, Although the proximal promoter containing AP-1 and C/EBP binding sites is capable of directing differentiation-dependent gene expression in cultured adipocytes, these constructs are essentially inactive in the tissues of transgenic mice. We found that -5.4 kb of the 5'-flanking region were required to direct heterologous gene (chloramphenicol acetyl transferase; CAT) expression to the adipose tissue of transgenic mice. By deletion analysis, we identified a 520 bp enhancer at -5.4 kb of the aP2 gene. We show that this enhancer can direct high levels of gene expression specifically to the adipose tissue of transgenic mice. This enhancer also functions in a differentiation-dependent manner in cultured adipocytes and cannot be transactivated in preadipocytes by C/EBP. Molecular analysis indicates that several cis- and trans- acting acting elements, though not C/EBP, contribute to the specificity and potency of this enhancer. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. UNIV ILLINOIS,SCH MED,DEPT BIOCHEM,CHICAGO,IL 60612. FU NIDDK NIH HHS [DK31405] NR 20 TC 56 Z9 57 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 JUL PY 1992 VL 49 IS 3 BP 219 EP 224 DI 10.1002/jcb.240490303 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JC616 UT WOS:A1992JC61600001 PM 1644859 ER PT J AU KOKETSU, N MOSKOWITZ, MA KONTOS, HA YOKOTA, M SHIMIZU, T AF KOKETSU, N MOSKOWITZ, MA KONTOS, HA YOKOTA, M SHIMIZU, T TI CHRONIC PARASYMPATHETIC SECTIONING DECREASES REGIONAL CEREBRAL BLOOD-FLOW DURING HEMORRHAGIC HYPOTENSION AND INCREASES INFARCT SIZE AFTER MIDDLE CEREBRAL-ARTERY OCCLUSION IN SPONTANEOUSLY HYPERTENSIVE RATS SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE SPHENOPALATINE GANGLION; VASOACTIVE INTESTINAL POLYPEPTIDE; MIDDLE CEREBRAL ARTERY OCCLUSION ID VASOACTIVE INTESTINAL POLYPEPTIDE; CEREBROVASCULAR NERVE-FIBERS; GENE-RELATED PEPTIDE; SUBSTANCE-P; SPHENOPALATINE GANGLION; STIMULATION; CAT; IMMUNOREACTIVITY; INVITRO; RELEASE AB Regional cerebral blood flow (rCBF) during controlled hemorrhagic hypotension (140-20 mm Hg) was assessed 10-14 days after chronic unilateral sectioning of parasympathetic and/or sensory fibers innervating pial vessels in spontaneously hypertensive rats (SHR). rCBF was measured in the cortical barrel fields bilaterally by laser Doppler blood flowmetry. Immunohistochemistry of middle cerebral artery (MCA) whole mount preparations was used to verify the surgical lesion. During hemorrhagic hypotension, rCBF was equivalent on the two sides in shams, after selective sensory denervation, or in parasympathetically sectioned animals exhibiting small decreases (less-than-or-equal-to 30%) in immunoreactive vasoactive intestinal peptide (VIP)-containing fibers. After chronic parasympathetic denervation, decreases in perfusion pressure were accompanied by greater reductions in rCBF on the lesioned side; changes in vascular resistance were also attenuated on that side. The rCBF response to hypercapnia (P(a)CO2 50 mm Hg), however, was symmetrical and robust. To examine the effects of impaired neurogenic vasodilation on the pathophysiology of cerebral ischemia, infarct size was measured 24 h following tandem MCA occlusion in denervated animals. Infarction volume was larger after selective parasympathetic sectioning (sham, 156 +/- 27 vs. 196 +/- 32 mm3, respectively) but only in those denervated animals demonstrating greater-than-or-equal-to 40% decrease in immunoreactive VIP-containing fibers within the ipsilateral MCA. Lower than expected blood flow/perfusion pressure in the cortex distal to an occluded blood vessel may relate the observed blood flow responses to the occurrence of larger cortical infarcts in parasympathetically denervated animals. If true, the findings suggest a novel role for neurogenic vasodilation in the pathophysiology of cerebral ischemia and in rCBF regulation within the periinfarction zone. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,DIV CARDIOL,RICHMOND,VA 23298. FU NINDS NIH HHS [NS 26361, NS 10828] NR 26 TC 52 Z9 53 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 JUL PY 1992 VL 12 IS 4 BP 613 EP 620 PG 8 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA JC365 UT WOS:A1992JC36500009 PM 1618940 ER PT J AU ZENG, XN LEYDEN, JJ BRAND, JG SPIELMAN, AI MCGINLEY, KJ PRETI, G AF ZENG, XN LEYDEN, JJ BRAND, JG SPIELMAN, AI MCGINLEY, KJ PRETI, G TI AN INVESTIGATION OF HUMAN APOCRINE GLAND SECRETION FOR AXILLARY ODOR PRECURSORS SO JOURNAL OF CHEMICAL ECOLOGY LA English DT Article DE HUMAN AXILLARY ODORS; HUMAN APOCRINE GLAND SECRETION; (E)-3-METHYL-2-HEXENOIC ACID; AXILLARY ODOR PRECURSORS; ANDROSTENOL AB Recently completed studies from our laboratories have demonstrated that the characteristic human male axillary odors consist of C6 to C-11 normal, branched, and unsaturated aliphatic acids, with (E)-3-methyl-2-hexenoic acid being the most abundant. To investigate the mechanism by which the odor is formed, it is necessary to determine the nature of the odorless precursor(s) found in the apocrine secretion which is converted by the cutaneous microorganisms to the characteristic axillary odor. Pooled apocrine secretion was obtained from several male volunteers by intracutaneous injection of epinephrine. Partitioning this secretion into aqueous and organic soluble fractions was followed by hydrolysis of each fraction with NaOH or incubation with axillary microorganisms (cutaneous lipophilic corynebacterium). Analysis by gas chromatography/mass spectrometry (GC/MS) revealed the presence of (E)- and (Z)-3-methyl-2-hexenoic acid in the aqueous phase hydrolysate and aqueous phase incubated with bacteria; however, only a trace amount was seen in the resultant organic phase mixtures. These results suggest that a water-soluble precursor(s) is converted by the axillary flora to the characteristic axillary odors. C1 MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT DERMATOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNIV PENN,SCH DENT MED,DEPT BIOCHEM,PHILADELPHIA,PA 19104. NYU,COLL DENT,NEW YORK,NY 10003. NR 18 TC 59 Z9 62 U1 1 U2 5 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0098-0331 J9 J CHEM ECOL JI J. Chem. Ecol. PD JUL PY 1992 VL 18 IS 7 BP 1039 EP 1055 DI 10.1007/BF00980061 PG 17 WC Biochemistry & Molecular Biology; Ecology SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology GA JD590 UT WOS:A1992JD59000008 PM 24254146 ER PT J AU GOLDMAN, RS AXELROD, BN GIORDANI, BJ FOSTER, N BERENT, S AF GOLDMAN, RS AXELROD, BN GIORDANI, BJ FOSTER, N BERENT, S TI LONGITUDINAL SENSITIVITY OF THE FULD CHOLINERGIC PROFILE TO ALZHEIMERS-DISEASE SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article ID MEMORY FUNCTIONS; DEMENTIA AB The diagnostic sensitivity of a profile (Fuld, 1984) thought to mark cholinergic changes in Alzheimer's Disease (AD) was examined in a sample of 53 patients meeting criteria for AD on two occasions and in 19 patients for three occasions. The low obtained sensitivities of the Fuld profile (17%-26%) across testings is consistent with previous studies that used a single time point. The findings also revealed unstable positive and negative profiles over time. There were no performance differences on intellectual or memory measures when comparing subjects identified as positive or negative by the Fuld index. The results demonstrate that the index is insensitive to the dementing process and is a poor diagnostic marker for AD. C1 US DEPT VET AFFAIRS,ALLEN PK,MI. UNIV MICHIGAN,ANN ARBOR,MI 48109. RP GOLDMAN, RS (reprint author), DEPT VET AFFAIRS MED CTR,PSYCHOL SERV 116B,2215 FULLER RD,ANN ARBOR,MI 48105, USA. NR 23 TC 3 Z9 3 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JUL PY 1992 VL 14 IS 4 BP 566 EP 574 DI 10.1080/01688639208402845 PG 9 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA JK552 UT WOS:A1992JK55200010 PM 1400919 ER PT J AU VACANTI, CA SILBERT, BS VACANTI, FX AF VACANTI, CA SILBERT, BS VACANTI, FX TI FENTANYL-INDUCED MUSCLE RIGIDITY AS AFFECTED BY PRETREATMENT WITH AMANTADINE HYDROCHLORIDE SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Article DE AMANTADINE; FENTANYL; MUSCLE RIGIDITY, PRETREATMENT AB Study Objective: To determine whether the degree of muscle rigidity in humans caused by the administration of high-dose fentanyl is affected by pretreatment with amantadine hydrochloride, a drug that stimulates the release of dopamine in the basal ganglia. Design: Randomized, observer-blinded comparison of regimes. Setting: Inpatient surgery at a university-affiliated teaching hospital. Patients: Sixteen patients scheduled for elective surgery in whom the administration of high-dose fentanyl was felt to be appropriate. Interventions: Eight patients in the control group were given diazepam 5 mg orally 1 hour prior to induction of anesthesia. Eight patients in an experimental group were given the same dose of diazepam and also were treated with amantadine 1 g orally in divided doses over a period of 25 hours prior to their scheduled surgery. At the time of surgery, all patients were given fentanyl 50 mug/kg intravenously at a rate of 1 mg/min and were clinically evaluated for the degree of muscle rigidity of the chest wall, abdomen, and extremities. Measurements and Main Results: A single observer, blinded to the technique, evaluated and recorded the degree of muscle rigidity present in the chest wall, abdomen, and upper extremities immediately after administration of the fentanyl and 3 minutes later. The observer was the same individual in all instances. In no case did the muscle rigidity compromise our ability to adequately oxygenate the patient. Conclusions: Muscle rigidity associated with the administration of high-dose fentanyl is not attenuated by prior administration of amantadine in the dose range studied. RP VACANTI, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD JUL-AUG PY 1992 VL 4 IS 4 BP 282 EP 284 DI 10.1016/0952-8180(92)90129-O PG 3 WC Anesthesiology SC Anesthesiology GA JP816 UT WOS:A1992JP81600004 PM 1419008 ER PT J AU SZABO, MD CROSBY, G AF SZABO, MD CROSBY, G TI EXCESSIVE ATLANTOOCCIPITAL FLEXION AS A CAUSE OF COMPLETE AIRWAY-OBSTRUCTION FOLLOWING ANTERIOR CERVICAL-SPINE FUSION SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Article DE AIRWAY, OBSTRUCTION; COMPLICATIONS, AIRWAY OBSTRUCTION; SURGERY, ORTHOPEDIC, NEUROLOGIC AB This report describes complete airway obstruction following anterior cervical fusion caused by extreme, fixed flexion of the neck in a halo device. The causes and treatment Of such an airway complication are reviewed. RP SZABO, MD (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD JUL-AUG PY 1992 VL 4 IS 4 BP 328 EP 330 DI 10.1016/0952-8180(92)90140-V PG 3 WC Anesthesiology SC Anesthesiology GA JP816 UT WOS:A1992JP81600015 PM 1419015 ER PT J AU THORENS, B WU, YJ LEAHY, JL WEIR, GC AF THORENS, B WU, YJ LEAHY, JL WEIR, GC TI THE LOSS OF GLUT2 EXPRESSION BY GLUCOSE-UNRESPONSIVE BETA-CELLS OF DB/DB MICE IS REVERSIBLE AND IS INDUCED BY THE DIABETIC ENVIRONMENT SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ANTIPEPTIDE ANTIBODIES; IMMUNOFLUORESCENCE MICROSCOPY; NON-INSULIN-DEPENDENT DIABETES MELLITUS; PANCREAS PERFUSION; TRANSPLANTATION ID INSULIN-RESPONSE; TRANSPORTER; LIVER; MELLITUS; RATS; SEQUENCE AB Glucose-induced insulin secretion by beta-cells of diabetic db/db mice was studied by a pancreas perfusion technique, an d the levels of GLUT2 protein in pancreatic islets were assessed by immunofluorescence microscopy and protein blot analysis. Beta-cells from diabetic mice had a high basal rate of insulin secretion; they did not respond to glucose stimulation but displayed a normal secretory response to arginine. At the same time, GLUT2 expression by db/db islets was lost whereas beta-cells from nondiabetic db/+ mice expressed high levels of this transporter. GLUT2 levels in liver or kidney of diabetic mice were, however, mostly unaltered. Transplanting islets from db/db mice under the kidney capsule of db/+ mice restored normal GLUT2 levels. Conversely, transplantation of db/+ islets into db/db mice induced the disappearance of GLUT2 expression. When islets from db/+ mice were transplanted under the kidney capsule of streptozocin-diabetic mice, the immunodetection of GLUT2 also disappeared. We conclude that: (a) GLUT2 expression is decreased in glucose-unresponsive beta-cells from db/db mice; (b) the decreased expression of GLUT2 is reversible; (c) the loss of GLUT2 expression is induced by the diabetic environment of db/db and streptozocin-induced diabetic mice. These observations together with previously published data suggest that a factor different from glucose or insulin regulates the beta-cell expression of GLUT2. C1 WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. FU NHLBI NIH HHS [HL-41484]; NIDDK NIH HHS [DK-35449]; NIGMS NIH HHS [GM-40916] NR 29 TC 128 Z9 129 U1 0 U2 6 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 JUL PY 1992 VL 90 IS 1 BP 77 EP 85 DI 10.1172/JCI115858 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA JE390 UT WOS:A1992JE39000011 PM 1634622 ER PT J AU KITZ, RJ AF KITZ, RJ TI CAN TECHNOLOGY EDUCATION DURING MEDICAL-SCHOOL MAKE BETTER DOCTORS SO JOURNAL OF CLINICAL MONITORING LA English DT Editorial Material DE RESEARCH; EDUCATION-MEDICAL STUDENTS C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIOL,BOSTON,MA 02115. RP KITZ, RJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,BOSTON,MA 02114, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0748-1977 J9 J CLIN MONITOR JI J. Clin. Monit. PD JUL PY 1992 VL 8 IS 3 BP 243 EP 249 DI 10.1007/BF01616784 PG 7 WC Anesthesiology SC Anesthesiology GA JD595 UT WOS:A1992JD59500011 PM 1494932 ER PT J AU LOEHRER, PJ EINHORN, LH ELSON, PJ CRAWFORD, ED KUEBLER, P TANNOCK, I RAGHAVAN, D STUARTHARRIS, R SAROSDY, MF LOWE, BA BLUMENSTEIN, B TRUMP, D AF LOEHRER, PJ EINHORN, LH ELSON, PJ CRAWFORD, ED KUEBLER, P TANNOCK, I RAGHAVAN, D STUARTHARRIS, R SAROSDY, MF LOWE, BA BLUMENSTEIN, B TRUMP, D TI A RANDOMIZED COMPARISON OF CISPLATIN ALONE OR IN COMBINATION WITH METHOTREXATE, VINBLASTINE, AND DOXORUBICIN IN PATIENTS WITH METASTATIC UROTHELIAL CARCINOMA - A COOPERATIVE GROUP-STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID TRANSITIONAL-CELL-CARCINOMA; URINARY-TRACT; BLADDER-CANCER; ONCOLOGY-GROUP; CHEMOTHERAPY; CYCLOPHOSPHAMIDE; TRIAL; CIS-DICHLORODIAMMINEPLATINUM(II); EXPERIENCE; TUMORS C1 UNIV OKLAHOMA, OKLAHOMA CITY, OK USA. ROYAL PRINCE ALFRED HOSP, SYDNEY, AUSTRALIA. DEPT BIOSTAT, SEATTLE, WA USA. INDIANA UNIV, MED CTR, DEPT MED, INDIANAPOLIS, IN 46204 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT BIOSTAT, BOSTON, MA 02115 USA. UNIV COLORADO, DENVER, CO 80202 USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. PRINCESS MARGARET HOSP, TORONTO M4X 1K9, ONTARIO, CANADA. WESTMEAD HOSP, SYDNEY, AUSTRALIA. OREGON HLTH SCI UNIV, PORTLAND, OR 97201 USA. DUKE UNIV, RALEIGH, NC USA. FU NCI NIH HHS [2 R 35 CA 39844-02, R10 CA 28171-04]; NCRR NIH HHS [MO 1 RR 00 750-06] NR 32 TC 589 Z9 596 U1 1 U2 2 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X EI 1527-7755 J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUL PY 1992 VL 10 IS 7 BP 1066 EP 1073 PG 8 WC Oncology SC Oncology GA JA771 UT WOS:A1992JA77100007 PM 1607913 ER PT J AU SOIFFER, RJ MURRAY, C MAUCH, P ANDERSON, KC FREEDMAN, AS RABINOWE, SN TAKVORIAN, T ROBERTSON, MJ SPECTOR, N GONIN, R MILLER, KB RUDDERS, RA FREEMAN, A BLAKE, K CORAL, F NADLER, LM RITZ, J AF SOIFFER, RJ MURRAY, C MAUCH, P ANDERSON, KC FREEDMAN, AS RABINOWE, SN TAKVORIAN, T ROBERTSON, MJ SPECTOR, N GONIN, R MILLER, KB RUDDERS, RA FREEMAN, A BLAKE, K CORAL, F NADLER, LM RITZ, J TI PREVENTION OF GRAFT-VERSUS-HOST DISEASE BY SELECTIVE DEPLETION OF CD6-POSITIVE LYMPHOCYTES-T FROM DONOR BONE-MARROW SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CHRONIC MYELOGENOUS LEUKEMIA; NATURAL-KILLER-CELLS; CHRONIC MYELOID-LEUKEMIA; TOTAL-BODY IRRADIATION; TERM FOLLOW-UP; LYMPHOBLASTIC-LEUKEMIA; RISK-FACTORS; TRANSPLANTATION; RECIPIENTS; RELAPSE C1 HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL & MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. TUFTS UNIV,SCH MED,BOSTON,MA 02111. NEW ENGLAND MED CTR HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA. RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [K08-CA01105]; NIAID NIH HHS [P01-AI29530, N01-AI62531] NR 53 TC 109 Z9 109 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 JUL PY 1992 VL 10 IS 7 BP 1191 EP 1200 PG 10 WC Oncology SC Oncology GA JA771 UT WOS:A1992JA77100024 PM 1607923 ER PT J AU HAFFAJEE, AD SOCRANSKY, SS GOODSON, JM AF HAFFAJEE, AD SOCRANSKY, SS GOODSON, JM TI SUBGINGIVAL TEMPERATURE .1. RELATION TO BASE-LINE CLINICAL-PARAMETERS SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE SUBGINGIVAL TEMPERATURE; PERIODONTITIS ID GINGIVAL AB 44 subjects ranging in age from 14-71 years were measured at 6 sites per tooth for gingival redness, plaque accumulation, suppuration, bleeding on probing, pocket depth and attachment level. Subgingival temperatures were measured at the same 6 sites per tooth using a periodontal temperature probe (Perio-temp(TM), Abiodent(SM), Danvers, MA). This instrument was also used to measure each subject's sublingual temperature in order to compute the differences between sublingual and subgingival temperature. Relationships were sought between the baseline clinical parameters and the temperature variables in subjects and at sites. The mean and standard deviation of the sublingual temperatures for the 44 subjects was 36.6+/-0.4-degrees-C (range 35.8-37.6-degrees-C). The mean of each subject's mean whole mouth subgingival temperature was 1.9-degrees-C lower, 34.8+/-0.6-degrees-C (range 33.4-36.1-degrees-C). The differences of the mean subgingival temperature from sublingual ranged from -0.8 to -3.2-degrees-C (average -1.9+/-0.5-degrees-C). Mean temperature difference for a subject correlated with % of sites with plaque (r(s) = 0.45), redness (r(s) = 0.33), bleeding on probing (r(s) = 0.44), % of sites with attachment level > 3 mm (r(s) = 0.44), mean pocket depth (r(s) = 0.44) and meanattachment level (r(s) = 0.39). There were higher mean temperatures at sites exhibiting or not exhibiting plaque (35.0, 34.5-degrees-C), redness (34.9, 34.6), bleeding on probing (35.1, 34.7) and suppuration (35.4, 34.8). Sites with pockets < 4, 4-6 and > 6 mm had mean temperatures of 34.6, 35.2, 35.8-degrees-C, respectively. Site temperature showed a similar relationship with attachment level. The data indicated that subjects differed in their mean subgingival temperature and that some of the differences were indicative of the extent of prior periodontitis and current levels of gingival inflammation. Similarly, temperature at a site related to location of the site in the mouth, pocket depth, attachment level and inflammatory status. RP HAFFAJEE, AD (reprint author), FORSYTH DENT CTR,140 THE FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-02847, DE-04881] NR 9 TC 35 Z9 35 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD JUL PY 1992 VL 19 IS 6 BP 401 EP 408 DI 10.1111/j.1600-051X.1992.tb00670.x PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JB767 UT WOS:A1992JB76700008 PM 1634630 ER PT J AU HAFFAJEE, AD SOCRANSKY, SS GOODSON, JM AF HAFFAJEE, AD SOCRANSKY, SS GOODSON, JM TI SUBGINGIVAL TEMPERATURE .2. RELATION TO FUTURE PERIODONTAL ATTACHMENT LOSS SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE SUBGINGIVAL TEMPERATURE; PERIODONTITIS; RISK INDICATOR; LONGITUDINAL AB The purpose of the present investigation was to determine whether subgingival temperature was a risk indicator of periodontal attachment loss (detected in the following 2 months) in a subject or at a site. 29 subjects were measured at 6 sites per tooth for clinical parameters as well as subgingival temperature using a periodontal temperature probe (Periotemp(TM), ABIODENT(SM), Danvers, MA). The same instrument was used to measure sublingual temperature in order to compute differences between subgingival and sublingual temperature. Clinical and temperature parameters were measured at 2-month intervals. A total of 49 subject visits which had both baseline temperature and subsequent attachment level change measurements were available for analysis. Attachment level loss > 2.5 mm occurred at 1 or more sites at 16 of 49 subject visits. Elevated mean subgingival temperature was related to subsequent attachment loss particularly in individuals who exhibited more than 1 progressing site. The odds ratios of a subject exhibiting new attachment loss at 1 or more sites or at 2 or more sites were 14.5 and 64.0 if the subject's mean subgingival temperature exceeded 35.5-degrees-C. Subjects with high mean subgingival temperatures and widespread periodontal destruction appeared to be at greatest risk for new attachment loss. Discriminant analysis using % of sites with suppuration, redness and attachment level > 3 mm and mean site temperature correctly "predicted" disease activity with a sensitivity, specificity and overall agreement of 0.75, 0.76 and 0.82 respectively. Of 7243 sites, 43 (0.59%) and 160 (2.2%) showed attachment loss of either 2.5 mm or more or 2 mm or more respectively. Unchanging sites exhibited lower mean site temperature and higher deviations from sublingual than sites which lost or "gained" attachment. % of sites showing new attachment loss increased with increasing site temperature, decreasing site temperature deviation and a change in the indicator value from green to yellow to red. For example, % of sites exhibiting loss of attachment of 2.5 mm or more was 0.23 at < 34-degrees-C, 0.36 at 34-35-degrees-C, 0.82 at 35-36-degrees-C and 1.04 at > 36-degrees-C. This pattern was observed for subsets of sites with pocket depths < 4 mm and 4-6 mm, but was weaker for pockets > 6 mm. Most striking was the high risk (8.9% of sites) of new attachment loss at sites with shallow pockets (< 4 mm), which bled on probing and had red temperature indicator values compared with the lower risk (1.4%) at shallow, non-bleeding sites with green indicator values. The findings of the present investigation suggest that knowledge of the subgingival temperature will be useful in identifying subjects and sites at risk for new attachment loss. RP HAFFAJEE, AD (reprint author), FORSYTH DENT CTR,140 THE FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-04881, DE-02847] NR 5 TC 32 Z9 33 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD JUL PY 1992 VL 19 IS 6 BP 409 EP 416 DI 10.1111/j.1600-051X.1992.tb00671.x PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JB767 UT WOS:A1992JB76700009 PM 1634631 ER PT J AU HAFFAJEE, AD SOCRANSKY, SS SMITH, C DIBART, S GOODSON, JM AF HAFFAJEE, AD SOCRANSKY, SS SMITH, C DIBART, S GOODSON, JM TI SUBGINGIVAL TEMPERATURE .3. RELATION TO MICROBIAL COUNTS SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE SUBGINGIVAL TEMPERATURE; PERIODONTITIS; BACTERIA ID FLURBIPROFEN TREATMENT; PERIODONTITIS; VIRULENCE AB The present investigation examined the relationship of selected bacterial species and subgingival temperature. 35 subjects were measured at 6 sites per tooth for clinical parameters and subgingival temperature. Measurements were repeated for 21 subjects at 2 month intervals providing a total of 66 subjects visits. At each visit, subgingival plaque samples were taken from the mesial aspect of each tooth and anaerobically dispersed, diluted and plated on non-selective media. After anaerobic incubation, colonies were lifted to nylon filters and specific species detected using digoxigenin-labeled whole chromosomal DNA probes. Species enumerated were; A. actinomycetemcomitans serotypes a and b, B. forsythus, B. gingivalis, B. intermedius I and II, C. ochracea, F. nucleatum ss. vincentii, P. micros, S. intermedius, S. sanguis I and II, V. parvula and W. recta. Total viable counts and counts of Capnocytophaga sp. were determined directly from the primary isolation plates. A total of 1581 samples were evaluated. Subject visits with higher mean subgingival temperatures had significantly higher mean %s of B. intermedius I and P. micros, and lower mean %s of Capnocytophaga sp. Sites with higher subgingival temperatures had elevated proportions of B. intermedius I and II, A. actinomycetemcomitans serotype a and B. gingivalis more frequently than sites with lower temperatures, while Capnocytophaga sp. were elevated more often at cooler sites. 43 of the subject visits had follow up attachment level measurements at 2 months. The 1026 microbial samples and the subgingival temperature measurements from these visits were related to longitudinal attachment change. Discriminant analysis indicated that combinations of temperature and microbial parameters were more effective in predicting subjects at risk and sites at risk for new attachment loss than either group of variables alone. RP HAFFAJEE, AD (reprint author), FORSYTH DENT CTR,140 THE FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-02847, DE-04881] NR 13 TC 27 Z9 28 U1 0 U2 2 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD JUL PY 1992 VL 19 IS 6 BP 417 EP 422 DI 10.1111/j.1600-051X.1992.tb00672.x PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JB767 UT WOS:A1992JB76700010 PM 1321846 ER PT J AU KENT, R SMITH, DJ JOSHIPURA, K SOPARKAR, P TAUBMAN, MA AF KENT, R SMITH, DJ JOSHIPURA, K SOPARKAR, P TAUBMAN, MA TI HUMORAL IGG ANTIBODIES TO ORAL MICROBIOTA IN A POPULATION AT RISK FOR ROOT-SURFACE CARIES SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID PERIODONTALLY TREATED PATIENTS; CREVICULAR FLUID ANTIBODY; STREPTOCOCCUS-MUTANS; DENTAL-CARIES; MICROORGANISMS; ASSOCIATION; PLAQUE; SERUM; SPECIFICITY; RESPONSES AB Mutans streptococci have been strongly implicated in the initiation of dental caries on coronal surfaces. Their role in development of root-surface caries is less clear. The etiologic agents of both types of dental caries are likely to elicit systemic immune responses. The objective of the present study, therefore, was to study the association of clinical variables of disease with humoral IgG antibodies to nine oral micro-organisms in 314 adult subjects, aged 45-65 years, who were at risk for root-surface caries. Antibody activity to Streptococcus mutans strain Ingbritt, S. mutans/S. sobrinus GTFs, S. faecalis strain 19433, Actinomyces viscosus strain WVU 626, Actinomyces naeslundii strain 12, Lactobacillus casei, Actinobacillus actinomycetemcomitans strain Y4, Porphyromonas gingivalis strain 381, Eikenella corrodens strain 1073, and Wolinella recta strain 371 was measured by ELISA. Pearson correlation coefficients among log10 antibody levels within subjects revealed marked positive correlations among subgingival bacteria, generally weak positive correlations among supragingival micro-organisms, and no correlations between elements of the supragingival battery with the subgingival battery. IgG antibody levels to mutans streptococcal antigens were significantly correlated with subject DMF scores (r = 0.23; p < 0.0001). No significant correlation was seen between DMF scores and antibody to any other supragingival micro-organism tested. Further relationships between levels of S. mutans antibody and individual clinical variables were analyzed by step-wise multiple linear regression, resulting in a model that was highly significant (p = 0.0001), with an r2 = 0.14. Numbers of missing teeth, coronal caries, root-surface caries, and root-surface restorations were each positively associated with antibody levels to mutans streptococci. The model indicated that the associations seen with S. mutans antibody reflected previous encounters with S. mutans antigens, since this model emphasized cumulative caries experience over measures reflecting a subject's current status. These observations strengthen the association between S. mutans and dental caries on coronal surfaces and suggest a further association with caries on root surfaces. C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. FORSYTH DENT CTR,DEPT CLIN TRIALS,BOSTON,MA 02115. FU NIDCR NIH HHS [DE-07009] NR 35 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JUL PY 1992 VL 71 IS 7 BP 1399 EP 1407 DI 10.1177/00220345920710070801 PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JE838 UT WOS:A1992JE83800008 PM 1321176 ER PT J AU HOWARD, FD MOINGEON, P MOEBIUS, U MCCONKEY, DJ YANDAVA, B GENNERT, TE REINHERZ, EL AF HOWARD, FD MOINGEON, P MOEBIUS, U MCCONKEY, DJ YANDAVA, B GENNERT, TE REINHERZ, EL TI THE CD3-ZETA CYTOPLASMIC DOMAIN MEDIATES CD2-INDUCED T-CELL ACTIVATION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID RECEPTOR ZETA-CHAIN; ANTIGEN RECEPTOR; LYMPHOCYTE-T; CD2; COMPLEX AB CD2-mediated T lymphocyte activation requires surface expression of CD3-Ti, the T cell receptor (TCP) for antigen major histocompatibility complex protein. Given the importance of CD3-zeta in TCR signaling, we have directly examined the ability of the CD3-zeta cytoplasmic domain to couple CD2 to intracellular signal transduction pathways. A cDNA encoding a chimeric protein consisting of the human CD3-zeta cytoplasmic domain (amino acid residues 31-142) fused to the CD8-alpha extracellular and transmembrane domains (amino acid residues 1-187) was transfected into a CD2+CD3-CD8- variant of the human T cell line Jurkat. The resulting transfectants expressed the CD8-alpha/CD3-zeta chimeric receptor at the cell surface in the absence of other TCR subunits. Stimulation of these transfectants with anti-T11(2) + anti-T11(3) Monoclonal antibodies (mAbs) initiated both a prompt cytosolic free calcium ([Ca2+]i) rise and protein tyrosine kinase activation. Stimulation with either intact anti-T11(2) + anti-T11(3) mAbs or purified F(ab')2 fragments resulted in interleukin 2 (IL-2) secretion. In contrast, control cell lines transfected with a cDNA encoding wild-type CD8-alpha, and thus lacking surface expression of the CD3-zeta cytoplasmic domain, failed to show any [Ca2+]i rise, protein tyrosine kinase activation, or IL-2 secretion after identical stimulation. These data directly establish the CD3-zeta cytoplasmic domain as a necessary and sufficient component of the CD3-Ti complex involved in T lymphocyte activation through CD2. Moreover, they show that CD2 signaling can function in the absence of Fc receptors. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP HOWARD, FD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-19807] NR 27 TC 70 Z9 70 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 JUL 1 PY 1992 VL 176 IS 1 BP 139 EP 145 DI 10.1084/jem.176.1.139 PG 7 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA JA759 UT WOS:A1992JA75900015 PM 1351920 ER EF