FN Thomson Reuters Web of Science™ VR 1.0 PT J AU OKEN, BS KISHIYAMA, SS KAYE, JA HOWIESON, DB AF OKEN, BS KISHIYAMA, SS KAYE, JA HOWIESON, DB TI ATTENTION-DEFICIT IN ALZHEIMERS-DISEASE IS NOT SIMULATED BY AN ANTICHOLINERGIC/ANTIHISTAMINERGIC DRUG AND IS DISTINCT FROM DEFICITS IN HEALTHY AGING SO NEUROLOGY LA English DT Article; Proceedings Paper CT 45th Annual Meeting of the American-Academy-of-Neurology CY APR, 1993 CL NEW YORK, NY SP AMER ACAD NEUROL ID MINI-MENTAL-STATE; SENILE DEMENTIA; DIVIDED ATTENTION; VISUAL-ATTENTION; AGE-DIFFERENCES; HUMAN-MEMORY; TIME COURSE; SCOPOLAMINE; HYPERSENSITIVITY; SENSITIVITY AB Objective. To evaluate attention deficit in Alzheimer's disease (AD) and its relationship to attention deficits associated with aging and with medications altering alertness. Methods, Ten patients with probable AD, 10 healthy old controls, and 15 young controls performed a covert orienting of spatial attention task. Young controls performed the task an additional time after ingestion of diphenhydramine 1 mg/kg. Reaction times were obtained following valid, neutral, and invalid cues. Results. In all groups, the reaction times were shortest for the validly cued stimuli and longest for the invalidly cued stimuli. Additionally, the AD patients performed disproportionately worse following the invalid cue than did the control groups. Young controls given diphenhydramine had decreased subjective alertness, performed worse than they did before drug but better than the old controls or AD patients, and had no disproportionate impairment with the invalid cue. Conclusions, AD patients have disproportionate problems shifting spatial attention compared with age-matched controls. Impaired attentional performance in AD cannot be simulated in young subjects by ingestion of a combined antihistamine/anticholinergic agent at a dose sufficient to produce significant changes in alertness. C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP OKEN, BS (reprint author), OREGON HLTH SCI UNIV,DEPT NEUROL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. OI Kaye, Jeffrey/0000-0002-9971-3478 FU NIA NIH HHS [1P30 AG08017, R01 AG08714] NR 58 TC 43 Z9 44 U1 1 U2 3 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1994 VL 44 IS 4 BP 657 EP 662 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA NG065 UT WOS:A1994NG06500013 PM 8164820 ER PT J AU BIELAMOWICZ, S BERKE, GS WATSON, D GERRATT, BR KREIMAN, J AF BIELAMOWICZ, S BERKE, GS WATSON, D GERRATT, BR KREIMAN, J TI EFFECTS OF RLN AND SLN STIMULATION ON GLOTTAL AREA SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID VOICE; PHONATION; FEMALE; INVIVO; LARYNX; FLOW AB In vivo canine experiments have demonstrated that vocal fold stiffness varies proportionately with changing levels of recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) stimulation. This study evaluated the morphologic changes in the glottis at varying levels of nerve stimulation and the presumed effects on laryngeal air particle velocity. Stroboscopic data from the in vivo canine model of phonation were examined under varying conditions of RLN and SLN stimulation. Computerized analysis of stroboscopic images was used to reconstruct the glottal area vs. time waveforms. As RLN stimulation increased, glottal area per cycle decreased (p < 0.05). However, as SLN stimulation increased, glottal area per cycle increased (p < 0.05). These results support the hypothesis that increasing RLN stimulation at similar levels of SLN stimulation produces an increase in air particle velocity, whereas an increase in SLN stimulation causes a decrease in air particle velocity. C1 UNIV CALIF LOS ANGELES,MED CTR,DIV HEAD & NECK SURG,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DIV HEAD & NECK SURG,LOS ANGELES,CA. OI Kreiman, Jody/0000-0002-5360-1729 NR 20 TC 7 Z9 7 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD APR PY 1994 VL 110 IS 4 BP 370 EP 380 PG 11 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA NG807 UT WOS:A1994NG80700003 PM 8170680 ER PT J AU HERBERT, V AF HERBERT, V TI FOLATE SUPPLEMENTS SHOULD BE APPROPRIATELY LABELED TO PROTECT CONSUMERS SO PEDIATRICS LA English DT Letter C1 BRONX VET AFFAIRS MED CTR,BRONX,NY 10468. RP HERBERT, V (reprint author), MT SINAI MED CTR,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 3 TC 3 Z9 3 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 APR PY 1994 VL 93 IS 4 BP 694 EP 695 PG 2 WC Pediatrics SC Pediatrics GA ND363 UT WOS:A1994ND36300037 PM 8155182 ER PT J AU TAKAHASHI, LK AF TAKAHASHI, LK TI STIMULUS-CONTROL OF BEHAVIORAL-INHIBITION IN THE PREWEANLING RAT SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE PREWEANLING RATS; BEHAVIORAL INHIBITION; ULTRASONIC VOCALIZATION; FREEZING; DEVELOPMENT; CONSPECIFIC THREAT; SOCIAL ISOLATION; CONSPECIFIC ODORS ID OLFACTORY CUES; ANTIPREDATOR BEHAVIOR; DEFENSIVE BEHAVIORS; ALARM CALLS; RESPONSES; PREDATOR; VOCALIZATIONS; FLOCKS; RECOGNITION; NORVEGICUS AB Previous studies demonstrate that 14-day-old rats reduce their emission of ultrasonic vocalizations and freeze when exposed to an unfamiliar adult male rat. This study sought to identify the stimulus characteristics of conspecific males that potentiate the display of behavioral inhibition. In Experiment 1, day 14 rats were isolated from the nest and exposed to either an unfamiliar prepubescent male rat or an unfamiliar adult male rat. Pups exposed to the unfamiliar adult male rat exhibited significantly elevated levels of freezing and reduced their emission of ultrasounds. In Experiment 2, pups were exposed to either a familiar or an unfamiliar adult male rat. Although several pups exposed to the familiar adult male rat exhibited freezing, pups tested with the unfamiliar adult rat showed a reliably higher duration of freezing and made fewer vocalizations. Results suggest that neither the unfamiliar factor nor cues associated with male adulthood are sufficient to account for the occurrence of behavioral inhibition when presented separately. However, the combination of unfamiliarity and adult male stimuli are highly potent stimulus features that elicit behavioral inhibition in preweanling rats. 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 [NIMH MH-43986] NR 49 TC 36 Z9 36 U1 0 U2 0 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 APR PY 1994 VL 55 IS 4 BP 717 EP 721 DI 10.1016/0031-9384(94)90050-7 PG 5 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA NA800 UT WOS:A1994NA80000018 PM 8190800 ER PT J AU BOWDEN, CL BRUGGER, AM SWANN, AC CALABRESE, JR JANICAK, PG PETTY, F DILSAVER, SC DAVIS, JM RUSH, AJ SMALL, JG GARZATREVINO, ES RISCH, SC GOODNICK, PJ MORRIS, DD AF BOWDEN, CL BRUGGER, AM SWANN, AC CALABRESE, JR JANICAK, PG PETTY, F DILSAVER, SC DAVIS, JM RUSH, AJ SMALL, JG GARZATREVINO, ES RISCH, SC GOODNICK, PJ MORRIS, DD TI EFFICACY OF DIVALPROEX VS LITHIUM AND PLACEBO IN THE TREATMENT OF MANIA SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID AFFECTIVE-DISORDERS; BIPOLAR DISORDER; DOUBLE-BLIND; FOLLOW-UP; VALPROATE; ILLNESS; CARBAMAZEPINE; ALCOHOL; STATES; SODIUM AB Objective.-To compare the effectiveness of divalproex sodium with that of lithium and placebo in patients with acute mania. Design.-Randomized, double-blind, parallel-group study of treatment outcomes in patients with manic-depressive illness. Patients.-A total of 179 hospitalized, acutely manic patients meeting the Research Diagnostic Criteria for manic disorder, approximately half of whom had been nonresponsive to lithium previously, were studied at nine university-affiliate hospitals. Interventions.-After a minimum 3-day washout period, random assignment for 21 days to divalproex, lithium, or placebo in a 2:1:2 ratio. Dosage of divalproex and lithium was increased if tolerated to a target concentration of 1041 mu mol/L (150 mu g/ mL) or 1.5 mmol/L (conventionally expressed as milliequivalents per liter), respectively. Main Outcome Measures.-Primary outcome measures were changes in the Mania Rating scale derived from the Schedule for Affective Disorders and Schizophrenia. Results.-lntent-to-treat analysis for efficacy was based on data from 68, 35, and 73 patients in the divalproex, lithium, and placebo groups, respectively. Groups were initially comparable except that all eight patients with four or more manic episodes in the previous year were in the divalproex group. In 30%, 33%, and 51% of the above groups, treatment was prematurely terminated due to lack of efficacy, with fewer premature terminations from divalproex than placebo (P=.017). The proportions of patients improving at least 50% were higher for divalproex and lithium groups than for the placebo group: 48% for divalproex (P=.004) and 49% for lithium (P=.025) vs 25% for placebo. Divalproex was as effective in rapid-cycling manic patients as in other patients. Conclusions.-Both divalproex and lithium were significantly more effective than placebo in reducing the symptoms of acute mania. The efficacy of divalproex appears to be independent of prior responsiveness to lithium. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX USA. ABBOTT LABS, CLIN RES SECT, N CHICAGO, IL USA. UNIV TEXAS, SCH MED, DEPT PSYCHIAT, HOUSTON, TX USA. CASE WESTERN RESERVE UNIV, SCH MED, DEPT PSYCHIAT, CLEVELAND, OH 44106 USA. ILLINOIS STATE PSYCHIAT INST, CHICAGO, IL USA. UNIV ILLINOIS, DEPT PSYCHIAT, CHICAGO, IL 60612 USA. VET AFFAIRS MED CTR, DALLAS, TX USA. UNIV TEXAS, SW MED CTR, DEPT PSYCHIAT, DALLAS, TX USA. INDIANA UNIV, SCH MED, DEPT PSYCHIAT, INDIANAPOLIS, IN 46202 USA. EMORY UNIV, SCH MED, DEPT PSYCHIAT, ATLANTA, GA 30322 USA. UNIV MIAMI, DEPT PSYCHIAT, CORAL GABLES, FL USA. RP BOWDEN, CL (reprint author), UNIV TEXAS, HLTH SCI CTR, DEPT PSYCHIAT, DIV BIOL PSYCHIAT, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. OI Rush, Augustus/0000-0003-2004-2382 NR 45 TC 740 Z9 751 U1 2 U2 22 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 EI 1538-3598 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 23 PY 1994 VL 271 IS 12 BP 918 EP 924 DI 10.1001/jama.271.12.918 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA NA743 UT WOS:A1994NA74300027 PM 8120960 ER PT J AU MCBRIDE, R CHESEBRO, JH WIEBERS, DO HOLLAND, AE LINKER, S BARDSLEY, WT KOPECKY, S LITIN, SC MEISSNER, I ZERBE, DM FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J JENKINS, JS WRIGHT, W ANDERSON, DC ASINGER, RW NEWBURG, SM BUNDLIE, SR FARMER, CC KOLLER, RL HAUGLAND, JM NANCE, MA TARREL, RM DUNBAR, DN JORGENSEN, CR SHARKEY, SW LEONARD, ADS KANTER, MC SOLOMON, DH ZABALGOITIA, M MCANULTY, JH MARCHANT, C COULL, BM KELLEY, RE CHAHINE, R PALERMO, M TEIXEIRO, P FELDMAN, G HAYWARD, A MACMILLAN, K GANDARA, E ANDERSON, W BLANK, N STRAUSS, R FEINBERG, WM VOLD, BK KERN, KB APPLETON, C BRUCK, D DORR, S DITTRICH, HC ROTHROCK, JF KERRIDGE, C LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS HELGASON, CM KONDOS, GT HOFF, J MCRAE, RP HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME MILLER, VT HOCKERSMITH, CJ COHEN, BA JANOSIK, DL CADELL, DJ KELLERMAN, L GOMEZ, CR LABOVITZ, AJ ROTHBART, RM BAILEY, GH BURKHARDT, C HORWITZ, L BLACKSHEAR, JL WEAVER, L BAKER, V LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA PEARCE, LA FLETCHER, KA NASCO, E HART, RG SHERMAN, DG TALBERT, RL DACY, TL HERBERLING, PA AF MCBRIDE, R CHESEBRO, JH WIEBERS, DO HOLLAND, AE LINKER, S BARDSLEY, WT KOPECKY, S LITIN, SC MEISSNER, I ZERBE, DM FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J JENKINS, JS WRIGHT, W ANDERSON, DC ASINGER, RW NEWBURG, SM BUNDLIE, SR FARMER, CC KOLLER, RL HAUGLAND, JM NANCE, MA TARREL, RM DUNBAR, DN JORGENSEN, CR SHARKEY, SW LEONARD, ADS KANTER, MC SOLOMON, DH ZABALGOITIA, M MCANULTY, JH MARCHANT, C COULL, BM KELLEY, RE CHAHINE, R PALERMO, M TEIXEIRO, P FELDMAN, G HAYWARD, A MACMILLAN, K GANDARA, E ANDERSON, W BLANK, N STRAUSS, R FEINBERG, WM VOLD, BK KERN, KB APPLETON, C BRUCK, D DORR, S DITTRICH, HC ROTHROCK, JF KERRIDGE, C LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS HELGASON, CM KONDOS, GT HOFF, J MCRAE, RP HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME MILLER, VT HOCKERSMITH, CJ COHEN, BA JANOSIK, DL CADELL, DJ KELLERMAN, L GOMEZ, CR LABOVITZ, AJ ROTHBART, RM BAILEY, GH BURKHARDT, C HORWITZ, L BLACKSHEAR, JL WEAVER, L BAKER, V LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA PEARCE, LA FLETCHER, KA NASCO, E HART, RG SHERMAN, DG TALBERT, RL DACY, TL HERBERLING, PA TI WARFARIN VERSUS ASPIRIN FOR PREVENTION OF THROMBOEMBOLISM IN ATRIAL-FIBRILLATION - STROKE PREVENTION IN ATRIAL-FIBRILLATION-II STUDY SO LANCET LA English DT Article ID COMPLICATIONS; THERAPY AB Warfarin is an established treatment for prevention of ischaemic stroke in patients with atrial fibrillation, but the value of this agent relative to aspirin is unclear. In the first Stroke Prevention in Atrial Fibrillation (SPAF-I) study, direct comparison of warfarin with aspirin was limited by the small number of thromboembolic events. SPAF-II aims to address this issue and also to assess the differential effects of the two treatments according to age. We compared warfarin (prothrombin time ratio 1.3-1.8, international normalised ratio 2.0-4.5) with aspirin 325 mg daily for prevention of ischaemic stroke and systemic embolism (primary events) in two parallel randomised trials involving 715 patients aged 75 years or less and 385 patients older than 75; we sought reductions in the absolute rate of primary events by warfarin compared with aspirin of 2% per year and 4% per year, respectively. In the younger patients, warfarin decreased the absolute rate of primary events by 0.7% per year (95% Cl - 0.4 to 1.7). The primary event rate per year was 1.3% with warfarin and 1.9% with aspirin (relative risk [RR] 0.67, p = 0.24). The absolute rate of primary events in low-risk younger patients (without hypertension, recent heart failure, or previous thromboembolism) on aspirin was 0.5% per year (95% Cl 0.1 to 1.9). Among older patients, warfarin decreased the absolute rate of primary events by 1.2% per year (95% Cl - 1.7 to 4.1). The primary event rate per year was 3.6% with warfarin and 4.8% with aspirin (RR 0.73, p = 0.39). In this older group, the rate of all stroke with residual deficit (ischaemic or haemorrhagic) was 4.3% per year with aspirin and 4.6% per year with warfarin (RR 1.1). Warfarin may be more effective than aspirin for prevention of ischaemic stroke in patients with atrial fibrillation, but the absolute reduction in stroke rate by warfarin is small. Younger patients without risk factors had a low rate of stroke when treated with aspirin. In older patients the rate of stroke (ischaemic and haemorrhagic) was substantial, irrespective of which agent was given. Patient age and the inherent risk of thromboembolism should be considered in the choice of antithrombotic prophylaxis for patients with atrial fibrillation. C1 MAYO CLIN & MAYO FDN, ROCHESTER, MN USA. UNIV MISSOURI, COLUMBIA, MO USA. HENNEPIN CTY MED CTR, MINNEAPOLIS, MN USA. ABBOTT NW HOSP, MINNEAPOLIS, MN USA. PARK NICOLLET MED CTR, MINNEAPOLIS, MN USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. OREGON HLTH SCI UNIV, PORTLAND, OR 97201 USA. UNIV MIAMI, SCH MED, MIAMI, FL USA. KAISER PERMANENTE CTR HLTH RES, PORTLAND, OR USA. UNIV ARIZONA, COLL MED, TUCSON, AZ USA. UNIV CALIF SAN DIEGO, MED CTR, SAN DIEGO, CA 92103 USA. ST JOHNS MERCY MED CTR, ST LOUIS, MO USA. UNIV CHICAGO, COLL MED, CHICAGO, IL 60637 USA. UNIV ILLINOIS, COLL MED, PEORIA, IL 61656 USA. MT SINAI MED CTR, NEW YORK, NY 10029 USA. NORTHWESTERN UNIV, SCH MED, CHICAGO, IL USA. ST LOUIS UNIV, MED CTR, ST LOUIS, MO USA. UNIV COLORADO, SCH MED, DENVER, CO USA. MAYO CLIN, JACKSONVILLE, FL USA. UNIV WASHINGTON, SEATTLE, WA USA. RP MCBRIDE, R (reprint author), STAT & EPIDEMIOL RES CORP, 1107 NE 45TH ST, SUITE 520, SEATTLE, WA 98105 USA. NR 20 TC 610 Z9 617 U1 0 U2 10 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0140-6736 EI 1474-547X J9 LANCET JI Lancet PD MAR 19 PY 1994 VL 343 IS 8899 BP 687 EP 691 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA NB809 UT WOS:A1994NB80900006 ER PT J AU DUPONTVERSTEEGDEN, EE MCCARTER, RJM KATZ, MS AF DUPONTVERSTEEGDEN, EE MCCARTER, RJM KATZ, MS TI PULMONARY-FUNCTION IS DECREASED IN MDX MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UT,HLTH SCI CTR,DEPT PHYSIOL,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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A901 EP A901 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701830 ER PT J AU HERBERT, V SHAW, S JAYATILLEKE, E AF HERBERT, V SHAW, S JAYATILLEKE, E TI VITAMIN-C SUPPLEMENTS ARE HARMFUL TO LETHAL FOR THE OVER 10-PERCENT OF AMERICANS WITH HIGH IRON STORES SO FASEB JOURNAL LA English DT Meeting Abstract C1 MT SINAI VA MED CTR,NEW YORK,NY 10468. BRONX VET ADM MED CTR,NEW YORK,NY 10468. NR 3 TC 8 Z9 8 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A678 EP A678 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700541 ER PT J AU WANG, W ZHOU, T MOUNTZ, JD AF WANG, W ZHOU, T MOUNTZ, JD TI BOTH CD3 AND FAS SIGNALS ARE REQUIRED TO INDUCE DELETION OF CD4+ CD8+ THYMOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. UNIV ALABAMA,BIRMINGHAM,AL 35294. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A740 EP A740 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700901 ER PT J AU GULLEY, ML EAGAN, PA QUINTANILLAMARTINEZ, L PICADO, AL SMIR, BN CHILDS, C DUNN, CD CRAIG, FE WILLIAMS, JW BANKS, PM AF GULLEY, ML EAGAN, PA QUINTANILLAMARTINEZ, L PICADO, AL SMIR, BN CHILDS, C DUNN, CD CRAIG, FE WILLIAMS, JW BANKS, PM TI EPSTEIN-BARR-VIRUS DNA IS ABUNDANT AND MONOCLONAL IN THE REED-STERNBERG CELLS OF HODGKINS-DISEASE - ASSOCIATION WITH MIXED CELLULARITY SUBTYPE AND HISPANIC AMERICAN ETHNICITY SO BLOOD LA English DT Article ID POLYMERASE CHAIN-REACTION; INSITU HYBRIDIZATION; VIRAL GENOMES; SAN-ANTONIO; EBV; LYMPHOMA; EXPRESSION; GENE; SIBLINGS; TISSUE C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. INST NACL NUTR,DEPT PATOL,THALPAN,DF,MEXICO. HOSP SAN JUAN DIOS,DEPT PATOL,SAN JOSE,COSTA RICA. SW TEXAS METHODIST HOSP,SAN ANTONIO,TX. WILFORD HALL USAF MED CTR,SAN ANTONIO,TX 78236. RP GULLEY, ML (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU AHRQ HHS [U01-HS07397]; NCI NIH HHS [K08-CA01615] NR 51 TC 105 Z9 106 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1994 VL 83 IS 6 BP 1595 EP 1602 PG 8 WC Hematology SC Hematology GA NA491 UT WOS:A1994NA49100021 PM 8123850 ER PT J AU DALLAS, SL PARKSNYDER, S MIYAZONO, K TWARDZIK, D MUNDY, GR BONEWALD, LF AF DALLAS, SL PARKSNYDER, S MIYAZONO, K TWARDZIK, D MUNDY, GR BONEWALD, LF TI CHARACTERIZATION AND AUTOREGULATION OF LATENT TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) COMPLEXES IN OSTEOBLAST-LIKE CELL-LINES - PRODUCTION OF A LATENT COMPLEX LACKING THE LATENT TGF-BETA-BINDING PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOLECULAR-WEIGHT COMPLEX; MARFAN-SYNDROME; HUMAN-PLATELETS; BONE-FORMATION; MESSENGER-RNA; FACTOR-BETA-1; EXPRESSION; PRECURSOR; SEQUENCES; INVIVO AB We have previously shown that bone organ cultures produce large amounts of latent transforming growth factor beta (TGF beta), which lacks latent TGF beta-binding protein (LTBP). In this study we used the known osteoblastlike cell lines UMR-106, ROS 17/2.8, and MG63 as models to further examine latent TGF beta expression in bone. We found that the osteosarcoma cell line UMR-106 secreted latent TGF beta almost exclusively as a 100-kDa complex lacking LTBP. ROS 17/2.8 cells produced both the 100-kDa complex and also a 290-kDa complex containing the fibroblastic (190 kDa) form of LTBP. MG63 cells (like human foreskin fibroblasts) expressed almost exclusively the 290-kDa complex. To investigate the regulation of latent TGF beta complexes in bone cells we assessed the effects of TGF beta 1 treatment on expression of active and latent TGF beta. TGF beta 1 induced secretion of latent but not active TGF beta in all cell types examined. In human foreskin fibroblast cells, TGF beta 1 and LTBP mRNA were expressed concomitantly. In contrast, in osteosarcoma cell lines autoinduction of TGF beta 1 mRNA was associated with either a delayed increase or no change in LTBP mRNA In UMR-106 cells LTBP message was virtually undetectable. We postulate that the expression of different latent TGF beta forms by osteoblast-like cells may reflect their maturation states and that different latent TGF beta complexes may have different functions, for example as secretory forms or as matrix storage forms. C1 LUDWIG INST CANC RES,UPPSALA,SWEDEN. BRISTOL MYERS SQUIBB,SEATTLE,WA 98121. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DALLAS, SL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV ENDOCRINOL & METAB,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [DE-08569] NR 29 TC 135 Z9 139 U1 0 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 1994 VL 269 IS 9 BP 6815 EP 6822 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MZ503 UT WOS:A1994MZ50300088 PM 8120044 ER PT J AU SMALL, GW ROSENTHAL, M TOURTELLOTTE, WW AF SMALL, GW ROSENTHAL, M TOURTELLOTTE, WW TI CENTRAL-NERVOUS-SYSTEM IGG SYNTHESIS RATES IN ALZHEIMER-DISEASE - POSSIBLE DIFFERENCES IN EARLY-ONSET AND LATE-ONSET SUBGROUPS SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article DE IGG SYNTHESIS RATE; ALZHEIMER DISEASE; AGE AT ONSET ID MULTI-INFARCT DEMENTIA; BLOOD-BRAIN-BARRIER; CEREBROSPINAL-FLUID; OLIGOCLONAL BANDS; ALBUMIN; IMMUNOGLOBULIN; SERUM; AUTOANTIBODIES; ANTIBODIES; SCLEROSIS AB Central nervous system IgG synthesis rates were determined for 51 patients with autopsy-confirmed Alzheimer disease and 23 age-matched controls. Rates were no different between patients and controls when overall groups were compared. Age-at-dementia-onset data were available on 37 patients. Comparisons of 11 early-onset (<65 years of age) patients with 26 late-onset patients revealed significantly increased intrathecal IgG synthesis rates for the late-onset group. These results suggest that IgG synthesis may be a contributing pathogenic factor in a subgroup of patients with late-onset Alzheimer disease. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA USA. VET AFFAIRS MED CTR, CTR GERIATR RES EDUC & CLIN, SEPULVEDA, CA USA. FU NIA NIH HHS [NIA AG10123]; NIMH NIH HHS [NIMH 1R29 MH46424] NR 42 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD SPR PY 1994 VL 8 IS 1 BP 29 EP 37 DI 10.1097/00002093-199408010-00006 PG 9 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA MZ515 UT WOS:A1994MZ51500005 PM 8185879 ER PT J AU FREEMAN, GL HARRIS, MM GHIDONI, JJ PAGE, A CANTU, TL YOUNG, E AF FREEMAN, GL HARRIS, MM GHIDONI, JJ PAGE, A CANTU, TL YOUNG, E TI ANALYSIS OF MYOCARDIAL RESPONSE TO SIGNIFICANT WEIGHT-LOSS IN OBESE RATS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE CARDIAC MASS; MYOCARDIAL REGRESSION; OBESITY; ENERGY RESTRICTION ID SEMISTARVATION DIETS; LEFT-VENTRICLE; REDUCTION; HYPERTROPHY; CAPTOPRIL; SUDDEN; DEATH AB We evaluated cardiac response to weight loss induced by a very-low-energy (VLE) diet similar to commercially available protein-sparing diets. Such diets have been implicated in sudden death, and whether organ and tissue responses to them are untoward is not known. Rapid weight loss was induced in rats with weights ranging from obese to normal, and cardiac mass and myocardial histomorphometry were assessed. Over 3 wk body weight dropped from 544 +/- 12 to 417 +/- 21 g (P < 0.001). Heart weight was less in the VLE group than in obese controls (1246 +/- 115 vs 1625 +/- 179 mg, P < 0.001), as were the weights of the left ventricle (805 +/- 81 vs 1061 +/- 134 mg, P < 0.001) and right ventricle (198 +/- 27 vs 265 +/- 40 mg, P < 0.002). Reduction in heart weight was commensurate with loss of body weight (r = 0.89). Myocyte cross-sectional area was reduced in the VLE group (452.6 +/- 108.6 to 331.8 +/- 41.5 mu m(2), P < 0.05), with no structural abnormalities. We conclude that weight loss in the weight range studied is accompanied by proportional reduction in cardiac mass and myocyte size. Myocardial regression is not accompanied by myocyte dropout or edema, and likely represents a simple adaptation to reduced body size. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP FREEMAN, GL (reprint author), UNIV TEXAS,HLTH SCI CTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [5 RO1 DK35039-03] NR 29 TC 10 Z9 10 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAR PY 1994 VL 59 IS 3 BP 566 EP 571 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MZ669 UT WOS:A1994MZ66900004 PM 8116532 ER PT J AU WEINSTOCK, R LEONG, GB SILVA, JA AF WEINSTOCK, R LEONG, GB SILVA, JA TI COMPETENCE TO TERMINATE LIFE-SUSTAINING CARE - ETHICAL AND LEGAL CONSIDERATIONS SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article ID ADVANCE DIRECTIVES; HEALTH-CARE; CONSENT; DILEMMA; ORDERS AB Recent federal legislation requires that patients be provided with information about advance directives for terminating health care. Although the mental status of patients executing these directives is crucial, and states require competence to make such a directive, no clear criteria or mandated procedures exist to evaluate the patient's competence to make these decisions. No explicit criteria exist for competence of surrogates either. The authors propose guidelines for such competence determinations. They also consider psychiatric factors surrounding decisions to terminate life-sustaining care. Such decisions have particular importance for geriatric patients. Further research is needed to guide both physicians and policymakers in determining the frequency and types of psychiatric problems in such patients and resultant ''irrational'' decisions to die. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV,SAN ANTONIO,TX 78284. RP WEINSTOCK, R (reprint author), W LOS ANGELES VET ADM ADM CTR,PSYCHIAT SERV,116AC,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 36 TC 4 Z9 4 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD SPR PY 1994 VL 2 IS 2 BP 95 EP 106 PG 12 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA NF320 UT WOS:A1994NF32000002 PM 11652962 ER PT J AU ROYALL, DR MAHURIN, R AF ROYALL, DR MAHURIN, R TI QUALITATIVE DEMENTIA TYPES SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Letter C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD SPR PY 1994 VL 2 IS 2 BP 178 EP 179 PG 2 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA NF320 UT WOS:A1994NF32000015 ER PT J AU RUMBAUT, RE KROLL, MH GYORKEY, F SCHAFER, AI AF RUMBAUT, RE KROLL, MH GYORKEY, F SCHAFER, AI TI ACQUIRED PLATELET STORAGE POOL DEFICIENCY DUE TO SEVERE VALVULAR DISEASE CORRECTED BY PROSTHETIC VALVE-REPLACEMENT SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Letter ID AGGREGATION C1 BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. HOUSTON VA MED CTR,HOUSTON,TX. RP RUMBAUT, RE (reprint author), BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030, USA. NR 4 TC 3 Z9 3 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 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD MAR PY 1994 VL 45 IS 3 BP 272 EP 273 DI 10.1002/ajh.2830450322 PG 2 WC Hematology SC Hematology GA MT449 UT WOS:A1994MT44900021 PM 8296805 ER PT J AU BONADONNA, RC GROOP, LC SIMONSON, DC DEFRONZO, RA AF BONADONNA, RC GROOP, LC SIMONSON, DC DEFRONZO, RA TI FREE FATTY-ACID AND GLUCOSE-METABOLISM IN HUMAN AGING - EVIDENCE FOR OPERATION OF THE RANDLE CYCLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INSULIN; LIPID METABOLISM; SUBSTRATE COMPETITION ID INSULIN RESISTANCE; ELDERLY SUBJECTS; TURNOVER; OXIDATION; PLASMA; MEN; OBESITY; AGE; SENSITIVITY AB Free fatty acid and glucose metabolism in human aging: evidence for operation of the Randle cycle. Am. J. Physiol. 266 (Endocrinol. Metab. 29): E501-E509, 1994. - We assessed insulin effects on plasma free fatty acid (FFA) and glucose metabolism in seven elderly (71 +/- 2 yr) and in seven younger (21 +/- 1 yr) subjects matched for body weight and body mass index but not for percent body fat (32.4 +/- 3.8% in elderly vs. 20.4 +/- 3.5% in young, P < 0.05), by performing sequential euglycemic clamps at five insulin doses (0.6, 1.5, 3, 6, and 15 pmol.min(-1).kg(-1)) in combination with indirect calorimetry and [1-C-14]palmitate plus [3-H-3]glucose infusion. At baseline, plasma FFA concentration, turnover and oxidation, and total lipid oxidation were all increased in the elderly (897 +/- 107 vs. 412 +/- 50 mu mol/l and 11.2 +/- 1.4 vs. 5.14 +/- 0.86, 3.45 +/- 0.65 vs. 1.37 +/- 0.25, and 4.63 +/- 0.72 vs. 3.01 +/- 0.33 mu mol.min(-1).kg(-1) lean body mass, P < 0.05 for all comparisons), whereas glucose turnover was similar as a result of decreased glucose oxidation (8.2 +/- 1.4 vs. 13 +/- 1.9 mu mol.min(-1).kg(-1) lean body mass, P < 0.05) and increased glucose storage (6.6 +/- 1.4 vs. 1.7 +/- 1.3 mmol.min(-1).kg(-1) lean body mass, P < 0.05). At all insulin infusions, plasma FFA concentration, turnover and oxidation, and total lipid oxidation were higher in the elderly than in the younger group (P < 0.05). However, if normalized per fat mass, all FFA and lipid metabolic fluxes, both in the postabsorptive state and during hyperinsulinemia, were comparable in the two groups. Insulin-mediated inhibition of hepatic glucose production and stimulation of glucose storage were similar in the two groups, but glucose oxidation was lower in the elderly than in the young at all insulin concentrations tested (P < 0.05). Plasma FFA turnover rate and total lipid oxidation were negatively correlated with whole body glucose uptake and oxidation in the two groups (P < 0.05-0.01). Thus, in human aging, abnormalities in insulin regulation of FFA/lipid metabolism may be secondary to increased fat mass and substrate competition between fat and glucose and may play a role in determining a reduction in insulin-mediated glucose oxidation. C1 UNIV PISA,CNR,INST CLIN PHYSIOL,METAB UNIT,I-156100 PISA,ITALY. UNIV HELSINKI,DEPT MED 4,SF-00170 HELSINKI,FINLAND. UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 39 TC 64 Z9 64 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP E501 EP E509 PN 1 PG 9 WC Physiology SC Physiology GA NF859 UT WOS:A1994NF85900058 PM 8166272 ER PT J AU KLEYMAN, TR ERNST, SA COUPAYEGERARD, B AF KLEYMAN, TR ERNST, SA COUPAYEGERARD, B TI ARGININE-VASOPRESSIN AND FORSKOLIN REGULATE APICAL CELL-SURFACE EXPRESSION OF EPITHELIAL NA+ CHANNELS IN A6 CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE AMILORIDE; ANTIDIURETIC HORMONE; ANTI-SODIUM CHANNEL ANTIBODY; BREFELDIN A ID BREFELDIN-A; SODIUM-TRANSPORT; HORMONAL-CONTROL; URINARY-BLADDER; LINE A6; ALDOSTERONE; MEMBRANE; PROTEINS; PHOSPHORYLATION; LOCALIZATION AB Both arginine vasopressin (AVP) and forskolin regulate vectorial Na+ transport across high-resistance epithelia by increasing the Na+ conductance of the apical membrane mediated by amiloride-sensitive Na+ channels. Pretreatment of A6 cells with brefeldin A partially inhibited the increase in Na+ transport in response to forskolin, suggesting recruitment of Na+ channels from an intracellular pool. The activation of Cl- secretion was not affected. Apical cell surface expression of Na+ channels was examined following activation of transepithelial Na+ transport across the epithelial cell line A6 by AVP or forskolin. Apical cell surface radioiodinated Na+ channels were immunoprecipitated to quantify the biochemical pool of Na+ channels at the apical plasma membrane and to determine whether an increment in the biochemical pool of Naf channels expressed at the apical cell surface is a potential mechanism by which AVP and forskolin increase apical membrane Na+ conductance. The activation of Na+ transport across A6 cells by AVP was accompanied by a significant increase in the biochemical pool of Na+ channels at the apical plasma membrane within 5 min after addition of hormone, which was sustained for at least 30 min. The increase in apical cell surface expression of Na+ channels was also observed 30 min after application of forskolin. No changes in the oligomeric subunit composition of the channel were noted. Brefeldin A inhibited the forskolin-stimulated increase in apical cell surface expression of Na+ channels. These results suggest that AVP and forskolin regulate Na+ transport, in part, via rapid recruitment of Na+ channels to the cell surface, perhaps from a pool of channels in the subapical cytoplasm. C1 UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. UNIV MICHIGAN,DEPT ANAT & CELL BIOL,ANN ARBOR,MI 48109. RP KLEYMAN, TR (reprint author), DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. FU NIDDK NIH HHS [DK-34933] NR 35 TC 74 Z9 74 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP F506 EP F511 PN 2 PG 6 WC Physiology SC Physiology GA NF861 UT WOS:A1994NF86100127 PM 8160801 ER PT J AU PORSA, E FREEMAN, GL HERLIHY, JT AF PORSA, E FREEMAN, GL HERLIHY, JT TI TACHYCARDIA HEART-FAILURE ALTERS RABBIT AORTIC SMOOTH-MUSCLE RESPONSIVENESS TO ANGIOTENSIN-II SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE POTASSIUM DEPOLARIZATION; CALCIUM; ISOPROTERENOL; PHENYLEPHRINE; VASCULAR SMOOTH MUSCLE ID CHRONIC SUPRAVENTRICULAR TACHYCARDIA; INOSITOL TRISPHOSPHATE; NOREPINEPHRINE; RECEPTORS; VASOCONSTRICTION; CALCIUM; CELLS; DOGS AB The effects of heart failure on the responsiveness of aortic smooth muscle tissue to various vasoactive agents were examined. Heart failure was induced in rabbits by sustained rapid ventricular pacing (400 beats/min) for 6-7 wk. After the rabbits were killed, strips of thoracic aorta were prepared and mounted in tissue baths. Responsiveness of these aortic strips to potassium depolarization and cumulative additions of vasoactive agents was determined. Aortic strips from control and tachycardia heart failure (THF) rabbits developed similar maximum forces to stimulation by potassium depolarization (0.77 +/- 0.08 vs. 0.96 +/- 0.16 kg/cm(2)), calcium chloride (0.71 +/- 0.09 vs. 0.88 +/- 0.06 kg/cm(2)), and phenylephrine (0.90 +/- 0.08 vs. 1.14 +/- 0.09 kg/cm(2)). The maximum relaxation to isoproterenol was also unaffected by THF (0.08 +/- 0.02 vs. 0.07 +/- 0.01 kg/cm(2)). In contrast, the maximum response of aortic strips from THF rabbits to angiotensin II was significantly lower than control (0.37 +/- 0.07 vs. 0.069 +/- 0.09 kg/cm(2)). With regard to aortic smooth muscle sensitivity, no differences in the concentrations at which 50% of the maximal response is achieved (EC(50)) were observed between THF and control strips for calcium chloride (0.10 +/- 0.01 vs. 0.16 +/- 0.04 mM), isoproterenol (51.5 +/- 13.5 vs. 51.0 +/- 5.4 nM), and phenylephrine (65.2 +/- 12.3 vs. 92.5 +/- 18.0 nM). However, THF was associated with a significant increase in the EC(50) value for angiotensin II response (2.03 +/- 0.25 vs. 0.58 +/- 0.05 nM). These results demonstrate that THF is associated with a specific and significant reduction in the sensitivity and maximal responsiveness of aortic smooth muscle to angiotensin II. THF-induced alterations in the characteristics of angiotensin II receptors may be responsible for these changes. 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,SAN ANTONIO,TX 78284. NR 30 TC 5 Z9 5 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP H1228 EP H1232 PN 2 PG 5 WC Physiology SC Physiology GA NF861 UT WOS:A1994NF86100049 ER PT J AU OOKHTENS, M MITTUR, AV ERHART, NA AF OOKHTENS, M MITTUR, AV ERHART, NA TI CHANGES IN PLASMA GLUTATHIONE CONCENTRATIONS, TURNOVER, AND DISPOSAL IN DEVELOPING RATS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GLUTATHIONE; PLASMA; TURNOVER; KINETICS; DEVELOPMENT; AGING ID HEPATIC GLUTATHIONE; EFFLUX; LIVER; HEPATOCYTES; HOMEOSTASIS; INHIBITION; MECHANISM; STRESS; STATE; FORMS AB We have previously shown that sinusoidal reduced glutathione (GSH) efflux declines during development because of a declining maximum transport rate [Am. J. Physiol. 261 (Gastrointest. Liver Physiol. 24): G648-G656, 1991]. Because rat liver serves as the principal source of plasma GSH, we studied the response of plasma GSH to this declining inflow from liver. In immature (28- to 42-day) and mature (90- to 151-day) rats we injected tracer boluses of [S-35]GSH intravenously and collected arterial samples over a 0.75- to 8-mi:n interval while plasma GSH pool remained at steady state!. Concentrations and radioactivities of GSH, oxidized glutathione (GSSG), cysteine (CYSH), cystine (CYSS), and cysteine-glutathione disulfides (CYSSG) and the radioactivities of proteins were measured in plasma. Our results show the following changes in plasma concentrations (mu M): decreases in unbound (free) GSH (26.0 +/- 2.1 to 12.4 +/- 0.98; P < 0.001), total unbound GSH equivalents GSH + 2GSSG (29.1 +/- 2.1 to 15.3 +/- 1.2; P < 0.001), total reducible (unbound + bound) GSH (39.3 +/- 2.2 to 28.9 +/- 2.6; P < 0.025!, and free CYSH (57.6 +/- 8.5 to 29.9 +/- 4.0; P < 0.05); no changes in GSSG (1.57 +/- 0.27 vs. 1.47 +/- 0.41), CYSS (36.7 +/- 12 vs;. 43.4 +/- 17), and total unbound CYSH equivalents CYSH - 2CYSS (131 +/- 15 vs. 117 +/- 18); increases in total reducible (unbound + bound) CYSH (158 +/- 8.1 to 203 +/- 24; P < 0.05) and CYSSG (1.80 +/- 0.42 to 4.94 +/- 1.4 in IJ,M GSH equivalents; P < 0.05). A concurrent decline occurred in irreversible disposal rate (IDR) of plasma GSH from 38.5 +/- 4.9 to 16.4 +/- 1.4 nmol.min(-1).ml(-1) (P < 0.001) as determined by compartmental analysis of tracer data. This 57% decrease in IDR parallels a decrease of 53% in the inflow of GSH estimated by perfused livers (17.0 to 8.0 nmol.min(-1).ml plasma(-1)). However, perfused liver estimates do not match >44-49% of plasma IDR. Thus perfused liver appears to underestimate the true rate of sinusoidal GSH efflux taking place in vivo. Some earlier arteriovenous data and our present portal vein-to-hepatic vein difference measurements appear to corroborate this view. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES OUTPATIENT CLIN,RES SERV,LOS ANGELES,CA 90012. RP OOKHTENS, M (reprint author), UNIV SO CALIF,SCH MED,DEPT MED,DIV GASTROINTESTINAL & LIVER DIS,GI & LIVER RES L,LOS ANGELES,CA 90033, USA. FU NIA NIH HHS [AG-074667] NR 28 TC 22 Z9 22 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP R979 EP R988 PN 2 PG 10 WC Physiology SC Physiology GA NF861 UT WOS:A1994NF86100097 PM 8160895 ER PT J AU GREEN, MF HUGDAHL, K MITCHELL, S AF GREEN, MF HUGDAHL, K MITCHELL, S TI DICHOTIC-LISTENING DURING AUDITORY HALLUCINATIONS IN PATIENTS WITH SCHIZOPHRENIA SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID ACUTE PSYCHOTIC ILLNESS; CEREBRAL LATERALITY; FORCED-ATTENTION; TEMPORAL-LOBE; CHILDREN; RELIABILITY AB Objective: Auditory hallucinations are a serious problem for a large subgroup of psychotic patients who do not respond optimally to neuroleptic medication. It has been hypothesized that hearing imaginary voices involves the same physiological processes as those involved in hearing real voices, but this hypothesis has not been conclusively confirmed. Method: In this study a consonant-vowel version of the Dichotic Listening Test was used to assess the functional integration of the left hemisphere in hallucinating and nonhallucinating psychotic patients. The test was administered under three conditions: a nonforced attention condition, a condition in which attention was forced to the left ear, and one in which attention was forced to the right ear. Results: The nonhallucinating patients showed the normal right ear advantage, which indicates a left hemisphere superiority in the processing of linguistic stimuli. In contrast, the hallucinating patients showed no ear advantage, Neither group was able to modify its performance when instructed to attend to either the left or the right ear. A subgroup of patients was tested in both hallucinating and nonhallucinating states, but the ear asymmetry was not noticeably different between these states. Conclusions: The results suggest that auditory hallucinations are associated with abnormalities in left hemisphere functioning and that these abnormalities might not be limited to the time of the auditory hallucinations. It is hypothesized that a relatively enduring left hemisphere abnormality may leave some patients at risk for auditory hallucinations. C1 W LOS ANGELES VA MED CTR, LOS ANGELES, CA USA. UNIV BERGEN, DEPT MED & BIOL PSYCHOL, BERGEN, NORWAY. RP GREEN, MF (reprint author), UNIV CALIF LOS ANGELES, RES CTR, DEPT PSYCHIAT & BIOBEHAV SCI, BOX 6022, CAMARILLO, CA 93011 USA. FU NIMH NIH HHS [NIMH MH-4392, NIMH MH-30911] NR 28 TC 90 Z9 92 U1 0 U2 3 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 1994 VL 151 IS 3 BP 357 EP 362 PG 6 WC Psychiatry SC Psychiatry GA MY317 UT WOS:A1994MY31700006 PM 8109643 ER PT J AU BOHN, MJ KRANZLER, HR BEAZOGLOU, D STAEHLER, BA AF BOHN, MJ KRANZLER, HR BEAZOGLOU, D STAEHLER, BA TI NALTREXONE AND BRIEF COUNSELING TO REDUCE HEAVY DRINKING - RESULTS OF A SMALL CLINICAL-TRIAL SO AMERICAN JOURNAL ON ADDICTIONS LA English DT Article; Proceedings Paper CT Annual Meeting of the International Conference on Psychoneuroendocrinology CY AUG, 1992 CL MADISON, WI ID ALCOHOL DEPENDENCE; CONSUMPTION; POPULATION; STRATEGIES; MORPHINE AB Naltrexone (NTX) has been shown to be safe and effective in reducing relapses among alcoholics. Among nondependent heavy drinkers, who are more numerous in the general population than are alcohol-dependent drinkers, brief counseling has been shown to reduce alcohol consumption. The authors conducted a 6-week randomized study of the effects of adding 25-mg or 50-mg daily doses of NTX to brief counseling in 14 nondependent heavy drinkers. NTX was well-tolerated. Desire for alcohol, drinking frequency, frequency of heavy drinking, total alcohol consumption, and serum gamma-glutamyl transpeptidase all decreased significantly during treatment. A placebo-controlled trial is warranted to evaluate further the efficacy of NTX in this group of problem drinkers. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV CONNECTICUT,ALCOHOL RES CTR,FARMINGTON,CT 06030. RP BOHN, MJ (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 28 TC 42 Z9 45 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1055-0496 J9 AM J ADDICTION JI Am. J. Addict. PD SPR PY 1994 VL 3 IS 2 BP 91 EP 99 PG 9 WC Substance Abuse SC Substance Abuse GA NH408 UT WOS:A1994NH40800001 ER PT J AU SPRUANCE, SL PAVIA, AT PETERSON, D BERRY, A POLLARD, R PATTERSON, TF FRANK, I REMICK, SC THOMPSON, M MACARTHUR, RD MOREY, GE RAMIREZRONDA, CH BERNSTEIN, BM SWEET, DE CRANE, L PETERSON, EA PACHUCKI, CT GREEN, SL BRAND, J RIOS, A DUNKLE, LM CROSS, A BROWN, MJ INGRAHAM, P GUGLIOTTI, R SCHINDZIELORZ, AH SMALDONE, L BECKER, T BIA, FJ BUJWIT, C DONABEDIAN, H EVANS, TG FIELLIN, M KAEMPFER, S OKEEFE, JP LIPTON, L MARK, RJ OTT, G REIMER, LG RIES, K WATERMAN, K WEST, MM AF SPRUANCE, SL PAVIA, AT PETERSON, D BERRY, A POLLARD, R PATTERSON, TF FRANK, I REMICK, SC THOMPSON, M MACARTHUR, RD MOREY, GE RAMIREZRONDA, CH BERNSTEIN, BM SWEET, DE CRANE, L PETERSON, EA PACHUCKI, CT GREEN, SL BRAND, J RIOS, A DUNKLE, LM CROSS, A BROWN, MJ INGRAHAM, P GUGLIOTTI, R SCHINDZIELORZ, AH SMALDONE, L BECKER, T BIA, FJ BUJWIT, C DONABEDIAN, H EVANS, TG FIELLIN, M KAEMPFER, S OKEEFE, JP LIPTON, L MARK, RJ OTT, G REIMER, LG RIES, K WATERMAN, K WEST, MM TI DIDANOSINE COMPARED WITH CONTINUATION OF ZIDOVUDINE IN HIV-INFECTED PATIENTS WITH SIGNS OF CLINICAL DETERIORATION WHILE RECEIVING ZIDOVUDINE - A RANDOMIZED, DOUBLE-BLIND CLINICAL-TRIAL SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS INFECTIONS; DIDANOSINE; ZIDOVUDINE; AIDS-RELATED COMPLEX; ACQUIRED IMMUNODEFICIENCY SYNDROME ID IMMUNODEFICIENCY-VIRUS INFECTION; 2',3'-DIDEOXYINOSINE; RESISTANCE; TYPE-1; AZT AB Objective: To determine the benefits of switching to didanosine compared with continuing zidovudine among patients infected with human immunodeficiency virus (HIV) who have previously used zidovudine and have signs of clinical deterioration. Design:Randomized, double-blind, two-armed, parallel, comparative clinical trial with a blinded, compassionate crossover provision at 12 weeks. Setting: Outpatient clinics at 19 tertiary care medical centers. Patients: 312 patients infected with HIV who had received zidovudine for 6 months or more, had CD4 cell counts of 300/mm(3) or less, and had signs of clinical deterioration within 12 weeks before study entry. Intervention: Peroral didanosine tablets (600 mg/d adjusted for weight, ''high dose'') or zidovudine capsules (600 mg/d). Measurements: Primary study end points were death, a new acquired immunodeficiency syndrome (AIDS)-defining event, or the combination of two new or recurrent HIV-related diagnoses with a 50% decrease in CD4 cells. Results: Switching to didanosine was associated with fewer end points than continuing zidovudine (relative risk [RR] for zidovudine:didanosine = 1.5; 95% Cl, 1.1 to 2.0). This benefit was consistent across subgroups of patients with either AIDS-related complex or AIDS and was most apparent among those with a CD4 count at entry of 100/mm(3) or more (RR = 2.2; Cl, 1.1 to 4.4). Conclusions: This study shows a positive treatment effect for switching from zidovudine to didanosine among patients with either AIDS-related complex or AIDS and validates the common practice of using clinical signs or a decrease in the CD4 count as an indication for changing therapy. C1 HOLY CROSS HOSP,SALT LAKE CITY,UT 84102. UNIV TEXAS,SW MED CTR DALLAS,DALLAS,TX 75235. UNIV ARIZONA,HLTH SCI CTR,INFECT DIS SECT,TUCSON,AZ 85724. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. YALE UNIV,SCH MED,NEW HAVEN,CT. UNIV PENN,IMMUNODEFICIENCY PROGRAM,PHILADELPHIA,PA 19104. ALBANY MED CTR,ALBANY,NY. AIDS RES CONSORTIUM ATLANTA,ATLANTA,GA. MED COLL OHIO,DEPT MED,TOLEDO,OH 43614. VET AFFAIRS MED CTR,SAN JUAN,PR 00927. MED COLL WISCONSIN,MILWAUKEE,WI 53226. UNIV KANSAS,SCH MED,WICHITA,KS 67214. VET AFFAIRS EDWARD HINES JR HOSP,INFECT DIS SECT,HINES,IL 60141. UNIV ARIZONA,HLTH SCI CTR,TUCSON,AZ 85724. HOME HLTH CARE SERV,RES INST,ORLANDO,FL. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,WALLINGFORD,CT 06492. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77555. HARPER GRACE HOSP,DETROIT,MI 48201. UNIV PUERTO RICO,SCH MED & AFFILIATED HOSP,SAN JUAN,PR. RP SPRUANCE, SL (reprint author), UNIV UTAH,HLTH SCI AIDS CTR,MC 4B322,50 N MED DR,SALT LAKE CITY,UT 84132, USA. NR 24 TC 72 Z9 72 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 MAR 1 PY 1994 VL 120 IS 5 BP 360 EP 368 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA MY497 UT WOS:A1994MY49700002 PM 7905722 ER PT J AU HOLLIDAY, S ROMERO, J AF HOLLIDAY, S ROMERO, J TI ANTERIOR COMMUNICATING ARTERY (ACOA) ANEURYSM - A LONGITUDINAL CASE-STUDY EXAMINING THE EFFECTS OF PREEXISTING PSYCHIATRIC-ILLNESS AND MEDICATION EFFECTS OF THE ACOA SYNDROME SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6177 J9 ARCH CLIN NEUROPSYCH JI Arch. Clin. Neuropsychol. PD MAR-APR PY 1994 VL 9 IS 2 BP 141 EP 141 PG 1 WC Psychology, Clinical; Psychology SC Psychology GA NM848 UT WOS:A1994NM84800060 ER PT J AU SADEK, J JOHNSON, SA PAULSEN, JS SALMON, DP SWENSON, MP BUTTERS, N AF SADEK, J JOHNSON, SA PAULSEN, JS SALMON, DP SWENSON, MP BUTTERS, N TI DIFFERENTIATION OF HUNTINGTONS-DISEASE AND ALZHEIMERS-DISEASE - DISTINCT COGNITIVE PROFILES REMAIN IN ADVANCED ILLNESS SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. US DEPT VET AFFAIRS,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6177 J9 ARCH CLIN NEUROPSYCH JI Arch. Clin. Neuropsychol. PD MAR-APR PY 1994 VL 9 IS 2 BP 179 EP 180 PG 2 WC Psychology, Clinical; Psychology SC Psychology GA NM848 UT WOS:A1994NM84800126 ER PT J AU ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH AF ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH TI TRANSCRIPTIONAL REGULATION OF THE TARTRATE-RESISTANT ACID-PHOSPHATASE (TRAP) GENE BY IRON SO BIOCHEMICAL JOURNAL LA English DT Article ID LYMPHOBLASTOID T-CELLS; MESSENGER-RNA; TRANSFERRIN RECEPTOR; EXPRESSION; PROTEIN; INDUCTION; UTEROFERRIN; FERRITIN; PROGESTERONE; ISOENZYME AB Tartrate-resistant acid phosphatase (TRAP) was first identified in cells from patients with hairy cell leukaemia. Subsequently, it has been found in other leukaemias, B-lymphoblastoid cell lines, osteoclasts and subsets of normal lymphocytes, macrophages, and granulocytes. Recent data indicate that TRAP and porcine uteroferrin, a placental iron-transport protein, represent a single gene product. However, the intracellular role of TRAP is unknown. We used a full-length human placental TRAP cDNA probe to examine TRAP expression in human peripheral mononuclear cells (PMCs). TRAP mRNA increased 50-75-fold after 24 h in unstimulated PMC cultures. Cell-fractionation experiments indicated that monocytes were the main cell population accounting far increased TRAP mRNA transcripts, and this was confirmed by histochemical staining for TRAP enzyme activity. Because expression of other iron-binding and -transport proteins is controlled by iron availability, we examined the role of iron in regulating TRAP expression. Increase of TRAP mRNA transcripts in PMCs was inhibited by 50 mu M desferrioxamine, a potent iron chelator. The 5' flanking region of the TRAP gene was cloned from a mouse genomic library. In preliminary transient transfection experiments, it was determined that the 5'-flanking region of the TRAP gene contained iron-responsive elements. Therefore, a series of stably transfected HRE H9 cell lines was developed bearing genetic constructs containing various segments of the murine TRAP 5' promoter region driving a luciferase reporter gene. Treatment of transfectants with 100 mu g/ml iron-saturated human transferrin (FeTF) was performed to assess iron responsiveness of the constructs. Constructs containing a full-length TRAP promoter (comprising base pairs -1846 to +2) responded to FeTF with a 4-5-fold increase of luciferase activity whereas constructs containing only base pairs -363 to +2 of the TRAP promoter did not respond. Constructs containing 1240 or 881 bp of the TRAP promoter gave only a 1.5- to 2-fold increase of luciferase activity with FeTF. In all cases, increase of luciferase activity was blocked by desferrioxamine. Cells transfected with another luciferase construct driven by a simian virus 40 promoter did not show any increase of luciferase activity with FeTF. These data indicate that expression of TRAP is regulated by iron and that this regulation is exerted at the level of gene transcription. The transfection experiments also suggest that the region of the TRAP 5'-flanking sequence between base pairs - 1846 and - 1240 contains an iron regulatory element. C1 UNIV TEXAS,AUDIE L MURPHY VET ADM HOSP,HLTH SCI CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV HEMATOL,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM 35188]; NIAMS NIH HHS [AR 41336, AR 3539] NR 31 TC 32 Z9 32 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 MAR 1 PY 1994 VL 298 BP 421 EP 425 PN 2 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA073 UT WOS:A1994NA07300026 PM 8135751 ER PT J AU LEVINE, SM ANZUETO, A PETERS, JI CALHOON, JH JENKINSON, SG BRYAN, CL AF LEVINE, SM ANZUETO, A PETERS, JI CALHOON, JH JENKINSON, SG BRYAN, CL TI SINGLE-LUNG TRANSPLANTATION IN PATIENTS WITH SYSTEMIC-DISEASE SO CHEST LA English DT Article ID PRIMARY PULMONARY-HYPERTENSION AB Objective: To report functional results and survival in patients undergoing single lung transplantation (SLT) for pulmonary involvement associated with systemic disease or prior malignancy, criteria traditionally considered contraindications to SLT. Design: Case series. Setting: The University of Texas Health Science Center at San Antonio. Patients: Nine patients who have undergone SLT for end-stage lung disease: four patients with sarcoidosis; two patients with limited scleroderma; and three patients with prior malignancies (two with prior lymphoma and bleomycin-induced pulmonary fibrosis and one who received two bone marrow transplants for acute lymphocytic leukemia and subsequently developed chemotherapy-induced pulmonary fibrosis). Measurements: Pulmonary function testing, exercise oximetry, quantitative ventilation-perfusion lung scanning. Actuarial survival. Results: All patients had marked improvement in pulmonary function, exercise oximetry, and quantitative ventilation perfusion to the SLT. One patient with scleroderma died 90 days postoperatively from Pseudomonas pneumonia with a sepsis syndrome. One patient with sarcoidosis died 150 days postoperatively from disseminated aspergillosis. At autopsy, there was no evidence of recurrent fibrosis or sarcoidosis in the transplanted lungs in either of these two patients. The seven surviving patients have returned to work or school and are conducting all activities of daily living without pulmonary disability. The 1- and 2-year actuarial survival rates in these nine patients is 68.6 percent as compared with the 1- and e-year actuarial survival rates of 66.3 percent and 55.8 percent in the remainder of our SLT group as a whole (n=49). Despite pharmacologic immunosuppression, there is no evidence of recurrent malignancy in the 3 patients with prior malignancies. Conclusions: We conclude that carefully selected patients with end-stage lung involvement related to systemic disease or chemotherapy-induced fibrosis may benefit from SLT. C1 UNIV TEXAS,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP LEVINE, SM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS,PULM DIS SECT 111B,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NHLBI NIH HHS [HL-32824] NR 13 TC 45 Z9 45 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1994 VL 105 IS 3 BP 837 EP 841 DI 10.1378/chest.105.3.837 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NA618 UT WOS:A1994NA61800037 PM 7510601 ER PT J AU ANZUETO, A LEVINE, SM TILLIS, WP CALHOON, JH BRYAN, CL AF ANZUETO, A LEVINE, SM TILLIS, WP CALHOON, JH BRYAN, CL TI USE OF THE FLOW-VOLUME LOOP IN THE DIAGNOSIS OF BRONCHIAL STENOSIS AFTER SINGLE-LUNG TRANSPLANTATION SO CHEST LA English DT Note ID MANAGEMENT; REJECTION; GRAFT; LASER AB Bronchial complications, including stricture, stenosis, and/or anastomotic dehiscence, are a major cause of morbidity following single lung transplantation. This report describes a 19-year-old man with a diagnosis of end-stage pulmonary fibrosis secondary to prior chemotherapy for non-Hodgkins lymphoma who underwent single lung transplantation, The immunosuppressive regimen included cyclosporine, azathioprine, and methylprednisolone sodium succinate (Solu-Medrol) intravenously for six doses during the first 3 days postoperatively followed by oral prednisone. Sixteen weeks following transplantation, the patient complained of dyspnea. Spirometry revealed a decrease in FEF25-75 and the flow-volume curve demonstrated a bioconcave appearance. The now-volume loop showed a relatively high initial flow phase occurring over the first 2 to 3 s followed by a low-flow phase. The expiratory phase also showed the same characteristics. Bronchoscopy revealed 75 percent stenosis of the bronchial lumen to the transplanted lung. A transbronchial biopsy specimen obtained at that time was consistent with acute rejection. The patient was treated with a methylprednisolone bolus. A repeated bronchoscopy showed the persistence of stenosis distal to the anastomosis. The patient underwent several bronchoplastic balloon dilatations without complete resolution of the stenosis and a stainless steel mesh stent was placed. Repeated spirometry showed marked improvement of the FEF25-75 and normalization of the flow-volume loop. We conclude that the flow-volume loop curve is a noninvasive procedure that may help monitor the patency of the bronchial anastomoses following single lung transplantation. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. RP ANZUETO, A (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 14 TC 19 Z9 20 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 MAR PY 1994 VL 105 IS 3 BP 934 EP 936 DI 10.1378/chest.105.3.934 PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NA618 UT WOS:A1994NA61800058 PM 7510602 ER PT J AU JOHNSON, TB KENT, RL BUBOLZ, BA MCDERMOTT, PJ AF JOHNSON, TB KENT, RL BUBOLZ, BA MCDERMOTT, PJ TI ELECTRICAL-STIMULATION OF CONTRACTILE ACTIVITY ACCELERATES GROWTH OF CULTURED NEONATAL CARDIOCYTES SO CIRCULATION RESEARCH LA English DT Article DE HYPERTROPHY; CARDIOCYTES; CONTRACTION; ELECTRICAL STIMULATION ID RIBOSOMAL-RNA SYNTHESIS; RAT CARDIAC MYOCYTES; ADULT FELINE CARDIOCYTES; HEART-CELLS; GENE-EXPRESSION; 2,3-BUTANEDIONE MONOXIME; MAMMALIAN MYOCARDIUM; PROTEIN-SYNTHESIS; MYOSIN SYNTHESIS; SKELETAL-MUSCLE AB An electrical stimulation system was designed to regulate synchronized contractile activity of neonatal rat cardiocytes and to examine the effects of mechanical contraction on cardiocyte growth. Continuous electrical stimulation at a pulse duration of 5 milliseconds and frequency of 3 Hz resulted in a time-dependent accumulation of cell protein that reached 34% above initial values, as measured by the protein-to-DNA ratio. The growth response did not occur using voltage amplitudes that were subthreshold for contraction and was independent of contraction frequencies set at greater than or equal to 0.5 Hz. The RNA-to-DNA ratio increased in parallel to cell protein, indicating that the capacity for protein synthesis was enhanced by contraction. Rates of 28S rRNA synthesis were accelerated twofold in contracting cardiocytes. By comparison, protein and RNA accumulation did not occur in electrically stimulated cardiocytes in which contraction was blocked by either 10 mu mol/L verapamil or by 5 mmol/L 2,3-butanedione monoxime, an inhibitor of actomyosin crossbridge cycling. Electrical stimulation of cardiocyte contraction did not enhance alpha-cardiac actin or myosin heavy chain (alpha+beta) mRNA transcript levels relative to 28S rRNA during the period of rapid growth that occurred over the first 48 hours. It is concluded that (1) electrical stimulation of contraction accelerates cardiocyte growth and RNA accumulation, (2) mechanical contraction is involved in regulating the growth of electrically stimulated cardiocytes, and (3) the levels of cu-actin and myosin heavy chain mRNA increase in proportion to rRNA during the growth of contracting cardiocytes. (Circ Res. 1994;74:448-459.) C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CARDIOL SECT,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT CELL BIOL & ANAT,CHARLESTON,SC. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. GAZES CARDIAC RES INST,CHARLESTON,SC. NR 45 TC 40 Z9 40 U1 1 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD MAR PY 1994 VL 74 IS 3 BP 448 EP 459 PG 12 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA MZ583 UT WOS:A1994MZ58300010 PM 8118953 ER PT J AU ZHOU, SR HAN, Q LAGANKE, CC WHITAKER, JN AF ZHOU, SR HAN, Q LAGANKE, CC WHITAKER, JN TI COMPARISON OF PROPERTIES OF MURINE MONOCLONAL ANTIIDIOTYPIC ANTIBODIES GENERATED WITH IDIOTYPE-BEARING MONOCLONAL-ANTIBODIES TO MYELIN BASIC-PROTEIN PEPTIDES OR THEIR COMPLEMENTARY PEPTIDES SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID MESSENGER-RNA; IMMUNIZATION; IDIOTOPES; REGION AB The present study was undertaken to compare the features of monoclonal antibody (mAb) anti-idiotope (Id) induced by complementary peptides, synthesized on the basis of inverted hydropathy for a myelin basic protein (MBP) peptide, or by conventional methodology using Id-bearing antibodies to the same MBP peptide as immunogen. The six reagents studied consisted of mAbs reactive with MBP peptide acetyl 1-9 and MBP peptide 80-89 and anti-Id reagents against these two mAbs prepared by either the complementary peptide or the conventional approach. ELISA, immunoblotting, immunoinhibition of hybridoma cell production of Id-bearing mAb to MBP, and FACS indicated that the anti-Ids generated by either technique were similar although existing in a range reflecting biologic phenomena. mAbs anti-Id prepared by either method continued to show an IgM isotype preference, possibly related to technical considerations, and continued to recognize a cross-reactive Id on the K light chain of the mAbs to MBP peptides acetyl 1-9 and 80-89. There was no indication that the anti-Ids prepared by the complementary peptide approach were restrictive or selective in a manner different from those made by the conventional approach. (C) 1994 Academic Press, Inc. C1 UNIV ALABAMA,DEPT CELL BIOL,BIRMINGHAM,AL. UNIV ALABAMA,CTR NEUROIMMUNOL,BIRMINGHAM,AL. BIRMINGHAM VA MED CTR,NEUROL & RES SERV,BIRMINGHAM,AL 35294. RP ZHOU, SR (reprint author), UNIV ALABAMA,DEPT NEUROL,BIRMINGHAM,AL, USA. FU NINDS NIH HHS [NS 29719, NS 23240]; PHS HHS [T3207335] NR 23 TC 14 Z9 14 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 MAR PY 1994 VL 70 IS 3 BP 251 EP 259 DI 10.1006/clin.1994.1037 PG 9 WC Immunology; Pathology SC Immunology; Pathology GA MY664 UT WOS:A1994MY66400011 PM 7508836 ER PT J AU WILLIAMS, M VANREMMEN, H RICHARDSON, A AF WILLIAMS, M VANREMMEN, H RICHARDSON, A TI EFFECT OF CULTURING ON GENE-EXPRESSION IN RAT HEPATOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A22 EP A22 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19600125 ER PT J AU DANKO, I FRITZ, JD JIAO, SS HOGAN, K LATENDRESSE, JS WOLFF, JA AF DANKO, I FRITZ, JD JIAO, SS HOGAN, K LATENDRESSE, JS WOLFF, JA TI PHARMACOLOGICAL ENHANCEMENT OF IN-VIVO FOREIGN GENE-EXPRESSION IN MUSCLE SO GENE THERAPY LA English DT Article ID MOUSE SKELETAL-MUSCLE; MUSCULAR-DYSTROPHY; LOCAL-ANESTHETICS; MAMMALIAN-CELLS; PLASMID DNA; LONG-TERM; REGENERATION; INVIVO; RAT; BUPIVACAINE AB Intramuscular injection of naked plasmid DNA provides a means for gene transfer and expression in striated muscle. in this study, the effects oi treating muscle with normal saline, etidocaine, mepivacaine, acetic anhydride, sodium bicarbonate, Notechis scutatus venom, cardiotoxin and bupivacaine before plasmid DNA injection on foreign gene expression were evaluated Dose dependence, strain and species specificity, the time interval between pharmacological agent and plasmid DNA injection, the stability of gene expression and the Tate of the injected plasmid DNA were studied using reporter gene expression, by histological examination and semi-quantitative polymerase chain reaction. Of the various gents tested, the best enhancement of foreign gene expression occurred in muscle treated with 0.75% bupivacaine five to seven days before plasmid DNA injection. Rat and mouse quadriceps muscle treated with 0.75% bupivacaine had levels of luciferase activity four- to 40-times greater than non-bupivacaine-treated muscle. Also, beta-galactosidase expressing myofibers were observed throughout the length of the muscle in samples treated with 0.75% bupivacaine before reporter gene injection. Muscle treated with 0.75% bupivacaine fully recovered from the degeneration caused by its injection with no long-term effects histologically. The heightened level of reporter gene expression persisted in 0.75% bupivacaine-treated muscle for one month, but decreased to that of non-bupivacaine-treated muscle by two months after plasmid DNA injection. Enhancement oi foreign gene expression may be particularly advantageous in vaccination protocols employing intramuscular plasmid injection. C1 UNIV WISCONSIN,WAISMAN CTR,DEPT PEDIAT,MADISON,WI 53705. UNIV WISCONSIN,WAISMAN CTR,DEPT MED GENET,MADISON,WI 53705. UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET ADM HOSP,DEPT ANESTHESIOL,MADISON,WI 53706. UNIV WISCONSIN,CTR CLIN SCI,MADISON,WI 53706. NR 39 TC 136 Z9 148 U1 0 U2 4 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0969-7128 J9 GENE THER JI Gene Ther. PD MAR PY 1994 VL 1 IS 2 BP 114 EP 121 PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA PT946 UT WOS:A1994PT94600006 PM 7584066 ER PT J AU HAMNER, MB AF HAMNER, MB TI EXACERBATION OF POSTTRAUMATIC-STRESS-DISORDER SYMPTOMS WITH MEDICAL ILLNESS SO GENERAL HOSPITAL PSYCHIATRY LA English DT Note ID POST-TRAUMATIC STRESS; KOREAN WAR PRISONERS; FOLLOW-UP; MORTALITY AB Chronic posttraumatic stress disorder (PTSD) may increase the risk for associated psychiatric and medical illnesses. In turn, the onset of medical illness may result in an exacerbation of PTSD symptoms leading to excessive or maladaptive psychological and physiological reactions. Five combat veterans with PTSD and medical disease are presented to illustrate this potential for worsening of PTSD with concurrent medical illness. Health care workers in general hospital settings should be aware of unique psychological vulnerabilities in PTSD patients. Prospective studies are needed to assess the impact of medical comorbidity on the course of PTSD. C1 RALPH HENRY JOHNSON DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV,CHARLESTON,SC. MED UNIV S CAROLINA,DEPT PSYCHIAT & HLTH BEHAV SCI,CHARLESTON,SC 29425. NR 13 TC 15 Z9 15 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD MAR PY 1994 VL 16 IS 2 BP 135 EP 137 DI 10.1016/0163-8343(94)90058-2 PG 3 WC Psychiatry SC Psychiatry GA NL442 UT WOS:A1994NL44200012 PM 8039692 ER PT J AU WALLACE, JE MOJAVERIAN, P LIN, CC KIM, HK HARRIS, SC CHEN, TJH RINALDI, MG AF WALLACE, JE MOJAVERIAN, P LIN, CC KIM, HK HARRIS, SC CHEN, TJH RINALDI, MG TI DETERMINATION OF SCH-39304 BY MEGABORE CAPILLARY GAS-LIQUID-CHROMATOGRAPHY SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article C1 SCHERING PLOUGH CORP,RES,DEPT DRUG METAB,KENILWORTH,NJ. VET ADM MED CTR,CHICAGO,IL 60612. PRECIS ANALYT LABS INC,SAN ANTONIO,TX 78216. AUDIE L MURPHY MEM VET ADM MED CTR,LAB SERV,SAN ANTONIO,TX 78284. RP WALLACE, JE (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU PRESTON PUBLICATIONS INC PI NILES PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 SN 0146-4760 J9 J ANAL TOXICOL JI J. Anal. Toxicol. PD MAR-APR PY 1994 VL 18 IS 2 BP 118 EP 121 PG 4 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA NB984 UT WOS:A1994NB98400011 PM 8207932 ER PT J AU BRYAN, CL PATEFIELD, AJ COHEN, D NIELSEN, JL EMANUEL, B CALHOON, JH AF BRYAN, CL PATEFIELD, AJ COHEN, D NIELSEN, JL EMANUEL, B CALHOON, JH TI ASSESSMENT OF INJURY IN TRANSPLANTED AND NONTRANSPLANTED LUNGS AFTER 6 H OF COLD-STORAGE WITH GLUTATHIONE SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE LUNG INJURY; TRANSPLANTATION; NEUTROPHIL; FREE RADICAL; CANINE; PULMONARY EDEMA; LIPID PEROXIDATION ID PULMONARY REIMPLANTATION RESPONSE; ARTERY OCCLUSION; REPERFUSION; EDEMA; PERMEABILITY; DISULFIDE; TRANSPORT; PRESSURE; RAT AB Single-lung transplantation after 3 h of hypothermic storage produces bilateral lung injury [pulmonary reimplantation response (PRR)]. We hypothesized that glutathione (GSH) hypothermic storage would protect both lungs from PRR for extended preservation times and that differences in injury and protection would be realized between the graft and the nontransplanted lung. Mongrel dogs underwent left single-lung autotransplantation after preservation for 5-6 h in Euro-Collins (EC) solution, EC plus exogenous GSH (EC + GSH), or Viaspan (VIA) at 4 degrees C. Lung injury was measured in both lungs after 1 h of reperfusion. EC dogs demonstrated significant increases in lung edema, lipid peroxidation, and alveolar neutrophil recruitment in the lung graft and to a less extent in the nontransplanted right lung compared with control dogs (P < 0.05). Edema, lipid peroxidation, and alveolar neutrophils were significantly reduced in both lungs from EC + GSH and VIA dogs compared with lungs from EC dogs (P < 0.05). An increase in large-pore permeability was measured in the lung graft from EC dogs compared with all other lungs. Bronchoalveolar lavage fluid lactate dehydrogenase and total protein concentrations were elevated in both lungs from all three groups of transplanted dogs compared with those of control dogs (P < 0.05). These data suggest that GSH-containing solutions attenuate the PRR after 6 h of ischemic hypothermic storage but that the protection is incomplete. Mechanisms of injury affecting the lung graft during the PRR appear to differ from those affecting the nontransplanted lung. C1 UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. USAF,MED CTR,DEPT MED,SAN ANTONIO,TX 78284. USAF,MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RP BRYAN, CL (reprint author), UNIV TEXAS,AUDIE L MURPHY VET HOSP,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE MED,SAN ANTONIO,TX 78284, USA. NR 33 TC 12 Z9 12 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD MAR PY 1994 VL 76 IS 3 BP 1232 EP 1241 PG 10 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA NB204 UT WOS:A1994NB20400037 PM 8005867 ER PT J AU PEACOCK, MD SCHENK, DA LAWRENCE, RA MORGAN, JA JENKINSON, SG AF PEACOCK, MD SCHENK, DA LAWRENCE, RA MORGAN, JA JENKINSON, SG TI ELIMINATION OF GLUTATHIONE-INDUCED PROTECTION FROM HYPERBARIC HYPEROXIA BY ACIVICIN SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE GAMMA-GLUTAMYL TRANSPEPTIDASE; HYPERBARIC OXYGEN TOXICITY; RAT ID GLUTAMYL-TRANSFERASE TRANSPEPTIDASE; ISOLATED RAT HEPATOCYTES; OXYGEN-TOXICITY; SELENIUM DEFICIENCY; OXIDATIVE INJURY; EXOGENOUS GLUTATHIONE; PLASMA GLUTATHIONE; LUNG GLUTATHIONE; SMALL-INTESTINE; LYMPHOID-CELLS AB Glutathione (GSH) administered intraperitoneally significantly prolongs the time to initial seizure and survival time of rats exposed to hyperbaric hyperoxia (HBO). Acivicin is an antitumor antibiotic that is an inhibitor of gamma-glutamyl transpeptidase (GGT), an enzyme necessary for the breakdown and transport across cell membranes of GSH. To determine whether acivicin treatment alters GSH-induced protection from HBO, rats were dosed with 25 mg/kg of acivicin or vehicle 1 h before O-2 exposure at an inspired O-2 fraction at 1.0 at 4 ATA. Immediately before exposure, rats received GSH (1 mmol/kg) or vehicle. Time to seizure and time to death were recorded during exposure by direct observation. In separate groups of rats on the same dosing schedule, plasma GSH, renal GGT, and brain GGT were measured 15 min after the GSH injection without HBO exposure and 100 min after the beginning of HBO exposure. Renal GGT was decreased to 2.5% of control and brain GGT to 37% of control in the acivicin-dosed rats. Plasma GSH increased 3-fold in rats given acivicin alone, 52-fold in rats given GSH alone, and 84-fold in rats receiving both acivicin and GSH. Rats dosed with GSH alone had significantly prolonged times to seizure and death compared with all other groups. Rats dosed with GSH after receiving acivicin were not protected from HBO despite the large increase in plasma GSH that occurred in these animals. GSH treatment did not increase tissue GSH in lung, liver, or brain at 160 or 200 min of exposure. These data support the hypothesis that acivicin treatment abolishes GSH-induced protection from HBO and that elevations in plasma GSH do not protect acivicin-treated animals. C1 UNIV TEXAS,HLTH SCI CTR,BROOKE ARMY MED CTR,WILFORD HALL USAF MED CTR,LUNG METAB UNIT,SAN ANTONIO,TX. AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. NR 44 TC 12 Z9 12 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD MAR PY 1994 VL 76 IS 3 BP 1279 EP 1284 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA NB204 UT WOS:A1994NB20400044 PM 7911799 ER PT J AU FREEDMAN, JE WIRSHING, WC RUSSELL, AT BRAY, MP UNUTZER, J AF FREEDMAN, JE WIRSHING, WC RUSSELL, AT BRAY, MP UNUTZER, J TI ABSENCE STATUS SEIZURES DURING SUCCESSFUL LONG-TERM CLOZAPINE TREATMENT OF AN ADOLESCENT WITH SCHIZOPHRENIA SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article AB This article reports the appearance of complex partial seizures during the course of successful use of the atypical neuroleptic clozapine in a 15 year old with neuroleptic-resistant schizophrenia. After 7 months of clozapine treatment, and 1 week after a gradual increase in dose to 550 mg, the adolescent began to develop periods of nausea and a ''spacey feeling'' that lasted for several minutes to hours at a time. A diagnosis of absence status was confirmed by electroencephalography (EEG). It was treated effectively by dose reduction (to 400 mg daily) without the use of anticonvulsant medications. A 3-year follow-up showed the generally sustained efficacy of this treatment, without recurrence of absence status seizures. This appears to be the first report of an absence seizure apparently associated with clozapine treatment. Published reports on 80 adolescents suggest an estimated prevalence of clozapine-induced seizures at about 4% (compared to 1-5% in adults, depending on dose), whereas 60% developed mild to marked EEG abnormalities. The current data on the safety and efficacy of clozapine for treating adolescents with schizophrenia remain preliminary. These data support the clinical recommendation that an EEG be obtained before adolescents are started on treatment with clozapine. RP FREEDMAN, JE (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,11301 WILSHIRE BLVD,BLDG 20,LOS ANGELES,CA 90073, USA. NR 0 TC 11 Z9 11 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD SPR PY 1994 VL 4 IS 1 BP 53 EP 62 DI 10.1089/cap.1994.4.53 PG 10 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA NE990 UT WOS:A1994NE99000005 ER PT J AU LORR, M STRACK, S AF LORR, M STRACK, S TI PERSONALITY PROFILES OF POLICE CANDIDATES SO JOURNAL OF CLINICAL PSYCHOLOGY LA English DT Article ID OFFICERS; CLUSTERS AB Recently, Eber (1991) reported on several large-scale studies of law enforcement candidates. The main measures were the two parts of the Clinical Analysis Questionnaire (Krug, Cattell, & IPAT, 1980). Part I consists of the 16 Personality Factor Questionnaire Scales, while Part II is devoted to 12 measures of psychopathology. The most striking finding was a clear personality profile characterized by a strong pattern of self-discipline or Control, Tough Poise, and low Anxiety. Our study hypothesis was that several police personality profiles would be found. This conjecture was tested on the 16PF scores of two samples of 275 police candidates by means of the Ward (1963) hierarchical clustering procedure and the Milligan/Sokal (1980) nonhierarchical K-means cluster procedures. Three distinct score profiles were isolated in both samples. C1 US DEP VET AFFAIRS,OUTPATIENT CLIN,LOS ANGELES,CA. RP LORR, M (reprint author), CATHOLIC UNIV AMER,LIFE CYCLE INST,WASHINGTON,DC 20064, USA. NR 26 TC 6 Z9 6 U1 2 U2 6 PU CLINICAL PSYCHOLOGY PUBL CO PI BRANDON PA 4 CONANT SQUARE, BRANDON, VT 05733 SN 0021-9762 J9 J CLIN PSYCHOL JI J. Clin. Psychol. PD MAR PY 1994 VL 50 IS 2 BP 200 EP 207 DI 10.1002/1097-4679(199403)50:2<200::AID-JCLP2270500208>3.0.CO;2-1 PG 8 WC Psychology, Clinical SC Psychology GA NE675 UT WOS:A1994NE67500007 PM 8014241 ER PT J AU LEONG, GB AF LEONG, GB TI DECLERAMBAULT SYNDROME (EROTOMANIA) IN THE CRIMINAL-JUSTICE SYSTEM - ANOTHER LOOK AT THIS RECURRING PROBLEM SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; EROTOMANIA; DECLERAMBAULTS SYNDROME; DANGEROUSNESS; DELUSIONS ID LOVE AB While de Clerambault syndrome (crotomania) has long been a subject of scientific study, it has only recently become a frequent topic of media attention. A series of five individuals who were arrested for crimes related to their erotomanic delusion are presented. The psychiatric findings from this sample have potential social policy implication. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. RP LEONG, GB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIATRY SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 19 TC 20 Z9 20 U1 1 U2 2 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD MAR PY 1994 VL 39 IS 2 BP 378 EP 385 PG 8 WC Medicine, Legal SC Legal Medicine GA ND048 UT WOS:A1994ND04800010 PM 8195752 ER PT J AU MACKINNEY, AA AF MACKINNEY, AA TI ON TEACHING BEDSIDE DIAGNOSTIC AND THERAPEUTIC PROCEDURES TO MEDICAL-STUDENTS - AN ANNOTATED-BIBLIOGRAPHY OF AUDIOVISUAL MATERIALS SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Bibliography DE BEDSIDE PROCEDURES; MEDICAL STUDENTS; TEACHING; VIDEO-TAPES; AUDIOVISUAL MATERIALS AB Objective: The teaching of procedures that involve risk of pain or morbidity deserves special care. The author set out to develop a teaching program for medical students to ensure quality control of bedside diagnostic and therapeutic procedures. Design: A bibliography of available videotapes and related audiovisual teaching materials on 15 common bedside procedures was assembled following requests for materials from all U.S. medical schools. Audiovisual materials from nine institutions were reviewed. Setting: Medical schools and teaching institutions. Participants: Medical schools and libraries. Main results: Seventy-three percent (24/33) of responding schools had no visual material on the procedures. There was ten times more material on physical diagnosis than on bedside procedures. About 20 videotapes were reviewed in an annotated bibliography. Some videos contained valuable insights on how to make good teaching materials. A set of criteria for quality videotapes is listed. Conclusions: Considerable work needs to be done to develop audiovisual materials and curricula for teaching bedside procedures. Videotape is a valuable medium for introducing procedures and ensuring uniformity of technique. After reviewing all available videotapes, the author decided that videotapes should be the initial part of a multidimensional program for teaching procedures. RP MACKINNEY, AA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD MAR PY 1994 VL 9 IS 3 BP 153 EP 157 DI 10.1007/BF02600031 PG 5 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA ND613 UT WOS:A1994ND61300006 PM 7515107 ER PT J AU VELAMOOR, VR NORMAN, RMG CAROFF, SN MANN, SC SULLIVAN, KA ANTELO, RE AF VELAMOOR, VR NORMAN, RMG CAROFF, SN MANN, SC SULLIVAN, KA ANTELO, RE TI PROGRESSION OF SYMPTOMS IN NEUROLEPTIC MALIGNANT SYNDROME SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID CATATONIA; DANTROLENE AB The neuroleptic malignant syndrome (NMS) is a rare but potentially fatal disorder characterized by mental-status changes, muscle rigidity, hyperthermia, and autonomic dysfunction. Systematic examination of early signs and the progression of symptoms in NMS may be worthwhile to facilitate prompt recognition and interventions to abort the syndrome in its incipient stage. The authors present the results of a preliminary review of the temporal sequence of the four predominant signs of NMS as described in 340 clinical reports of NMS in the literature. Of all order implications, 70.5% were consistent with the sequence of mental-status changes, rigidity, hyperthermia, and autonomic dysfunction. Changes in either mental status or rigidity were the initial manifestations of NMS in 82.3% of cases with a single presenting sign and were significantly more Likely to be observed before hyperthermia and autonomic dysfunction. Methodological limitations of these data and clinical implications are discussed. C1 UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP VELAMOOR, VR (reprint author), VICTORIA HOSP,DEPT PSYCHIAT,375 SOUTH ST,LONDON N6A 4G5,ON,CANADA. NR 25 TC 70 Z9 72 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD MAR PY 1994 VL 182 IS 3 BP 168 EP 173 DI 10.1097/00005053-199403000-00007 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NA763 UT WOS:A1994NA76300007 PM 7906709 ER PT J AU SALLOWAY, S CUMMINGS, J AF SALLOWAY, S CUMMINGS, J TI SUBCORTICAL DISEASE AND NEUROPSYCHIATRIC ILLNESS SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Editorial Material ID OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; HUNTINGTONS-DISEASE; BEHAVIORAL-CHANGES; MOOD DISORDER; LESIONS; INFARCTION; DEPRESSION; SYMPTOMS; GLUCOSE AB The relationship between neuropsychiatric disorders and dysfunction of subcortical structures is the theme of the 1994 joint meeting of the British and American Neuropsychiatric Associations, to be held July 21-24, 1994, in Newport, Rhode Island. In this essay Dr. Salloway, chair of the Scientific Program Committee, and Dr. Cummings, director-elect of The American Neuropsychiatric Association, define the structures embraced in the ''subcortical'' concept and summarize the relationship between specific neuropsychiatric symptoms and regional subcortical dysfunction. These concepts and observations will be expanded, challenged, and refined at the meeting. C1 BUTLER HOSP, PROVIDENCE, RI 02906 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHIAT SERV, BEHAV NEUROSCI SECT, LOS ANGELES, CA USA. RP SALLOWAY, S (reprint author), BROWN UNIV, SCH MED, PROVIDENCE, RI 02912 USA. FU NIA NIH HHS [AG10123] NR 36 TC 36 Z9 36 U1 1 U2 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SPR PY 1994 VL 6 IS 2 BP 93 EP 99 PG 7 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ963 UT WOS:A1994NJ96300001 PM 8044049 ER PT J AU AMES, D CUMMINGS, JL WIRSHING, WC QUINN, B MAHLER, M AF AMES, D CUMMINGS, JL WIRSHING, WC QUINN, B MAHLER, M TI REPETITIVE AND COMPULSIVE BEHAVIOR IN FRONTAL-LOBE DEGENERATIONS SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID KLUVER-BUCY SYNDROME; NON-ALZHEIMER TYPE; PICKS DISEASE; BASAL GANGLIA; DIAGNOSIS; DEMENTIA; DISORDER AB The authors review the relationship of repetitive behaviors to frontal lobe degenerations and report the repetitive and compulsive behaviors, radiologic imaging findings, and neuropathology of 3 patients with dementia secondary to frontal lobe degeneration. These 3 patients and 78% of 46 proven pathologic cases of frontal lobe degeneration described in the literature demonstrate repetitive behaviors ranging from motor stereotypies to complex obsessive-compulsive disorder. This review suggests that combined damage to the frontal lobe, caudate nucleus, and globus pallidus may account for the repetitive behaviors seen in frontal lobe degenerations, idiopathic obsessive-compulsive disorder, and other neuropsychiatric diseases. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PATHOL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHIAT SERV, LOS ANGELES, CA USA. FU NIA NIH HHS [AG10123] NR 49 TC 87 Z9 87 U1 1 U2 4 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SPR PY 1994 VL 6 IS 2 BP 100 EP 113 PG 14 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ963 UT WOS:A1994NJ96300002 PM 8044031 ER PT J AU FREEMAN, GL COLSTON, JT MILLER, DD AF FREEMAN, GL COLSTON, JT MILLER, DD TI ALTERATIONS IN MYOCARDIAL FREE FATTY-ACID CLEARANCE PRECEDE MECHANICAL ABNORMALITIES IN CANINE TACHYCARDIA-INDUCED HEART-FAILURE SO JOURNAL OF NUCLEAR CARDIOLOGY LA English DT Article DE ENERGETICS; MYOCARDIAL; DEPRESSION; CONTRACTILITY; CARDIAC METABOLISM ID CHRONIC SUPRAVENTRICULAR TACHYCARDIA; I-123 PHENYLPENTADECANOIC ACID; CONGESTIVE CARDIOMYOPATHY; HYPERTENSIVE RATS; PRESSURE; DOGS; TOMOGRAPHY; INJURY; TRACER AB Background. The purpose of this study was to evaluate whether abnormalities of free fatty acid metabolism are present before the onset of overt mechanical dysfunction in dogs with tachycardia-induced heart failure. We studied six dogs chronically instrumented to allow assessment of left ventricular function in the pressure-volume plane. Methods and Results. Free fatty acid clearance was assessed according to the washout rate of a free fatty acid analog, iodophenylpentadecanoic acid ([I-123]PPA or IPPA). IPPA clearance was measured within 1 hour of the hemodynamic assessment, The animals were studied under baseline conditions and 11.7 +/- 3.6 days after ventricular pacing at a rate of 240 beats/min. Hemodynamic studies after pacing showed a nonsignificant increase in left ventricular end-diastolic pressure (11.7 +/- 4.7 to 17.4 +/- 6.5 mm Hg) and a nonsignificant decrease in the maximum derivative of pressure with respect to time (1836 +/- 164 vs 1688 +/- 422 mm Hg/sec). There was also no change in the time constant of left ventricular relaxation, which was 34.8 +/- 7.67 msec before and 35.3 +/- 7.3 msec after pacing. However, a significant prolongation in the clearance half-time of [I-123]PPA, from 86.1 +/- 23.9 to 146.5 +/- 22.6 minutes (p < 0.01) was found. Thus abnormal lipid clearance appears before the onset of significant mechanical dysfunction in tachycardia-induced heart failure. Conclusion. This suggests that abnormal substrate metabolism may play an important role in the pathogenesis of this condition. C1 ST LOUIS UNIV,CTR HLTH SCI,DEPT MED,DIV CARDIOL,ST LOUIS,MO 63110. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CARDIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 25 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1071-3581 J9 J NUCL CARDIOL JI J. Nucl. Cardiol. PD MAR-APR PY 1994 VL 1 IS 2 BP 171 EP 179 DI 10.1007/BF02984089 PN 1 PG 9 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA PU845 UT WOS:A1994PU84500007 PM 9420684 ER PT J AU GRAVENSTEIN, S DRINKA, P DUTHIE, EH MILLER, BA BROWN, CS HENSLEY, M CIRCO, R LANGER, E ERSHLER, WB AF GRAVENSTEIN, S DRINKA, P DUTHIE, EH MILLER, BA BROWN, CS HENSLEY, M CIRCO, R LANGER, E ERSHLER, WB TI EFFICACY OF AN INFLUENZA HEMAGGLUTININ DIPHTHERIA TOXOID CONJUGATE VACCINE IN ELDERLY NURSING-HOME SUBJECTS DURING AN INFLUENZA OUTBREAK SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ANTIBODY-RESPONSE; INTERLEUKIN-2 PRODUCTION; MORTALITY; AGE; IMMUNOGENICITY; REACTOGENICITY; PREVENTION; AMANTADINE; POPULATION; REDUCTION AB Objective: To compare the efficacy of an influenza hemagglutinin-diphtheria toroid conjugate vaccine with the commercially available influenza hemagglutinin-subunit vaccine in preventing influenza in older adults living in a nursing home. Design: A prospective, randomized, double-blind vaccine trial with 5 months of follow-up after vaccination. Setting: Fourteen Wisconsin nursing homes. Participants: Nursing home residents at least 65 years old who were able to give informed consent and were free of malignancy and not receiving immunosuppressive therapy. Interventions: Participants received, by intramuscular injection, 0.5 mt of a trivalent influenza vaccine containing 15 mu g each of A/Leningrad/360/86 (H3N2), A/Taiwan/1/86 (H1N1), and B/Ann Arbor/1/86 (HA) or 0.5 mt of an influenza vaccine containing the same antigens conjugated to diphtheria toroid (HA-D). Measurements: Blood was obtained pre- and 1 month postvaccination to assess for any vaccine-induced antibody titer change. Clinical surveillance for respiratory illness was performed twice weekly for 5 months. A record was kept of all signs and symptoms of new respiratory illness, and a viral culture and acute and convalescent sera were obtained. Results: 204 participants received HA and 204 received HA-D. Both groups had similar baseline antibody levels to all influenza antigens. HA-D recipients seroconverted more frequently based on serum neutralizing activity (P < 0.05), had a greater increase in geometric mean titer (GMT), and sustained the increase in antibody titer longer than HA recipients. Vaccine hemagglutinin recall was greater in a subset of HA-D recipients as measured by lymphocyte proliferative assays (P < 0.05). During an outbreak of influenza A (H3N2 A/Shanghai/11/87-like and A/Victoria/7/87-like), fewer HA-D (29/195) than HA (43/204) recipients had laboratory-confirmed infection (P = 0.053), and, of these, fewer HA-D-treated subjects had lower respiratory tract involvement (5/29 HA-D and 17/43 HA) (P = 0.022). Conclusions: HA-D was more immunogenic in institutionalized elderly recipients and produced greater protection from influenza infection. Superior protection may be due to HA-D's ability to stimulate and recruit antigen-presenting cells, thus enabling the recipient to achieve and maintain functional antibody titers. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. WISCONSIN VET HOME,KING,WI. MED COLL WISCONSIN,MILWAUKEE,WI. ZABLOCKI VET ADM MED CTR,MILWAUKEE,WI. WISCONSIN STATE LAB HYG,MADISON,WI. CONNAUGHT LABS LTD,SWIFTWATER,PA. RP GRAVENSTEIN, S (reprint author), UNIV WISCONSIN,DEPT MED,INST AGING & ADULT LIFE,GERIATR SECT,1300 UNIV AVE,ROOM 2245,MADISON,WI 53706, USA. RI Gravenstein, Stefan/G-1681-2011 FU NIA NIH HHS [AG 09632, AG 00548, AG 007831] NR 31 TC 79 Z9 81 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAR PY 1994 VL 42 IS 3 BP 245 EP 251 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NA038 UT WOS:A1994NA03800002 PM 8120307 ER PT J AU MAHONEY, J SAGER, M DUNHAM, NC JOHNSON, J AF MAHONEY, J SAGER, M DUNHAM, NC JOHNSON, J TI RISK OF FALLS AFTER HOSPITAL DISCHARGE SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID HIP FRACTURE; ELDERLY PEOPLE; COMMUNITY; STRENGTH; DELIRIUM; HOME AB Objectives: To determine the incidence of falls within the first month after hospitalization and risk factors associated with falling during this period. Design: Cohort study with 1-month follow-up after hospital discharge. Setting: 370-bed community hospital. Patients: Consecutive sample of 214 patients, aged 70 years and over, hospitalized for medical illness more than 48 hours and discharged to the community. Exclusion criteria: terminal illness, neurologic diagnosis, discharge to skilled nursing facility. Measurements: Information was obtained at hospital admission, discharge, and 1 month after discharge. Initial assessment included demographic data, vision, mood, pre-admission function, and use of assistive device. Discharge assessment included length of hospital stay, use of assistive device, need for professional help after discharge, medications, cognition, and functional status. Patients were assessed 1 month after discharge for history of confusion and falls. Main outcome measure was falls in the first month after discharge. Main Results: Twenty-nine patients (13.6%) fell during the month after discharge. Major risk factors for falls included, at discharge, decline in mobility (P = 0.005), use of assistive device (P = 0.002), and cognitive impairment (P = 0.05), and after hospital discharge, self-report of confusion (P = 0.002). Patients who were functionally dependent and needed professional help after discharge had the highest rate of falls (20.2%). In contrast, only 8.4% of independent patients not requiring professional help fell (P = 0.01). Conclusions: There is a high incidence of falls after hospital discharge, particularly among patients who are functionally dependent. Further study is needed to determine to what extent acute illness and hospitalization may influence falls risk. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI. UNIV WISCONSIN,DEPT PREVENT MED,MADISON,WI. HOME HLTH UNITED,MADISON,WI. RP MAHONEY, J (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,GRECC,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NIA NIH HHS [1T32AG00213-02] NR 43 TC 95 Z9 97 U1 0 U2 6 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAR PY 1994 VL 42 IS 3 BP 269 EP 274 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NA038 UT WOS:A1994NA03800006 PM 8120311 ER PT J AU CHIODO, LK KANTEN, DN GERETY, MB MULROW, CD CORNELL, JE AF CHIODO, LK KANTEN, DN GERETY, MB MULROW, CD CORNELL, JE TI FUNCTIONAL STATUS OF MEXICAN-AMERICAN NURSING-HOME RESIDENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article AB Objective: To compare sociodemographic characteristics, physical function, and cognition of Mexican American and non-Hispanic white nursing home residents. Design and Setting: Cross-sectional survey of residents in eight proprietary nursing homes and one Veterans Affairs nursing home in San Antonio, Texas. Subjects: Residents with lengths of stay greater than or equal to 90 days. Measurements: Sociodemographic characteristics, residence prior to admission, and dependency in activities of daily living (ADL) were abstracted from the medical record. The Folstein Mini-Mental State Examination (MMSE) was administered in the resident's self-selected language to a subset of residents. Main Results: There were 1160 participants, 261 Mexican American (23%) and 899 non-Hispanic white residents (77%). Mexican Americans were younger (77.1 vs 80.7 years), more often men (44% vs 30%), less educated (6.2 vs 10.8 years), and more often dependent on Medicaid funding (66% vs 40%) than non-Hispanic whites. Mexican Americans were less independent in feeding (34% vs 49%), transfers (18% vs 30%), toileting (19% vs 29%), and dressing (12% vs 19%). Mean MMSE scores were different in Mexican Americans and non-Hispanic whites (8.93 vs 11.85), and this difference remained significant after adjustment for age and education (P = 0.04). ADL function was strongly associated with MMSE (P = 0.0001) and less strongly associated with ethnicity (P = 0.056) in multiple regression analysis. Conclusions: This study provides the strongest evidence to date that Mexican American nursing home residents are more cognitively and functionally impaired than non-Hispanic white residents. Further studies should explore whether medical conditions, selection and referral patterns or cultural factors explain functional differences between Mexican American and non-Hispanic white nursing home residents. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX. RP CHIODO, LK (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU PHS HHS [NIA U01A09117-01] NR 11 TC 19 Z9 19 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAR PY 1994 VL 42 IS 3 BP 293 EP 296 PG 4 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NA038 UT WOS:A1994NA03800010 PM 8120314 ER PT J AU ANDERSON, RJ SPONSEL, HT KROLL, DJ JACKSON, S BRECKON, R HOEFFLER, JP AF ANDERSON, RJ SPONSEL, HT KROLL, DJ JACKSON, S BRECKON, R HOEFFLER, JP TI ESCAPE FROM THE ANTIPROLIFERATIVE EFFECT OF TRANSFORMING GROWTH FACTOR-BETA(1) IN LLC-PK1 RENAL EPITHELIAL-CELLS SO KIDNEY INTERNATIONAL LA English DT Article ID FACTOR-BETA; TGF-BETA; C-MYC; GENE-EXPRESSION; EXPERIMENTAL GLOMERULONEPHRITIS; INHIBITORY RESPONSES; PROXIMAL TUBULE; PROLIFERATION; SUPPRESSION; RECEPTORS AB Transforming growth factor-beta(1) (TGF-beta(1)) usually inhibits proliferation of epithelial cells. We find that LLC-PK1 renal tubular epithelial cells develop rapid in vitro resistance to the inhibitory effects of TGF-beta(1) and subsequently proliferate in response to TGF-beta(1). This unique response to TGF-beta(1) is not observed in another renal tubular epithelial cell line (MDCK cells). The proliferative response to TGF-beta(1) is additive to that produced by other growth factors. The proliferative response to TGF-beta(1) occurs despite an effect of TGF-beta(1) to suppress epidermal growth factor stimulated c-myc mRNA as determined by Northern analyses. These results suggest that LLC-PK1 cells develop rapid resistance to TGF-beta(1) inhibition of proliferation in vitro and that this resistance occurs despite continued suppression of c-myc mRNA. C1 UNIV COLORADO,HLTH SCI CTR,DIV MED ONCOL,DENVER,CO 80262. RP ANDERSON, RJ (reprint author), UNIV COLORADO,HLTH SCI CTR,DENVER VET AFFAIRS MED CTR,DEPT MED,DENVER,CO, USA. NR 42 TC 8 Z9 8 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD MAR PY 1994 VL 45 IS 3 BP 642 EP 649 DI 10.1038/ki.1994.86 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA MW173 UT WOS:A1994MW17300003 PM 8196265 ER PT J AU HARDIN, TC BUTLER, SC ROSS, S WAKEFORD, JH JORGENSEN, JH AF HARDIN, TC BUTLER, SC ROSS, S WAKEFORD, JH JORGENSEN, JH TI COMPARISON OF AMPICILLIN-SULBACTAM AND TICARCILLIN-CLAVULANIC ACID IN PATIENTS WITH CHRONIC-RENAL-FAILURE - EFFECTS OF DIFFERENTIAL PHARMACOKINETICS ON SERUM BACTERICIDAL ACTIVITY SO PHARMACOTHERAPY LA English DT Article ID TISSUE PENETRATION; PHARMACOLOGY AB Study Objectives. To evaluate the pharmacodynamic antibacterial activity of ticarcillin-clavulanic acid (T-C) and ampicillin-sulbactam (A-S) combinations against reference bacterial strains in patients with end-stage renal disease maintained on long-term hemodialysis. Design. Randomized, crossover, controlled study. Setting. National Institutes of Health-funded general clinical research unit in a Veterans Administration Medical Center. Patients. Nine adult men with end-stage renal disease maintained on long-term hemodialysis. Two subjects did not complete the study due to problems of vascular access, and another withdrew for personal reasons. Interventions. On a nondialysis day, each subject was randomly administered either T-C 3.1 g or A-S 3 g as a slow intravenous infusion over 30 minutes. Serial blood samples were collected for measurement of antibiotic serum concentrations and determination of serum bactericidal titers. Following a washout period, the study was repeated with the alternative antibiotic combination. Measurements and Main Results. The mean observed apparent beta-half-life of clavulanic acid was substantially shorter than that for the other three drugs. The bactericidal activity of both A-S and T-C against non-beta-lactamase-producing (Nbeta-LP) strains of S. aureus and E. coli was consistently high, as indicated by geometric mean SBTs of at least 1:5 at 24 hours. Against beta-lactamase-producing (beta-LP) S. aureus, the geometric mean SBTs for A-S were at least 1:25 throughout the study period, while the geometric mean SBTs for T-C decreased over 24 hours from 1:29 to 1:6. Against beta-LP E. coli, the bactericidal activities for both A-S and T-C were poor, with geometric mean peak SBTs of only 1:6 and 1:3, respectively. The geometric mean SBT for T-C against this E. coli strain had declined to 1:1 at 6 hrs. Conclusion. Increasing the dosing interval for T-C in patients with end-stage renal disease may lead to periods of insufficient clavulanic acid to protect ticarcillin from beta-lactamase degradation. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RP HARDIN, TC (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PHARM SERV 119,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NCRR NIH HHS [M01-RR-01346] NR 11 TC 11 Z9 11 U1 0 U2 3 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER BOX 806 171 HARRISON AVE, BOSTON, MA 02111 SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD MAR-APR PY 1994 VL 14 IS 2 BP 147 EP 152 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA ND068 UT WOS:A1994ND06800003 PM 8197032 ER PT J AU HISNANICK, JJ AF HISNANICK, JJ TI COMPARATIVE-ANALYSIS OF VIOLENT DEATHS IN AMERICAN-INDIANS AND ALASKA NATIVES SO SOCIAL BIOLOGY LA English DT Article ID UNITED-STATES; SUICIDE; HOMICIDE; FIREARM AB Accidents, injuries, and outcomes from adverse effects have been identified as the second leading cause of death for American Indians and Alaska Natives (AI/AN). However, no studies have been done which analyze violent deaths (homicides, suicides, and other accidents) for this population with a focus on time trends. For this study, overall and gender-specific mortality rates due to violent deaths were computed for 1973-88. The results indicate that overall and gender-specific mortality rates for violent deaths in AI/AN have been decreasing on average per year: homicide, 4.3%; suicide, 2.7%; other accidents, 5.6%. Similarly, age-adjusted rates have been declining, and at faster rates than those of the U.S. general population: homicide, 4.5% vs. 1.4%; suicide, 2.5% vs. 0.6%; other accidents, 6.2% vs. 2.6%. However, the male-female ratio for homicides and other accidents has remained unchanged, and the ratio for suicide has been increasing. While the gap between age-adjusted rates have been narrowing, the age-adjusted rates for AI/AN have remained consistently above those of the U.S. general population. RP HISNANICK, JJ (reprint author), US DEPT VET AFFAIRS,DIV BIOMETR 008C12,WASHINGTON,DC 20420, USA. NR 19 TC 5 Z9 5 U1 0 U2 2 PU SOC STUDY SOCIAL BIOLOGY PI PORT ANGELES PA P O BOX 2349, PORT ANGELES, WA 98362 SN 0037-766X J9 SOC BIOL JI Soc. Biol. PD SPR-SUM PY 1994 VL 41 IS 1-2 BP 96 EP 109 PG 14 WC Demography; Social Sciences, Biomedical; Sociology SC Demography; Biomedical Social Sciences; Sociology GA PG814 UT WOS:A1994PG81400007 PM 7973844 ER PT J AU MCCULLOUGH, LB ASHTON, CM AF MCCULLOUGH, LB ASHTON, CM TI A METHODOLOGY FOR THE TEACHING ETHICS IN THE CLINICAL SETTING - A CLINICAL HANDBOOK FOR MEDICAL-ETHICS SO THEORETICAL MEDICINE LA English DT Article DE BIOETHICS; CLINICAL ETHICS; TEACHING; HANDBOOK; PREVENTIVE ETHICS AB The pluralism of methodologies and severe time constraints pose important challenges to pedagogy in clinical ethics. We designed a step-by-step student handbook to operate within such constraints and to respect the methodological pluralism of bioethics and clinical ethics. The handbook comprises six steps: Step 1: What are the facts of the case?; Step 2: What are your obligations to your patient?; Step 3: What are your obligations to third parties to your relationship with the patient?; Step 4: Do your obligations converge or conflict?; Step 5: What is the strongest objection that could be made to the identification of convergence in step 4 or the arguments in step 4? How can this objection be effectively countered?; and Step 6: How could the ethical conflict, or perceived ethical conflict, have been prevented? C1 HOUSTON VET AFFAIRS MED CTR,VET ADM HLTH SERV RES & DEV FIELD PROGRAM,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. RP MCCULLOUGH, LB (reprint author), BAYLOR COLL MED,CR ETHICS MED & PUBL ISSUES,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. NR 6 TC 18 Z9 18 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-9902 J9 THEOR MED JI Theor. Med. PD MAR PY 1994 VL 15 IS 1 BP 39 EP 52 DI 10.1007/BF00999218 PG 14 WC Medicine, Legal; Social Issues SC Legal Medicine; Social Issues GA NQ703 UT WOS:A1994NQ70300004 PM 8059431 ER PT J AU HERSHMAN, JM AF HERSHMAN, JM TI HIGHLIGHTS OF THIS ISSUE SO THYROID LA English DT Editorial Material RP HERSHMAN, JM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BLDG 114,ROOM 200,WILSHIRE & SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD SPR PY 1994 VL 4 IS 1 BP 1 EP 1 DI 10.1089/thy.1994.4.1 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NJ425 UT WOS:A1994NJ42500001 ER PT J AU OBERLEY, TD SEMPF, JM OBERLEY, MJ MCCORMICK, ML MUSE, KE OBERLEY, LW AF OBERLEY, TD SEMPF, JM OBERLEY, MJ MCCORMICK, ML MUSE, KE OBERLEY, LW TI IMMUNOGOLD ANALYSIS OF ANTIOXIDANT ENZYMES IN HUMAN RENAL-CELL CARCINOMA SO VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY LA English DT Article DE MANGANESE SUPEROXIDE DISMUTASE; NEOPLASIA; MITOCHONDRIA ID MANGANESE SUPEROXIDE-DISMUTASE; SYRIAN-HAMSTER TISSUES; FREE-RADICALS; IMMUNOHISTOCHEMICAL LOCALIZATION; KIDNEY DEVELOPMENT; TRANSGENIC MICE; TUMOR; PROLIFERATION; EXPRESSION; RADIATION AB Analysis of activities of the antioxidant enzyme manganese superoxide dismutase in human renal cell carcinomas often showed greatly altered enzyme levels (either elevated or depressed) compared to the cell of origin, the kidney proximal tubule. In order to better understand the variability observed, immunogold studies were performed on human renal cell carcinomas using a polyclonal antibody to human kidney manganese superoxide dismutase. For comparison, studies were also performed using antibodies to other antioxidant enzymes. For histologic studies, renal cell carcinomas were subclassified on the basis of light microscopy and ultrastructural analysis into clear cell, granular cell, or mixed clear and granular cell variants. In all three types of tumor, immunogold studies showed little staining using antibodies to copper, zinc superoxide dismutase or glutathione-dependent enzymes. However, intensity of labelling for manganese superoxide dismutase and catalase depended on the cell type(s) in the tumor. Clear cell variants demonstrated trace staining for manganese superoxide dismutase and catalase, while granular cell variants exhibited heavy staining for both of these enzymes. Mixed types of tumors showed clear cells with trace staining for all antioxidant enzymes examined, while granular cells again showed intense labelling for manganese superoxide dismutase and catalase. Using normal kidney proximal tubule as a comparison, immunogold ultrastructural analysis using antibody to manganese superoxide dismutase demonstrated infrequent small lightly labelled mitochondria in clear cell variants, while granular cell variants exhibited numerous medium-sized heavily labelled mitochondria. These data suggest that: 1) the variability in activity values for manganese superoxide dismutase may be due to heterogeneity of cell types in these tumors and 2) manganese superoxide dismutase immunoreactive protein was elevated in granular cells both because of an increase in number of mitochondria and because the labelling density in mitochondria was increased compared to mitochondria in clear cell types or in normal proximal tubular cells. C1 UNIV IOWA,COLL MED,RADIAT RES LAB,IOWA CITY,IA 52242. UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53706. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL & LAB MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA 41267] NR 43 TC 34 Z9 34 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0945-6317 J9 VIRCHOWS ARCH JI Virchows Arch. Int. J. Pathol. PD MAR PY 1994 VL 424 IS 2 BP 155 EP 164 PG 10 WC Pathology SC Pathology GA NZ498 UT WOS:A1994NZ49800006 PM 8180777 ER PT J AU RUBIN, RA FALESTINY, M MALET, PF AF RUBIN, RA FALESTINY, M MALET, PF TI CHRONIC HEPATITIS-C - ADVANCES IN DIAGNOSTIC TESTING AND THERAPY SO ARCHIVES OF INTERNAL MEDICINE LA English DT Review ID NON-B-HEPATITIS; RECOMBINANT ALPHA-INTERFERON; AUTOIMMUNE CHRONIC HEPATITIS; NON-A; VIRUS-ANTIBODIES; VIRAL-RNA; MECHANISMS; SERUM; ALFA; HIV AB The methods for diagnosing hepatitis C virus infection have been evolving since the first-generation enzyme-linked immunosorbent assay antibody test was devised in 1989. In addition to assaying for serum antibodies against viral proteins, serum and liver tissue can be tested for viral RNA, evidence of ongoing viral replication. The improving ability to diagnose hepatitis C has furthered the understanding of the natural history of this infection. Acute hepatitis C results in chronic elevations of serum transaminase levels following nearly one half of cases. Cirrhosis complicates approximately 20% of chronic infections. Long-standing chronic hepatitis C may play a role in the pathogenesis of hepatocellular carcinoma. Sustained normalization of serum transaminase levels, often accompanied by a decrease in or disappearance of viral RNA, occurs in approximately 25% of patients with chronic hepatitis C who are treated with a 6-month course of recombinant interferon alfa. This treatment can occasionally be complicated by hematologic, endocrinologic, and psychiatric adverse effects but is usually fairly well tolerated. Whether interferon therapy will diminish the risk of cirrhosis or carcinoma is not yet known. This article reviews the diagnosis of chronic hepatitis C infection as well as the mechanisms of action, efficacy, and adverse effects associated with interferon alfa therapy. C1 HOSP UNIV PENN,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. RP RUBIN, RA (reprint author), VET AFFAIRS MED CTR,DIV GASTROENTEROL,PHILADELPHIA,PA 19104, USA. NR 33 TC 34 Z9 34 U1 1 U2 1 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 FEB 28 PY 1994 VL 154 IS 4 BP 387 EP 392 DI 10.1001/archinte.154.4.387 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA MY631 UT WOS:A1994MY63100005 PM 7509593 ER PT J AU BUSSEY, HI LINN, WD AF BUSSEY, HI LINN, WD TI WARFARIN AND ASPIRIN AFTER HEART-VALVE REPLACEMENT SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 AUDIE MURPHY VET AFFAIRS MED CTR,SAN ANTONIO,TX 78284. RP BUSSEY, HI (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 0 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 FEB 17 PY 1994 VL 330 IS 7 BP 508 EP 508 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MW480 UT WOS:A1994MW48000026 PM 8289865 ER PT J AU MULROW, CD GERETY, MB KANTEN, D CORNELL, JE DENINO, LA CHIODO, L AGUILAR, C ONEIL, MB ROSENBERG, J SOLIS, RM AF MULROW, CD GERETY, MB KANTEN, D CORNELL, JE DENINO, LA CHIODO, L AGUILAR, C ONEIL, MB ROSENBERG, J SOLIS, RM TI A RANDOMIZED TRIAL OF PHYSICAL REHABILITATION FOR VERY FRAIL NURSING-HOME RESIDENTS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID RESOURCE UTILIZATION GROUPS; LONG-TERM CARE; IMPACT; MUSCLE; EFFICACY; THERAPY; UNIT AB Background.-Past studies suggest multidisciplinary interventions that include physical therapy (PT) can improve function of nursing home residents. This trial specifically evaluates effects of PT for frail long-stay nursing home residents. Design.-Randomized, controlled trial. Setting.-One academic nursing home and eight community nursing homes. Patients.-A total of 194 elderly nursing home residents dependent in at least two activities of daily living residing in the nursing home for at least 3 months. Interventions.-Patients were randomized to individually tailored one-on-one PT sessions or friendly visits (FVs) three times a week for 4 months. Physical therapy included range-of-motion, strength, balance, transfer, and mobility exercises. Main Outcome Measures.-Performance-based physical function assessed by the Physical Disability Index; self-perceived health status assessed with the Sickness Impact Profile; observer-reported activities of daily living; and falls. Results.-Eighty-nine percent and 92% of PT and FV sessions, respectively, were attended; 5% and 9% of subjects dropped out in the PT group and FV group, respectively. Compared with the FV group, the PT group experienced no significant improvements in overall Physical Disability Index, Sickness Impact Profile, or activities of daily living scores. A 15.5% improvement in the mobility subscale of the Physical Disability Index was seen (95% confidence interval [CI], 6.4% to 24.7%); no benefits in range-of-motion, strength, or balance subscales were found. Compared with the FV group, the PT group used assistive devices for bed mobility tasks less often (P=.06) and were less likely to use assistive devices and wheelchairs for locomotion (P<.005). There were 79 falls in the PT group vs 60 falls in the FV group (P=.11). Charge for the 4-month PT program was $1220 per subject (95% CI, $412 to $1832). Conclusion.-This standardized physical therapy program provided modest mobility benefits for very frail long-stay nursing home residents with physical disability due to multiple comorbid conditions. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,2400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [UO1AG09117] NR 41 TC 176 Z9 176 U1 9 U2 18 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 16 PY 1994 VL 271 IS 7 BP 519 EP 524 DI 10.1001/jama.271.7.519 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA MV423 UT WOS:A1994MV42300034 PM 8301766 ER PT J AU KASINATH, BS BLOCK, JA SINGH, AK TERHUNE, WC MALDONADO, R DAVALATH, S KALLGREN, MJ WANNA, L AF KASINATH, BS BLOCK, JA SINGH, AK TERHUNE, WC MALDONADO, R DAVALATH, S KALLGREN, MJ WANNA, L TI REGULATION OF RAT GLOMERULAR EPITHELIAL-CELL PROTEOGLYCANS BY HIGH-GLUCOSE MEDIUM SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID HEPARAN-SULFATE PROTEOGLYCAN; BASEMENT-MEMBRANE GLYCOSAMINOGLYCANS; INDUCED DIABETIC RATS; GROWTH-FACTOR-BETA; INCREASED PERMEABILITY; MESANGIAL CELLS; COMPLICATIONS; CULTURE; TISSUE; HEPARAN-(SO4)-S-35 AB In diabetic nephropathy the heparan sulfate proteoglycan (HSPG) content of the glomerular basement membrane (GBM) is reduced but the cellular mechanisms involved have not been studied. Glomerular epithelial cells (GEC) are thought to be the source of HSPG present in the GBM. In this study we examined if proteoglycan metabolism of the rat GEC in culture is dysregulated in a metabolic environment simulating diabetes. Following incubation for 8 days with a serum-supplemented medium containing 30 mM glucose and no added insulin, a significant increase in the overall synthesis of (SO4)-S-35-labeled molecules by the GEC was seen compared to control monolayers incubated with medium containing 5 mM glucose and insulin. Ion exchange chromatography revealed that 30 mM glucose did not alter the anionic charge density of proteoglycans, but significantly increased the amount of S-35-labeled low-anionic macromolecules in the medium; mannitol induced similar changes. Sepharose CL-4B chromatography, glycosaminoglycan analysis and immunoprecipitation of control cell layer proteoglycans demonstrated the presence of HSPG of hydrodynamic size, K-av 0.4, resembling rat GBM HSPG in size and antigenic nature. Incubation of GEC with 30 mM glucose resulted in a significant reduction (58%) in this HSPG species, an effect not seen with equimolar mannitol. Additionally, 30 mM glucose induced a significant increment in synthesis of a small HS species (K-av 0.71 on Sepharose CL-4B column) present in the cell layer. Our findings suggest that both osmotic and nonosmotic mechanisms are operative in dysregulation of glycopeptide metabolism by high-glucose medium and that reduced synthesis by the GEC may contribute to decreased content of GBM HSPG in diabetic nephropathy. (C) 1994 Academic Press, Inc. C1 RUSH MED COLL,CHICAGO,IL. LOYOLA UNIV,SCH MED,CHICAGO,IL. RP KASINATH, BS (reprint author), UNIV TEXAS,AUDIE L MURPHY MEM VET ADM HOSP,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK 41517] NR 47 TC 12 Z9 12 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 15 PY 1994 VL 309 IS 1 BP 149 EP 159 DI 10.1006/abbi.1994.1097 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MY517 UT WOS:A1994MY51700023 PM 8117103 ER PT J AU JENSEN, DM CHENG, S KOVACS, TOG RANDALL, G JENSEN, ME REEDY, T FRANKL, H MACHICADO, G SMITH, J SILPA, M VANDEVENTER, G AF JENSEN, DM CHENG, S KOVACS, TOG RANDALL, G JENSEN, ME REEDY, T FRANKL, H MACHICADO, G SMITH, J SILPA, M VANDEVENTER, G TI A CONTROLLED-STUDY OF RANITIDINE FOR THE PREVENTION OF RECURRENT HEMORRHAGE FROM DUODENAL-ULCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID BLEEDING PEPTIC-ULCERS; HISTAMINE2-RECEPTOR ANTAGONISTS; MAINTENANCE TREATMENT; STANDARD THERAPY; CONTROLLED TRIAL; DRUG-THERAPY; CIMETIDINE; MULTICENTER; DISEASE; RELAPSE AB Background. Hemorrhage is the most common complication of duodenal ulcer disease, but there is little information about the effectiveness and safety of long-term maintenance therapy with histamine H-2-receptor blockers. Methods. We conducted a double-blind study in patients with endoscopically documented hemorrhage from duodenal ulcers. Patients were randomly assigned to maintenance therapy with ranitidine (150 mg at night) or placebo and were followed for up to three years. Endoscopy was performed at base line (to document that the ulcers had healed), at exit from the study, and when a patient had persistent ulcer symptoms unrelieved by antacids or had gastrointestinal bleeding. Symptomatic relapses without bleeding were treated with ranitidine; if the ulcer healed within eight weeks, the patient resumed taking the assigned study medication. Results. The two groups were similar at entry, which usually occurred about three months after the index hemorrhage. After a mean follow-up of 61 weeks, 3 of the 32 patients treated with ranitidine had recurrent hemorrhage, as compared with 12 of the 33 given placebo (P<0.05). Half the episodes of recurrent bleeding were asymptomatic. One patient in the ranitidine group withdrew from the study because of asymptomatic thrombocytopenia during the first month. Conclusions. For patients whose duodenal ulcers heal after severe hemorrhage, long-term maintenance therapy with ranitidine is safe and reduces the risk of recurrent bleeding. C1 UNIV CALIF LOS ANGELES, CTR ULCER RES & EDUC, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA USA. VALLEY MED CTR, VAN NUYS, CA USA. ALTON OCHSNER MED FDN & OCHSNER CLIN, NEW ORLEANS, LA 70121 USA. HIGHLAND HOSP, OAKLAND, CA USA. RI smith, james/C-9922-2016 FU NIADDK NIH HHS [AM 41301, AM 33273] NR 27 TC 101 Z9 103 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 10 PY 1994 VL 330 IS 6 BP 382 EP 386 DI 10.1056/NEJM199402103300602 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MV279 UT WOS:A1994MV27900002 PM 8284002 ER PT J AU VONREYN, CF BROWN, ST ARBEIT, RD AF VONREYN, CF BROWN, ST ARBEIT, RD TI RIFABUTIN PROPHYLAXIS AGAINST MYCOBACTERIUM-AVIUM COMPLEX INFECTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 BRONX VET AFFAIRS MED CTR,BRONX,NY 10468. BOSTON VET AFFAIRS MED CTR,BOSTON,MA 02130. RP VONREYN, CF (reprint author), DARTMOUTH COLL,HITCHCOCK MED CTR,HANOVER,NH 03756, USA. NR 2 TC 4 Z9 4 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 10 PY 1994 VL 330 IS 6 BP 437 EP 437 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MV279 UT WOS:A1994MV27900026 PM 8129826 ER PT J AU SCHWARTZ, GG GREYSON, CR WISNESKI, JA GARCIA, J STEINMAN, S AF SCHWARTZ, GG GREYSON, CR WISNESKI, JA GARCIA, J STEINMAN, S TI RELATION AMONG REGIONAL O-2 CONSUMPTION, HIGH-ENERGY PHOSPHATES, AND SUBSTRATE UPTAKE IN PORCINE RIGHT VENTRICLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY; ENERGY METABOLISM; CORONARY CIRCULATION; PHOSPHOCREATINE; ADENOSINE 5'-TRIPHOSPHATE; ISOPROTERENOL ID P-31 NMR-SPECTROSCOPY; FREE FATTY-ACIDS; HEART INVIVO; CREATINE-KINASE; MITOCHONDRIAL RESPIRATION; OXYGEN-CONSUMPTION; ATP SYNTHESIS; RAT-HEART; METABOLISM; MYOCARDIUM AB Changes in phosphate metabolites may play a role in the regulation of myocardial oxidative phosphorylation in vivo. We tested the hypothesis that changes in phosphate metabolites with increased myocardial oxygen consumption (MVO(2)) depend on the mechanism by which MVO(2) is increased. In 17 open-chest pigs, regional MVO(2) of the right ventricular (RV) free wall was increased from control by isoproterenol infusion (Iso) and by pulmonary artery constriction (PAC). The phosphocreatine-to-ATP ratio (PCr/ATP), which is inversely related to free ADP concentration ([ADP]), was determined by P-31-nuclear magnetic resonance (NMR) spectroscopy. Regional MVO(2) and lactate, glucose, and free fatty acid (FFA) uptake were determined in the myocardium directly beneath the NMR coil. Iso and PAC increased MVO(2) nearly equally, to approximately twice control, but produced directionally opposite changes in PCr/ATP: a significant decrease with PAC (control 1.52 +/- 0.06, PAC 1.35 +/- 0.06, means +/- SE) but a significant increase with Iso (to 1.72 +/- 0.07). Thus increased [ADP] may have stimulated oxidative phosphorylation during PAC but could not have done so during Iso. With Iso, uptake of FFA was more than three times that with PAC, and the sum of the oxygen extraction ratios for lactate, glucose, and FFA was more than double that with PAC. Enhanced substrate uptake during Iso may have increased mitochondrial NADH, which in turn may have provided an alternative stimulus to the rate of oxidative phosphorylation. These results support multifactorial control of RV oxidative phosphorylation in vivo. C1 UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94121. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94121. RP SCHWARTZ, GG (reprint author), SAN FRANCISCO VET AFFAIRS MED CTR,CARDIOL SECT 111C,4150 CLEMENT ST,SAN FRANCISCO,CA 94121, USA. FU NHLBI NIH HHS [HL-02155, HL-07192] NR 37 TC 17 Z9 17 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1994 VL 266 IS 2 BP H521 EP H530 PN 2 PG 10 WC Physiology SC Physiology GA NA803 UT WOS:A1994NA80300022 PM 8141353 ER PT J AU JENKINSON, SG LAWRENCE, RA ZAMORA, CA DENEKE, SM AF JENKINSON, SG LAWRENCE, RA ZAMORA, CA DENEKE, SM TI INDUCTION OF INTRACELLULAR GLUTATHIONE IN ALVEOLAR TYPE-II PNEUMOCYTES FOLLOWING BCNU EXPOSURE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE N,N'-BIS(2-CHLOROETHYL)-N-NITROSOUREA; CYSTINE TRANSPORT; OXYGEN TOXICITY ID PERFORMANCE LIQUID-CHROMATOGRAPHY; CYSTINE TRANSPORT ACTIVITY; GLUTAMIC-ACID UPTAKE; ENDOTHELIAL-CELLS; DIETHYL MALEATE; 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA BCNU; ELECTROPHILIC AGENTS; HUMAN-FIBROBLASTS; EPITHELIAL-CELLS; RAT HEPATOCYTES AB N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU) is a potent inhibitor of glutathione reductase (GSSG-Red) activity in both tissues and cells. We examined the effects of treating alveolar type II cells with BCNU and found that a marked decrease in cellular GSSG-Red activity occurred in these cells associated with a time-dependent increase in cellular glutathione (GSH) concentrations. The increase in GSH was not found to be related to changes in cellular gamma-glutamyl transpeptidase activity, gamma-glutamylcysteine synthetase activity, nor increased intracellular transport of cystine. When the BCNU-exposed cells were incubated with hydrogen peroxide to produce oxidant stress, the cells exhibited increased susceptibility to oxidant damage when compared with controls, despite the fact that cellular concentrations of GSH were markedly elevated. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE MED,SAN ANTONIO,TX 78284. RP JENKINSON, SG (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT 111E,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NHLBI NIH HHS [HL-30556, HL-32824] NR 41 TC 19 Z9 19 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1994 VL 266 IS 2 BP L125 EP L130 PN 1 PG 6 WC Physiology SC Physiology GA NA801 UT WOS:A1994NA80100072 PM 7908172 ER PT J AU MCKAY, JR ALTERMAN, AI MCLELLAN, AT SNIDER, EC AF MCKAY, JR ALTERMAN, AI MCLELLAN, AT SNIDER, EC TI TREATMENT GOALS, CONTINUITY OF CARE, AND OUTCOME IN A DAY HOSPITAL SUBSTANCE-ABUSE REHABILITATION PROGRAM SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID ADDICTION SEVERITY INDEX; DRUG-ABUSE; ALCOHOLISM AB Objective: Relationships between day hospital treatment goals, self-help group participation, and substance use outcome were examined for 180 alcohol- or cocaine-dependent male patients in a day hospital Veterans Administration substance abuse program. Method: The primary goals assessed were completion of the day hospital program and participation in posttreatment self-help groups. For subjects who completed the day hospital program, progress toward three other goals was also assessed: decreased denial, endorsement of 12-Step beliefs, and participation in self-help groups during the day hospital program. The outcome measures were urine toxicology and self-reports of alcohol or cocaine use at 4- and 7-month post-intake follow-up interviews. Results: Day hospital completion and participation in posttreatment self-help groups predicted better outcome. Self-help participation also predicted outcome after day hospital completion was controlled. Among subjects who completed the day hospital program, the other three goals did not predict substance use outcome. However, involvement with self-help groups during the day hospital program and decreases in denial Predicted continued involvement with self-help groups. Conclusions: Patients who complete day hospital substance abuse rehabilitation and then continue to participate in self-help groups are likely to have lower rates of alcohol and cocaine use during follow-up. Furthermore, the beneficial effect of self-help group participation does not appear to be strictly the result of motivation or some other patient characteristic. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP MCKAY, JR (reprint author), UNIV PENN,SCH MED,DEPT PSYCHIAT,TREATMENT RES CTR,3900 CHESTNUT ST,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [DA-05186] NR 21 TC 93 Z9 93 U1 1 U2 5 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD FEB PY 1994 VL 151 IS 2 BP 254 EP 259 PG 6 WC Psychiatry SC Psychiatry GA MV488 UT WOS:A1994MV48800018 PM 8296899 ER PT J AU TAGLIENTE, TM AF TAGLIENTE, TM TI HALOTHANE-INDUCED ALTERATIONS IN RAT-BRAIN NITRIC-OXIDE SYNTHASE ACTIVITY ARE CONCENTRATION AND REGION DEPENDENT SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 MT SINAI SCH MED,NEW YORK,NY. BRONX VET ADM MED CTR,NEW YORK,NY. NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1994 VL 78 IS 2 SU S BP U225 EP U225 PG 1 WC Anesthesiology SC Anesthesiology GA NA406 UT WOS:A1994NA40600420 ER PT J AU NELSON, S PRITT, A MARLAR, RA AF NELSON, S PRITT, A MARLAR, RA TI RAPID PREPARATION OF PLASMA FOR STAT COAGULATION-TESTING SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article AB We undertook to confirm and extend the previous work on the use of microcentrifugation (2 minutes at 11000g) to prepare platelet-poor plasma for assay of the prothrombin time, partial thromboplastin time, fibrinogen level, D-dimer, antithrombin Ill, and dilute Russell viper venom time. We compared results of routinely submitted blood samples by both high-speed and routine (15 minutes at 1800g) centrifugation. We found no significant differences in assay results and concluded that the high-speed technique is a reliable and useful option for minimizing turnaround times for these coagulation assays. C1 UNIV COLORADO,HLTH SCI CTR,DENVER VET AFFAIRS MED CTR,LAB SERV 113,DENVER,CO 80220. NR 4 TC 13 Z9 14 U1 0 U2 1 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 FEB PY 1994 VL 118 IS 2 BP 175 EP 176 PG 2 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MV289 UT WOS:A1994MV28900020 PM 8311659 ER PT J AU ROSS, RJ BALL, WA DINGES, DF KRIBBS, NB MORRISON, AR SILVER, SM MULVANEY, FD AF ROSS, RJ BALL, WA DINGES, DF KRIBBS, NB MORRISON, AR SILVER, SM MULVANEY, FD TI RAPID EYE-MOVEMENT SLEEP DISTURBANCE IN POSTTRAUMATIC-STRESS-DISORDER SO BIOLOGICAL PSYCHIATRY LA English DT Article DE POSTTRAUMATIC STRESS DISORDER; RAPID EYE MOVEMENT SLEEP; NIGHTMARES; PHASIC ACTIVITY; MAJOR DEPRESSION; ALCOHOL ABUSE ID CORTISOL EXCRETION; DEPRESSED-PATIENTS; STARTLE RESPONSE; REM; HYPOTHESIS; SPIKES; BRAIN; STATE AB The subjective sleep disturbance in posttraumatic stress disorder (PTSD), including the repetitive, stereotypical anxiety dream, suggests dysfunctional rapid eye movement (REM) sleep mechanisms. The polysomnograms of a group of physically healthy combat veterans with current PTSD were compared with those of an age-appropriate normal control group. Tonic and phasic REM sleep measures in the PTSD subjects were elevated on the second night of recorded sleep. Increased phasic REM sleep activity persisted in the PTSD group on the subsequent night. During the study, an anxiety dream occurred in a PTSD subject in REM sleep. The results are consistent with the view that a dysregulation of the REM sleep control system, particularly phasic event generation, may be involved in the pathogenesis of PTSD. The finding of a specific disturbance of sleep unique to PTSD may have significant implications for the design of effective treatments for PTSD. C1 PHILADELPHIA VET AFFAIRS MED CTR,RES SERV,PHILADELPHIA,PA. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH VET MED,DEPT ANIM BIOL,PHILADELPHIA,PA 19104. COATESVILLE VET AFFAIRS MED CTR,COATESVILLE,PA. FU NIMH NIH HHS [MH-42903, F32-MH-09584-01] NR 36 TC 123 Z9 126 U1 0 U2 8 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD FEB 1 PY 1994 VL 35 IS 3 BP 195 EP 202 DI 10.1016/0006-3223(94)91152-5 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MY642 UT WOS:A1994MY64200007 PM 8173020 ER PT J AU MARGOLIS, ML HYZY, JB SCHENKEN, LL SCHEPART, BS AF MARGOLIS, ML HYZY, JB SCHENKEN, LL SCHEPART, BS TI SERUM TUMOR-MARKERS IN NONSMALL CELL LUNG-CANCER - A COMPARATIVE-ANALYSIS SO CANCER LA English DT Article DE TUMOR MARKERS; MONOCLONAL ANTIBODIES; NONSMALL CELL LUNG CANCER ID MULTIPLE BIOMARKER ASSAY; MONOCLONAL-ANTIBODIES; CLINICAL-SIGNIFICANCE; CARCINOMA; DIAGNOSIS; ANTIGENS AB Background. The role of serum tumor markers in non-small cell lung cancer (NSCLC) remains undefined. New proposed markers have seldom been rigorously compared with existing standards. The authors prospectively compared the performance of three new monoclonal antibodies (MoAb) (5E8, 5C7, and 1F10) with the established serum markers carcinoembryonic antigen (CEA) and squamous cell carcinoma antigen (SCC). Methods. The cohort consisted of 45 consecutive outpatients with newly diagnosed NSCLC. Control subjects were 38 outpatients with non-neoplastic chronic pulmonary diseases. Blood from each patient and control subject was assayed for all five tumor markers. An enzyme linked immunosorbent assay (ELISA) was used to determine 5E8, 5C7, and 1F10 reactivity. Commercially available kits were used to measure SCC by radioimmunoassay and CEA by ELISA. Individual and combinations of tumor markers were compared in terms of sensitivity, specificity, and accuracy for NSCLC diagnosis. Results. 5E8 plus 5C7 plus 1F10 significantly surpassed SCC plus CEA in terms of sensitivity (P < 0.05) and proved the most accurate marker combination. Among single markers, 5E8 was most specific, 5C7 most sensitive, and 5C7 and 1F10 each most accurate, but differences from CEA alone were not significant. Subgroup analysis by histologic type and stage demonstrated similar findings, and marker combinations yielded little additional diagnostic benefit. Conclusions. 5E8, 5C7, and 1F10 performed marginally better than did CEA and SCC in patients with newly diagnosed NSCLC. Many limitations apply in defining a clinical niche for these tumor markers in NSCLC, although 5E8, 5C7, and 1F10 previously have demonstrated a modest prognostic value. An adjunctive role in a few specific clinical contexts remains possible. C1 MED COLL PENN,PHILADELPHIA,PA. MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. ALLEGHENY GEN HOSP,CLIN ONCOL LAB,PITTSBURGH,PA. RP MARGOLIS, ML (reprint author), VET AFFAIRS MED CTR,PULM DIS SECT,PHILADELPHIA,PA 19104, USA. NR 20 TC 26 Z9 27 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1994 VL 73 IS 3 BP 605 EP 609 DI 10.1002/1097-0142(19940201)73:3<605::AID-CNCR2820730317>3.0.CO;2-T PG 5 WC Oncology SC Oncology GA MU681 UT WOS:A1994MU68100016 PM 8299082 ER PT J AU NAGATSU, M ZILE, MR TSUTSUI, H SCHMID, PG DEFREYTE, G COOPER, G CARABELLO, BA AF NAGATSU, M ZILE, MR TSUTSUI, H SCHMID, PG DEFREYTE, G COOPER, G CARABELLO, BA TI NATIVE BETA-ADRENERGIC SUPPORT FOR LEFT-VENTRICULAR DYSFUNCTION IN EXPERIMENTAL MITRAL REGURGITATION NORMALIZES INDEXES OF PUMP AND CONTRACTILE FUNCTION SO CIRCULATION LA English DT Article DE CONTRACTILITY; MITRAL VALVE; REGURGITATION RECEPTORS; ADRENERGIC; BETA ID CONGESTIVE HEART-FAILURE; SYSTOLIC PRESSURE-VOLUME; IDIOPATHIC DILATED CARDIOMYOPATHY; CANINE LEFT-VENTRICLE; WALL STRESS; PLASMA NOREPINEPHRINE; OVERLOAD HYPERTROPHY; MYOCARDIAL STIFFNESS; REGIONAL WORK; END-SYSTOLE AB Background It is generally accepted that the adrenergic nervous system provides inotropic support for the failing heart. However, the magnitude of this support has never been studied extensively. The present study was performed to test the hypothesis that the adrenergic nervous system is capable of maintaining indexes of pump and contractile function in the normal range despite significant innate myocardial depression. Methods and Results We used our model of experimental canine mitral regurgitation, which produces left ventricular dysfunction after 3 months of volume overload. We studied indexes of contractile function on and off beta-blockade at baseline and again on and off beta-blockade 3 months after chronic mitral regurgitation had induced significant contractile dysfunction. At baseline, acute beta-blockade caused insignificant reductions in the mass-corrected slope of the end-ejection stress-volume relation (EESVR), the end-systolic stiffness constant, and the ejection fraction-end-systolic stress and the mean velocity of circumferential fiber shortening (VCF)-end-systolic stress relations. After 3 months of chronic mitral regurgitation, all indexes of contractile function were normal in the unblocked state except for the VCF-stress relation, which was mildly reduced. However, after acute beta-blockade after 3 months of chronic mitral regurgitation, the EESVR fell to 303+/-27 versus 443+/-24 during acute beta-blockade before mitral regurgitation was created (P<.05), and the end-systolic stiffness constant was reduced to 2.54+/-0.15 versus 3.27+/-0.11 (P<.05). Only after beta-blockade was the ejection fraction-stress relation significantly reduced for dogs with chronic mitral regurgitation. The VCF-stress relation became markedly more abnormal. The viscosity-velocity relation of myocytes isolated from the ventricles of the dogs with mitral regurgitation confirmed that substantial innate contractile depression was present. Conclusions After 3 months of chronic mitral regurgitation, the adrenergic nervous system was able to maintain most indexes of contractile function in the normal range despite significant depression in innate contractile function. Thus, in the absence of beta-blockade, significant innate contractile depression may be obscured by adrenergic support. C1 MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT MED,DIV CARDIOL,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. UNIV IOWA,DEPT MED,IOWA CITY,IA 52242. RI Tsutsui, Hiroyuki/A-4070-2012 FU NHLBI NIH HHS [HL-38185] NR 46 TC 40 Z9 40 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 818 EP 826 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200036 PM 8313571 ER PT J AU DRAYTON, J DICKINSON, G RINALDI, MG AF DRAYTON, J DICKINSON, G RINALDI, MG TI COADMINISTRATION OF RIFAMPIN AND ITRACONAZOLE LEADS TO UNDETECTABLE LEVELS OF SERUM ITRACONAZOLE SO CLINICAL INFECTIOUS DISEASES LA English DT Letter C1 DEPT VET AFFAIRS MED CTR,DIV INFECT DIS,MIAMI,FL 33125. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 1 TC 43 Z9 44 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 FEB PY 1994 VL 18 IS 2 BP 266 EP 266 PG 1 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MU350 UT WOS:A1994MU35000032 PM 8161649 ER PT J AU SCHILLER, JH SABATINI, L BITTNER, G PINKERMAN, CL MAYOTTE, J LEVITT, M MEISNER, L AF SCHILLER, JH SABATINI, L BITTNER, G PINKERMAN, CL MAYOTTE, J LEVITT, M MEISNER, L TI PHENOTYPIC, MOLECULAR AND GENETIC-CHARACTERIZATION OF TRANSFORMED HUMAN BRONCHIAL EPITHELIAL-CELL STRAINS SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE TRANSFORMATION; HUMAN BRONCHIAL EPITHELIAL CELLS ID RAS ONCOGENE ACTIVATION; LUNG-CANCER PATIENTS; SQUAMOUS DIFFERENTIATION; NEOPLASTIC PROGRESSION; CLINICAL-SIGNIFICANCE; PROGNOSTIC MARKER; P53 MUTATIONS; RETINOIC ACID; LINES; ADENOCARCINOMA AB In order to study the phenotypic, genetic, and molecular characteristics of normal human bronchial epithelial cells (HBE) so as to establish a model of HBE cell carcinogenesis, we established six HBE cell strains by transfection with either the SV40 virus or an origin of replication defective large T plasmid. Tracheobronchial specimens were obtained from autopsy samples or heart donors from noncancer patients, cultured, and transfected using strontium chloride. Three cell strains were established by transfection with the whole SV40 virus (NL4SV, NL11SV, and NL20SV) and three cell strains were established with the origin of replication depleted T antigen (NL25, NL30-0, NL30-N). All of the cell strains senesced between passages 19-28. None of the cell strains formed colonies in 0.15% agarose. All required epidermal growth factor, whereas their requirement for fetal bovine serum was variable. None of the cell strains formed tumors in nude mice. Cytogenetic analysis revealed that none of the cell strains were diploid. They ranged from having few random changes to extreme chromosomal instability. Only one cell strain (NL30-N) had two consistent markers. About one-third of the NL30-O cells, derived from independent cultures from the same donor, had the same markers. No DNA amplification for c-myc was observed in any of the transformed HBE cell strains. No mutations were detected in K-ras codons 12, 13, and 61 using primer engineered restriction fragment-length polymorphism analysis. No mutations were detected in exons 5-9 of the p53 gene by single strand conformation polymorphism (SSCP) analysis. We conclude that despite differences in morphology, phenotype, differentiation, and karyotype between six nontumorigenic HBE cell strains, none have activation of dominant oncogenes or inactivation of tumor suppressor genes that have been described in human lung tumors. These cells should be useful as a model for molecular studies of HBE cell carcinogenesis. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI 53792. UNIV WISCONSIN HOSP & CLIN,DEPT PATHOL & LAB MED,MADISON,WI 53792. UNIV PITTSBURGH,PITTSBURGH,PA 15260. NR 59 TC 4 Z9 4 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD FEB PY 1994 VL 4 IS 2 BP 461 EP 470 PG 10 WC Oncology SC Oncology GA MT110 UT WOS:A1994MT11000026 PM 21566947 ER PT J AU CHEN, TH PRATT, SA SHOBACK, DM AF CHEN, TH PRATT, SA SHOBACK, DM TI INJECTION OF BOVINE PARATHYROID POLY(A)(+) RNA INTO XENOPUS-OOCYTES CONFERS SENSITIVITY TO HIGH EXTRACELLULAR CALCIUM SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID INOSITOL PHOSPHATES; HORMONE SECRETION; MOLECULAR-CLONING; DIVALENT-CATIONS; CYTOSOLIC CA-2+; MESSENGER-RNA; CELLS; RECEPTOR; EXPRESSION; ACCUMULATION AB Parathyroid cells detect increments in the extracellular [Ca2+], which lead to substantial increases in intracellular free Ca2+ ([Ca2+](i)) and, ultimately, to suppression of parathyroid hormone (PTH) secretion. To determine whether mRNA from parathyroid tissue could confer sensitivity to high extracellular Ca2+, we isolated and injected total bovine parathyroid poly(A)(+) RNA into Xenopus laevis oocytes. To assess translational activity of the RNA, PTH released into the media was measured. Intact PTH was detected in the medium for less than or equal to 48 h, and injection of increasing amounts of RNA (similar to 0.5-50 ng/oocyte) led to the release of greater quantities of PTH. We screened for the expression of a putative Ca2+ sensor molecule by measuring Ca-45 efflux from preloaded oocytes, in response to raising extracellular [Ca2+] from 0.7 to 5.7 mM. This increment in [Ca2+] stimulated Ca-45 efflux by 249 +/- 52 cpm over 20 min from eggs injected with parathyroid poly(A)(+) RNA (n = 22). This response was significantly greater than Ca-45 efflux from any group of controls exposed to the same change in extracellular Ca2+ (p < 0.02), including oocytes injected with either water, cRNA for the platelet-derived growth factor (PDGF) BB receptor, or T cell poly(A)(+) RNA. Size-fractionation of poly(A)(+) RNA over sucrose gradients demonstrated that mRNA, which induced responsiveness to high extracellular Ca2+ was present in fractions with transcripts of similar to 5-9 kB. Injection of these fractions also conferred sensitivity to the presence of Ba2+ or Sr2+ (both at 5 mM) in the media. These findings establish that parathyroid cells express mRNA for a molecule capable of detecting changes in the extracellular divalent cation concentration. This molecule may play a role in secretory responses mediated by Ca2+ in the parathyroid. C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO VA MED CTR,ENDOCRINE RES UNIT,SAN FRANCISCO,CA 94121. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA. FU NIDDK NIH HHS [R29 DK39594, DK43400] NR 30 TC 13 Z9 13 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD FEB PY 1994 VL 9 IS 2 BP 293 EP 300 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MW246 UT WOS:A1994MW24600018 PM 7511319 ER PT J AU MARGOLIN, K ARONSON, FR SZNOL, M ATKINS, MB GUCALP, R FISHER, RI SUNDERLAND, M DOROSHOW, JH ERNEST, ML MIER, JW DUTCHER, JP GAYNOR, ER WEISS, GR AF MARGOLIN, K ARONSON, FR SZNOL, M ATKINS, MB GUCALP, R FISHER, RI SUNDERLAND, M DOROSHOW, JH ERNEST, ML MIER, JW DUTCHER, JP GAYNOR, ER WEISS, GR TI PHASE-II STUDIES OF RECOMBINANT HUMAN INTERLEUKIN-4 IN ADVANCED RENAL-CANCER AND MALIGNANT-MELANOMA SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE INTERLEUKIN-4; RENAL CANCER; MALIGNANT MELANOMA; CYTOKINES; IMMUNOTHERAPY ID TUMOR-NECROSIS-FACTOR; GAMMA-INTERFERON; CELL-GROWTH; LYMPHOCYTES; ALPHA; IL-4; PROLIFERATION; EXPRESSION; MONOCYTES; INVITRO AB Interleukin (IL)-4 is a pluripotent cytokine that stimulates proliferation of activated T-cells and has antineoplastic activity against human renal tumors in animal systems. In phase I trials, IL-4 could be tolerated at doses up to 20 mu g/kg, with dose-limiting toxicities consisting of fever, fluid retention, nasal congestion, and mucositis. We report the results of two separate Phase II trials of IL-4 in 30 patients with metastatic malignant melanoma and 19 patients with advanced renal cancer. IL-4 was administered intravenously every 8 h for 14 doses in two 5-day courses separated by a 9-day interval. The first 27 patients were treated at a dose of 800 mu g/m(2), but after three of these patients developed cardiac toxicities, the dose was decreased to 600 mu g/m(2). One complete response occurred in a patient with metastatic melanoma (duration greater than or equal to 30 months). No responses were seen among the patients with renal cancer. The most frequent side effects were fever, nausea, malaise, nasal congestion, and diarrhea. Reversible hepatic and renal dysfunction were also common. Hypotension was infrequent, but transient weight gain due to fluid retention was common. The major life-threatening toxicities were cardiac and gastrointestinal. Suspected cardiac ischemia was observed in two patients, pericarditis in one, and arrhythmias in two. Three patients had major upper gastrointestinal bleeding without evidence of local tumor. We conclude that IL-4, when given as a single agent on this schedule at maximum tolerated dose, does not possess meaningful activity in renal cancer or melanoma. C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. NCI,CANC THERAPY PROGRAM,BETHESDA,MD. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. MONTEFIORE MED CTR,ALBERT EINSTEIN CANC CTR,BRONX,NY 10467. LOYOLA UNIV,STRITCH SCH MED,CHICAGO,IL. UNIV TEXAS,AUDIE MURPHY VET ADM HOSP,HLTH SCI CTR,SAN ANTONIO,TX. RP MARGOLIN, K (reprint author), CITY HOPE NATL MED CTR,DEPT MED ONCOL,1500 E DUARTE RD,DUARTE,CA 91010, USA. NR 22 TC 52 Z9 52 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD FEB PY 1994 VL 15 IS 2 BP 147 EP 153 DI 10.1097/00002371-199402000-00009 PG 7 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA MT386 UT WOS:A1994MT38600009 PM 8136948 ER PT J AU GRANDALIANO, G VALENTE, AJ ROZEK, MM ABBOUD, HE AF GRANDALIANO, G VALENTE, AJ ROZEK, MM ABBOUD, HE TI GAMMA-INTERFERON STIMULATES MONOCYTE CHEMOTACTIC PROTEIN (MCP-1) IN HUMAN MESANGIAL CELLS SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article ID HUMAN ENDOTHELIAL-CELLS; ACTIVATING FACTOR MCAF; SMOOTH-MUSCLE CELLS; GROWTH-FACTOR; MONOCLONAL-ANTIBODIES; T-CELLS; CHEMOATTRACTANT; INTERLEUKIN-8; MACROPHAGES; GLOMERULONEPHRITIS AB Cell-mediated immunity and monocyte infiltration is a prominent histologic feature of several different types of glomerulonephritis. Monocyte influx to the glomerulus correlates with glomerular hypercellularity and proteinuria. Glomerular mesangial cells, in addition to being targets for inflammatory stimuli, are also effector cells that actively participate in glomerular pathology. Mesangial cells release monocyte chemotactic protein (MCP-I). In the present article, we characterized and studied the regulation of MCP-1 released by cultured human mesangial cells. Serum-deprived mesangial cells constitutively release chemotactic activity that is neutralized by specific anti-MCP-1 antibody. An antibody to baboon MCP-I recognized 16, 15, and II kd proteins from concentrated conditioned medium that were consistent with the presence of different forms of MCP-1. Gamma interferon (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-l [II-I) markedly stimulate the release of MCP-1 as measured by a specific and sensitive radioimmunoassay. The release of MCP-1 in response to these cytokines is at least partially dependent on de novo synthesis of the protein because all three cytokines markedly stimulate the expression of MOP-I mRNA. These data demonstrate that human mesangial cells synthesize and release at least three different forms of MCP-I and that IFN-gamma and other cytokines regulate the secretion of MOP-1. IFN-gamma and MCP-I may play a major role in the recruitment and activation of monocytes to the inflamed glomerulus. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RI Grandaliano, Giuseppe/G-2963-2012 FU NHLBI NIH HHS [HL 26890]; NIDDK NIH HHS [DK 33665] NR 35 TC 62 Z9 62 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD FEB PY 1994 VL 123 IS 2 BP 282 EP 289 PG 8 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA MZ689 UT WOS:A1994MZ68900021 PM 8301205 ER PT J AU ASCH, DA PATTON, JP AF ASCH, DA PATTON, JP TI CONFLICTS OVER POSTEXPOSURE TESTING FOR HUMAN-IMMUNODEFICIENCY-VIRUS - CAN NEGOTIATED SETTLEMENTS HELP SO JOURNAL OF MEDICINE AND PHILOSOPHY LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; CONFIDENTIALITY; ETHICS; GAME THEORY; HEALTH POLICY; HUMAN IMMUNODEFICIENCY VIRUS; PRIVACY; PROFESSIONAL PATIENT RELATIONS ID PROGNOSTIC INFORMATION; INFECTION; HIV AB Health care workers with needlestick exposures to patients' blood often request a test of the patient for evidence of infection with human immunodeficiency virus. If the patient refuses the test, a conflict develops between the interests of the health care worker and those of the patient. Traditional approaches to this dilemma attempt to balance the rights or utilities of abstract patients and health care workers. While these approaches have the advantage of offering clear guidelines in advance of conflict, the interests of the actual participants may differ from those used to create the guidelines. In nonmedical settings, conflicts are often resolved efficiently through negotiation and monetary exchanges. Although negotiated monetary settlements between health care workers and patients may be an impractical way to resolve medical conflicts, models developed from these perspectives provide insights into the individual interests of physicians and patients. Changing existing rules about medical record documentation, or increasing the penalties for the misuse of medical information, may satisfy the interests on both sides of the conflict and so represent integrative bargaining solutions. Even so, as the relationship between health care workers and their patients evolves, more explicit strategies for negotiation may become a reasonable solution to the problem of conflict. C1 UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,MED SERV,PHILADELPHIA,PA 19104. RP ASCH, DA (reprint author), UNIV PENN,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104, USA. NR 14 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 0360-5310 J9 J MED PHILOS JI J. Med. Philos. PD FEB PY 1994 VL 19 IS 1 BP 41 EP 59 PG 19 WC Ethics; Social Sciences, Biomedical SC Social Sciences - Other Topics; Biomedical Social Sciences GA NC715 UT WOS:A1994NC71500004 PM 8201289 ER PT J AU CASON, BA HICKEY, RF SHUBAYEV, I AF CASON, BA HICKEY, RF SHUBAYEV, I TI ATP-K CHANNEL BLOCKADE IMPROVES CORONARY AUTOREGULATION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Meeting Abstract C1 SAN FRANCISCO VET AFFAIRS MED CTR,SAN FRANCISCO,CA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD FEB PY 1994 SI SI BP A379 EP A379 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PP518 UT WOS:A1994PP51801499 ER PT J AU NAGATSU, M ISHIHARA, K ZILE, MR TSUTSUI, H TAGAWA, H DEFREYTE, G TANAKA, R COOPER, G CARABELLO, BA AF NAGATSU, M ISHIHARA, K ZILE, MR TSUTSUI, H TAGAWA, H DEFREYTE, G TANAKA, R COOPER, G CARABELLO, BA TI THE EFFECTS OF COMPLETE VERSUS INCOMPLETE MITRAL-VALVE REPAIR IN EXPERIMENTAL MITRAL REGURGITATION SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID LEFT-VENTRICULAR PERFORMANCE; VOLUME OVERLOAD HYPERTROPHY; CONTRACTILE FUNCTION; CHORDAE TENDINEAE; REPLACEMENT; PRESERVATION; SURGERY; RECONSTRUCTION; CELLS AB Severe mitral regurgitation (regurgitant fraction 0.75 +/- 0.02) was created in eight dogs by our closed-chest chordal rupture technique. After 3 months of chronic mitral regurgitation all indices of contractile function were depressed. Mitral valve repair was then attempted. Postoperative regurgitant fraction was reduced compared with the preoperative value in; all eight dogs. Concomitantly, forward cardiac output increased in all, dogs and pulmonary capillary wedge pressure fell in all dogs. However, in some dogs, significant regurgitation persisted despite repair. Postoperative regurgitant fraction ranged from 0% to 60%. Postoperative residual regurgitant fraction was related significantly to postoperative cardiac output (r = 0.99), pulmonary capillary wedge pressure (r = 0.77), ejection fraction (v 3;0.75), and two indices of contractile function-the mass-corrected end-systolic stress volume relationship (r = 0.87) and end-systolic stiffness (r = 0.93). In general, these parameters returned to their normal values before mitral regurgitation when postoperative regurgitant fraction was less than 30%. Myocytes isolated from the ventricles at the end of study also demonstrated normal contractile function when regurgitant fraction was less than 30%. C1 MED UNIV S CAROLINA,DEPT MED,DIV CARDIOL,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,CHARLESTON,SC 29425. RI Tsutsui, Hiroyuki/A-4070-2012 FU NHLBI NIH HHS [NHLBI R01 HL38185] NR 32 TC 16 Z9 18 U1 0 U2 1 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 FEB PY 1994 VL 107 IS 2 BP 416 EP 423 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA MW492 UT WOS:A1994MW49200010 PM 8302060 ER PT J AU CUMMINGS, JL HEGARTY, A AF CUMMINGS, JL HEGARTY, A TI NEUROLOGY, PSYCHIATRY, AND NEUROPSYCHIATRY SO NEUROLOGY LA English DT Editorial Material ID DISORDERS; MOOD C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHIAT SERV, BEHAV NEUROSCI SECT, LOS ANGELES, CA USA. ALBERT EINSTEIN COLL MED, DEPT PSYCHIAT, BRONX, NY USA. ALBERT EINSTEIN COLL MED, DEPT NEUROL, BRONX, NY USA. RP CUMMINGS, JL (reprint author), UNIV CALIF LOS ANGELES, SCH MED, REED NEUROL RES CTR, DEPT NEUROL, 710 WESTWOOD PLAZA, LOS ANGELES, CA 90024 USA. FU NIA NIH HHS [AG10123] NR 31 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD FEB PY 1994 VL 44 IS 2 BP 209 EP 213 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA MW890 UT WOS:A1994MW89000003 PM 8309560 ER PT J AU SHEVELL, MI EVANS, BK AF SHEVELL, MI EVANS, BK TI THE SCHALTENBRAND EXPERIMENT, WURZBURG, 1940 - SCIENTIFIC, HISTORICAL, AND ETHICAL PERSPECTIVES SO NEUROLOGY LA English DT Article C1 UNIV ALABAMA,SCH MED,DEPT NEUROL,BIRMINGHAM,AL. MCGILL UNIV,MONTREAL CHILDRENS HOSP,DEPT PEDIAT,DIV PEDIAT NEUROL,MONTREAL,PQ,CANADA. BIRMINGHAM VA MED CTR,NEUROL SERV,BIRMINGHAM,AL. RP SHEVELL, MI (reprint author), MCGILL UNIV,MONTREAL CHILDRENS HOSP,DEPT NEUROL NEUROSURG,DIV PEDIAT NEUROL,A-514,MONTREAL H3H 1P3,PQ,CANADA. NR 43 TC 18 Z9 18 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD FEB PY 1994 VL 44 IS 2 BP 350 EP 356 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA MW890 UT WOS:A1994MW89000035 PM 8309591 ER PT J AU KAHN, RS TRESTMAN, R LAWLOR, BA GABRIEL, S DAVIDSON, M SIEVER, L AF KAHN, RS TRESTMAN, R LAWLOR, BA GABRIEL, S DAVIDSON, M SIEVER, L TI EFFECTS OF IPSAPIRONE IN HEALTHY-SUBJECTS - A DOSE-RESPONSE STUDY SO PSYCHOPHARMACOLOGY LA English DT Article DE IPSAPIRONE; DOSE-RESPONSE; SEROTONIN ID OBSESSIVE-COMPULSIVE DISORDER; SEROTONIN RECEPTOR HYPERSENSITIVITY; PITUITARY-ADRENAL AXIS; PANIC DISORDER; META-CHLOROPHENYLPIPERAZINE; NEURO-ENDOCRINE; 5-HT1A RECEPTORS; HUMANS; ACTIVATION; PROLACTIN AB A dose-response study of ipsapirone (IFS), a 5HT(1a) partial agonist, was conducted in healthy male subjects. IPS was administered in doses of 5,10 and 20 mg PO in a placebo-controlled, double-blind design to 15 subjects on 4 test days separated by at least 3 days. Oral temperature, ACTH, cortisol, prolactin, blood pressure, pulse rate and behavioral variables were assessed every 30 min for 3 h after administration of tablets (at 10:00 A.M.). IPS at 20 mg significantly decreased temperature and increased cortisol levels. Although IPS increased ACTH levels at 20 mg, this effect was variable and not significant. IPS did not affect prolactin levels nor did it have any behavioral effects. Although 20 mg IPS decreased blood pressure and pulse rate in one subject, overall it had no significant effect on these parameters. IPS at 20 mg PO appears a useful probe to test 5HT(1a) function when temperature and cortisol are used as response variables. These results replicate earlier studies on the effect of IPS in healthy human subjects. C1 ST JAMES HOSP,DEPT PSYCHIAT,DUBLIN 8,IRELAND. RP KAHN, RS (reprint author), BRONX VET AFFAIRS MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 51 TC 29 Z9 29 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD FEB PY 1994 VL 114 IS 1 BP 155 EP 160 DI 10.1007/BF02245457 PG 6 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA MW866 UT WOS:A1994MW86600020 PM 7846198 ER PT J AU ORTIZBRAVO, E BAKER, DG SCHUMACHER, HR AF ORTIZBRAVO, E BAKER, DG SCHUMACHER, HR TI MECHANISMS INVOLVED IN THE INITIATION, PERPETUATION AND SELF-LIMITED NATURE OF ACUTE GOUTY-ARTHRITIS SO REVUE DU RHUMATISME LA French DT Article DE GOUT ID MONOSODIUM URATE CRYSTALS; CALCIUM PYROPHOSPHATE DIHYDRATE; MICROCRYSTALLINE SODIUM URATE; INDUCED INFLAMMATION; HUMAN-NEUTROPHILS; SYNOVIAL FIBROBLAST; PROTEIN ADSORPTION; SERUM-PROTEINS; MESSENGER-RNA; CELLS C1 HOP UNIV PENN,SERV RHUMATOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,CTR RHUMATOL & IMMUNOL,PHILADELPHIA,PA 19104. NR 73 TC 0 Z9 0 U1 0 U2 1 PU EXPANSION SCI FRANCAISE PI PARIS PA 31 BLVD LATOUR MAUBOURG, 75007 PARIS, FRANCE SN 1169-8446 J9 REV RHUM JI Rev. Rhum. PD FEB PY 1994 VL 61 IS 2 BP 132 EP 138 PG 7 WC Rheumatology SC Rheumatology GA MY832 UT WOS:A1994MY83200009 PM 7920501 ER PT J AU ORAK, JK SINGH, AK RAJAGOPALAN, PR SINGH, I AF ORAK, JK SINGH, AK RAJAGOPALAN, PR SINGH, I TI MORPHOLOGICAL ANALYSIS OF MITOCHONDRIAL INTEGRITY IN PROLONGED COLD RENAL ISCHEMIA UTILIZING EURO-COLLINS VERSUS UNIVERSITY-OF-WISCONSIN PRESERVATION SOLUTION IN A WHOLE ORGAN MODEL SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 1st International Congress on Pediatric Transplantation CY AUG 29-SEP 01, 1993 CL MINNEAPOLIS, MN ID KIDNEY-PRESERVATION; UW SOLUTION; OF-WISCONSIN; SUPEROXIDE-DISMUTASE; RAT-KIDNEY; TRANSPLANTATION; STORAGE; PEROXISOMES; INJURY C1 RALPH JOHNSON VA HOSP,CHARLESTON,SC. RP ORAK, JK (reprint author), MED UNIV S CAROLINA,DIV PEDIAT NEPHROL,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 26 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 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1994 VL 26 IS 1 BP 122 EP 125 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA MW599 UT WOS:A1994MW59900062 PM 8108903 ER PT J AU GAIRE, M MAGBANUA, Z MCDONNELL, S MCNEIL, L LOVETT, DH MATRISIAN, LM AF GAIRE, M MAGBANUA, Z MCDONNELL, S MCNEIL, L LOVETT, DH MATRISIAN, LM TI STRUCTURE AND EXPRESSION OF THE HUMAN GENE FOR THE MATRIX METALLOPROTEINASE MATRILYSIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RHEUMATOID SYNOVIAL FIBROBLASTS; COLLAGENASE GENE; HUMAN STROMELYSIN; IV COLLAGENASE; CHROMOSOMAL LOCALIZATION; PHORBOL INDUCTION; MESSENGER-RNA; GROWTH-FACTOR; PROMOTER; TRANSIN AB Matrilysin, a member of the matrix metalloproteinase family, is structurally different from the other matrix metalloproteinases by virtue of the absence of a conserved COOH-terminal protein domain. In addition, matrilysin mRNA is regulated in a specific and distinct manner in normal and malignant tissues. Analysis of the genomic structure of the human matrilysin gene revealed that the organization of the first five exons is highly conserved among the different members of the matrix metalloproteinase family, but that matrilysin contains an atypical sixth exon. The promoter region of the matrilysin gene has several features that are conserved among several other matrix metalloproteinase family members, including the presence of TATA, AP-1, and PEA3 elements. Comparison of the expression of the human matrilysin promoter with rat stromelysin promoter/chloramphenicol acetyltransferase constructs in HeLa cells revealed that constructs containing AP-1 and PEA3 elements respond similarly to epidermal growth factor and tumor promoter (12-O-tetradecanoylphorbol-13-acetate) induction, but that the addition of upstream stromelysin sequences results in an increased transcriptional activity not observed with upstream matrilysin sequences. The similarities and differences observed between the promoters of matrilysin and the other metalloproteinases may provide insights into the molecular mechanisms that regulate the expression of this family of enzymes as a whole and the factors that distinguish the expression patterns of individual family members. C1 VANDERBILT UNIV,DEPT CELL BIOL,NASHVILLE,TN 37232. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO VET AFFAIRS MED CTR,DEPT MED,SAN FRANCISCO,CA 94121. FU NCI NIH HHS [CA46843]; NIDDK NIH HHS [DK39776] NR 51 TC 214 Z9 217 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 JAN 21 PY 1994 VL 269 IS 3 BP 2032 EP 2040 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MR988 UT WOS:A1994MR98800074 PM 8294454 ER PT J AU TAKAYAMA, K MITCHELL, DH DIN, ZZ MUKERJEE, P LI, C COLEMAN, DL AF TAKAYAMA, K MITCHELL, DH DIN, ZZ MUKERJEE, P LI, C COLEMAN, DL TI MONOMERIC RE LIPOPOLYSACCHARIDE FROM ESCHERICHIA-COLI IS MORE ACTIVE THAN THE AGGREGATED FORM IN THE LIMULUS AMEBOCYTE LYSATE ASSAY AND IN INDUCING EGR-1 MESSENGER-RNA IN MURINE PERITONEAL-MACROPHAGES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ENDOTOXIN; DIFFERENTIATION; PROTEIN; GROWTH AB Using the equilibrium dialysis apparatus, an aqueous suspension of predominantly aggregated Re lipopolysaccharide (ReLPS) from Escherichia coli D31 m4 (99.9% at 82.5 muM) can be processed to yield a solution of monomeric ReLPS at a saturation concentration of 77 ng/ml (3.4 x 10(-8) m). We compared the in vitro biological activities of these two physically distinct types of ReLPS preparations in two select assays, reaction in the Limulus amebocyte lysate (LAL) assay and induction of Egr-1 mRNA in macrophages. These assays were chosen for their rapid response times and relatively short incubation periods. The monomeric ReLPS was 179- and 1000-fold more active than the aggregated ReLPS preparation in the LAL assay and induction of Egr-1 mRNA by thioglycollate-elicited murine peritoneal macrophages, respectively. These results clearly showed that the monomeric ReLPS is the more active form. The lower biological activities of the aggregated ReLPS preparation might be due to the presence of a small amount of monomeric ReLPS (0.01-0.6%) produced during its preparation and the incubation periods in the biological assays. Thus, aggregated ReLPS may be relatively inactive. C1 UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. UNIV COLORADO,HLTH SCI CTR,DIV INFECT DIS,DENVER,CO 80262. VET ADM MED CTR,INFECT DIS SECT,DENVER,CO 80220. RP TAKAYAMA, K (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NIGMS NIH HHS [GM-36054] NR 18 TC 90 Z9 91 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 21 PY 1994 VL 269 IS 3 BP 2241 EP 2244 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MR988 UT WOS:A1994MR98800102 PM 8294481 ER PT J AU HIRAYAMA, F CLARK, SC OGAWA, M AF HIRAYAMA, F CLARK, SC OGAWA, M TI NEGATIVE REGULATION OF EARLY B-LYMPHOPOIESIS BY INTERLEUKIN-3 AND INTERLEUKIN-1-ALPHA SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MULTIPOTENTIAL HEMATOPOIETIC PROGENITORS; COLONY-STIMULATING FACTOR; BONE-MARROW CULTURES; FACTOR-I; INTERLEUKIN-3-DEPENDENT PROLIFERATION; SYNERGISTIC INTERACTIONS; MURINE HEMATOPOIESIS; C-KIT; CELLS; GROWTH AB We recently developed a two-step methyl cellulose culture system for murine lymphohemopoietic progenitors that are capable of differentiation along the myeloid and B-lymphoid lineages. In this system, two-factor combinations, which include steel factor plus interleukin (IL) 6, IL-11, or granulocyte colony-stimulating factor effectively supported the lymphomyeloid potential of primary colonies. Interestingly, IL-3 could neither replace nor act synergistically with steel factor in maintaining the B-lymphoid potential of the primary colonies although the frequency of colony formation was the same with IL-3 and steel factor. We now report that addition of IL-3 or IL-1 alpha to a permissive system suppresses the B-lymphoid potential of primitive progenitor cells in primary culture in dose-dependent fashion. In vivo transfer of the primary colonies to scid mice confirmed the suppressive effects of 11-3 and IL-1 alpha. In addition, IL-1 alpha inhibited pre-B-cell colony formation in the secondary culture. Once pre-B-cell colonies had formed in secondary culture, neither factor affected the proliferation of the pre-B cells. These results suggest negative regulatory roles for IL-3 and IL-1 alpha in early stages of B lymphopoiesis. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. GENET INST INC,CAMBRIDGE,MA 02140. FU NIDDK NIH HHS [DK32294] NR 33 TC 82 Z9 83 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 18 PY 1994 VL 91 IS 2 BP 469 EP 473 DI 10.1073/pnas.91.2.469 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MR989 UT WOS:A1994MR98900010 PM 7507246 ER PT J AU BHANDARI, B GRANDALIANO, G ABBOUD, HE AF BHANDARI, B GRANDALIANO, G ABBOUD, HE TI PLATELET-DERIVED GROWTH-FACTOR (PDGF) BB HOMODIMER REGULATES PDGF A-CHAIN AND PDGF B-CHAIN GENE-TRANSCRIPTION IN HUMAN MESANGIAL CELLS SO BIOCHEMICAL JOURNAL LA English DT Article ID FACTOR-A-CHAIN; MICROVASCULAR ENDOTHELIAL-CELLS; CULTURED 3T3-L1 ADIPOCYTES; C-SIS GENE; GLUTAMINE-SYNTHETASE GENE; HUMAN GLIOBLASTOMA CELLS; MESSENGER-RNA STABILITY; CYCLIC-AMP; FACTOR-BETA; EXPRESSION AB Mesangial cells express platelet-derived growth factor (PDGF) A- and B-chain mRNA and release PDGF. Several polypeptide growth factors, including PDGF itself, induce PDGF A- and B-chain mRNA abundance. To understand the molecular mechanisms associated with the changes in mRNA abundance, we measured the effects of PDGF BB homodimer on PDGF A- and B-chain gene transcription in cultured mesangial cells. The data demonstrate 2- and 4-fold increases in PDGF A-chain gene transcription in response to PDGF BB homodimer at 5 and 24 h time points respectively. PDGF B-chain gene transcription was also induced approximately 3-fold at 2, 5 and 24 h time points in response to treatment with PDGF BB homodimer. The effect of PDGF BB on the half-life of PDGF A- as well as PDGF B-chain mRNA was measured directly by the pulse-chase method. There was no effect on PDGF A-chain mRNA half-life whereas PDGF B-chain mRNA half-life was increased 1.5-fold. These studies indicate that, in human mesangial cells, the increase in the levels of PDGF A- and B-chain mRNA in response to PDGF-receptor(s) activation is mediated at the level of gene transcription. In addition, the regulation of PDGF B- but not PDGF A-chain gene involves increased mRNA stability. Mesangial cells are a useful model for studying molecular mechanisms of PDGF-gene regulation in non-transformed human cells. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP BHANDARI, B (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,SAN ANTONIO,TX 78284, USA. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK 43988] NR 34 TC 8 Z9 8 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 JAN 15 PY 1994 VL 297 BP 385 EP 388 PN 2 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MT892 UT WOS:A1994MT89200021 PM 8297346 ER PT J AU SUHL, J SIMONS, P REEDY, T GARRICK, T AF SUHL, J SIMONS, P REEDY, T GARRICK, T TI MYTH OF SUBSTITUTED JUDGMENT - SURROGATE DECISION-MAKING REGARDING LIFE-SUPPORT IS UNRELIABLE SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID PROXY AB Objective: To identify factors predicting the accuracy of surrogate decision making in life support decisions. Design: Questionnaire. Setting: Urban Veterans Affairs hospital. Patients and Design: Fifty hospitalized patients and their chosen surrogates were given questionnaires describing life support modalities and four common medical scenarios in which life support would be contemplated. An additional 50 patients also completed the questionnaire. Patients gave their choices of life support in the different scenarios. Surrogates guessed the patients' answers (substituted judgment). Details of the patient-surrogate relationship were asked. Patients completed a depression inventory. Main Outcome Measure: Patient-surrogate agreement. Main Results: Surrogates correctly guessed patients' wishes about life support overall on 59.3% of the questions, not better than random chance (kappa=.09). The only predictor of accurate surrogate decision making was specific discussion between patient and surrogate about life support. Secondary Results: Patients had an overall low desire for life support (35%), and a majority favored euthanasia under some circumstances (62%). There was no relationship between depression score and desire for life support. Conclusions: Substituted judgment by surrogates is not more accurate than random chance. Discussion between patient and surrogate about life support correlated with more accurate substituted judgment. C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT, LOS ANGELES, CA USA. NR 16 TC 144 Z9 144 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD JAN 10 PY 1994 VL 154 IS 1 BP 90 EP 96 DI 10.1001/archinte.154.1.90 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA MQ203 UT WOS:A1994MQ20300011 PM 8267493 ER PT B AU OBRIEN, CP JONES, RT AF OBRIEN, CP JONES, RT BE Pletscher, A Ladewig, D TI METHODOLOGICAL ISSUES IN THE EVALUATION OF A MEDICATION FOR ITS POTENTIAL BENEFITS IN ENHANCING PSYCHOTHERAPY SO 50 YEARS OF LSD: CURRENT STATUS AND PERSPECTIVES OF HALLUCINOGENS LA English DT Proceedings Paper CT Symposium of the Swiss-Academy-of-Medical-Science - 50-Years of LSD - Current Status and Perspectives of Hallucinogens CY OCT 21-22, 1993 CL LUGANO-AGNO, SWITZERLAND SP SWISS ACAD MED SCI C1 UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA BN 1-85070-569-0 PY 1994 BP 213 EP 221 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA BC46P UT WOS:A1994BC46P00015 ER PT J AU STROOP, WG BANKS, MC AF STROOP, WG BANKS, MC TI HERPES-SIMPLEX VIRUS TYPE-1 STRAIN KOS-63 DOES NOT CAUSE ACUTE OR RECURRENT OCULAR DISEASE AND DOES NOT REACTIVATE GANGLIONIC LATENCY IN-VIVO SO ACTA NEUROPATHOLOGICA LA English DT Article DE CORNEA; HSV-1; HERPESVIRUS; KERATITIS OCULAR DISEASE ID CENTRAL-NERVOUS-SYSTEM; INSITU HYBRIDIZATION; INFECTED NEURONS; DELETION MUTANT; RABBIT; MOUSE; TRANSCRIPT; ENCEPHALITIS; MODEL; RNA AB The virological, clinical, and histopathological manifestations of acute and experimentally reactivated infections of eyes and trigeminal ganglia have been studied following intranasal infection of rabbits with herpes simplex virus type 1 (strain KOS-63). All animals shed virus in nasal secretions, but only three shed virus in tear film during the first 12 days of infection. No animal developed clinical or histological evidence of corneal or retinal ocular disease at any time after infection. KOS-63 established trigeminal ganglionic latency; viral RNA, restricted to neuronal nuclei, was detected by in situ hybridization, and virus was recovered from co-cultivation cultures of nervous tissue, but not from cell-free homogenates. Reactivation of latent trigeminal ganglionic infection was attempted by intravenous administration of cyclophosphamide, followed by dexamethasone 24 h later. Injection of the drugs failed to reactivate KOS-63 latency; no animal shed virus in nasal or ocular secretions, and no animal developed gross or microscopic corneal lesions. In addition, viral antigens were not detected by immunofluorescence microscopy in ganglia from rabbits subjected to the drug protocol, and virus was only recovered from ganglia by in vitro co-cultivation reactivation techniques. The failure of KOS-63 to reactivate was not due to an inherent failure of populate and infect the ganglion, because the virus did not reactivate from ganglia that contained many latently infected cells. These studies demonstrate that, although KOS-63 is neuroinvasive and capable of establishing latency, it is virtually nonvirulent for the eye, and cannot be reactivated by a systemic immunosuppressive trigger known to reactivate other HSV-1 strains. C1 BAYLOR COLL MED,DEPT NEUROL,DEPT OPHTHALMOL,DIV MOLEC VIROL,HOUSTON,TX 77030. RP STROOP, WG (reprint author), BAYLOR COLL MED,CULLEN EYE INST,DEPT VET AFFAIRS MED CTR,OPHTHALMOL RES LAB,6501 FANNIN NC200,HOUSTON,TX 77030, USA. FU NIDCD NIH HHS [1R01 DC1706] NR 41 TC 13 Z9 13 U1 2 U2 4 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PD JAN PY 1994 VL 87 IS 1 BP 14 EP 22 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA MP030 UT WOS:A1994MP03000003 PM 8140892 ER PT J AU NUECHTERLEIN, KH DAWSON, ME GREEN, MF AF NUECHTERLEIN, KH DAWSON, ME GREEN, MF TI INFORMATION-PROCESSING ABNORMALITIES AS NEUROPSYCHOLOGICAL VULNERABILITY INDICATORS FOR SCHIZOPHRENIA SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE SCHIZOPHRENIA; VULNERABILITY; INFORMATION PROCESSING; ATTENTION; MEMORY; NEUROPSYCHOLOGY ID CONTINUOUS PERFORMANCE-TEST; SUSTAINED ATTENTION; STARTLE-REFLEX; BACKWARD-MASKING; CHILDREN; RISK; DISORDERS AB Studies of schizophrenic patients in psychotic and clinically remitted states and of biological relatives indicate that subtle anomalies in information processing may be critical components of neuropsychological vulnerability to schizophrenia. We describe a conception of possible abnormalities and several recent strategies to differentiate these possibilities. Within Continuous Performance Test conditions, varying the perceptual load vs. the active, working memory load yields a distinction between a stable vulnerability factor across clinical states and a potential mediating vulnerability factor. Specialized backward masking paradigms offer ways to separate two initial sensory-perceptual processes from attentional shifting processes. Top-down attentional influences on sensorimotor gating allow examination of the role of central executive processes in modulating early sensory processes. Initial results are discussed. C1 UNIV SO CALIF, DEPT PSYCHOL, LOS ANGELES, CA 90089 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. RP UNIV CALIF LOS ANGELES, DEPT PSYCHIAT & BIOBEHAV SCI, 300 UCLA MED PLAZA, LOS ANGELES, CA 90024 USA. NR 40 TC 98 Z9 100 U1 1 U2 3 PU WILEY PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0001-690X EI 1600-0447 J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PY 1994 VL 90 SU 384 BP 71 EP 79 DI 10.1111/j.1600-0447.1994.tb05894.x PG 9 WC Psychiatry SC Psychiatry GA PW216 UT WOS:A1994PW21600011 PM 7879647 ER PT J AU MARDER, SR AF MARDER, SR TI THE ROLE OF DOSAGE AND PLASMA-LEVELS IN NEUROLEPTIC RELAPSE PREVENTION SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article; Proceedings Paper CT Lundbeck Symposium on the Role of Compliance in the Treatment of Schizophrenia CY NOV 12-13, 1993 CL COPENHAGEN, DENMARK SP LUNDBECK A S DE SCHIZOPHRENIA; ANTIPSYCHOTIC; FLUPHENAZINE; HALOPERIDOL ID FLUPHENAZINE DECANOATE; SCHIZOPHRENICS; THERAPY AB Recent research has focused on strategies for optimizing the long-term treatment of schizophrenia by decreasing relapse rates at the same time that antipsychotic drug side effects are minimized. Studies have suggested that substantially lowering the dose by as much as 80% can result in fewer side effects, less anxiety and depression, and improved compliance. However, dosage reduction can also lead to increases in the vulnerability to mild exacerbation of psychosis. A recent study from our laboratory indicates that supplementing low dose depot antipsychotic medications with oral supplementation at the time of prodromal symptoms may improve the safety of low doses. For patients who are treated with fluphenazine decanoate, monitoring plasma fluphenazine levels may also help to minimize relapse rates. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP MARDER, SR (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV 116A,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 9 TC 8 Z9 8 U1 6 U2 6 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PY 1994 VL 89 SU 382 BP 25 EP 27 DI 10.1111/j.1600-0447.1994.tb05861.x PG 3 WC Psychiatry SC Psychiatry GA NU464 UT WOS:A1994NU46400005 ER PT B AU YOSHIKAWA, TT AF YOSHIKAWA, TT BE Powers, DC Morley, JE Coe, RM TI INFECTIOUS DISEASES, IMMUNITY, AND AGING - PERSPECTIVES AND PROSPECTS SO AGING, IMMUNITY, AND INFECTION LA English DT Proceedings Paper CT Aging, Immunity, and Infection Symposium CY SEP, 1992 CL ST LOUIS, MO C1 US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE,WASHINGTON,DC. NR 0 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER PUBL CO PI NEW YORK PA 536 BROADWAY, NEW YORK, NY 10012 BN 0-8261-8180-5 PY 1994 BP 1 EP 11 PG 11 WC Geriatrics & Gerontology; Immunology SC Geriatrics & Gerontology; Immunology GA BB77C UT WOS:A1994BB77C00001 ER PT J AU RABINOWITZ, JL BRAND, JG COWART, BJ ENGEN, RL AF RABINOWITZ, JL BRAND, JG COWART, BJ ENGEN, RL TI HEPATIC LIPID PROFILES IN MINIATURE PIGS AFTER ALCOHOL FEEDING SO ALCOHOL LA English DT Article DE ALCOHOL; LIVER LIPIDS; NEUTRAL LIPIDS; POLAR LIPIDS; PHOSPHOLIPIDS; SATURATED FATTY ACIDS; UNSATURATED FATTY ACIDS; MINIATURE PIG AB Changes in lipid profiles have not been reported for the known increases in total lipid content in livers of alcoholics. We have reported a lowering of the P-oxidative capacity of alcoholic livers, and therefore would expect a lower turnover of fatty acids in these livers, and thus a change in lipid profile. The percentage composition of saturated and unsaturated fatty acids in the liver of alcohol-fed miniature pigs versus the controls, as well as the function of distance from the main hepatic vein, have both been determined in this study involving the feeding of ethanol for one year. Livers of alcohol-fed miniature pigs contained more total lipids than those of controls. Results also indicated significantly higher percentages of free fatty acids and triglycerides in the alcohol-fed miniature pigs, and also an increase in percentage total neutral lipids. The effect of distance from the main blood source (and therefore oxygenation) gave a fatty acid profile that showed an increase in the ratio of saturated to unsaturated fatty acids with increasing distance from the right hepatic vein. This change in ratio was independent of alcohol feeding. C1 UNIV PENN,SCH DENT MED,PHILADELPHIA,PA 19104. MONELL CHEM SENSES CTR,PHILADELPHIA,PA 19104. IOWA STATE UNIV,DEPT VET PHYSIOL,AMES,IA 50011. RP RABINOWITZ, JL (reprint author), VET AFFAIRS MED CTR,UNIV & WOODLANDS AVE,PHILADELPHIA,PA 19104, USA. NR 27 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0741-8329 J9 ALCOHOL JI Alcohol PD JAN-FEB PY 1994 VL 11 IS 1 BP 25 EP 29 DI 10.1016/0741-8329(94)90007-8 PG 5 WC Substance Abuse; Pharmacology & Pharmacy; Toxicology SC Substance Abuse; Pharmacology & Pharmacy; Toxicology GA MV745 UT WOS:A1994MV74500005 PM 8142063 ER PT J AU WORNER, TM AF WORNER, TM TI PROPRANOLOL VERSUS DIAZEPAM IN THE MANAGEMENT OF THE ALCOHOL-WITHDRAWAL SYNDROME - DOUBLE-BLIND CONTROLLED TRIAL SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID CLINICAL MANAGEMENT; CEREBROSPINAL-FLUID; DRUG-THERAPY; IV-CLONIDINE; BENZODIAZEPINES; INTOXICATION; LOFEXIDINE AB Thirty-seven male alcoholics admitted electively for detoxification were randomized to treatment with either diazepam or propranolol. Subjects were comparable both in age and in duration and quantity of alcohol consumed. Admission laboratory parameters did not distinguish between the groups. Eleven subjects required no medication to control withdrawal signs/symptoms. Both groups showed improvement in blood pressure, pulse, and withdrawal tremor. None of the subjects randomized to diazepam manifested withdrawal seizures or hallucinations. By contrast, one subject in the propranolol group had a single withdrawal seizure. Another subject manifested increasing withdrawal that required parenteral paraldehyde treatment. Thus, this study confirms that a significant number of subjects admitted electively for alcohol withdrawal can be managed without medication. Minor tranquilizers still remain the ''gold standard'' for management of the withdrawal syndrome. C1 BRONX VET ADM MED CTR,DEPT MED,BRONX,NY. MT SINAI SCH MED,DEPT MED,NEW YORK,NY. NR 29 TC 25 Z9 25 U1 3 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1994 VL 20 IS 1 BP 115 EP 124 DI 10.3109/00952999409084061 PG 10 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA MY615 UT WOS:A1994MY61500009 PM 8192130 ER PT J AU TSUANG, JW SHAPIRO, E SMITH, TL SCHUCKIT, MA AF TSUANG, JW SHAPIRO, E SMITH, TL SCHUCKIT, MA TI DRUG-USE AMONG PRIMARY ALCOHOLIC VETERANS SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID TREATMENT PROGRAM; YOUNG ADULTHOOD; PATTERNS; ABUSE; PROGRESSION; ADOLESCENCE; RELAPSE; INVOLVEMENT; POPULATION; DEPENDENCE AB Many people with alcohol dependence use other drugs. However, not much is known about the relationship between their past drug use (not necessarily dependence) and their prognosis following treatment. The goal of this study is first to determine the drug use rates among primary alcoholic men and then to evaluate the possible relationship between past drug use and future alcohol or drug use relapse. As a result, 630 primary alcoholic veterans were recruited from a 28-day inpatient Alcohol and Drug Treatment Program at the San Diego VA Medical Center. Among them, almost two-thirds also had a history of drug use. Subjects were divided into the following four groups which were determined by their lifetime drug use histories: Group I (N = 226) consisted of drug abstainers, Group 2 (N = 142) was made up of alcoholics who had used only marijuana, Group 3 (N = 210) contained stimulant users who had never used opiates, and Group 4 (N = 52) included all opiate users. Comparisons of the four groups at a 3-month follow-up revealed that alcoholic men who had a history of stimulant or opiate use (Groups 3 and 4) were more likely to have had a drug use relapse. However, the four groups had similar alcohol relapse rates. C1 VET AFFAIRS MED CTR,DEPT PSYCHIAT,PSYCHIAT SERV 116A,SAN DIEGO,CA 92161. UNIV CALIF SAN DIEGO,SCH MED,SAN DIEGO,CA 92103. W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. FU NIAAA NIH HHS [NIAAA 05226, NIAAA 08401, NIAAA 08403] NR 35 TC 11 Z9 11 U1 4 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1994 VL 20 IS 4 BP 483 EP 493 DI 10.3109/00952999409109185 PG 11 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA PN615 UT WOS:A1994PN61500006 PM 7832181 ER PT J AU CRAIG, DJ AF CRAIG, DJ TI JOHNNY COMES HOME SO AMERICAN JOURNAL OF NURSING LA English DT Editorial Material RP CRAIG, DJ (reprint author), PORTLAND VET AFFAIRS MED CTR,NURSING HOME CARE UNIT,VANCOUVER,WA, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-936X J9 AM J NURS JI Am. J. Nurs. PD JAN PY 1994 VL 94 IS 1 BP 50 EP 51 PG 2 WC Nursing SC Nursing GA MQ529 UT WOS:A1994MQ52900020 PM 8273816 ER PT J AU LAKE, FR DEMPSEY, EC SPAHN, JD RICHES, DWH AF LAKE, FR DEMPSEY, EC SPAHN, JD RICHES, DWH TI INVOLVEMENT OF PROTEIN-KINASE-C IN MACROPHAGE ACTIVATION BY POLY(I-CENTER-DOT-C) SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE COMPLEMENT BF; INTERFERON-BETA; TUMOR NECROSIS FACTOR-ALPHA ID TUMOR-NECROSIS-FACTOR; MURINE PERITONEAL-MACROPHAGES; MESSENGER-RNA EXPRESSION; TUMORICIDAL ACTIVITY; INTERFERON-BETA; BACTERIAL LIPOPOLYSACCHARIDE; DOWN-REGULATION; PHORBOL ESTERS; CALCIUM; GAMMA AB The expression of cytocidal activity is initiated by the interaction of macrophages with priming [e.g., interferon (IFN)] and triggering stimuli (polyinosinic-polycytidylic acid). We have shown that the triggering step can be initiated in a Ca2+-dependent fashion and hypothesized that protein kinase C (PKC) may couple the Ca2+ signal to the expression of a gene product, Bf, that accompanies the expression of macrophage cytocidal activity. Exposure of IFN-primed macrophages to polyinosinic-polycytidylic acid in the presence of the PKC inhibitors H-7 or sphingosine or after downregulation of PKC with phorbol myristate acetate markedly inhibited Bf synthesis. Western blots of macrophage lysates revealed the presence of the alpha-, delta-, and zeta-isozymes of PKC, and all were found to be downregulated by phorbol myristate acetate. Inhibition of PKC also prevented the increase in IFN-beta mRNA levels and partially blocked the response to IFN-beta. These data suggest that the alpha-, delta-, and zeta-isozymes of PKC are involved in signaling leading to Bf expression and that the level of involvement is restricted to the induction and response to IFN-beta. C1 DENVER VET AFFAIRS MED CTR,DEPT MED,DIV PULM SCI,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,CARDIOVASC PULM RES LAB,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT BIOCHEM BIOPHYS & GENET,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT PHARMACOL,DENVER,CO 80262. RP LAKE, FR (reprint author), NATL JEWISH CTR IMMUNOL & RESP MED,DEPT PEDIAT,DIV BASIC SCI,DENVER,CO 80206, USA. FU DRS NIH HHS [BRSG-05357]; NCI NIH HHS [CA-50107] NR 37 TC 11 Z9 11 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP C134 EP C142 PN 1 PG 9 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100015 PM 8304411 ER PT J AU PIQUERAS, AI SOMERS, M HAMMOND, TG STRANGE, K HARRIS, HW GAWRYL, M ZEIDEL, ML AF PIQUERAS, AI SOMERS, M HAMMOND, TG STRANGE, K HARRIS, HW GAWRYL, M ZEIDEL, ML TI PERMEABILITY PROPERTIES OF RAT RENAL LYSOSOMES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE KIDNEY; MEMBRANE PERMEABILITY; PROTON ADENOSINE-TRIPHOSPHATASE; WATER PERMEABILITY; WATER CHANNELS ID LIPID BILAYER-MEMBRANES; CELL CHIP28 PROTEIN; WATER CHANNELS; TOAD BLADDER; PROTON PUMP; NONELECTROLYTE PERMEATION; URINARY-BLADDER; H+-ATPASE; VESICLES; INHIBITORS AB Although lysosomes maintain large pH gradients and may be subjected to significant osmotic gradients in vivo, little is known about their passive permeability properties. In recent studies, vacuolar H+-adenosinetriphosphatases (ATPases), such as those found in lysosomes, have been suggested to act as water channels. In addition, the erythrocyte and proximal tubule water channel CHIP28 is present on the plasma membrane of proximal tubule cells and may undergo endocytosis so that it is incorporated in lysosomes. We therefore examined water, proton, and small nonelectrolyte permeabilities in freshly purified lysosomes from rat renal proximal tubule. Lysosomes were purified by differential and Percoll gradient centrifugation. The preparation contained only lysosomes when examined by electron microscopy. Moreover, analysis by flow cytometry showed virtually all particles to be positive for acid phosphatase and cathepsin B activities. Permeabilities were measured on a stopped-flow fluorimeter by monitoring the self-quenching or pH-sensitive quenching of entrapped fluorescein derivatives. Osmotic water permeability (P-f) averaged 0.011 +/- 0.003 cm/s (n = 6), a value similar to that of biological membranes containing water channels. However, P-f was insensitive to the organic mercurial reagent p-chloromercuribenzene-sulfonate and to HgCl2 and exhibited an activation energy of 10.8 +/- 0.8 kcal/mol. These results indicate that water flux in lysosomes occurred via the lipid bilayer, and not via water channels. Addition of ATP led to lysosomal acidification (proton flux = 4.6 +/- 0.8 x 10(-11) mmol H+.s(-1).cm(-2)), which was completely inhibited by 0.1 mu M bafilomycin. P-f was insensitive to this agent as was the passive proton permeability (0.36 +/- 0.18 cm/s, n = 4). Permeabilities to small nonelectrolytes varied in proportion to the oil-water partition coefficient, confirming the applicability of Overton's rule to lysosomes. We conclude that proximal tubular lysosomes exhibit high P-f, which occurs via the lipid bilayer and not via vacuolar H+-ATPase. C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. BIOPURE CORP,BOSTON,MA 02111. VET ADM MED CTR W ROXBURY,BOSTON,MA 02132. UNIV WISCONSIN,MED & RES SERV,WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP PIQUERAS, AI (reprint author), CHILDRENS HOSP MED CTR,DEPT MED,BOSTON,MA 02111, USA. FU NIDDK NIH HHS [DK-46117, DK-43955, DK-38744] NR 55 TC 18 Z9 19 U1 1 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP C121 EP C133 PN 1 PG 13 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100014 PM 8304410 ER PT J AU JAFFA, AA LEROITH, D ROBERTS, CT RUST, PF MAYFIELD, RK AF JAFFA, AA LEROITH, D ROBERTS, CT RUST, PF MAYFIELD, RK TI INSULIN-LIKE GROWTH-FACTOR-I PRODUCES RENAL HYPERFILTRATION BY A KININ-MEDIATED MECHANISM SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE RENAL KALLIKREIN; KININ RECEPTOR ANTAGONIST; RENAL VASODILATION ID GLOMERULAR MESANGIAL CELLS; DIETARY-PROTEIN; FILTRATION RATE; PLASMA-FLOW; KIDNEY; KALLIKREIN; EXPRESSION; BINDING; RNA AB Insulin-like growth factor-I (IGF-I) infusion into rats and humans reduces renal vascular resistance and raises glomerular filtration rate (GFR) and renal plasma flow (RPF). To investigate whether kinins mediate the renal vasodilatory effects of IGF-I, we infused rats with IGF-I alone or in the presence of a B-2 kinin receptor antagonist. Left kidney GFR, RPF, and kinin excretion were measured during infusion of vehicle and subsequently during 60-min infusion ofIGF-I or IGF-I plus kinin antagonist. IGF-I was given as a bolus (150 mu g/kg body wt), followed by infusion at a rate of 8.3 mu g.kg(-1).min(-1) for 60 min. The kinin antagonist was infused at a dose of 1 mu g.kg(-1).min(-1) for 60 min before the start of IGF-I infusion. GFR and RPF increased significantly after IGF-I infusion was begun, from baseline levels of 1.70 +/- 0.12 and 6.21 +/- 0.34 to 2.12 +/- 0.11 and 7.91 +/-: 0.29 ml/min, respectively, at 20 min (P < 0.001). This effect was maintained throughout 60 min of infusion. The increase in GFR and RPF was associated with a marked rise in urinary kinin excretion, from a baseline of 8.51 +/- 6.7 to 24.7 +/- 6.7 pg/min at 20 min and 40.3 +/- 10.4 pg/min at 40 min (P < 0.001). Pretreatment with the kinin receptor antagonist blocked the rise in GFR and RPF in response to IGF-I. These data suggest that the renal vasodilatory effect of IGF-I is mediated by kinins. C1 MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT BIOMETRY,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. RP JAFFA, AA (reprint author), MED UNIV S CAROLINA,DEPT MED,DIV ENDOCRINOL DIABET & METAB,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 27 TC 26 Z9 26 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP F102 EP F107 PN 2 PG 6 WC Physiology SC Physiology GA NA598 UT WOS:A1994NA59800096 PM 8304475 ER PT J AU EUBANKS, PJ SAWICKI, MP SAMARA, GJ GATTI, R NAKAMURA, Y TSAO, D JOHNSON, C HURWITZ, M WAN, YJY PASSARO, E AF EUBANKS, PJ SAWICKI, MP SAMARA, GJ GATTI, R NAKAMURA, Y TSAO, D JOHNSON, C HURWITZ, M WAN, YJY PASSARO, E TI PUTATIVE TUMOR-SUPPRESSOR GENE ON CHROMOSOME-11 IS IMPORTANT IN SPORADIC ENDOCRINE TUMOR-FORMATION SO AMERICAN JOURNAL OF SURGERY LA English DT Article ID NEOPLASIA TYPE-1; PARATHYROID TUMORS; SMALL REGION; GASTRINOMA; ALLELES; CANCER; HETEROZYGOSITY; IDENTIFICATION; LOCALIZATION; ASSOCIATION AB Endocrine tumors arising sporadically or as a manifestation of the multiple endocrine neoplasia type I syndrome (MEN I) have been shown to have mutations on chromosome 11. These mutations can be detected at the molecular level by loss of heterozygosity (LOH) for DNA markers from chromosome 11. This study represents one of the largest collections of sporadic endocrine tumors in which LOH was systematically assessed on chromosome 11 for the loci flanking the proposed MEN I region. DNA was isolated from 39 endocrine tumors and probed with ? DNA probes spanning the region of chromosome 11q13 from the loci PYGM to INT-2. Eleven tumors demonstrated LOH at any two loci in this region. The remaining 28 tumors showed no LOH or were noninformative at these loci. Thus, nearly 30% of these tumors showed LOH in the region (from PYGM to INT-2) that is thought to contain the MEN I gene(s). Previous studies of sporadic endocrine tumors have suggested that these tumors may arise via the same mechanism as tumors of the MEN I syndrome. Namely, these sporadic tumors are thought to result from mutations leading to genetic loss on the long arm of chromosome 11, thereby inactivating a possible tumor-suppressor gene (or genes). These findings strongly support the hypothesis that sporadic pancreatic endocrine tumors share a similar etiology of tumorigenesis with tumors of the MEN I syndrome, which principally involves deletion of a tumor-suppressor element (or elements). C1 UNIV CALIF LOS ANGELES, VET ADM WADSWORTH MED CTR W112, HARBOR MED CTR, DEPT SURG, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, HARBOR MED CTR, DEPT PATHOL, LOS ANGELES, CA USA. W LOS ANGELES VAMC, DEPT SURG, LOS ANGELES, CA USA. W LOS ANGELES VAMC, DEPT PATHOL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. ALBERTA CHILDRENS PROV GEN HOSP, DEPT GENET, CALGARY DIV BIOCHEM, CALGARY, AB, CANADA. CANC INST, TOKYO, TOKYO, JAPAN. NR 29 TC 59 Z9 59 U1 0 U2 1 PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC PI BRIDGEWATER PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD JAN PY 1994 VL 167 IS 1 BP 180 EP 185 DI 10.1016/0002-9610(94)90071-X PG 6 WC Surgery SC Surgery GA MV407 UT WOS:A1994MV40700026 PM 7906100 ER PT J AU ALBERT, MM RUSNAK, J LUTHER, MF GRAYBILL, JR AF ALBERT, MM RUSNAK, J LUTHER, MF GRAYBILL, JR TI TREATMENT OF MURINE CRYPTOSPORIDIOSIS WITH ANTICRYPTOSPORIDIAL IMMUNE RAT BILE SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID BOVINE COLOSTRUM; GIARDIA-MURIS; MONOCLONAL-ANTIBODIES; NEONATAL MICE; NUDE-MICE; PARVUM; IMMUNOCOMPETENT; NEUTRALIZATION; SPOROZOITES; PROTOZOAN AB Persistent cryptosporidiosis was established in nu/nu BALB/c mice by oral inoculation with Cryptosporidium parvum oocysts. The model was used to determine the impact of anticryptosporidial immune rat bile on the resolution of the disease. Presence of C. parvum-specific IgA in the immune rat bile was determined by enzyme-linked immunosorbent assay. Infection of mice was verified by stool analysis for oocysts and by hematoxylin and eosin-stained intestinal sections from control mice (infected but untreated). Efficacy of treatment was determined in control and treated mice by analysis of identical, hematoxylin and eosin-stained sections of the small intestine and cecum. Semiquantitative comparisons were made by determining the percent of crypts infected with Cryptosporidium organisms. The scores of treated mice were significantly lower then controls. Microscopic analysis of intestinal sections showed less villus atrophy, crypt hyperplasia, and fewer organisms per crypt in the immune bile-treated mice than in controls. These results support a role for humoral immunity in the eradication of cryptosporidiosis. C1 WILFORD HALL USAF MED CTR,DEPT INFECT DIS,LACKLAND AFB,TX 78236. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. RP ALBERT, MM (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT RES,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 35 TC 6 Z9 7 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD JAN PY 1994 VL 50 IS 1 BP 112 EP 119 PG 8 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA MW296 UT WOS:A1994MW29600017 PM 8304566 ER PT B AU SMITH, ME FEILD, TC AF SMITH, ME FEILD, TC GP AMER STAT ASSOC TI Veterans and VA system users classified by federal poverty guidelines and thresholds and the VA means test SO AMERICAN STATISTICAL ASSOCIATION 1994 PROCEEDINGS OF THE GOVERNMENT STATISTICS SECTION LA English DT Proceedings Paper CT Annual Meeting of the American-Statistical-Association, Government-Statistics-Section CY AUG 13-18, 1994 CL TORONTO, CANADA SP Amer Stat Assoc, Govt Stat Sect DE POVERTY; HEALTH CARE REFORM C1 US DEPT VET AFFAIRS,WASHINGTON,DC 20420. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-11-X PY 1994 BP 28 EP 33 PG 6 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA BD50Y UT WOS:A1994BD50Y00010 ER PT J AU EBERT, SC CRAIG, WA AF EBERT, SC CRAIG, WA TI RETAIN INTERMITTENT DOSING OF CARBAPENEMS - REPLY SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Letter ID IMIPENEM C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. RP EBERT, SC (reprint author), UNIV WISCONSIN,MERITER HOSP,SCH PHARM,DEPT PHARM,MADISON,WI 53715, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JAN PY 1994 VL 38 IS 1 BP 159 EP 160 PG 2 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA MP524 UT WOS:A1994MP52400030 ER PT J AU FOSSEY, MD HAMNER, MB AF FOSSEY, MD HAMNER, MB TI CLONAZEPAM-RELATED SEXUAL DYSFUNCTION IN MALE VETERANS WITH PTSD SO ANXIETY LA English DT Note DE ALPRAZOLAM; ANTIDEPRESSANTS; ANXIETY; BENZODIAZEPINES; DIAZEPAM; LORAZEPAM ID POSTTRAUMATIC-STRESS-DISORDER; PANIC DISORDER; SOCIAL PHOBIA; ALPRAZOLAM; AGORAPHOBIA; THERAPY AB Medication-induced sexual dysfunction can significantly interfere with patients' quality of life and lead to poor compliance. This retrospective study examined the records of 100 male veterans with post-traumatic stress disorder (PTSD) selected in alphabetical order from an active treatment file of 230 patients. Forty-two patients had received clonazepam (mean maximum dose: 3.4 +/- 1.6 mg/day) at some point during their treatment. Of these, 18 (42.9%) complained of significant sexual dysfunction (primarily erectile dysfunction). Eighty-four patients received diazepam (mean maximum dose: 52.1 +/- 29.7 mg/day), nine received alprazolam (mean maximum dose: 5.2 +/- 2.8 mg/day) and eight received lorazepam (mean maximum dose: 3.8 +/- 2.4 mg/day). None of these patients complained of sexual dysfunction during treatment with these three other benzodiazepines. Our findings suggest that benzodiazepines, particularly clonazepam in the current study, can be a cause of sexual dysfunction in many male patients. Prospective studies comparing the overall clinical utility of various benzodiazepines are indicated in this and other clinic populations. (C) 1995 Wiley-Liss, Inc. C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. RP FOSSEY, MD (reprint author), RALPH H JOHNSON VA MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. NR 28 TC 18 Z9 18 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 5 BP 233 EP 236 PG 4 WC Psychiatry; Psychology SC Psychiatry; Psychology GA RK515 UT WOS:A1994RK51500007 PM 9160580 ER PT J AU KAGAN, BL SOKOLOV, Y AF KAGAN, BL SOKOLOV, Y TI USE OF LIPID BILAYER-MEMBRANES TO DETECT PORE FORMATION BY TOXINS SO BACTERIAL PATHOGENESIS, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID FRAGMENTED SARCOPLASMIC-RETICULUM; PLANAR PHOSPHOLIPID-BILAYERS; DIPHTHERIA-TOXIN; ELECTRICAL-PROPERTIES; CHANNELS; INSERTION; MECHANISM; FUSION C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,BRAIN RES INST,LOS ANGELES,CA 90024. PURDUE UNIV,LAB ANIM PROGRAM,W LAFAYETTE,IN 47907. RP KAGAN, BL (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024, USA. FU NIMH NIH HHS [MH43433] NR 26 TC 12 Z9 12 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 235 BP 691 EP 705 PG 15 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88R UT WOS:A1994BA88R00056 PM 7520122 ER PT J AU SCHROEDER, MM HANDELSMAN, L TORRES, L DORFMAN, D RINALDI, P JACOBSON, J WIENER, J RITTER, W AF SCHROEDER, MM HANDELSMAN, L TORRES, L DORFMAN, D RINALDI, P JACOBSON, J WIENER, J RITTER, W TI EARLY AND LATE COGNITIVE EVENT-RELATED POTENTIALS MARK STAGES OF HIV-1 INFECTION IN THE DRUG-USER RISK GROUP SO BIOLOGICAL PSYCHIATRY LA English DT Article DE EVENT-RELATED POTENTIALS; HIV-1 INFECTION; AIDS; DEMENTIA; ADC ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS DEMENTIA COMPLEX; ELECTROPHYSIOLOGICAL DIFFERENCES; DISCRIMINATION TASKS; MISMATCH NEGATIVITY; PARKINSONS-DISEASE; BRAIN; MANIFESTATIONS; P300; SCHIZOPHRENIA AB HIV-1 (Human immunodeficiency virus) infection of the brain causes delays in auditory event-related potential (ERP) components. We recorded auditory ERPs from 38 former parenteral drug users (PDUs) at three stages of HIV-1 infection: seronegative; seropositive; stage II; and seropositive, stage IV. There were five response conditions: Go Nogo, Count, Simple Response, Simple Count, and Ignore. P3 peak latencies were significantly delayed and P3 amplitudes were significantly reduced for all seropositives, including asymptomatics, when compared to PDU seronegative controls. In contrast, the P1 and N1 peak latency measures were delayed only for seropositives with acquired immunodeficiency syndrome (AIDS) qualifying illnesses. There was a significant negative correlation between the CD4 count and the latency of P1, N1, and the MMN. Also, increased P1 and N1 amplitudes correlated with indices of disease progression (Choice RT and CD4 counts, respectively). The results extend previous findings by clarifying the pattern of auditory ERP markers of disease progression. Early, as well as late, brain involvement caused by HIV-1 is marked by delays and decreased amplitudes in cognitive components. In addition, late brain involvement is marked by delays and increased amplitudes in specific, automatic, and/or obligatory components. C1 VET AFFAIRS MED CTR,NEUROL SERV,BRONX,NY. VET AFFAIRS MED CTR,INFECT DIS SERV,BRONX,NY. MT SINAI SCH MED,NEW YORK,NY. ALBERT EINSTEIN COLL MED,DEPT NEUROL,BRONX,NY. ALBERT EINSTEIN COLL MED,DEPT NEUROSCI,BRONX,NY. CUNY,LEHMAN COLL,DEPT PSYCHOL,NEW YORK,NY. RP SCHROEDER, MM (reprint author), BRONX VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 65 TC 24 Z9 24 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JAN 1 PY 1994 VL 35 IS 1 BP 54 EP 69 DI 10.1016/0006-3223(94)91168-1 PG 16 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MW336 UT WOS:A1994MW33600010 PM 8167205 ER PT J AU BYRD, TF AF BYRD, TF TI CYTOKINES AND LEGIONELLOSIS SO BIOTHERAPY LA English DT Article DE FERRITIN; INTERFERON GAMMA; IRON; LACTOFERRIN; MONOCYTE; TRANSFERRIN ID COLONY-STIMULATING FACTOR; RECOMBINANT INTERFERON-GAMMA; HUMAN-MONOCYTES INHIBIT; INTRACELLULAR MULTIPLICATION; LEGIONNAIRES-DISEASE; MONONUCLEAR PHAGOCYTES; PNEUMOPHILA; IRON; MACROPHAGES; TRANSFERRIN AB Recent studies have led to an enhanced understanding of the role of cell-mediated immunity and cytokines in Legionnaires' disease. In particular, the effect of interferon gamma on human mononuclear phagocyte iron metabolism and the role of iron availability in Legionella pneumophila intracellular multiplication in human monocytes has been elucidated. With this knowledge it is now possible to develop treatment strategies for Legionnaires' disease using interferon gamma and/or agents affecting human mononuclear phagocyte iron metabolism. RP BYRD, TF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,WILSHIRE & SAWTELLE,BLDG 500,ROOM 4469,W111F,LOS ANGELES,CA 90073, USA. NR 21 TC 7 Z9 7 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0921-299X J9 BIOTHERAPY JI Biotherapy PY 1994 VL 7 IS 3-4 BP 179 EP 186 DI 10.1007/BF01878484 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA PQ405 UT WOS:A1994PQ40500005 PM 7865349 ER PT J AU HIRAYAMA, F KATAYAMA, N NEBEN, S DONALDSON, D NICKBARG, EB CLARK, SC OGAWA, M AF HIRAYAMA, F KATAYAMA, N NEBEN, S DONALDSON, D NICKBARG, EB CLARK, SC OGAWA, M TI SYNERGISTIC INTERACTION BETWEEN INTERLEUKIN-12 AND STEEL FACTOR IN SUPPORT OF PROLIFERATION OF MURINE LYMPHOHEMATOPOIETIC PROGENITORS IN CULTURE SO BLOOD LA English DT Article ID CELL STIMULATORY FACTOR; MULTIPOTENTIAL HEMATOPOIETIC PROGENITORS; LYMPHOCYTE MATURATION FACTOR; INTERLEUKIN-3-DEPENDENT PROLIFERATION; FACTOR NKSF; C-KIT; ENHANCEMENT; COLONIES; IDENTIFICATION; IMMUNOGLOBULIN C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. GENET INST INC,CAMBRIDGE,MA. FU NIDDK NIH HHS [DK32294] NR 31 TC 80 Z9 82 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 1994 VL 83 IS 1 BP 92 EP 98 PG 7 WC Hematology SC Hematology GA MQ098 UT WOS:A1994MQ09800013 PM 7506084 ER PT J AU OGAWA, M SHIH, JP KATAYAMA, N AF OGAWA, M SHIH, JP KATAYAMA, N TI ENRICHMENT FOR PRIMITIVE HEMATOPOIETIC PROGENITORS OF MARROW-CELLS FROM 5-FLUOROURACIL-TREATED MICE AND NORMAL MICE SO BLOOD CELLS LA English DT Article; Proceedings Paper CT Symposium on Frontiers in Stem Cell Biology CY MAY 14-16, 1993 CL SANTA FE, NM DE PRIMITIVE HEMATOPOIETIC PROGENITORS; 5-FLUOROURACIL; C-KIT ID HEMATOPOIETIC STEM-CELLS; C-KIT; BONE-MARROW; SEPARATION; EXPRESSION; RECONSTITUTION; PURIFICATION; FLUORESCENCE; COLONIES AB Study of the mechanisms regulating stem cells would be significantly facilitated if a purified population of stem cells were available. During the last 4 years, our laboratory has been engaged in enrichment of murine marrow cells for primitive hemopoietic progenitors. We primarily used marrow cells from mice treated with 150 mg/kg of 5-fluorouracil (5-FU), and our assay for the primitive progenitors was formation of multilineage colonies supported by a combination of interleukin-3 (IL-3) and IL-6. First, we found that post-5-FU marrow cells with a density of 1.0631-1.0770 g/cm(3), negative for lineage-specific markers and positive for Ly-6A/E are routinely enriched for multipotential progenitors by approximately 800-fold. We then observed that J11d.2 and c-kit are additional useful markers for further enrichment of the primitive hemopoietic progenitors. Cell cycle-dormant primitive progenitors are primarily in the J11d.2(+) fraction, whereas more mature progenitors are J11d.2(-). The primitive progenitors express relatively low levels of c-kit, while more mature, actively cycling progenitors express high levels of c-kit. Combinations of these markers may be useful in enrichment of marrow cells of normal mice for primitive hemopoietic progenitors. C1 MED UNIV S CAROLINA,DEPT MED,DIV EXPTL HEMATOL,CHARLESTON,SC 29425. RP OGAWA, M (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. FU NIDDK NIH HHS [DK32294] NR 21 TC 12 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 1 BP 7 EP 13 PG 7 WC Hematology SC Hematology GA NX139 UT WOS:A1994NX13900002 PM 7994063 ER PT J AU HIRAYAMA, F OGAWA, M AF HIRAYAMA, F OGAWA, M TI CYTOKINE REGULATION OF EARLY B-LYMPHOPOIESIS ASSESSED IN CULTURE SO BLOOD CELLS LA English DT Article DE B LYMPHOPOIESIS; STEEL FACTOR; INTERLEUKIN-6; GRANULOCYTE COLONY-STIMULATING FACTOR ID CELLS; PROGENITORS AB Lymphohemopoietic progenitors that are capable of expressing B-cell and myeloid lineages may be cultured from bone marrow cells of adult mice by using a two-step methylcellulose culture system, In this system, the primary colonies expressing myeloid lineages are plated in secondary culture for B-lymphoid colony formation, We have observed that combinations of two factors based on steel factor (SLF), such as SLF plus interleukin (IL)-6, SLF plus granulocyte colony-stimulating factor (G-CSF), and SLF plus IL-11 support the differentiation and proliferation of B-cell progenitors from the lymphohemopoietic progenitors, Surprisingly, IL-3 failed to support B lymphopoiesis either alone or in combination with other factors, In addition, when added to permissive culture conditions, IL-3 and IL-1 independently inhibited the B-cell potential of the primary colonies, The inhibitory effects of IL-3 and IL-1 observed in this in vitro system may be significant in the selection of cytokine combinations for in vitro expansion of hemopoietic stem cells. C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. NR 5 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 2-3 BP 341 EP 347 PG 7 WC Hematology SC Hematology GA PZ375 UT WOS:A1994PZ37500020 PM 7538338 ER PT S AU CHIAPPELLI, F MANFRINI, E FRANCESCHI, C COSSARIZZA, A BLACK, KL AF CHIAPPELLI, F MANFRINI, E FRANCESCHI, C COSSARIZZA, A BLACK, KL BE deKloet, ER Azmitia, EC Landfield, PW TI STEROID REGULATION OF CYTOKINES - RELEVANCE FOR TH1-TO-TH2 SHIFT SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID HUMAN T-CELLS; ALZHEIMERS-DISEASE; GLUCOCORTICOID RECEPTORS; LYMPHOKINE PRODUCTION; HUMAN-LYMPHOCYTES; ANOREXIA-NERVOSA; BRAIN-TUMORS; DEHYDROEPIANDROSTERONE; HELPER; INVITRO C1 UNIV CALIF LOS ANGELES, SCH MED, BRAIN & DENT RES INST, DEPT NEUROBIOL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, HUMAN IMMUNOL & PSYCHONEUROIMMUNOL LAB, LOS ANGELES, CA 90073 USA. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES, SCH DENT, BRAIN & DENT RES INST, LOS ANGELES, CA 90024 USA. OI Cossarizza, Andrea/0000-0002-5381-1558 FU NIAID NIH HHS [AI07126]; NIDA NIH HHS [DA07683] NR 92 TC 33 Z9 33 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 204 EP 215 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00017 PM 7825877 ER PT S AU CHIAPPELLI, F MANFRINI, E GWIRTSMAN, H GARCIA, C PHAM, L LEE, P FROST, P AF CHIAPPELLI, F MANFRINI, E GWIRTSMAN, H GARCIA, C PHAM, L LEE, P FROST, P BE deKloet, ER Azmitia, EC Landfield, PW TI STEROID RECEPTOR-MEDIATED MODULATION OF CD4+CD62L+ CELL HOMING - IMPLICATIONS FOR DRUG-ABUSERS SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID PRODUCTS; ADHESION C1 UNIV CALIF LOS ANGELES, SCH MED, BRAIN RES INST, DEPT NEUROBIOL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, HUMAN IMMUNOL & PSYCHOEUROIMMUNOL LAB, LOS ANGELES, CA 90073 USA. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES, SCH DENT, DENT RES INST, HUMAN ORAL & MOLEC IMMUNOL LAB, LOS ANGELES, CA 90024 USA. OI Frost, Patrick/0000-0003-3348-5983 FU NIAID NIH HHS [AI07126]; NIDA NIH HHS [DA07683] NR 11 TC 5 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 421 EP 425 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00043 PM 7529973 ER PT J AU ROWAN, AB FOY, DW RODRIGUEZ, N RYAN, S AF ROWAN, AB FOY, DW RODRIGUEZ, N RYAN, S TI POSTTRAUMATIC-STRESS-DISORDER IN A CLINICAL-SAMPLE OF ADULTS SEXUALLY ABUSED AS CHILDREN SO CHILD ABUSE & NEGLECT LA English DT Article DE PTSD; CHILD SEXUAL ABUSE; EXPOSURE LEVELS ID POST-TRAUMATIC STRESS; CHILDHOOD; IMPACT; INCEST; SCALE; PTSD AB Forty-seven help-seeking, adult survivors of childhood sexual abuse (CSA) were assessed to examine the relationship between the level of CSA exposure and the subsequent development of posttraumatic stress disorder. CSA exposure was operationalized to include the overall level of exposure, frequency and duration of the abuse, age of onset, use of force, perceived life threat, and the occurrence of penetration. Participants were administered standardized measures of PTSD, including the Structured Clinical Interview of DSM-III-R (SCID). On the SCID, 69% of the survivors met full DSM-III-R criteria for PTSD. Significant correlations were found between several overall exposure measures and PTSD diagnostic status and the intensity of PTSD symptomatology. Similar relationships were identified with the duration and frequency of the abuse, the age of onset, and the use of force. This study is important in that it utilized standardized measures of PTSD and found a significant incidence of PTSD among adult CSA survivors. C1 FULLER THEOL SEMINARY,GRAD SCH PSYCHOL,180 N OAKLAND AVE,PASADENA,CA 91101. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,BRENTWOOD,CA. NR 33 TC 104 Z9 104 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PD JAN PY 1994 VL 18 IS 1 BP 51 EP 61 DI 10.1016/0145-2134(94)90095-7 PG 11 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA MQ185 UT WOS:A1994MQ18500006 PM 8124598 ER PT J AU NEWTON, TF LEUCHTER, AF MILLER, EN WEINER, H AF NEWTON, TF LEUCHTER, AF MILLER, EN WEINER, H TI QUANTITATIVE EEG IN PATIENTS WITH AIDS AND ASYMPTOMATIC HIV-INFECTION SO CLINICAL ELECTROENCEPHALOGRAPHY LA English DT Article DE AIDS; HIV INFECTION; QUANTITATIVE EEG ID IMMUNODEFICIENCY-VIRUS-INFECTION; EARLY NEUROLOGIC ABNORMALITIES; DEMENTIA COMPLEX; NEUROPSYCHOLOGICAL PERFORMANCE; ELECTROENCEPHALOGRAPHY; DIAGNOSIS; COHERENCE; COHORT; MACS; MEN C1 UNIV CALIF LOS ANGELES, NEUROPSYCHIAT INST & HOSP, DEPT BIOBEHAV, LOS ANGELES, CA USA. RP NEWTON, TF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, DEPT PSYCHIAT W116AC, WILSHIRE & SAWTELLE BLVD, LOS ANGELES, CA 90073 USA. OI newton, thomas/0000-0002-3198-5901 FU NIAID NIH HHS [N01 AI 72631]; NIMH NIH HHS [5T32 MH 119200-2] NR 22 TC 11 Z9 12 U1 0 U2 0 PU EEG & CLINICAL NEUROSCIENCE SOC (E C N S) PI WHEATON PA 805 W LIBERTY DR, PO BOX 725, WHEATON, IL 60187 USA SN 0009-9155 J9 CLIN ELECTROENCEPHAL JI Clin. Electroencephalogr. PD JAN PY 1994 VL 25 IS 1 BP 18 EP 25 PG 8 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA MQ846 UT WOS:A1994MQ84600004 PM 8174287 ER PT J AU SINGH, BN AF SINGH, BN TI ANTIARRHYTHMIC ACTIONS OF CALCIUM-ANTAGONISTS SO CORONARY ARTERY DISEASE LA English DT Review DE ANTIARRHYTHMIC DRUGS; CALCIUM ANTAGONISTS; POSTMYOCARDIAL INFARCTION SURVIVAL ID PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA; CHRONIC ATRIAL-FIBRILLATION; SUSTAINED VENTRICULAR-TACHYCARDIA; ACUTE MYOCARDIAL-INFARCTION; CONGESTIVE-HEART-FAILURE; INTRAVENOUS DILTIAZEM; CARDIAC-ARRHYTHMIAS; TRIGGERED ACTIVITY; ORAL VERAPAMIL; DOUBLE-BLIND C1 W LOS ANGELES VAMC,DEPT CARDIOL,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA. NR 51 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD JAN PY 1994 VL 5 IS 1 BP 27 EP 36 DI 10.1097/00019501-199401000-00005 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NA049 UT WOS:A1994NA04900005 PM 8136929 ER PT J AU KLEIN, GL COBURN, JW AF KLEIN, GL COBURN, JW TI TOTAL PARENTERAL-NUTRITION AND ITS EFFECTS ON BONE METABOLISM SO CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES LA English DT Review DE HORMONE; OSTEOMALACIA; METABOLIC BONE DISEASE; OSTEOPOROSIS; CYTOCHROME P450; OSTEOCALCIN; CALCITONIN; PARATHYROID HORMONE; VITAMIN-D; ALKALINE PHOSPHATASE; ALUMINUM ID VITAMIN-D; PARATHYROID-HORMONE; GLA-PROTEIN; HEMODIALYSIS-PATIENTS; RENAL OSTEODYSTROPHY; SELENIUM DEFICIENCY; CALCIUM-METABOLISM; DIALYSIS PATIENTS; ALUMINUM CONTENT; DRUG-METABOLISM AB Total parenteral nutrition (TPN) may affect bone metabolism in a variety of ways. These may include potential indirect effects such as on gastrointestinal hormone secretion, liver function, especially cytochrome P450 isoenzymes, metabolic biorhythms where established, and the continuous compared with the intermittent supply of nutrients. More substantial evidence exists for the reduction of bone formation, parathyroid hormone secretion, and calcitriol production in TPN patients along with high urinary calcium excretion. This review considers both aluminum loading and vitamin D sensitivity as etiologic factors and suggests that aluminum may have played a primary role in the pathogenesis of these abnormalities in bone and mineral metabolism, but that vitamin D may have potentiated the deleterious actions of aluminum. While the sources of aluminum contamination of TPN solutions have been identified and efforts are under way to reduce its contamination of TPN solutions, the persistence of low bone mass measurement in TPN patients is a problem that has been identified repeatedly, does not have a current explanation, and requires further study. C1 W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. RP KLEIN, GL (reprint author), UNIV TEXAS,MED BRANCH,DEPT PEDIAT,DIV PEDIAT GASTROENTEROL,CHILDRENS HOSP ROOM C353,GALVESTON,TX 77555, USA. OI Klein, Gordon/0000-0002-3011-4186 NR 129 TC 14 Z9 15 U1 1 U2 1 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, JOURNALS CUSTOMER SERVICE, BOCA RATON, FL 33431 SN 1040-8363 J9 CRIT REV CL LAB SCI JI Crit. Rev. Clin. Lab. Sci. PY 1994 VL 31 IS 2 BP 135 EP 167 DI 10.3109/10408369409084675 PG 33 WC Medical Laboratory Technology SC Medical Laboratory Technology GA NV034 UT WOS:A1994NV03400002 PM 7917007 ER PT J AU JENKINSON, SG LEVINE, SM AF JENKINSON, SG LEVINE, SM TI LUNG TRANSPLANTATION SO DM DISEASE-A-MONTH LA English DT Article ID OBSTRUCTIVE PULMONARY-DISEASE; TRANS-BRONCHIAL BIOPSIES; HIGH-RESOLUTION CT; HEART-LUNG; OBLITERATIVE BRONCHIOLITIS; BRONCHOALVEOLAR LAVAGE; CHRONIC REJECTION; NATURAL-HISTORY; RECIPIENTS; EMPHYSEMA AB Solid-organ transplantation has flourished during the last decade, with transplantation of heart and lungs becoming available to patients with end-stage cardiac or pulmonary diseases. The first lung transplant was performed in 1963 on a 58-year-old man with bronchogenic carcinoma. He survived for 18 days. During the next two decades, approximately 40 lung transplant procedures were attempted without success. These early attempts at lung transplantation were unsuccessful because of the development of lung rejection anastomotic complications, or infection in the transplant recipients. In the early 1980s, human heart-lung transplantation was successfully performed for the treatment of pulmonary vascular disease. After this procedure, single-lung transplantation for the treatment of end-stage interstitial lung disease and obstructive lung disease was developed. More recently, the technique of double-lund transplantation has come into existence. This article reviews various aspects of lung transplantation, including immunosuppression, lund graft preservation, the various surgical techniques and types of lund transplant procedures available, recipient and donor selection criteria and postoperative care of the transplant recipient. In addition, infectious and noninfectious complications seen in this particular patient population including acute and chronic rejection, will be discussed. C1 AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT,MED INTENS CARE UNIT,SAN ANTONIO,TX. RP JENKINSON, SG (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 78 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0011-5029 J9 DM-DIS MON JI DM-Dis.-a-Mon. PD JAN PY 1994 VL 40 IS 1 BP 3 EP 38 PG 36 WC Medicine, General & Internal SC General & Internal Medicine GA MR398 UT WOS:A1994MR39800001 ER PT J AU DRINKA, TJK AF DRINKA, TJK TI INTERDISCIPLINARY GERIATRIC TEAMS - APPROACHES TO CONFLICT AS INDICATORS OF POTENTIAL TO MODEL TEAMWORK SO EDUCATIONAL GERONTOLOGY LA English DT Article ID WORK TEAMS AB Interdisciplinary health care teams (IHTs) are essential for the delivery of health care to frail elderly persons. Teaching professionals how to function in health care teams is difficult. Educators often, use linear group development theories for teaching about IHTs. However, distinguishing features of the health care field, such as the diversity of the health professions, the ongoing nature of IHTs, high turnover in health care facilities, and incongruous development of the team and its members, may render linear group theories insufficient as models for IHTs. A team that has moved through its basic developmental phases once or twice may not be an, effective role model for teaching health professionals about IHTs. IHTs develop and function in unpredictable ways and, depending on their cultural depth, may be negative role models for professionals. As a team develops, long-term members should assume leadership roles as teachers of teamwork. Methods for constructively confronting conflict with a focus on integrative problem solving allow team members to move beyond basic group development tasks and to promote continuous reassessment of the team's established norms. Skills in conflict management, problem solving, and assumption of functional leadership are necessary for team members who assume the leadership role of teaching teamwork. In addition, evidence of constructive confrontation may be a good indicator of an IHT's readiness to model teamwork. RP DRINKA, TJK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON GERIATR RES EDUC & CLIN CTR,MADISON,WI 53705, USA. NR 28 TC 4 Z9 4 U1 1 U2 4 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0360-1277 J9 EDUC GERONTOL JI Educ. Gerontol. PD JAN-FEB PY 1994 VL 20 IS 1 BP 87 EP 103 DI 10.1080/0360127940200107 PG 17 WC Education & Educational Research; Gerontology SC Education & Educational Research; Geriatrics & Gerontology GA MR478 UT WOS:A1994MR47800007 ER PT J AU CLARK, PG DRINKA, TJK AF CLARK, PG DRINKA, TJK TI SPECIAL ISSUE ON CONCEPTUAL FOUNDATIONS FOR INTERDISCIPLINARY EDUCATION IN GERONTOLOGY AND GERIATRICS - INTRODUCTION SO EDUCATIONAL GERONTOLOGY LA English DT Editorial Material C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP CLARK, PG (reprint author), UNIV RHODE ISL,KINGSTON,RI 02881, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0360-1277 J9 EDUC GERONTOL JI Educ. Gerontol. PD JAN-FEB PY 1994 VL 20 IS 1 BP R3 EP R8 PG 6 WC Education & Educational Research; Gerontology SC Education & Educational Research; Geriatrics & Gerontology GA MR478 UT WOS:A1994MR47800001 ER PT J AU CASALE, L CARDOZO, C KALB, T LESSER, M AF CASALE, L CARDOZO, C KALB, T LESSER, M TI QUANTITATION OF ENDOPEPTIDASE-24.11 AND ENDOPEPTIDASE-24.15 IN HUMAN BLOOD LEUKOCYTES SO ENZYME & PROTEIN LA English DT Article DE B LYMPHOCYTES; ENDOPEPTIDASE 24.11; ENDOPEPTIDASE 24.15; MONOCYTES; NEUTROPHILS; T LYMPHOCYTES ID LYMPHOBLASTIC-LEUKEMIA ANTIGEN; MEMBRANE-BOUND METALLOENDOPEPTIDASE; ENKEPHALIN-CONTAINING PEPTIDES; NEUTRAL ENDOPEPTIDASE; HUMAN-NEUTROPHILS; SOLUBLE METALLOENDOPEPTIDASE; RAT-BRAIN; ALVEOLAR MACROPHAGES; NATURAL PEPTIDES; LYMPHOID-CELLS AB Endopeptidase 24.11 (EP 24.11; also called neutral endopeptidase, enkephalinase, CALLA, or CD10) and endopeptidase 24.15 (EP 24.15) are widely distributed neutral metalloendopeptidases that degrade a number of bioactive peptides including substance P, bradykinin, neurotensin, and chemotactic peptides. In this study we used sensitive substrates and specific inhibitors to quantitate the levels of these enzymes in purified peripheral human blood leukocytes obtained from healthy blood donors. We found that neutrophils did not contain detectable amounts of EP 24.15. In contrast, T lymphocytes, B lymphocytes, and monocytes contained significant amounts of the enzyme (446 +/- 248,314 +/- 183, and 484 +/- 212 nmol/mg protein/h, respectively). Neutrophils contained significant amounts of EP 24.11 (266 +/- 130 nmol/mg protein/h). Significantly lower levels of the enzyme were found in T lymphocytes, B lymphocytes, and monocytes (94 +/- 31, 87 +/- 38, and 20 +/- 13 nmol/mg protein/h, respectively). These findings suggest that the effects of some bioactive peptides on peripheral blood leukocyte function may be modulated by these enzymes. C1 BRONX VET AFFAIRS MED CTR,PULM SECT,BRONX,NY 10468. MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. MT SINAI SCH MED,DEPT PHARMACOL,NEW YORK,NY 10029. NR 41 TC 5 Z9 5 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1019-6773 J9 ENZYME PROTEIN JI Enzyme Protein PY 1994 VL 48 IS 3 BP 143 EP 148 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TE523 UT WOS:A1994TE52300002 PM 8589801 ER PT J AU YOSHIMURA, M PEKARY, AE PANG, XP BERG, L COLE, LA KARDANA, A HERSHMAN, JM AF YOSHIMURA, M PEKARY, AE PANG, XP BERG, L COLE, LA KARDANA, A HERSHMAN, JM TI EFFECT OF PEPTIDE NICKING IN THE HUMAN CHORIONIC-GONADOTROPIN BETA-SUBUNIT ON STIMULATION OF RECOMBINANT HUMAN THYROID-STIMULATING HORMONE RECEPTORS SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article ID NORMAL PREGNANT-WOMEN; THYROTROPIN; BINDING; CELLS; HETEROGENEITY; HCG; FRAGMENTATION; SERA AB It is now generally accepted that human chorionic gonadotropin (hCG) has thyroid-stimulating activity. Heterologous forms of the hCG molecule occur in the purified preparations extracted from urine of pregnant women and patients with trophoblastic diseases. This work was undertaken to determine the effect of peptide nicking in the hCG-beta subunit on its thyrotropic potency. Using Chinese hamster ovary cells expressing functional human thyroid-stimulating hormone (TSH) receptors, we examined the effect of nicked hCG on cyclic AMP (cAMP) production and receptor binding. The effect of human leukocyte elastase (hLE), a nicking enzyme, on standard hCG also was examined in the cAMP assay and on receptor binding. We studied five hCG preparations extracted from the urine of normal pregnancy (CR-127 and P8) and trophoblastic diseases (C2, C5 and M4). Two preparations (C2, 96% nicked and M4, 100% nicked in the beta 44-49 region) showed about a 1.5-fold potency of standard hCG CR-127, which is also 20% nicked in the same region. Non-nicked hCG (P8) had the weakest potency among all of the samples tested. Treatment of standard hCG with hLE increased the cAMP response about two-fold. Dose-dependent displacement of bovine [I-125]TSH by standard hCG and hLE-digested hCG was observed and was almost identical. We have confirmed the increased in vitro thyrotropic activity of hCG nicked in the beta-intercysteine loop on recombinant human TSH receptors. These data suggest that peptide heterogeneity of the hCG molecule may modulate the in vivo thyrotropic activity of hCG in pregnant women and patients with trophoblastic diseases. C1 W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINOL RES LAB W111D,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. YALE UNIV,SCH MED,DEPT OBSTET & GYNECOL,NEW HAVEN,CT 06510. NR 26 TC 17 Z9 17 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0804-4643 J9 EUR J ENDOCRINOL JI Eur. J. Endocrinol. PD JAN PY 1994 VL 130 IS 1 BP 92 EP 96 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NK507 UT WOS:A1994NK50700012 PM 7510202 ER PT J AU POWERS, PA SCHERER, SW TSUI, LC GREGG, RG HOGAN, K AF POWERS, PA SCHERER, SW TSUI, LC GREGG, RG HOGAN, K TI LOCALIZATION OF THE GENE ENCODING THE ALPHA(2)/DELTA SUBUNIT (CACNL2A) OF THE HUMAN SKELETAL-MUSCLE VOLTAGE-DEPENDENT CA2+ CHANNEL TO CHROMOSOME 7Q21-Q22 BY SOMATIC-CELL HYBRID ANALYSIS SO GENOMICS LA English DT Note ID CALCIUM-CHANNEL; SEQUENCE C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53705. UNIV WISCONSIN,DEPT PEDIAT,MADISON,WI 53705. UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO M5S 1A8,ON,CANADA. HOSP SICK CHILDREN,RES INST,DEPT GENET,TORONTO M5G 1X8,ON,CANADA. RP POWERS, PA (reprint author), UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV 707,1500 HIGHLAND AVE,MADISON,WI 53705, USA. RI Tsui, Lap-chee/A-1081-2010; Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Scherer, Stephen /0000-0002-8326-1999 NR 15 TC 17 Z9 17 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1994 VL 19 IS 1 BP 192 EP 193 DI 10.1006/geno.1994.1044 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NA601 UT WOS:A1994NA60100043 PM 8188232 ER PT J AU WEDDINGTON, WW MCLELLAN, AT AF WEDDINGTON, WW MCLELLAN, AT TI SUBSTANCE-ABUSE TREATMENT SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Letter RP WEDDINGTON, WW (reprint author), VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBST ABUSE TREATMENT UNIT,PHILADELPHIA,PA 19104, USA. NR 3 TC 0 Z9 0 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD JAN PY 1994 VL 45 IS 1 BP 80 EP 80 PG 1 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA MP418 UT WOS:A1994MP41800020 PM 8125471 ER PT J AU SMITH, MJ ROUSCULP, MD GOLDSMITH, KT CURIEL, DT GARVER, RI AF SMITH, MJ ROUSCULP, MD GOLDSMITH, KT CURIEL, DT GARVER, RI TI SURFACTANT PROTEIN A-DIRECTED TOXIN GENE KILLS LUNG-CANCER CELLS IN-VITRO SO HUMAN GENE THERAPY LA English DT Article ID INSITU HYBRIDIZATION; RETROVIRAL VECTOR; APOPROTEIN; EXPRESSION; EFFICIENCY; MODULATION; CARCINOMA; PROMOTER; THERAPY; INVITRO AB Human surfactant protein A (SPA) expression is considered a marker of respiratory epithelial differentiation. Non-small cell lung cancers (NSCLC) are respiratory epithelial derivatives, and it was previously shown that a minority of these cancers expressed SPA, presumably a consequence of their respiratory epithelial origin. In the studies reported here, SPA-I gene transcriptional regulatory sequences were localized to a 2.75-kb genomic 5'-flanking region fragment obtained by screening a human genomic library. The 2.75-kb fragment was used to direct a luciferase coding sequence transcriptionally within a plasmid construct. In plasmid transduction experiments, the SPA-directed luciferase plasmid produced significant luciferase activity in the SPA-expressing NSCLC cell line, H441, but only background levels in the non-SPA-expressing A549 cells. Because Northern blot analysis of resected NSCLC showed that the majority expressed SPA, an SPA-transcriptional targeting strategy was investigated using chimeric toxin genes comprising the coding sequence for herpes simplex virus thymidine kinase (HSV-TK) under transcriptional control of SPA or SV40 regulatory sequences. As expected, transduction of the constitutive, SV40-directed plasmid followed by ganciclovir treatment reduced numbers of both the A549 and H441 cells. In contrast, the SPA-directed plasmid reduced only the SPA-expressing H441 cells and had no significant effect on the A549 cells. The results of these in vivo experiments suggest the concept of transcriptionally directing toxin genes with SPA can produce targeted toxicity in NSCLC. C1 UAB,SCH MED,DIV PULM & CRIT CARE MED,BIRMINGHAM,AL 35294. UAB,SCH MED,INTERVENT GENET PROGRAM,BIRMINGHAM,AL 35294. UAB,SCH MED,BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. NR 23 TC 48 Z9 48 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JAN PY 1994 VL 5 IS 1 BP 29 EP 35 DI 10.1089/hum.1994.5.1-29 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA MT853 UT WOS:A1994MT85300005 PM 8155768 ER PT B AU MEYER, JS TAKASHIMA, S OBARA, K MURAMATSU, K MORTEL, KF AF MEYER, JS TAKASHIMA, S OBARA, K MURAMATSU, K MORTEL, KF BE Omae, T Chalmers, JP Gyarfas, I TI LONGITUDINAL OUTCOME FOLLOWING TREATMENT OF HYPERTENSION AMONG PATIENTS WITH ISCHEMIC VASCULAR DEMENTIA SO HYPERTENSION RESEARCH - CLINICAL AND EXPERIMENTAL, VOL 17, SUPPLEMENT 1, MAY 1994: PROCEEDINGS OF WHO/ISH MEETING ON HYPERTENSION AND CEREBROVASCULAR DISEASE LA English DT Proceedings Paper CT WHO/ISH Meeting on Hypertension and Cerebrovascular Disease CY MAY 25-27, 1993 CL NARA, JAPAN SP WHO, ISH DE CEREBRAL BLOOD FLOW; ISCHEMIC VASCULAR DEMENTIA; LEUKOARAIOSIS; WHITE MATTER; HYPERTENSION C1 BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JAPANESE SOC HYPERTENSION HYPERTENSION RES PUBL OFFICE PI TOYONAKA 565 PA CTR ACAD SOC, OSAKA, 14 FL SENRI LIFE SCI CTR BLDG 4-2 SHENSENRI-HIGASHI-MACHI, TOYONAKA 565 JAPAN PY 1994 BP S89 EP S96 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA BC36J UT WOS:A1994BC36J00015 ER PT J AU BEUTLER, AM WHITTUMHUDSON, JA NANAGARA, R SCHUMACHER, HR HUDSON, AP AF BEUTLER, AM WHITTUMHUDSON, JA NANAGARA, R SCHUMACHER, HR HUDSON, AP TI INTRACELLULAR LOCATION OF INAPPARENTLY INFECTING CHLAMYDIA IN SYNOVIAL TISSUE FROM PATIENTS WITH REITERS-SYNDROME SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT 2nd Molecular Aspects of the Rheumatic Diseases Symposium CY JUN 09-10, 1994 CL UNIV PENN, SCH MED, PHILADELPHIA, PA SP UNIV PENN, SCH MED, PHILADELPHIA VET ADM MED CTR, INST BIOTECHNOL & ADV MOLEC MED HO UNIV PENN, SCH MED DE CHLAMYDIA; REITERS SYNDROME; IN SITU HYBRIDIZATION; SYNOVIA ID INSITU HYBRIDIZATION; REACTIVE ARTHRITIS; TRACHOMATIS; CULTURE; DISEASE; RNA; DNA AB Culture of Chlamydia trachomatis from synovial tissues/fluids from Reiter's syndrome (RS) patients frequently yields negative results. However, we have identified chlamydial RNA at that site in such patients, suggesting that viable organisms may be present. Here we define the cellular location of chlamydia within the synovium via in situ hybridization. Using a chlamydial ribosomal RNA-directed probe, we show that synovial tissue from culture-negative RS patients gives strong hybridization which is often localized to a subsynovial cell layer, rather than to the synovial lining; in some cases, hybridizing cells are dispersed through the synovium. Ah hybridization signal is located within host cells, indicating that infectious extracellular elementary bodies are rare or absent. These data confirm the extensive intracellular presence of inapparent chlamydia in the synovia of RS patients and provide some insight into the usual culture negativity of synovial tissues for the organism. C1 DEPT VET AFFAIRS MED CTR,MED RES SERV,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,CTR ARTHRIT IMMUNOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. JOHNS HOPKINS UNIV,SCH MED,WILMER INST,BALTIMORE,MD 21205. FU NEI NIH HHS [EY-03324]; NIAMS NIH HHS [AR-42541] NR 26 TC 46 Z9 46 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1994 VL 13 IS 2-3 BP 163 EP 171 DI 10.1007/BF02918277 PG 9 WC Immunology SC Immunology GA QN404 UT WOS:A1994QN40400009 PM 7775807 ER PT J AU KELLEY, DM LICHTENSTEIN, A WANG, JY TAYLOR, AN DUBINETT, SM AF KELLEY, DM LICHTENSTEIN, A WANG, JY TAYLOR, AN DUBINETT, SM TI CORTICOTROPIN-RELEASING FACTOR REDUCES LIPOPOLYSACCHARIDE-INDUCED PULMONARY VASCULAR LEAK SO IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY LA English DT Article ID PITUITARY-ADRENAL AXIS; BETA-ENDORPHIN; THERMAL-INJURY; RAT PAWSKIN; HORMONE; MACROPHAGES; EXPRESSION; SECRETION; ADRENOCORTICOTROPIN; INTERLEUKIN-1 AB Previous studies have suggested that corticotropin-releasing factor (CRF) has immunoregulatory effects in addition to its neuroendocrine role. We examined the ability of CRF to inhibit lipopolysaccharide (LPS)-induced pulmonary vascular leak in vivo. Female BALB/C mice were treated with either normal saline (NS) or CRF prior to injection with LPS. Pulmonary vascular leak was inhibited by CRF as assessed by measurement of lung wet-to-dry ratios. The stress-induced increase in serum corticosterone levels in mice injected with LPS alone was not further increased by treatment with CRF. This indicates that the effect of CRF was not mediated centrally by stimulation of endogenous steroid release. Histologic examination of the lungs revealed that leukocyte infiltration was significantly depressed in CRF-treated mice thus confirming the protective effect of CRF. In addition, a modest prolongation of survival was demonstrated in CRF-treated mice following challenge with LPS (p=.08). These data indicate the potential utility of CRF as a modulator of pulmonary vascular leak. C1 UNIV CALIF LOS ANGELES,SCH MED,DIV PULM & CRIT CARE MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DIV ONCOL,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,IMMUNOL PULM LAB,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD RES DIV,LOS ANGELES,CA 90073. NR 35 TC 12 Z9 12 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0892-3973 J9 IMMUNOPHARM IMMUNOT JI Immunopharmacol. Immunotoxicol. PY 1994 VL 16 IS 2 BP 139 EP 148 DI 10.3109/08923979409007086 PG 10 WC Immunology; Pharmacology & Pharmacy; Toxicology SC Immunology; Pharmacology & Pharmacy; Toxicology GA NN361 UT WOS:A1994NN36100002 PM 8077603 ER PT J AU YOSHIKAWA, TT AF YOSHIKAWA, TT TI THE CHALLENGE AND UNIQUE ASPECTS OF TUBERCULOSIS IN OLDER PATIENTS SO INFECTIOUS DISEASES IN CLINICAL PRACTICE LA English DT Article ID IMMUNODEFICIENCY-VIRUS INFECTION; PULMONARY TUBERCULOSIS; MYCOBACTERIUM-TUBERCULOSIS; CLINICAL-FEATURES; ELDERLY PERSONS; SPECIMENS C1 GEORGE WASHINGTON UNIV,DIV AGING STUDIES & SERV,WASHINGTON,DC 20052. RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE,MAIL STOP 114,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 31 TC 9 Z9 9 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1056-9103 J9 INFECT DIS CLIN PRAC JI Infect. Dis. Clin. Pract. PD JAN-FEB PY 1994 VL 3 IS 1 BP 62 EP 66 DI 10.1097/00019048-199401000-00020 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MV769 UT WOS:A1994MV76900015 ER PT J AU BERLIN, J KING, AC TUTSCH, K FINDLAY, JW KOHLER, P COLLIER, M CLENDENINN, NJ WILDING, G AF BERLIN, J KING, AC TUTSCH, K FINDLAY, JW KOHLER, P COLLIER, M CLENDENINN, NJ WILDING, G TI A PHASE-II STUDY OF VINBLASTINE IN COMBINATION WITH ACRIVASTINE IN PATIENTS WITH ADVANCED RENAL-CELL CARCINOMA SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE RENAL CELL CARCINOMA; ACRIVASTINE; VINBLASTINE; DRUG RESISTANCE; P GLYCOPROTEIN ID MULTIDRUG-RESISTANCE; CONTINUOUS INFUSION; DRUG-RESISTANCE; TRIAL; CYCLOSPORINE; EXPRESSION; MODULATION; VERAPAMIL; ETOPOSIDE; CANCER AB Renal cell carcinoma exhibits chemoresistance attributable in part to the P-glycoprotein drug efflux mechanism. Acrivastine is a hydrophylic antihistamine that has been shown in vitro to reverse this form of resistance. After five patients were treated on a dose-finding study, seventeen patients with metastatic or unresectable renal cell carcinoma were entered into a phase II study of vinblastine in combination with acrivastine. Patients received oral acrivastine at doses of 400 mg every 4 hours for 6 days and a 96-hour continuous infusion of vinblastine at a dose of 1.6 mg/m(2)/24 h. Of 15 evaluable patients, no tumor responses were seen. The regimen was well-tolerated with the majority of toxicities being gastrointestinal and hematologic. Serum levels of acrivastine, its principal metabolite (270C81) and vinblastine were measured during the study. Based on in vitro data, the plasma levels of acrivastine were within a range adequate to block P-glycoprotein activity. High doses of acrivastine were well-tolerated clinically, however, the combination of acrivastine and vinblastine was not active against renal cell carcinoma. C1 UNIV WISCONSIN,CTR COMPREHENS CANC,DEPT HUMAN ONCOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. MERITER HOSP,MADISON,WI. BURROUGHS WELLCOME CO,DEPT CANC THERAPY,RES TRIANGLE PK,NC 27709. NR 17 TC 10 Z9 10 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1994 VL 12 IS 2 BP 137 EP 141 DI 10.1007/BF00874444 PG 5 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA PQ406 UT WOS:A1994PQ40600009 PM 7860231 ER PT B AU FOX, L FRIEDOKEN, M STAYER, J AF FOX, L FRIEDOKEN, M STAYER, J GP INT SOC AUGMENTAT & ALTERNAT COMMUN TI DETERMINING INDEPENDENT COMMUNICATION IN AN ADULT WITH SEVERE, NONFLUENT APHASIA AND A VOICE OUTPUT COMMUNICATION AID SO ISAAC '94 CONFERENCE BOOK AND PROCEEDINGS LA English DT Proceedings Paper CT 6th Biennial Conference of the International-Society-for-Augmentative-and-Alternative-Communication (ISAAC 94) CY OCT 09-13, 1994 CL MAASTRICHT, NETHERLANDS SP INT SOC AUGMENTAT & ALTERNAT COMMUN, IRV, INST RES DEV & KNOWLEDGE TRANSFER FIELD REHABIL & HANDICAP, DUTCH COUNCIL DISABLED DE ACQUIRED; LANGUAGE; DISORDER CASE; STUDIES TEACHING; AND OR; INTERVENTION TECHNOLOGY C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 0 TC 0 Z9 0 U1 0 U2 2 PU IRV, INST RES DEV & KNOWLEDGE TRANSF FIELD & REHAB HANDICAP PI HOENSBROEK PA PO BOX 192, 6430 AD HOENSBROEK, NETHERLANDS BN 90-74910-03-3 PY 1994 BP 81 EP 83 PG 3 WC Education, Special; Engineering, Biomedical; Language & Linguistics; Rehabilitation SC Education & Educational Research; Engineering; Linguistics; Rehabilitation GA BC07G UT WOS:A1994BC07G00025 ER PT J AU JONES, CLA DEMPSEY, EC KANE, MA AF JONES, CLA DEMPSEY, EC KANE, MA TI ABNORMAL PROTEIN KINASE-C-ALPHA IN HUMAN SMALL-CELL LUNG-CARCINOMA NCI-H345 CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DENVER VAMC,DENVER,CO 80220. UNIV COLORADO,HSC,DENVER,CO 80220. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 75 EP 75 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400191 ER PT J AU SAMUELS, MH LUTHER, M HENRY, P RIDGWAY, EC AF SAMUELS, MH LUTHER, M HENRY, P RIDGWAY, EC TI EFFECTS OF HYDROCORTISONE ON PULSATILE PITUITARY GLYCOPROTEIN-SECRETION SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; FOLLICLE-STIMULATING-HORMONE; LUTEINIZING-HORMONE; CUSHINGS-SYNDROME; THYROTROPIN SECRETION; THYROID-FUNCTION; ALPHA-SUBUNIT; TSH SECRETION; GONADOTROPIN-SECRETION; PLASMA TESTOSTERONE AB During states of stress, hypothalamic-pituitary-thyroid and hypothalamic-pituitary-gonadal function can be suppressed. One putative mediator of this stress response may be glucocorticoids, which have widespread effects on thyroid and gonadal function. To characterize dynamic pituitary glycoprotein secretion during glucocorticoid administration, 24-h TSH, LH, FSH, and ol-subunit pulses were measured in 10 healthy young subjects on 3 occassions: 1) at baseline, 2) during infusions of 100 mg hydrocortisone (HC) over 24 h, and 3) during infusions of 300 mg HC over 24 h. These HC infusions led to serum cortisol levels similar to the endogenous cortisol levels seen in moderate and severe stress. Both HC infusions had profound rapid effects on TSH levels, decreasing TSH pulse amplitude by 60% and abolishing the nocturnal TSH surge. However, TSH pulse frequency was unaltered. In contrast, HC infusions did not change mean or pulsatile LH, FSH, or alpha-subunit secretion. These results suggest that stress levels of cortisol acutely suppress TSH secretion at the pituitary level, with little effect on the TSH pulse generator. On the other hand, the effects of stress and/or hypercortisolism on the gonadal axis may require higher cortisol levels, more prolonged exposure, or other mediators of the stress response. C1 AUDIE L MURPHY MEM VET ADM MED CTR, RES SERV, SAN ANTONIO, TX 77030 USA. UNIV COLORADO, HLTH SCI CTR, DIV ENDOCRINOL, DENVER, CO 80262 USA. RP SAMUELS, MH (reprint author), OREGON HLTH SCI UNIV, DIV ENDOCRINOL L607, 3181 SW SAM JACKSON PK RD, PORTLAND, OR 97201 USA. FU NCRR NIH HHS [MO1-RR-00051] NR 44 TC 52 Z9 52 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1994 VL 78 IS 1 BP 211 EP 215 DI 10.1210/jc.78.1.211 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MR054 UT WOS:A1994MR05400040 PM 8288706 ER PT J AU JAINKITTIVONG, A YEH, CK JOHNSON, DA AF JAINKITTIVONG, A YEH, CK JOHNSON, DA TI SALIVARY HISTATIN LEVELS AND CANDIDA STATUS IN DENTURE PATIENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 192 EP 192 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500728 ER PT J AU TINER, BD VANSICKELS, JE MCANEAR, JT CASMEDES, HP AF TINER, BD VANSICKELS, JE MCANEAR, JT CASMEDES, HP TI EFFECT OF MAXILLOMANDIBULAR ADVANCEMENT ON OBSTRUCTIVE SLEEP-APNEA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 285 EP 285 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501461 ER PT J AU JAINKITTIVONG, A YEH, CK JOHNSON, DA AF JAINKITTIVONG, A YEH, CK JOHNSON, DA TI SALIVARY FUNCTION AND ORAL CANDIDA STATUS IN HEALTHY DENTURE PATIENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT DIAGNOST SCI & COMMUNITY DENT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 336 EP 336 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501868 ER PT J AU HOUSER, BE ALDER, ME MCANEAR, JT AF HOUSER, BE ALDER, ME MCANEAR, JT TI DENSITY VARIATIONS OF AUTOLOGOUS BONE-GRAFTS IN AUGMENTED MAXILLARY SINUSES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 447 EP 447 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502757 ER PT J AU LEONG, GB ETH, S SILVA, JA AF LEONG, GB ETH, S SILVA, JA TI TARASOFF DEFENDANTS - SOCIAL-JUSTICE OR ETHICAL DECAY SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; DUTY TO PROTECT; TESTIMONY; JUSTICE; ETHICS; PRIVILEGE; DANGEROUSNESS AB In 1976, the California Supreme Court ruled in Tarasoff v. Regents of the University of California that a duty to protect arises when a psychotherapist's patient poses a serious danger of physical harm to an identifiable third party. Discharging this duty by the issuance of a warning breaches the confidentiality of the psychotherapist-patient relationship. However, the potential benefit to society offsets the possible harm caused by the breach of confidentiality. Until recently, such warnings have served little purpose outside of possibly preventing harm. However, the cumulative effect of three recent California Supreme Court cases has been to permit the use of these confidentiality breaches in criminal proceedings to fulfill prosecutorial goals. Nonetheless, the cost of achieving social justice may be at the expense of other important ethical values for both the psychotherapeutic professions and society in general. C1 W LOS ANGELES VAMC,PSYCHIATRY SERV 116AA,LOS ANGELES,CA 90073. UNIV SO CALIF,SCH MED,LOS ANGELES,CA. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. NR 11 TC 5 Z9 5 U1 0 U2 2 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD JAN PY 1994 VL 39 IS 1 BP 86 EP 93 PG 8 WC Medicine, Legal SC Legal Medicine GA MT466 UT WOS:A1994MT46600009 PM 11644513 ER PT J AU KRAMER, BJ VITALIANO, PP AF KRAMER, BJ VITALIANO, PP TI COPING - A REVIEW OF THE THEORETICAL FRAMEWORKS AND THE MEASURES USED AMONG CAREGIVERS OF INDIVIDUALS WITH DEMENTIA SO JOURNAL OF GERONTOLOGICAL SOCIAL WORK LA English DT Article; Proceedings Paper CT 44th Annual Scientific Meeting of the Gerontological-Society-of-America CY NOV, 1992 CL SAN FRANCISCO, CA SP GERONTOL SOC AMER ID ALZHEIMERS-DISEASE; FAMILY CAREGIVERS; SPOUSE CAREGIVERS; STRESS; STRATEGIES; PREDICTORS; BURDEN; DEPRESSION; APPRAISAL; SUPPORT AB Gerontological social workers are often called upon to evaluate how family members are coping with caring for older adults with dementia. This paper examines the ways in which coping has been conceptualized and measured among caregivers. This review is intended to assist social workers in understanding the issues relevant to the assessment of caregiver coping given current theoretical formulations, to identify some of the gaps in the research conducted to date, and to help practitioners in deciding how to choose a comprehensive measure of coping. This review thereby compares and evaluates the conceptual and theoretical frameworks of 16 studies and examines the psychometric properties of the eight measures they have used to assess the coping of caregivers of older adults with dementia. Conclusions and implications for social work research and practice are discussed. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,GRECC,MADISON,WI. RP KRAMER, BJ (reprint author), UNIV WISCONSIN,SCH SOCIAL WORK,1350 UNIV AVE,MADISON,WI 53706, USA. NR 57 TC 21 Z9 21 U1 0 U2 6 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0163-4372 J9 J GERONTOL SOC WORK JI J. Gerontol. Soc. Work PY 1994 VL 23 IS 1-2 BP 151 EP 174 PG 24 WC Geriatrics & Gerontology; Social Work SC Geriatrics & Gerontology; Social Work GA QW960 UT WOS:A1994QW96000009 ER PT J AU GENTRY, RT BARAONA, E LIEBER, CS AF GENTRY, RT BARAONA, E LIEBER, CS TI GASTRIC FIRST PASS METABOLISM OF ALCOHOL SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Editorial Material ID HUMAN GASTROINTESTINAL-TRACT; DEHYDROGENASE-ACTIVITY; 1ST-PASS METABOLISM; H-2-RECEPTOR ANTAGONISTS; POSTPRANDIAL ABSORPTION; H2-RECEPTOR ANTAGONISTS; ENZYMATIC-PROPERTIES; ETHANOL-METABOLISM; CLASS-IV; RAT C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY. MT SINAI SCH MED,NEW YORK,NY. NR 55 TC 44 Z9 45 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD JAN PY 1994 VL 123 IS 1 BP 21 EP 26 PG 6 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA MZ688 UT WOS:A1994MZ68800013 PM 8288957 ER PT J AU GENTRY, RT BARAONA, E LIEBER, CS AF GENTRY, RT BARAONA, E LIEBER, CS TI REBUTTAL TO ANTAGONIST SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Editorial Material ID ALCOHOL-DEHYDROGENASE; ETHANOL-METABOLISM; RAT; ABSORPTION C1 BRONX VET AFFAIRS MED CTR,NEW YORK,NY. MT SINAI SCH MED,NEW YORK,NY. NR 15 TC 8 Z9 8 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD JAN PY 1994 VL 123 IS 1 BP 32 EP 33 PG 2 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA MZ688 UT WOS:A1994MZ68800016 ER PT J AU HOSTETLER, JS CATANZARO, A STEVENS, DA GRAYBILL, JR SHARKEY, PK LARSEN, RA TUCKER, RM ALHAIDARY, AD RINALDI, MG CLOUD, GA GALGIANI, JN AF HOSTETLER, JS CATANZARO, A STEVENS, DA GRAYBILL, JR SHARKEY, PK LARSEN, RA TUCKER, RM ALHAIDARY, AD RINALDI, MG CLOUD, GA GALGIANI, JN TI TREATMENT OF COCCIDIOIDOMYCOSIS WITH SCH-39304 SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID AMBULATORY PERITONEAL-DIALYSIS; FLUCONAZOLE; SCH-39304; THERAPY AB A new oral triazole antifungal, SCH 39304, was administered to 54 patients with progressive infections due to Coccidioides immitis from six collaborating centers. Patients were grouped according to site of infection including chronic pulmonary (25), bone/joint (17) and skin/soft tissue (12). The median age was 40 years; 83% were male, 52% white, 13% HIV-infected and 35% had failed previous therapy. The majority of patients were treated with either 100 mg or 200 mg day(-1). One patient on renal dialysis received 300 mg day(-1). Baseline abnormalities were reassessed for evidence of efficacy every 4 months and expressed in a standardized scoring system. Cumulative overall response rates at 4, 8 and 12 months were 7%, 36% and 66% respectively. Twelve month response rates by disease were 77% (pulmonary), 62% (skin/soft tissue) and 31% (bone/joint). Fifteen patients failed therapy although seven of these were still on treatment when the study was discontinued. Two failed due to toxicity. Possible symptoms or signs of toxicity occurred in 24 (44%) patients and were generally mild. SCH 39304 is an effective and well tolerated therapy for progressive forms of coccidioidomycosis. C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,DEPT MED,DIV INFECT DIS & GEOG MED,STANFORD,CA 94305. CALIF INST MED RES,SAN JOSE,CA 95128. NIAID,MYCOSES STUDY GRP,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DIV PULM MED,SAN DIEGO,CA 92103. AUDIE L MURPHY MEM VET ADM MED CTR,MED LAB,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV SO CALIF,LOS ANGELES CTY MED CTR,LOS ANGELES,CA 90033. WENATCHEE VALLEY CLIN,DIV CLIN RES,WENATCHEE,WA. VET AFFAIRS MED CTR,MED SERV,TUCSON,AZ. UNIV ARIZONA,DEPT MED,TUCSON,AZ. UNIV ALABAMA,CTR COMPREHENS CANC,BIOSTAT UNIT,BIRMINGHAM,AL 35294. FU NIAID NIH HHS [N01-AI-15082] NR 14 TC 9 Z9 9 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 IS 2 BP 105 EP 114 PG 10 WC Mycology SC Mycology GA NH896 UT WOS:A1994NH89600003 PM 8064541 ER PT J AU REQUINTINA, PJ OXENKRUG, GF YUWILER, A OXENKRUG, AG AF REQUINTINA, PJ OXENKRUG, GF YUWILER, A OXENKRUG, AG TI SYNERGISTIC SEDATIVE EFFECT OF SELECTIVE MAO-A, BUT NOT MAO-B, INHIBITORS AND MELATONIN IN FROGS SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article; Proceedings Paper CT 5th International Amine Oxidase Workshop - Amine Oxidases: Function and Dysfunction CY AUG 22-25, 1992 CL GALWAY, IRELAND AB Total suppression of righting reflex in frogs (Rana pipiens, 25-35 mg b.w.) was observed after combined administration of melatonin (12.5 mg/kg) and selective inhibitors of MAO-A: clorgyline (2.5 mg/kg) and moclobemide (50 mg/kg) but not MAO-B: selegiline (25 mg/kg) and Ro-19-6327 (50 mg/kg). None of these drugs alone affected the righting reflex. Clorgyline and selegiline selectively inhibited brain MAO-A and MAO-B activity (by more than 90%), resp. Frogs might represent a convenient model to study the selective MAO-A and B type inhibitors since they provide the opportunity to correlate behaviour and biochemical changes induced by MAO inhibitors. C1 BROWN UNIV,SCH MED,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,NEUROCHEM LAB,LOS ANGELES,CA 90073. RP REQUINTINA, PJ (reprint author), VET ADM MED CTR,PSYCHIAT SERV,PINEAL RES LAB,T-20,830 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. OI Oxenkrug, Gregory/0000-0002-7193-9117 NR 10 TC 5 Z9 5 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1994 IS 41 BP 141 EP 144 PG 4 WC Neurosciences SC Neurosciences & Neurology GA PW142 UT WOS:A1994PW14200021 ER PT J AU OXENKRUG, GF REQUINTINA, PJ CORREA, RM YUWILER, A AF OXENKRUG, GF REQUINTINA, PJ CORREA, RM YUWILER, A TI THE EFFECT OF 6-MONTHS L-DEPRENYL ADMINISTRATION ON PINEAL MAO-A AND MAO-B ACTIVITY AND ON THE CONTENT OF MELATONIN AND RELATED INDOLES IN AGED FEMALE FISHER 344N RATS SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article; Proceedings Paper CT 5th International Amine Oxidase Workshop - Amine Oxidases: Function and Dysfunction CY AUG 22-25, 1992 CL GALWAY, IRELAND ID LIFE AB Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night. Daytime values were unchanged by the treatment. The data suggest that stimulation of pineal melatonin biosynthesis might be one of the consequences of MAO-A inhibition contributing to life span prolongation induced by chronic selegiline treatment. C1 BROWN UNIV,SCH MED,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. W LOS ANGELES VET AFFAIRS MED CTR,NEUROCHEM LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP OXENKRUG, GF (reprint author), VET ADM MED CTR,PSYCHIAT SERV,PINEAL RES LAB,830 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. OI Oxenkrug, Gregory/0000-0002-7193-9117 NR 11 TC 6 Z9 7 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1994 IS 41 BP 249 EP 252 PG 4 WC Neurosciences SC Neurosciences & Neurology GA PW142 UT WOS:A1994PW14200034 ER PT J AU HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K AF HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K TI SPATIOTEMPORAL STAGES IN FACE AND WORD-PROCESSING .1. DEPTH RECORDED POTENTIALS IN THE HUMAN OCCIPITAL AND PARIETAL LOBES SO JOURNAL OF PHYSIOLOGY-PARIS LA English DT Article DE N400; P300; MEMORY; HIPPOCAMPUS; FUSIFORM-G ID EVENT-RELATED POTENTIALS; HUMAN HIPPOCAMPAL-FORMATION; RECOGNITION MEMORY; ENDOGENOUS POTENTIALS; BRAIN POTENTIALS; RHESUS-MONKEY; VISUAL-CORTEX; EVOKED-POTENTIALS; CORTICAL ACTIVITY; LANGUAGE AREA AB Evoked potentials (EPs) were used to help identify the timing, location, and intensity of the information-processing stages applied to faces and words in humans. EP generators were localized using intracranial recordings in 33 patients with depth electrodes implanted in order to direct surgical treatment of drug-resistant epilepsy. While awaiting spontaneous seizure onset, the patients gave their fully informed consent to perform cognitive tasks. Depth recordings were obtained from 1198 sites in the occipital. temporal and parietal cortices, and in the limbic system (amygdala, hippocampal formation and posterior cingulate gyrus). Twenty-three patients received a declarative memory recognition task in which faces of previously unfamiliar young adults without verbalizable distinguishing features were exposed for 300 ms every 3 s; 25 patients received an analogous task using words. For component identification, some patients also received simple auditory (21 patients) or visual (12 patients) discrimination tasks. Eight successive EP stages preceding the behavioral response (at about 600 ms) could be distinguished by latency, and each of 14 anatomical structures was found to participate in 2-8 of these stages. The earliest response, an N75-P105, focal in the most medial and posterior of the leads implanted in the occipital lobe (lingual g), was probably generated in visual cortical areas 17 and 18. These components were not visible in response to words, presumably because words were presented foveally. A focal evoked alpha rhythm to both words and faces was also noted in the lingual g. This was followed by an N130-P180-N240 focal and polarity-inverting in the basal occipitotemporal cortex (fusiform g, probably areas 19 and 37). In most cases, the P180 was evoked only by faces, and not by words, letters or symbols. Although largest in the fusiform g this sequence of potentials (especially the N240) was also observed in the supramarginal g, posterior superior and middle temporal g, posterior cingulate g, and posterior hippocampal formation. The N130, but not later components of this complex, was observed in the anterior hippocampus and amygdala. Faces only also evoked longer-latency potentials up to 600 ms in the right fusiform g. Words only evoked a series of potentials beginning at 190 ms and extending to 600 ms in the fusiform g and near the angular g (especially left). Both words and faces evoked a N150-P200-PN260 in the lingual g, and posterior inferior and middle temporal g. A N310-N430-P630 sequence to words and faces was largest and polarity-inverted in the hippocampal formation and amygdala, but was also probably locally-generated in many sites including the lingual g, lateral occipitotemporal cortex, middle and superior temporal g, temporal pole, supramarginal g, and posterior cingulate g. The P660 had the same distribution as has been noted for the P3b to rare target simple auditory and visual stimuli in 'oddball' tasks, with inversions in the hippocampus. In several sites, the N310 and N430 were smaller to repeated faces, and the P630 was larger. Putative information-processing functions were tentatively assigned to successive EP components based upon their cognitive correlates, as well as the functions and connections of their generating structures. For the N75-P105, this putative function is simple feature detection in primary visual cortex (V1 and V2). The N130-P180-N240 may embody structural face encoding in posterobasal inferotemporal cortex (homologous to V4?), with the results being spread widely to inferotemporal, multimodal and paralimbic cortices. For words, similar visual-form encoding (in fusiform g) or visual-phonemic encoding (in angular g) may occur between 150 and 280 ms. During the N310, faces and words may be multiply encoded for form and identity (inferotemporal), emotional (amygdala), recent declarative mnestic (hippocampal formation), and semantic (supramarginal and superior temporal sulcal supramodal cortices) characteristics. These multiple characteristics may be contextually integrated across inferotemporal, supramodal association, and limbic cortices during the N430, with cognitive closure following in the P630. In sum, visual information arrives at area 17 by about 75 ms, and is structurally-encoded in occipito-temporal cortex during the next 110 ms. By 150-200 ms after stimulus onset, activation has spread to parietal, lateral temporal, and limbic cortices, all of which continue to participate with the more posterior areas for the next 500 ms of event-encoding. Thus, face and word processing is serial in the sense that it can be divided into successive temporal stages, but highly parallel in that (after the initial stages where visual primitives are extracted) multiple anatomical areas with distinct perceptual, mnestic and emotional functions are engaged simultaneously. Consequently, declarative memory and emotional encoding can participate in early stages of perceptual, as well as later stages of cognitive integration. Conversely, occipitotemporal cortex is involved both early in processing (immediately after V1), as well as later, in the N430. That is, most stages of face and word processing appear to take advantage of the rich 'upstream' and 'downstream' anatomical connections in the ventral visual processing stream to link the more strictly perceptual networks with semantic, emotional, and mnestic networks. C1 CTR PAUL BROCA, INSERM, U97, F-75014 PARIS, FRANCE. UNIV CALIF LOS ANGELES, W LOS ANGELES VAMC, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90024 USA. STANFORD UNIV, STANFORD, CA 94305 USA. UNIV N TEXAS, DEPT PSYCHOL, DENTON, TX 76203 USA. UNIV CALIF LOS ANGELES, DEPT PSYCHOL, STANFORD, CA 94305 USA. RP HALGREN, E (reprint author), CHRU PONTCHAILLOU, NEUROL CLIN, INSERM, CJF 90-12, F-35033 RENNES, FRANCE. FU NINDS NIH HHS [R01 NS018741] NR 200 TC 279 Z9 281 U1 0 U2 14 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0928-4257 J9 J PHYSIOL-PARIS JI J. Physiol.-Paris PY 1994 VL 88 IS 1 BP 1 EP 50 DI 10.1016/0928-4257(94)90092-2 PG 50 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA NP319 UT WOS:A1994NP31900001 PM 8019524 ER PT J AU HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K CHAUVEL, P AF HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K CHAUVEL, P TI SPATIOTEMPORAL STAGES IN FACE AND WORD-PROCESSING .2. DEPTH-RECORDED POTENTIALS IN THE HUMAN FRONTAL AND ROLANDIC CORTICES SO JOURNAL OF PHYSIOLOGY-PARIS LA English DT Article DE N400; P300; MEMORY; ORBITOFRONTAL; CINGULATE ID MOVEMENT-RELATED POTENTIALS; HUMAN HIPPOCAMPAL-FORMATION; SUPPLEMENTARY MOTOR AREA; EVENT-RELATED POTENTIALS; VISUAL EVOKED-POTENTIALS; RHESUS-MONKEY; VOLUNTARY MOVEMENTS; ENDOGENOUS POTENTIALS; RECOGNITION MEMORY; BRAIN POTENTIALS AB Evoked potentials (EPs) were recorded directly from 650 frontal and peri-Rolandic sites in 26 subjects during face and/or word recognition, as well as during control tasks (simple auditory and visual discrimination). Electrodes were implanted in order to localize epileptogenic foci resistant to medication, and thus direct their surgical removal. While awaiting spontaneous seizure onset, the patients gave informed consent to perform cognitive tasks during intracerebral EEG recording. The earliest potentials appeared to be related to sensory stimulation, were prominent in lateral prefrontal cortex, and occurred at peak latencies of about 150 and 190 ms. A small triphasic complex beginning slightly later (peak latencies about 200-285-350 ms) appeared to correspond to the scalp N2-P3a-slow wave, associated with non-specific orienting. Multiple components peaking from 280 to 900 ms. and apparently specific to words were occasionally recorded in the left inferior frontal g, pars triangularis (Broca's area). Components peaking at about 430 and 600 ms were recorded in all parts of the prefrontal cortex, but were largest (up to 180 muV) and frequently polarity-inverted in the ventro-lateral prefrontal cortex. These components appeared to represent the N4-P3b, which have been associated with contextual integration and cognitive closure. Finally, a late negativity (650-900 ms) was recorded in precentral and premotor cortices, probably corresponding to a peri-movement readiness potential. In summary, EP components related to early sensory processing were most prominent in lateral prefrontal, to orienting in medial limbic, to word-specific processing in Broca's area, to cognitive integration in ventro-lateral prefrontal, and to response organization in premotor cortices. Thus, multiple frontal areas are involved in multiple stages of face and word processing, in a highly parallel but nonetheless differentiated manner. C1 CTR PAUL BROCA, INSERM, U97, F-75014 PARIS, FRANCE. UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, CTR EPILEPSY, LOS ANGELES, CA 90024 USA. STANFORD UNIV, DEPT NEUROSURG, STANFORD, CA 94305 USA. UNIV N TEXAS, DEPT PSYCHOL, DENTON, TX 76203 USA. UNIV CALIF LOS ANGELES, DEPT PSYCHOL, STANFORD, CA 94305 USA. RP HALGREN, E (reprint author), CHRU PONTCHAILLOU, NEUROL CLIN, INSERM, CJF 90-12, F-35033 RENNES, FRANCE. FU NINDS NIH HHS [NS18741] NR 154 TC 153 Z9 153 U1 0 U2 6 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0928-4257 J9 J PHYSIOL-PARIS JI J. Physiol.-Paris PY 1994 VL 88 IS 1 BP 51 EP 80 DI 10.1016/0928-4257(94)90093-0 PG 30 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA NP319 UT WOS:A1994NP31900002 PM 8019525 ER PT J AU LUPTON, JR ROBINSON, MC MORIN, JL AF LUPTON, JR ROBINSON, MC MORIN, JL TI CHOLESTEROL-LOWERING EFFECT OF BARLEY BRAN FLOUR AND OIL SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID SERUM-LIPID RESPONSE; BLOOD-PRESSURE; HYPERCHOLESTEROLEMIC MEN; METABOLISM; GRAIN; CEREALS; PRODUCT; WHEAT; FOODS; DIET AB Objective To compare the effects of adding barley bran flour and a barley oil extract to a fat-modified diet on serum lipids in persons with hypercholesterolemia. Design The basic design of the study was a randomized, 30-day intervention trial: it included a neutral-fiber control group and a 1-week preintervention period for the collection of baseline data. Subjects The subjects were 79 men aad women with hyper cholesterolemia. Subjects had a mean age of 48.2 years, and all completed the study. Intervention All participants were instructed to follow the National Cholesterol Education Program (NCEP) step I diet and were randomly assigned to one of three treatment groups: 20 g added cellulose; 3 g added barley oil extract, or 30 g added barley bran flour. Main outcome measures Total serum cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and very-low-density lipoprotein cholesterol were measured, along with serum triglycerides, before the intervention, at week I, at week 3, and at the end of the intervention. Statistical analyses performed Student's paired t test was used to detect significant changes within each treatment group from baseline to the end of the 30-day intervention. Ln addition, Pearson's correlation coefficients were used to detect significant correlations between the variables measured. Results Addition of barley bran flour significantly (P=.0001) decreased total serum cholesterol (-0.60 mmol/L as did addition of barley oil (-0.50 mmol/L, P=.002) after 30 days of intervention. Similarly, LDL-C decreased 6.5% with addition of barley bran flour (P=.036) and 9.2% with addition of barley oil (P=.003), Total serum cholesterol or LDL-C of the cellulose control group did not decrease significantly over the same period. HDL-C decreased significantly in the cellulose control group and the barley bran flour group (-0.15 mmol/L, P=.012, and -0.15 mmol/L, P=.006, respectively), but not in the barley oil group. Conclusion We conclude that addition of barley bran flour or barley oil enhances the cholesterol-lowering effect of the NCEP step 1 diet in individuals with hypercholesterolemia. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. OLIN E TEAGUE VET ADM MED CTR,TEMPLE,TX 76504. RP LUPTON, JR (reprint author), TEXAS A&M UNIV,FAC NUTR,COLL STN,TX 77843, USA. NR 34 TC 51 Z9 53 U1 0 U2 5 PU AMER DIETETIC ASSN PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD JAN PY 1994 VL 94 IS 1 BP 65 EP 70 DI 10.1016/0002-8223(94)92044-3 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MR351 UT WOS:A1994MR35100016 PM 8270757 ER PT J AU GERETY, MB CORNELL, JE MULROW, CD TULEY, M HAZUDA, HP LICHTENSTEIN, M AGUILAR, C KADRI, AA ROSENBERG, J AF GERETY, MB CORNELL, JE MULROW, CD TULEY, M HAZUDA, HP LICHTENSTEIN, M AGUILAR, C KADRI, AA ROSENBERG, J TI THE SICKNESS IMPACT PROFILE FOR NURSING-HOMES (SIP-NH) SO JOURNALS OF GERONTOLOGY LA English DT Article ID HEALTH-STATUS MEASURE; MEXICAN-AMERICANS; VALIDATION; IMPAIRMENT; VALIDITY AB Background. Valid, feasible measures of functional status are needed to evaluate the expanding nursing home population. This study attempts to increase relevance and reduce respondent burden of the Sickness Impact Profile (SIP) for nursing home residents while maintaining internal consistency and validity. Methods. 231 residents from one academic and four community nursing homes, aged greater-than-or-equal-to 60 with a Mini-Mental State Exam score greater-than-or-equal-to 11, were study participants. Nominal group process was used to identify items and/or categories for removal. Candidate items were those that: represented restrictions of the nursing home environment. had weak item-total score correlations, and/or made minimal contribution to category internal consistency. Reduction was constrained by: minimum correlation of r = .90 between SIP and Sickness Impact Profile for Nursing Homes (SIP-NH) scores, coefficients alpha that fell within 95% confidence regions about predicted alpha. Convergent and discriminant validity were evaluated with the Katz Activities of Daily Living, Physical Disability Index, Geriatric Depression Scale, and Folstein Mini-Mental State Exam. Results. The SIP-NH contains 66 items, a 51.5% reduction. Correlations between the SIP-NH and SIP were: total score r = .98, Physical dimension r = .97, and Psychosocial dimension r = .97. Alpha coefficients all fell within the 95% confidence regions. The SIP and the SIP-NH did not differ in correlations with validating instruments. Conclusions. The SIP-NH reduces respondent burden and has acceptable internal consistency and external validity. Potentially useful for discriminatory and predictive purposes, responsiveness to change will require longitudinal evaluation. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIAT & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN EPIDEMIOL,SAN ANTONIO,TX 78284. RP GERETY, MB (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIAT RES EDUC & CLIN,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [NIA UO1AG09117] NR 23 TC 28 Z9 28 U1 5 U2 5 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0022-1422 J9 J GERONTOL JI J. Gerontol. PD JAN PY 1994 VL 49 IS 1 BP M2 EP M8 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA MQ845 UT WOS:A1994MQ84500012 PM 8282976 ER PT J AU GULLEY, ML AMIN, MB BANKS, PM AYALA, AG EBLE, JN SRIGLEY, JR EAGAN, PA RO, JY AF GULLEY, ML AMIN, MB BANKS, PM AYALA, AG EBLE, JN SRIGLEY, JR EAGAN, PA RO, JY TI EPSTEIN-BARR-VIRUS IS DETECTED IN NASOPHARYNGEAL CARCINOMA BUT NOT IN LYMPHOEPITHELIOMA-LIKE CARCINOMA OF THE BLADDER SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX USA. HENRY FORD HOSP, DETROIT, MI 48202 USA. SUNNYBROOK MED CTR, TORONTO M4N 3M5, ON, CANADA. RICHARD L ROUDEBUSH VET AFFAIRS MED CTR, INDIANAPOLIS, IN USA. UNIV TEXAS, MD ANDERSON CANC CTR, HOUSTON, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0023-6837 EI 1530-0307 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A126 EP A126 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600748 ER PT S AU TALAL, N AF TALAL, N BE Sullivan, DA TI SJOGRENS-SYNDROME - CLOSE TO CAUSE AND CURE SO LACRIMAL GLAND, TEAR FILM, AND DRY EYE SYNDROMES: BASIC SCIENCE AND CLINICAL RELEVANCE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Conference on the Lacrimal Gland, Tear Film and Dry Eye Syndromes: Basic Science and Clinical Relevance CY NOV 14-17, 1992 CL SOUTHAMPTON, BERMUDA RP TALAL, N (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET HOSP,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [1R01 DE09311-01] NR 0 TC 1 Z9 1 U1 1 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44676-6 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 350 BP 679 EP 682 PG 4 WC Ophthalmology; Physiology SC Ophthalmology; Physiology GA BA17X UT WOS:A1994BA17X00114 PM 8030555 ER PT J AU BURKE, WJ RAGHU, G STRONG, R AF BURKE, WJ RAGHU, G STRONG, R TI TAXOL PROTECTS AGAINST CALCIUM-MEDIATED DEATH OF DIFFERENTIATED RAT PHEOCHROMOCYTOMA CELLS SO LIFE SCIENCES LA English DT Letter DE TAXOL; CALCIUM-MEDIATED CELL DEATH; PC12 CELLS; NERVE GROWTH FACTOR ID ALZHEIMERS-DISEASE; GLUTAMATE NEUROTOXICITY; DECREASED TRANSPORT; NITRIC-OXIDE; PHOSPHORYLATION; HYDROXYLASE; NERVE; TAU AB Elevated levels of intraneuronal calcium may contribute to neuronal death in both Alzheimer's disease and stroke. In part, this neuronal death may be due to calcium-induced disruption of microtubules and inhibition of axonal transport. Taxol stabilizes microtubules to disaggregation. To determine whether taxol could protect against calcium-mediated neuron eel death, a test system was established using a nerve growth factor-differentiated rat pheochromocytoma cell line (PC12 cells). PC12 cells were cultured with nerve growth factor to induce a neuronal phenotype. After 15 days, the cells were exposed to taxol, the calcium ionophore, A23187, or taxol plus ionophore for up to 24 h. Taxol alone reduced cell survival in a concentration dependent manner. At a concentration of 50 nM survival was reduced to between 63% and 84% of control after 4 h of exposure. The ionophore (1 mu M) variably reduced cell survival to between 10 and 55% at 4h. However, when taxol was added to the ionophore the cell survival was significantly increased by 1.5 to 4-fold. The protective effect of taxol lasted up to 24h. We conclude that taxol has a protective effect on calcium-mediated neurotoxicity. Drugs targeting underlying cellular mechanisms involved in calcium-mediated neuronal death may lead to successful therapy for Alzheimer's disease and stroke. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,SAN ANTONIO,TX 78284. ST LOUIS UNIV,SCH MED,DEPT NEUROL,ST LOUIS,MO. ST LOUIS UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63104. ST LOUIS UNIV,SCH MED,DEPT ANAT,ST LOUIS,MO. VET ADM MED CTR,ST LOUIS,MO 63125. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. NR 26 TC 3 Z9 3 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 55 IS 16 BP PL313 EP PL319 PG 7 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA PF351 UT WOS:A1994PF35100012 ER PT J AU GOODMAN, BM CARNES, M LENT, SJ AF GOODMAN, BM CARNES, M LENT, SJ TI MODEL SIMULATIONS OF ACTH PULSATILITY SO LIFE SCIENCES LA English DT Article DE ACTH; MODELING; PULSATILITY ID ADRENOCORTICOTROPIN SECRETION; HORMONE AB Using high intensity venous sampling (1-2 min integrated intervals) we have observed rapid (<10 min) large amplitude (up to 80 pg/ml) fluctuations in plasma ACTH concentrations in addition to variations at longer time scales. We developed a mathematical model to assess whether plausible physiological explanations could account for our observations and compared model simulations with time series from two human subjects. Three key features enabled the model to accurately simulate the observed time series. 1) The pattern of instantaneous secretory events comprising a pulse followed a Poisson process during baseline activity and rapidly shifted to a step function pattern during a pulsatile episode. 2) The fraction of secreted ACTH shunted between a fast and slow clearance mechanism varied biphasically between baseline and pulsatile states. 3) A brief rate-sensitive suppression of secretion was invoked when secretory rates increased above a threshold amount. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53792. RP GOODMAN, BM (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCRR NIH HHS [RR-03186]; NIDDK NIH HHS [DK-40759] NR 26 TC 4 Z9 4 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 54 IS 22 BP 1659 EP 1669 DI 10.1016/0024-3205(94)00606-7 PG 11 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA NH399 UT WOS:A1994NH39900003 PM 8177008 ER PT J AU FICHTNER, CG ARORA, RC OCONNOR, FL CRAYTON, JW AF FICHTNER, CG ARORA, RC OCONNOR, FL CRAYTON, JW TI PLATELET PAROXETINE BINDING AND FLUOXETINE PHARMACOTHERAPY IN POSTTRAUMATIC-STRESS-DISORDER - PRELIMINARY-OBSERVATIONS ON A POSSIBLE PREDICTOR OF CLINICAL TREATMENT RESPONSE SO LIFE SCIENCES LA English DT Letter ID PTSD; FLUVOXAMINE; IMIPRAMINE; TRIAL AB Recent open clinical trials have found the selective serotonin reuptake inhibitor (SSRI) fluoxetine to be beneficial in the treatment of posttraumatic stress disorder (PTSD) symptoms. We have reported previously that the binding of a newer SSRI, paroxetine, to blood platelets is decreased in PTSD patients compared to normal control subjects. In the current study, pretreatment platelet paroxetine binding data were analyzed for ten Vietnam combat veterans who were treated clinically with fluoxetine for PTSD, diagnosed on the basis of the Structured Clinical Interview for DSM-III-R. Specific binding of H-3-paroxetine is reported in terms of the dissociation constant (K(d)) and the maximum density of binding sites (B(max)). Based on our previous findings we hypothesized that decreased platelet H-3-paroxetine binding would be associated with positive therapeutic response to subsequent treatment with fluoxetine. Global clinical improvement ratings, conducted blind to the biochemical data, were used to separate patients into five maximal responders and five partial responders. The results indicated that maximal responders had lower pretreatment K(d) values (p=.016) and a trend toward lower pretreatment B(max) values (p=.075) than the partial responders. These preliminary findings may warrant further study of platelet SSRI binding as a possible predictor of SSRI treatment response in PTSD patients. C1 LOYOLA UNIV,STRITCH SCH MED,DEPT PSYCHIAT,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT PHARMACOL,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,PSYCHIAT SERV,BIOL PSYCHIAT SECT 116A7,HINES,IL 60141. RP FICHTNER, CG (reprint author), US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,PSYCHIAT SERV,POSTTRAUMAT STRESS DISORDER SECT,HINES,IL 60141, USA. NR 32 TC 9 Z9 9 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 54 IS 3 BP PL39 EP PL44 DI 10.1016/0024-3205(94)00592-3 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MM383 UT WOS:A1994MM38300010 PM 8289574 ER PT J AU CHIAPPELLI, F GARCIA, C MANFRINI, E FROST, P AF CHIAPPELLI, F GARCIA, C MANFRINI, E FROST, P TI MIGRATION OF HUMAN CD4+ LYMPHOCYTES - IMPLICATIONS FOR COCAINE AND ALCOHOL ABUSERS SO LYMPHOLOGY LA English DT Article; Proceedings Paper CT 14th International Congress of Lymphology CY SEP 20-26, 1993 CL WASHINGTON, DC SP INT SOC LYMPHOL, NIH ID NODE HOMING RECEPTOR; T-CELLS; HELPER-INDUCER; SUBSETS; DIFFERENTIATION; ACTIVATION; EXPRESSION; ADHESION; TQ1 AB T lymphocytes migrate across body tissues and organs, and home to sites where infection agents and tumors harbor. Cortisol and other glucocorticoids modulate the migration of helper T cells (CD4+), and particularly of CD4+ cells that expresses the homing receptor LECAM-1. A large proportion of these cells express the naive CD4 phenotype (CD4+CD45RA+), which in part determines their transit through the lymphatic system and the lymph nodes. We discuss implications for cocaine and alcohol abusers, who are at high risk for HIV infection and AIDS. C1 W LOS ANGELES VET AFFAIRS MED CTR,HUMAN IMMUNOL & PSYCHONEUROIMMUNOL LAB,LOS ANGELES,CA 90073. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES,SCH MED,BRI,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90024, USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU LYMPHOLOGY PI TUCSON PA C/O C L WITTE MD 1501 N CAMPBELL AVE DEPT SURGERY, TUCSON, AZ 85724 SN 0024-7766 J9 LYMPHOLOGY JI Lymphology PY 1994 VL 27 SU S BP 206 EP 211 PG 6 WC Immunology; Physiology SC Immunology; Physiology GA PK086 UT WOS:A1994PK08600055 ER PT J AU CHIAPPELLI, F TIO, DL FROST, P TAYLOR, AN AF CHIAPPELLI, F TIO, DL FROST, P TAYLOR, AN TI DIFFERENTIAL DISTRIBUTION OF THYMOCYTE SUBPOPULATIONS IN PREPUBERTAL MALE FETAL ALCOHOL EXPOSED RATS SO LYMPHOLOGY LA English DT Article; Proceedings Paper CT 14th International Congress of Lymphology CY SEP 20-26, 1993 CL WASHINGTON, DC SP INT SOC LYMPHOL, NIH ID PROLIFERATIVE RESPONSE; ETHANOL INUTERO; CELLS AB We reported significant differences in the response of thymocytes to mitogen stimulation among fetal alcohol exposed (FAE) and control male rats at postnatal day 45. We did not observe these differences in blood lymphocytes at any age tested. Thus, we have begun to test the hypothesis that the migration of thymocytes into peripheral blood is disturbed in FAE rats. We present preliminary flow cytometric analyses that suggest altered expression of the common leukocyte antigen (CD45RC) by thymocytes in prepubertal male FAE Sprague Dawley rats. This difference is not evident in peripheral blood, confirming the hypothesis that FAE disturbs the development of cellular immunity and the ''thymus-blood loop'' of lymphoid cell trafficking. C1 W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA 90073. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES,SCH MED,BRI,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90024, USA. NR 9 TC 1 Z9 1 U1 0 U2 0 PU LYMPHOLOGY PI TUCSON PA C/O C L WITTE MD 1501 N CAMPBELL AVE DEPT SURGERY, TUCSON, AZ 85724 SN 0024-7766 J9 LYMPHOLOGY JI Lymphology PY 1994 VL 27 SU S BP 212 EP 214 PG 3 WC Immunology; Physiology SC Immunology; Physiology GA PK086 UT WOS:A1994PK08600056 ER PT S AU TAKAYAMA, K QURESHI, N COTTER, RJ AF TAKAYAMA, K QURESHI, N COTTER, RJ BE Fenselau, C TI MASS-SPECTRAL ANALYSIS OF LIPID-A OF GRAM-NEGATIVE BACTERIA SO MASS SPECTROMETRY FOR THE CHARACTERIZATION OF MICROORGANISMS SE ACS SYMPOSIUM SERIES LA English DT Article; Proceedings Paper CT Symposium on Mass Spectrometry for the Characterization of Microorganisms, at the 204th National Meeting of the American-Chemical-Society CY AUG 23-28, 1992 CL WASHINGTON, DC SP AMER CHEM SOC, DIV ANAL CHEM ID LASER DESORPTION; SALMONELLA-TYPHIMURIUM; STRUCTURAL DETERMINATION; SPECTROMETRY; LIPOPOLYSACCHARIDES; FRAGMENTATION; MUTANT AB Positive ion FAB-MS, LD-MS, and PD-MS were utilized to obtain important structural information on the 4'-monophosphoryl lipid A (MPLA) derived from the lipopolysaccharides of Salmonella typhimurium and other Gram-negative bacterial strains which led to the elucidation of its chemical structure. The spectra of MPLA generated by these methods showed peaks corresponding to cationized molecular ions, losses of fatty acyl groups, and cleavage of the disaccharide yielding oxonium ions (FAB-MS and PD-MS), and several two-bond ring cleavages LD-MS and PD-MS). The distribution of the fatty acyl groups on the MPLA molecule was then deduced from its size and fragmentation pattern. We suggest that one could now identify and differentiate certain Gram-negative bacterial strains by performing mass spectral analysis of the isolated MPLA. C1 UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL,BALTIMORE,MD 21205. RP TAKAYAMA, K (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705, USA. NR 22 TC 2 Z9 2 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0097-6156 BN 0-8412-2737-3 J9 ACS SYM SER PY 1994 VL 541 BP 173 EP 184 PG 12 WC Chemistry, Multidisciplinary; Chemistry, Analytical; Microbiology SC Chemistry; Microbiology GA BZ67V UT WOS:A1994BZ67V00012 ER PT J AU SPARR, LF RUUD, DH HICKAM, DH COONEY, TG AF SPARR, LF RUUD, DH HICKAM, DH COONEY, TG TI THE EFFECT OF HOUSE OFFICER ROTATION ON INPATIENT SATISFACTION AND WARD ATMOSPHERE - PRELIMINARY FINDINGS SO MILITARY MEDICINE LA English DT Article AB Continual rotation of house officers builds discontinuity into the physician-patient relationship in teaching hospitals. This has led to speculation about the problem of residents and interns leaving their patients in the midst of hospital treatment. This article uses prospective data to assess the effect of house officer turnover on levels of patient satisfaction with hospital care and on patient perception of the hospital environment. Two inpatient cohorts defined by whether or not they had undergone a house officer change were matched by age and diagnostic category. Although survey instruments were significantly correlated, there was no significant difference between the two inpatient cohorts overall or on any of the survey subscales. The survey showed good satisfaction with the hospital, doctors, and nurses in both test groups. The authors draw a preliminary conclusion that patient satisfaction with medical care and with the hospital atmosphere remains constant, independent of termination of the doctor-patient relationship. Results from other reports linking patient satisfaction with continuity of care have been mixed, In discussing the limitations of their study, the authors point out that their findings are based on single-site data. RP SPARR, LF (reprint author), PORTLAND VA MED CTR,OUTPATIENT PSYCHIAT SECT,PORTLAND,OR 97201, USA. NR 0 TC 3 Z9 3 U1 1 U2 1 PU ASSN MILITARY SURG US PI BETHESDA PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0026-4075 J9 MIL MED JI Milit. Med. PD JAN PY 1994 VL 159 IS 1 BP 47 EP 53 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA MZ440 UT WOS:A1994MZ44000017 PM 8164867 ER PT S AU SATTIN, A PEKARY, AE LLOYD, RL AF SATTIN, A PEKARY, AE LLOYD, RL BE Strand, FL Beckwith, B Chronwall, B Sandman, CA TI TRH GENE-PRODUCTS ARE IMPLICATED IN THE ANTIDEPRESSANT MECHANISMS OF SEIZURES SO MODELS OF NEUROPEPTIDE ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 15th Annual Winter Neuropeptide Conference: Models of Neuropeptide Action CY FEB 05-08, 1994 CL BRECKENRIDGE, CO SP Int Neuropeptide Soc ID THYROTROPIN-RELEASING-HORMONE; RAT LIMBIC FOREBRAIN; ELECTROCONVULSIVE-THERAPY; BRAIN; EXPRESSION; DEPRESSION; RECEPTORS; THRESHOLD; EFFICACY; REGIONS C1 VET ADM MED CTR,RES SERV,SEPULVEDA,CA 91343. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,ENDOCRINOL RES LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. RP SATTIN, A (reprint author), VET ADM MED CTR,PSYCHIAT SERV,ANTIDEPRESSANT NEUROPHARMACOL RES LAB,116A-11,16111 PLUMMER ST,SEPULVEDA,CA 91343, USA. NR 36 TC 28 Z9 28 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-912-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 739 BP 135 EP 153 DI 10.1111/j.1749-6632.1994.tb19815.x PG 19 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD10Q UT WOS:A1994BD10Q00012 PM 7832467 ER PT S AU PEKARY, AE LLOYD, RL SATTIN, A AF PEKARY, AE LLOYD, RL SATTIN, A BE Strand, FL Beckwith, B Chronwall, B Sandman, CA TI PREDOMINANCE OF PGLU-HIS-PRO-GLY AMONG ALL TRH PRECURSOR PEPTIDES IN RAT LIMBIC FOREBRAIN AFTER ELECTROCONVULSIVE SEIZURES SO MODELS OF NEUROPEPTIDE ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 15th Annual Winter Neuropeptide Conference: Models of Neuropeptide Action CY FEB 05-08, 1994 CL BRECKENRIDGE, CO SP Int Neuropeptide Soc ID PITUITARY; BIOSYNTHESIS; INCREASES; BRAIN C1 UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. VET ADM MED CTR,PSYCHIAT & RES SERV,ANTIDEPRESSANT NEUROPHARMACOL RES LAB,SEPULVEDA,CA 91343. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP PEKARY, AE (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINOL RES LAB,RES SERV,BLDG 114,RM 200,LOS ANGELES,CA 90073, USA. NR 8 TC 7 Z9 7 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-912-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 739 BP 330 EP 333 DI 10.1111/j.1749-6632.1994.tb19838.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD10Q UT WOS:A1994BD10Q00034 PM 7832488 ER PT J AU SMALL, GW COLLINS, MT MAZZIOTTA, JC BAXTER, LR PHELPS, ME MANDELKERN, MA KAPLAN, A ADAMSON, CF CHANG, L GUZE, BH CORDER, EH SAUNDERS, AM CONNEALLY, PM HAINES, JL PERICAKVANCE, MA ROSES, AD AF SMALL, GW COLLINS, MT MAZZIOTTA, JC BAXTER, LR PHELPS, ME MANDELKERN, MA KAPLAN, A ADAMSON, CF CHANG, L GUZE, BH CORDER, EH SAUNDERS, AM CONNEALLY, PM HAINES, JL PERICAKVANCE, MA ROSES, AD TI APOLIPOPROTEIN-E TYPE-4 ALLELE LOWERS CEREBRAL PARIETAL METABOLISM IN RELATIVES AT RISK FOR FAMILIAL ALZHEIMER-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHARMACOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. INDIANA UNIV,MED CTR,DEPT MED & MOLEC GENET,INDIANAPOLIS,IN 46202. MASSACHUSETTS GEN HOSP E,MOLEC NEUROGEN UNIT,BOSTON,MA 02129. DUKE UNIV,MED CTR,ALZHEIMER DIS RES CTR,DURHAM,NC 27710. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S155 EP S155 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900638 ER PT J AU DASHEIFF, RM AF DASHEIFF, RM TI THE FIRST AMERICAN EPILEPTOLOGISTS - SPRATLING,WILLIAM,P.,MD, AND PARK,ROSWELL, MD SO NEUROLOGY LA English DT Editorial Material C1 UNIV PITTSBURGH,SCH MED,DEPT NEUROL,PITTSBURGH,PA 15261. US DEPT VET AFFAIRS,NEUROL SERV,PITTSBURGH,PA. RP DASHEIFF, RM (reprint author), UNIV PITTSBURGH,CTR EPILEPSY,3515 5TH AVE,ROOM 625,PITTSBURGH,PA 15213, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1994 VL 44 IS 1 BP 171 EP 174 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA MR371 UT WOS:A1994MR37100039 PM 8290059 ER PT J AU GRIFFITH, JM ADLER, LE FREEDMAN, R AF GRIFFITH, JM ADLER, LE FREEDMAN, R TI FINE MOTOR-PERFORMANCE IN SCHIZOPHRENIA SO NEUROPSYCHOBIOLOGY LA English DT Article DE SMOOTH PURSUIT EYE MOVEMENT; SCHIZOPHRENIA; NEUROMOTOR PERFORMANCE ID EYE-TRACKING DYSFUNCTIONS; PSYCHOTIC-PATIENTS; ABNORMALITIES AB Peripheral and central aspects of motor dysfunction were assessed in 12 schizophrenic and 12 normal subjects, using a test of control of finger movement based on the widely used smooth pursuit eye movement task. This was performed in order to investigate the basis of neuromotor dysfunction in schizophrenia. In this task, subjects used finger movement to track a visual target. Simultaneously, an electromyogram of the extensor digitorum communis, the primary muscle utilized in the task, was recorded. Smooth pursuit eye movements were also assessed. Accuracy of finger-based and smooth-pursuit eye movement tracking was analyzed by fast Fourier transform and expressed as a log signal-to-noise ratio. The electromyograms were analyzed by motor unit potential discrimination and by interspike interval histography. Schizophrenics demonstrated significantly poorer finger tracking than did controls, with a mean score of 2.01 +/- 0.63 (SD) versus 2.81 +/- 0.42 (t = 3.52, d.f. = 21, p < 0.005). However, there was no evidence for motor-unit dysfunction. Schizophrenics also performed more poorly on smooth-pursuit eye movement, with a mean score of 2.06 +/- 0.62 versus 3.33 +/- 1.21 (t = 3.21, d.f. = 22, p < 0.005). Severity of extrapyramidal symptoms was correlated with poorer performance on the finger tracking task, but not smooth-pursuit eye movement. These findings support the hypothesis that schizophrenics' tracking abnormalities are due to central nervous system deficits rather than peripheral pathology. C1 UNIV COLORADO,HLTH SCI CTR,DEPT PSYCHIAT,DENVER,CO 80262. DENVER VA MED CTR,DEPT PSYCHIAT,DENVER,CO. NR 15 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0302-282X J9 NEUROPSYCHOBIOLOGY JI Neuropsychobiology PY 1994 VL 29 IS 4 BP 179 EP 184 DI 10.1159/000119084 PG 6 WC Neurosciences; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA NP336 UT WOS:A1994NP33600005 PM 8047244 ER PT B AU GREEN, MF NUECHTERLEIN, KH AF GREEN, MF NUECHTERLEIN, KH BE David, AS Cutting, JC TI MECHANISMS OF BACKWARD-MASKING IN SCHIZOPHRENIA SO NEUROPSYCHOLOGY OF SCHIZOPHRENIA SE BRAIN DAMAGE, BEHAVIOUR AND COGNITION : DEVELOPMENTS IN CLINICAL NEUROPSYCHOLOGY LA English DT Proceedings Paper CT International Symposium on Neuropsychology of Schizophrenia CY OCT 10-11, 1991 CL INST PSYCHIAT LONDON, LONDON, ENGLAND SP INST PSYCHIAT LONDON, WELLCOME TRUST, LUNDBECK PHARM, SANDOZ HO INST PSYCHIAT LONDON C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RI David, Anthony/C-1315-2011 OI David, Anthony/0000-0003-0967-774X NR 0 TC 2 Z9 2 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC PUBL PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430 BN 0-86377-303-6 J9 BRAIN DAM B PY 1994 BP 79 EP 95 PG 17 WC Psychology, Clinical; Neurosciences; Psychiatry; Psychology SC Psychology; Neurosciences & Neurology; Psychiatry GA BA10R UT WOS:A1994BA10R00005 ER PT S AU LOPESVIRELLA, MF AF LOPESVIRELLA, MF BE Sakamoto, N Alberti, KGM Hotta, N TI INTERRELATED METABOLISM IMBALANCES LINKED TO HYPERGLYCEMIA-INDUCED VASCULAR DYSFUNCTION SO PATHOGENESIS AND TREATMENT OF NIDDM AND ITS RELATED PROBLEMS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 4th International Symposium on Treatment of Diabetes Mellitus: Pathogenesis and Treatment of NIDDM and Its Related Problems CY OCT 26-27, 1993 CL NAGOYA, JAPAN SP NAGOYA UNIV, JAPAN DIABETES SOC, FDN ADV INT SCI, AICHI PREFECTURE, NAGOYA CITY C1 MED UNIV S CAROLINA,RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81712-3 J9 INT CONGR SER PY 1994 VL 1057 BP 29 EP 36 PG 8 WC Endocrinology & Metabolism; Pathology SC Endocrinology & Metabolism; Pathology GA BB08V UT WOS:A1994BB08V00005 ER PT J AU TYAN, ML AF TYAN, ML TI FETAL WEIGHT AT TERM INFLUENCED BY H-2-ASSOCIATED LOCI SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; GROWTH; PHENOTYPE; STRAINS; RAT AB Pregnant mice which in theory differ only in the region of the major histocompatibility complex (MHC) on chromosome 17 (C57BL/10, the inbred partner [host strain], and B10.D2, B10.BR, B10.A, B10.A[2R], B10.A[5R], B10.A[15R] and B10.A[18R]) were sacrificed on the 11th and 18th days of gestation, and the fetuses were sexed and weighed. Fetuses from reciprocal crosses between B10.A and B10.BR, B10.D2 and C57BL/10 were weighed and sexed on the 18th day of gestation. It was found that (i) fetal weights were not significantly different among the strains examined on day 11 (B10.BR, B10.A[15R] and B10.A[18R]), (ii) B10.BR fetuses of both sexes weighed significantly less than fetuses from the other strains on day 18, (iii) B10.D2 18-day-old male but not female fetuses were heavier than the males from the other strains (this difference was not present when corrections for litter size were made), (iv) the fetuses from the B10.A x B10.BR cross were the smallest, those from the B10.D2 x B10.A cross the largest, and those from the B10.A x C57BL/10 crosses intermediate, and (v) maternal effects were noted in the B10.A x B10.BR and B10.A x B10.D2 but not the B10.A x C57BL/10 crosses. The results suggest that there are two or more MHC associated loci that influence growth rate in late gestation. Among the candidate genes are Ped and Igfr II. RP TYAN, ML (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073, USA. NR 17 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JAN PY 1994 VL 205 IS 1 BP 85 EP 88 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF384 UT WOS:A1994NF38400013 PM 8115355 ER PT J AU SAZON, DA SHARMA, O SANTIAGO, S WILLIAMS, AJ AF SAZON, DA SHARMA, O SANTIAGO, S WILLIAMS, AJ TI FLUORODEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY IN PULMONARY SARCOIDOSIS SO SARCOIDOSIS LA English DT Article ID LAVAGE RP SAZON, DA (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR, SCH MED, DIV PULM & CRIT CARE, LOS ANGELES, CA USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU PCA-PUBLISHING COMMUNICATION ADVERTISING PI MILAN PA VIA CLERICI 12, 20032 MILAN, ITALY SN 0393-1447 J9 SARCOIDOSIS JI Sarcoidosis PD JAN PY 1994 VL 11 SU 1 BP 363 EP 367 PG 5 WC Respiratory System SC Respiratory System GA NJ447 UT WOS:A1994NJ44700076 ER PT J AU KANE, JM MARDER, SR AF KANE, JM MARDER, SR TI CLOZAPINE - BENEFITS AND RISKS - REPLY SO SCHIZOPHRENIA BULLETIN LA English DT Letter C1 ALBERT EINSTEIN COLL MED,GLEN OAKS,NY 11004. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90073. RP KANE, JM (reprint author), LONG ISL JEWISH MED CTR,HILLSIDE HOSP,DEPT PSYCHIAT,GLEN OAKS,NY 11004, USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1994 VL 20 IS 1 BP 23 EP 24 PG 2 WC Psychiatry SC Psychiatry GA MY468 UT WOS:A1994MY46800004 ER PT J AU GREEN, MF SATZ, P CHRISTENSON, C AF GREEN, MF SATZ, P CHRISTENSON, C TI MINOR PHYSICAL ANOMALIES IN SCHIZOPHRENIA-PATIENTS, BIPOLAR PATIENTS, AND THEIR SIBLINGS SO SCHIZOPHRENIA BULLETIN LA English DT Article ID ADULT SCHIZOPHRENIA; PRENATAL EXPOSURE; INFLUENZA; CLASSIFICATION; DISORDERS; CHILDREN; ETIOLOGY; EPIDEMIC AB Minor physical anomalies (MPAs) are believed to reflect abnormalities in fetal neurodevelopment. Several studies have shown that schizophrenia patients have more MPAs than normal controls, but little is known about the meaning of this increased rate of MPAs. The current study first attempted to determine whether the increased MPAs are associated with schizophrenia in particular or with psychosis in general. Second, the study tested whether the patients' siblings also show an increased rate of MPAs by assessing MPAs in schizophrenia patients, bipolar manic patients, the siblings from each group of patients, and normal controls. The schizophrenia patients had significantly more MPAs than normal controls and bipolar patients. The rate of MPAs in bipolar patients did not differ from normal controls. This pattern suggests that MPAs have some degree of specificity to schizophrenia. Both sibling groups had fewer MPAs than the patients, and this difference was significant for the comparison between schizophrenia patients and their siblings. When viewed within a vulnerability-stress model, the results are consistent with the theory that MPAs may reflect early, largely extra-genetic, stressful events. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. FU NIMH NIH HHS [MH-43292] NR 30 TC 116 Z9 117 U1 2 U2 2 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1994 VL 20 IS 3 BP 433 EP 440 PG 8 WC Psychiatry SC Psychiatry GA PB173 UT WOS:A1994PB17300004 PM 7973464 ER PT J AU DAVIDSON, M HAROUTUNIAN, V GABRIEL, SM POWCHIK, P HARVEY, PD MOHS, RC DAVIS, KL AF DAVIDSON, M HAROUTUNIAN, V GABRIEL, SM POWCHIK, P HARVEY, PD MOHS, RC DAVIS, KL TI COGNITIVE IMPAIRMENT IN ELDERLY SCHIZOPHRENIC-PATIENTS SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT 116A,BRONX,NY 10468. NR 0 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1994 VL 11 IS 2 BP 162 EP 163 PG 2 WC Psychiatry SC Psychiatry GA MT535 UT WOS:A1994MT53500203 ER PT J AU GLASS, WF TROYER, DA KREISBERG, JI AF GLASS, WF TROYER, DA KREISBERG, JI TI REGULATION OF MESANGIAL CELL-FUNCTION BY THROMBIN SO SEMINARS IN THROMBOSIS AND HEMOSTASIS LA English DT Article ID EXTRACELLULAR-MATRIX; CYCLIC-AMP; TYROSINE PHOSPHORYLATION; PROTEIN-KINASE; SHAPE CHANGE; RECEPTOR; ADHESION; CAMP; TRANSFORMATION; FIBROBLASTS C1 UNIV TEXAS, HLTH SCI CTR, DEPT PATHOL, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP GLASS, WF (reprint author), UNIV VIRGINIA, HLTH SCI CTR, DEPT PATHOL, BOX 214, CHARLOTTESVILLE, VA 22908 USA. FU NIDDK NIH HHS [DK46735, DK29787, DK34234] NR 39 TC 1 Z9 1 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0094-6176 J9 SEMIN THROMB HEMOST JI Semin. Thromb. Hemost. PY 1994 VL 20 IS 4 BP 333 EP 338 DI 10.1055/s-2007-1001923 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA PW767 UT WOS:A1994PW76700006 PM 7899864 ER PT B AU TALAL, N AF TALAL, N BE Homma, M Sugai, S Tojo, T Miyasaka, N Akizuki, M TI SUMMARY - IV INTERNATIONAL-SYMPOSIUM ON SJOGRENS-SYNDROME SO SJOGREN'S SYNDROME: STATE OF THE ART LA English DT Proceedings Paper CT 4th International Symposium on Sjogrens Syndrome CY AUG 11-13, 1993 CL TOKYO, JAPAN C1 AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KUGLER PUBLICATIONS BV PI AMSTELVEEN PA PO BOX 516, 1180 AM AMSTELVEEN, NETHERLANDS BN 90-6299-107-6 PY 1994 BP 93 EP 98 PG 6 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BB01Y UT WOS:A1994BB01Y00018 ER PT S AU SEARLES, JS ALTERMAN, AI AF SEARLES, JS ALTERMAN, AI BE Babor, TF Hesselbrock, V Meyer, RE Shoemaker, W TI ENVIRONMENTAL DIFFERENCES IN YOUNG MEN WITH AND WITHOUT A FAMILY HISTORY OF ALCOHOLISM SO TYPES OF ALCOHOLICS: EVIDENCE FROM CLINICAL, EXPERIMENTAL, AND GENETIC RESEARCH SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Genetic Susceptibility, Biological Markers of Vulnerability and Alcoholic Subtypes CY OCT 22-23, 1992 CL FARMINGTON, CT SP NIAAA ID CROSS-FOSTERING ANALYSIS; ANTISOCIAL PERSONALITY; INHERITANCE; ABUSE C1 UNIV VERMONT,COLCHESTER,VT. UNIV PENN,VET AFFAIRS MED CTR,ADDICT RES CTR,PHILADELPHIA,PA 19104. RP SEARLES, JS (reprint author), VERMONT ALCOHOL RES CTR,2000 MT VIEW DR,COLCHESTER,VT, USA. NR 27 TC 8 Z9 8 U1 2 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-799-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 708 BP 147 EP 156 DI 10.1111/j.1749-6632.1994.tb24707.x PG 10 WC Substance Abuse; Genetics & Heredity; Multidisciplinary Sciences; Psychiatry SC Substance Abuse; Genetics & Heredity; Science & Technology - Other Topics; Psychiatry GA BA04C UT WOS:A1994BA04C00015 PM 8154675 ER PT B AU COBURN, JW AF COBURN, JW BE Norman, AW Bouillon, R Thomasset, M TI Use of calcitriol in treating the secondary hyperparathyroidism of uremia: What are the differences between oral and intravenous therapy? SO VITAMIN D: PLURIPOTENT STEROID HORMONE: STRUCTURAL STUDIES, MOLECULAR ENDOCRINOLOGY AND CLINICAL APPLICATIONS LA English DT Proceedings Paper CT 9th Workshop on Vitamin D CY MAY 28-JUN 02, 1994 CL ORLANDO, FL SP Chugai Pharm Co Ltd, Japan, Hoffmann La Roche Ltd, Switzerland, Hoffmann La Roche Inc, US, Inst Sci Roussel, France, Lab Leo SA, France, Leo Pharm Prod Ltd A S, Denmark, Novo Nordisk A S, Denmark, Procter & Gamble Pharm, US, Solvay Duphar BV, Netherlands, Sumitomo Pharm Co Ltd, Japan, Teijin Ltd, Japan, Westwood Squibb Pharm Res Inst, US C1 UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WALTER DE GRUYTER PI BERLIN 30 PA GENTHINER STRASSE 13, W-1000 BERLIN 30, GERMANY BN 3-11-014157-4 PY 1994 BP 649 EP 657 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD64B UT WOS:A1994BD64B00208 ER PT J AU DANG, H OGAWA, N TAKEI, M LAZARIDIS, K TALAL, N AF DANG, H OGAWA, N TAKEI, M LAZARIDIS, K TALAL, N TI INDUCTION OF LUPUS-ASSOCIATED AUTOANTIBODIES BY IMMUNIZATION WITH NATIVE AND RECOMBINANT IG POLYPEPTIDES EXPRESSING A CROSS-REACTIVE IDIOTYPE 4B4 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTI-SM AUTOANTIBODY; INTERSPECIES IDIOTYPE; DNA IDIOTYPE; NAIVE MICE; CELL LINES; ERYTHEMATOSUS; ANTIBODIES; ACTIVATION; DISEASE; GENE AB A human mAb designated 4B4 with anti-Sm activity was derived from a patient with systemic lupus erythematosus. This antibody expressed a lupus-associated cross-reactive Id, partially related to the monoclonal murine anti-Sm (Y2) from MRL/lpr mice. Studies were performed to investigate the ability of 4B4 to induce lupus in nonautoimmune-prone mice. BALB/c mice immunized with 4B4 produced antibodies to dsDNA, ssDNA, Sm ribonucleoprotein, and mouse Fc fragment. There was no antibody activity against SSA/Ro, SSB/La, and hen egg lysozyme. Ag inhibition studies show that the autoantibodies were not polyreactive. Mice were also immunized with r4B4 polypeptides representing the H/L heterodimer, H chain and L chain. Autoantibodies were induced in mice immunized against the H/L and H polypeptides. No autoantibodies were induced in mice immunized with recombinant L chain. Furthermore, from 20 to 68% of antibody activity to Sm or dsDNA could be inhibited with anti-Id antiserum (either anti-4B4 or Y2). The autoantibody was initially IgM and then underwent an isotype switch to IgG. These results show that lupus-associated autoantibodies can be induced by immunization with 4B4 and that the 4B4 V(H) region is important in this induction process. The finding of murine IgG autoantibody expressing a cross-reactive Id similar to the immunizing 4B4 suggests a role for anti-idiotypic Th cells in this autoimmune response. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DANG, H (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [DE 09311] NR 33 TC 46 Z9 46 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD DEC 15 PY 1993 VL 151 IS 12 BP 7260 EP 7267 PG 8 WC Immunology SC Immunology GA MM036 UT WOS:A1993MM03600066 PM 8258723 ER PT J AU BECKER, HC HALE, RL BOGGAN, WO RANDALL, CL AF BECKER, HC HALE, RL BOGGAN, WO RANDALL, CL TI EFFECTS OF PRENATAL ETHANOL EXPOSURE ON LATER SENSITIVITY TO THE LOW-DOSE STIMULANT ACTIONS OF ETHANOL IN MOUSE OFFSPRING - POSSIBLE ROLE OF CATECHOLAMINES SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE PRENATAL ETHANOL; ETHANOL-STIMULATED ACTIVITY; BRAIN CATECHOLAMINES; FETAL ALCOHOL SYNDROME; ETHANOL SENSITIVITY ID ALCOHOL EXPOSURE; ADULT-RATS; LOCOMOTOR-ACTIVITY; BEHAVIOR; INUTERO; MICE; CONSUMPTION; AMPHETAMINE; BRAIN; METHYLPHENIDATE AB The purpose of this study was to examine whether prenatal ethanol (EtOH) exposure alters later sensitivity to the low-dose stimulant effects of EtOH. Because the locomotor stimulant effects of EtOH are thought to be mediated, at least in part, by activation of brain monoamine systems, and because prenatal EtOH exposure has been shown to alter brain monoamine activity, it was hypothesized that prenatal EtOH exposure may alter sensitivity to the stimulant actions of EtOH. To test this hypothesis, sensitivity to the locomotor stimulant effects of various challenge doses of EtOH was examined in male and female offspring from prenatal alcohol (A), pair-fed (PF), and lab chow (LC) groups at different ages. In addition, to address the hypothesis further, sensitivity to the catecholamine synthesis inhibitor alpha-methyl-p-tyrosine (AMPT) was examined in these offspring, as well. Results indicated that male offspring prenatally exposed to EtOH exhibited reduced baseline activity and a blunted stimulant response to all challenge doses of EtOH (0.75-1.5 g/kg) in comparison with control offspring at 30 days of age, but these effects appeared to ''normalize'' at 70 days of age. Female EtOH-exposed offspring also exhibited a reduced baseline level of activity relative to control offspring, as well as a blunted stimulant response to the lowest challenge dose of EtOH (0.75 g/kg) at 30 days of age, and these effects persisted into adulthood. The stimulant response to higher doses of EtOH did not significantly differ among prenatal treatment groups in young or adult female offspring. However, because baseline activity was significantly lower in female EtOH exposed offspring than control offspring, the stimulant response to these doses of EtOH (1.125 and 1.5 g/kg) was relatively greater than that for PF and LC offspring. Importantly, none of the differences in performance among the prenatal treatment groups could be attributed to an alteration in EtOH pharmacokinetics, because blood ROH levels measured immediately following the 10-min test session were similar for all prenatal treatment groups across all of the EtOH test doses. Further, a similar response profile as that observed following EtOH challenge at 70 days of age was obtained following phenobarbital challenge (10-40 mg/kg). Finally, whereas AMPT (50-400 mg/ kg) dose-dependently antagonized the stimulant effects of EtOH in all prenatal treatment groups, this effect of AMPT was significantly greater in mice prenatally exposed to RON in comparison with control offspring. Thus, sensitivity to the stimulant effects of EtOH was significantly altered in adult male mice when these animals were additionally challenged with a drug that further reduced central catecholamine activity. Taken together, these results provide support for the hypothesis that prenatal EtOH exposure alters later sensitivity to the low-dose stimulant properties of the drug, and that this effect may be the result of an alteration in brain monoamine activity in these offspring. C1 MED UNIV S CAROLINA,RALPH H JOHNSON VET ADM MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC. FU NIAAA NIH HHS [AA07791] NR 48 TC 25 Z9 25 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD DEC PY 1993 VL 17 IS 6 BP 1325 EP 1336 DI 10.1111/j.1530-0277.1993.tb05249.x PG 12 WC Substance Abuse SC Substance Abuse GA MN395 UT WOS:A1993MN39500033 PM 8116850 ER PT J AU RABENECK, L RISSER, JMH MURRAY, NGB MCCABE, BK LACKE, CE LUCCO, LJ AF RABENECK, L RISSER, JMH MURRAY, NGB MCCABE, BK LACKE, CE LUCCO, LJ TI FAILURE OF PROVIDERS TO VACCINATE HIV-INFECTED MEN AGAINST HEPATITIS-B - A MISSED OPPORTUNITY SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID HOMOSEXUAL MEN; ANTIBODY; ANTIGEN AB Objective: To carry out an audit of hepatitis B immunization practices in an out patient HIV clinic. Methods: We reviewed the medical records of all new HIV-infected patients seen between October 1, 1990 and December 31, 1991. Results: The 125 patients were men with a mean age and CD4 count of 43 yr and 240 cells/mm3, respectively. Fourteen percent (14%) of men who showed a clear need for vaccine, having no HBV markers, were not vaccinated by the clinic staff. Further, 16% whose susceptibility to HBV infection was unclear, with anti-HBc as a sole HBV marker, were not evaluated with a booster dose of hepatitis B vaccine in an attempt to elicit an anamnestic response. Conclusions: In failing to vaccinate or evaluate the 30% of patients without HBsAg or anti-HBs, our providers are missing an important opportunity in preventive medicine. We urge others to examine their own hepatitis B screening and vaccination practices. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. VET ADM RES CTR AIDS & HIV INFECT,HOUSTON,TX. RP RABENECK, L (reprint author), VET ADM MED CTR 111D,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 18 TC 17 Z9 17 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD DEC PY 1993 VL 88 IS 12 BP 2015 EP 2018 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MK860 UT WOS:A1993MK86000006 PM 8249965 ER PT J AU BONADONNA, RC DELPRATO, S BONORA, E GULLI, G SOLINI, A DEFRONZO, RA AF BONADONNA, RC DELPRATO, S BONORA, E GULLI, G SOLINI, A DEFRONZO, RA TI EFFECTS OF PHYSIOLOGICAL HYPERINSULINEMIA ON THE INTRACELLULAR METABOLIC PARTITION OF PLASMA-GLUCOSE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INSULIN; GLYCOLYSIS; SUBSTRATE COMPETITION ID MAGNETIC-RESONANCE SPECTROSCOPY; MUSCLE GLYCOGEN-SYNTHESIS; WHOLE-BODY; INDIRECT CALORIMETRY; SUBSTRATE OXIDATION; SKELETAL-MUSCLE; INSULIN; HUMANS; INVIVO; TURNOVER AB Methodology for assessing the glycolytic and oxidative fluxes from plasma glucose, by measuring (H2O)-H-3 and (CO2)-C-14 rates of production during [3-H-3]- and [U-C-14]glucose infusion, was tested in healthy subjects. In study 1, during staircase (H2O)-H-3 infusion in six subjects, calculated rates of (H2O)-H-3 appearance agreed closely with (H2O)-H-3 infusion rates. In study 2, when [2-H-3]glucose and (NaHCO3)-C-14 were infused in four subjects in the basal state and during a 4-h euglycemic insulin (approximately 70 muU/ml) clamp, accurate estimates of the rates of [2-H-3]glucose detritiation were obtained (94-97% of the expected values), and the recovery factor of (NaHCO3)-C-14 did not change during hyperinsulinemia. In study 3, 11 subjects underwent a 4-h euglycemic insulin (approximately 70 muU/ml) clamp with [3-H-3]- and [U-C-14]glucose infusion and measurement of gaseous exchanges by indirect calorimetry to estimate the rates of total glycolysis, glycogen synthesis, glucose oxidation, nonoxidative glycolysis, hepatic glucose production, glucose recycling, and glucose conversion to fat. Hyperinsulinemia stimulated glycogen synthesis above baseline more than glycolysis [increment of 4.78 +/- 0.37 vs. 2.0 +/- 0. 17 mg . min-1 . kg-1 of lean body mass (LBM), respectively, P < 0.011 and incompletely suppressed (approximately 87%) hepatic glucose production. The major component of nonoxidative glycolysis shifted from glucose recycling in the postabsorptive state (approximately 57% of nonoxidative glycolysis) to glucose conversion to fat during hyperinsulinemia (approximately 59% of nonoxidative glycolysis). Lipid oxidation during the insulin clamp was negatively correlated with both isotopic glucose oxidation (r = -0.822, P < 0.002) and glycolysis (r = -0.582, P < 0.07). In conclusion, in healthy subjects, glycogen synthesis plays a greater role than glycolysis and glucose oxidation in determining insulin-mediated glucose disposal. Part of insulin-mediated increase in glycolysis/oxidation might be secondary to the relief of the competition between fat and glucose for oxidation. C1 UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. RP BONADONNA, RC (reprint author), CNR,INST CLIN PHYSIOL,METAB UNIT,VIA SAVI 8,I-56100 PISA,ITALY. RI Del Prato, Stefano/K-3405-2016; Solini, Anna/K-4666-2016 OI Del Prato, Stefano/0000-0002-5388-0270; Solini, Anna/0000-0002-7855-8253 FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 53 TC 24 Z9 24 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD DEC PY 1993 VL 265 IS 6 BP E943 EP E953 PN 1 PG 11 WC Physiology SC Physiology GA MQ656 UT WOS:A1993MQ65600052 PM 8279550 ER PT J AU ROBBINS, JA LEVINE, RL MASER, A ROSENBEK, JC KEMPSTER, GB AF ROBBINS, JA LEVINE, RL MASER, A ROSENBEK, JC KEMPSTER, GB TI SWALLOWING AFTER UNILATERAL STROKE OF THE CEREBRAL-CORTEX SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article ID RIGHT-HEMISPHERE STROKE; ASPIRATION; DYSPHAGIA C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV,MADISON,WI. GOVERNOR STATE UNIV,DIV COMMUN DISORDERS,UNIV PK,IL. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT SPEECH PATHOL & AUDIOL,MADISON,WI. UNIV WISCONSIN,HLTH SCI CTR,MADISON,WI 53706. RP ROBBINS, JA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,GRECC 11G,2500 OVERLOOK TERR,MADISON,WI 53705, USA. FU NINDS NIH HHS [NINDS NS24427] NR 34 TC 118 Z9 126 U1 0 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD DEC PY 1993 VL 74 IS 12 BP 1295 EP 1300 DI 10.1016/0003-9993(93)90082-L PG 6 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA ML134 UT WOS:A1993ML13400002 PM 8259895 ER PT J AU HUBBARD, JW MIDHA, KK HAWES, EM MCKAY, G MARDER, SR ARAVAGIRI, M KORCHINSKI, ED AF HUBBARD, JW MIDHA, KK HAWES, EM MCKAY, G MARDER, SR ARAVAGIRI, M KORCHINSKI, ED TI METABOLISM OF PHENOTHIAZINE AND BUTYROPHENONE ANTIPSYCHOTIC-DRUGS - A REVIEW OF SOME RECENT RESEARCH FINDINGS AND CLINICAL IMPLICATIONS SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID HALOPERIDOL PLASMA-LEVELS; REDUCED HALOPERIDOL; SCHIZOPHRENIC-PATIENTS; FLUPHENAZINE; GLUCURONIDE; INTERCONVERSIONS; IDENTIFICATION; DOPAMINE; BRAIN AB Whereas some metabolites of antipsychotic drugs are psychoactive and contribute to clinical improvement, recent studies have provided evidence that certain metabolites contribute to side-effects which can be disabling enough to negate clinical improvement as regards the psychosis. The route of administration of the drug can determine the amount of metabolite produced in the body and affect how the patient feels in response to the treatment. C1 UNIV SASKATCHEWAN, COLL PHARM, SASKATOON S7N 0W0, SASKATCHEWAN, CANADA. UNIV CALIF LOS ANGELES, CLIN RES CTR SCHIZOPHRENIA & PSYCHIAT REHABIL, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHOPHARMACOL LAB, LOS ANGELES, CA 90073 USA. UNIV SASKATCHEWAN, COLL MED, SASKATOON S7N 0W0, SASKATCHEWAN, CANADA. NR 18 TC 6 Z9 6 U1 0 U2 1 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON SW1X 8PG, ENGLAND SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD DEC PY 1993 VL 163 SU 22 BP 19 EP 24 PG 6 WC Psychiatry SC Psychiatry GA MN026 UT WOS:A1993MN02600003 ER PT J AU ASSEY, ME ZILE, MR USHER, BW KARAVAN, MP CARABELLO, BA AF ASSEY, ME ZILE, MR USHER, BW KARAVAN, MP CARABELLO, BA TI EFFECT OF CATHETER POSITIONING ON THE VARIABILITY OF MEASURED GRADIENT IN AORTIC-STENOSIS SO CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS LA English DT Article DE AORTIC STENOSIS; INTRAVENTRICULAR PRESSURE GRADIENTS; AORTIC VALVE GRADIENTS ID RESISTANCE; PRESSURE AB The purpose of this study was to quantify the variation in measured aortic valve gradient and calculated aortic valve area when different techniques of cardiac catheterization were utilized. Hemodynamic assessment of aortic stenosis severity requires an accurately determined pressure gradient. In aortic stenosis, the presence of intraventricular pressure gradients and downstream pressure recovery within the aorta means that a range of aortic valve gradients could be measured in a given patient depending upon catheter position and measurement technique. To quantify the degree of variation in measured gradient and calculated aortic valve area, we generated transvalvular gradients by nine different techniques in 15 patients (11 men, 4 women; 29-86 years old). Patients were divided into those with severe aortic stenosis (aortic valve area less than or equal to 0.6 cm(2), n = 6) and those with moderately severe aortic stenosis (aortic valve area 0.61-0.90 cm(2), n = 9). Considerable variation in measured gradient and calculated aortic valve area was observed. The maximum variation in gradient was similar in severe and moderately severe aortic stenosis groups (33 mm Hg. vs. 32 mm Hg., p = NS). However, the variation in gradient as a percent of maximum gradient was greater (P<0.05) in the moderately severe aortic stenosis group. The maximum variation in calculated aortic valve area was 0.1 cm(2) in the severe group and 0.3 cm(2) in the moderately severe group (P<0.01). An intraventricular gradient, present in 13 of 15 (87%) patients, was partially responsible for the variation in pressure gradient measurement and calculated aortic valve area. We conclude that in patients with valvular aortic stenosis, catheterization technique has an important impact on the hemodynamic assessment of aortic stenosis severity. This is particularly true in patients with moderately severe aortic stenosis where any variation tends to represent a larger percentage of the total gradient. (c) 1993 Wiley-Liss, Inc. RP ASSEY, ME (reprint author), MED UNIV S CAROLINA,RALPH H JOHNSON VET ADM MED CTR,GAZES CARDIAC RES INST,DIV CARDIOL,CHARLESTON,SC 29425, USA. NR 12 TC 21 Z9 21 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-6569 J9 CATHETER CARDIO DIAG JI Catheter. Cardiovasc. Diagn. PD DEC PY 1993 VL 30 IS 4 BP 287 EP 292 DI 10.1002/ccd.1810300405 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MJ794 UT WOS:A1993MJ79400003 PM 8287452 ER PT J AU BOKEN, DJ SWINDELLS, S RINALDI, MG AF BOKEN, DJ SWINDELLS, S RINALDI, MG TI FLUCONAZOLE-RESISTANT CANDIDA-ALBICANS SO CLINICAL INFECTIOUS DISEASES LA English DT Article AB Mucocutaneous candidiasis caused by Candida albicans is a common complication of human immunodeficiency virus (HIV) infection. Recent reports of isolation of resistant strains of C. albicans raise the specter of more widespread resistance, but limited series are available to analyze situations in which the likelihood of resistance is greatest. We present our experience with fluconazole-resistant candidiasis in patients with HIV infection obtained from retrospective chart review and by testing strains of C. albicans isolated during relapse for susceptibility to antifungal agents. The possible reasons for failure of antifungal therapy are discussed, as well the correlation between in vivo and in vitro data. Resistant candidiasis in patients with HIV disease is an emerging problem of considerable concern that merits further study. C1 UNIV NEBRASKA,MED CTR,DEPT INTERNAL MED,INFECT DIS SECT,600 S 42ND ST,OMAHA,NE 68198. AUDIE L MURPHY MEM VET ADM MED CTR,VET ADM,SAN ANTONIO,TX 78284. NR 19 TC 136 Z9 137 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD DEC PY 1993 VL 17 IS 6 BP 1018 EP 1021 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA ML918 UT WOS:A1993ML91800011 PM 8110924 ER PT J AU BARKLEY, B LICHTENSTEIN, MJ GARZA, C HAZUDA, HP AF BARKLEY, B LICHTENSTEIN, MJ GARZA, C HAZUDA, HP TI VALIDATION OF THE WELCH-ALLYN PNEUMOCHECK(TM) SPIROMETER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. UTHSC,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A752 EP A752 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800200 ER PT J AU DENINO, LA SMITH, T PINKSTON, M WILLIAMS, JW MULROW, CD AGUILAR, C AF DENINO, LA SMITH, T PINKSTON, M WILLIAMS, JW MULROW, CD AGUILAR, C TI DEVELOPMENT OF A PICTORIAL DIARY OF HEALTH-CARE UTILIZATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A750 EP A750 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800190 ER PT J AU FOUQUERAY, B KIYOMOTO, H GHOSHCHOUDHURY, G ABBOUD, HE AF FOUQUERAY, B KIYOMOTO, H GHOSHCHOUDHURY, G ABBOUD, HE TI GLUCOSE MODULATES TYROSINE PHOSPHATASE-ACTIVITY IN CULTURED MESANGIAL CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A809 EP A809 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800510 ER PT J AU GIBSON, S GERETY, MB WILLIAMS, JW MULROW, CD CORNELL, JE AF GIBSON, S GERETY, MB WILLIAMS, JW MULROW, CD CORNELL, JE TI DEPRESSION SCREENING SCALES - EFFECT OF FUNCTION, COGNITION, DISEASE NUMBER ON OPERATING CHARACTERISTICS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A817 EP A817 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800541 ER PT J AU HOLLEMAN, DR WILLIAMS, JW SIMEL, DL AF HOLLEMAN, DR WILLIAMS, JW SIMEL, DL TI USUAL CARE OF PATIENTS WITH SINUS COMPLAINTS LACKING RADIOGRAPHIC SINUSITIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET AFFAIRS MED CTR,LEXINGTON,KY. VET AFFAIRS MED CTR,SAN ANTONIO,TX. VET AFFAIRS MED CTR,DURHAM,NC. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A818 EP A818 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800546 ER PT J AU HOWARD, JP DRAKE, TR KELLOGG, DL AF HOWARD, JP DRAKE, TR KELLOGG, DL TI DELIVERY OF HYDROXOCOBALAMIN BY LECTRO-PATCH(R) IONTOPHORESIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A758 EP A758 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800233 ER PT J AU KANTEN, DN MULROW, CD GERETY, MB CORNELL, JE ROSENBERG, J AF KANTEN, DN MULROW, CD GERETY, MB CORNELL, JE ROSENBERG, J TI PREDICTORS OF FALLS IN FRAIL NURSING-HOME RESIDENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A751 EP A751 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800194 ER PT J AU WAI, W LICHTENSTEIN, MJ MONTERROSA, A ESPINO, DV HAZUDA, HP AF WAI, W LICHTENSTEIN, MJ MONTERROSA, A ESPINO, DV HAZUDA, HP TI CORRELATION OF STATIC AND DYNAMIC MEASURES OF BALANCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. UTHSC,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A752 EP A752 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800197 ER PT J AU WILLIAMS, JW HOLLEMAN, DR SAMSA, G SIMEL, DL AF WILLIAMS, JW HOLLEMAN, DR SAMSA, G SIMEL, DL TI RANDOMIZED DOUBLE-BLIND TRIAL OF 3 VERSUS 10 DAYS OF TRIMETHOPRIMSULFAMETHOXAZOLE FOR ACUTE SINUSITIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,SAN ANTONIO,TX. VET ADM MED CTR,LEXINGTON,KY 40511. VET ADM MED CTR,DURHAM,NC 27705. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A752 EP A752 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800201 ER PT J AU HUNT, LM AF HUNT, LM TI THE METASTASIS OF WITCHCRAFT - THE INTERRELATIONSHIP BETWEEN TRADITIONAL AND BIOMEDICAL CONCEPTS OF CANCER IN SOUTHERN MEXICO SO COLLEGIUM ANTROPOLOGICUM LA English DT Article ID ILLNESS; STRESS AB Patients receiving biomedical treatment for cancer in two provincial cities in Southern Mexico were observed in an ethnographic study, to rely primarily on biomedicine for diagnosis and treatment. However, close examination of their illness explanations and understandings revealed that they often incorporated traditional illness concepts (eg: witchcraft or susto) into these biomedically-based explanatory models. This paper explores their integration of traditional and biomedical models. It is proposed that, while biomedicine provides a basis for classifying illness and directing practical action, it leaves other needs unaddressed. An examination of case examples indicates that traditional illness models are incorporated with biomedical models because they address specific emotional, psychological, social and political-economic issues important to patients' experience of illness, but ignored by biomedical approaches. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP HUNT, LM (reprint author), UNIV N CAROLINA,DEPT SOCIOL ANTHROPOL & SOCIAL WORK,CHARLOTTE,NC 28223, USA. NR 32 TC 2 Z9 2 U1 1 U2 2 PU SCH BIOLOGICAL ANTHROPOLOGY PI ZAGREB PA MOSE PIJADE 158 P O BOX 291, 41001 ZAGREB, CROATIA SN 0350-6134 J9 COLLEGIUM ANTROPOL JI Coll. Anthropol. PD DEC PY 1993 VL 17 IS 2 BP 249 EP 256 PG 8 WC Anthropology SC Anthropology GA MP682 UT WOS:A1993MP68200008 ER PT J AU LUZI, L PETRIDES, AS DEFRONZO, RA AF LUZI, L PETRIDES, AS DEFRONZO, RA TI DIFFERENT SENSITIVITY OF GLUCOSE AND AMINO-ACID-METABOLISM TO INSULIN IN NIDDM SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; LEUCINE METABOLISM; PROTEIN-SYNTHESIS; SUBSTRATE AVAILABILITY; RESISTANCE; PATHOGENESIS; MUSCLE; OXIDATION; TURNOVER; DISPOSAL AB NIDDM subjects are characterized by impaired glucose tolerance and insulin resistance with respect to glucose metabolism. To examine whether the defect in glucose utilization extends to amino acid metabolism, 6 NIDDM subjects (64 +/- 4 yr of age; ideal body weight of 107 +/- 3%) and 7 control subjects (58 +/- 4 yr of age; ideal body weight of 105 +/- 2%) were studied with the euglycemic insulin clamp technique, in combination with [1-C-14]leucine and indirect calorimetry. All subjects participated in two studies. In study 1, after 3 h of tracer equilibration, a 3-h insulin clamp (40 mU.m-2.min-1) was performed to define the effect of insulin on leucine kinetics and glucose metabolism. In study 2, subjects received a repeat 3-h insulin clamp, and a balanced amino acid solution was infused to increase the plasma amino acid concentrations approximately 2-fold to examine the effect of combined physiological hyperinsulinemia-hyperaminoacidemia on the rate of leucine and glucose disposal, insulin-mediated total body glucose uptake was significantly reduced in NIDDM during both study 1 (5.6 +/- 0.4 vs. 6.9 +/- 0.6 mg.kg-1.min-1, P < 0.01) and study 2 (5.2 +/- 0.4 vs. 6.8 +/- 0.6, P < 0.01). Basal plasma leucine (120 +/- 10 vs. 123 +/- 11 muM) and alpha-ketoisocaproic acid concentrations (28 +/- 3 vs. 25 +/- 2 muM) were similar in NIDDM and control subjects, respectively. In contrast, the basal plasma glucose concentration (8.9 +/- 0.8 vs. 4.7 +/- 0.2 muM) and the HbA1c (8.5 +/- 0.2 vs. 5.7 +/- 0.2%) were significantly increased in NIDDM (P < 0.01). In the postabsorptive state, endogenous leucine flux, leucine oxidation, and nonoxidative leucine disposal were similar in NIDDM and control subjects. When insulin was infused without amino acids (study 1), the decrement in plasma leucine (53 +/- 5 vs. 48 +/- 4 muM), endogenous leucine flux (13 +/- 2 vs. 11 +/-1 mumol.m-2.min-1), leucine oxidation (1.6 +/- 0.2 vs. 1.3 +/- 0.1 mumol.m-2.min-1), and nonoxidative leucine disposal (10 +/- 1 vs. 8 +/- 1 mumol.m-2.min-1) was comparable in both groups. During combined insulin and amino acid infusion (study 2), plasma leucine concentration (185 +/- 20 vs. 190 +/- 15 muM) rose similarly in NIDDM and control subjects. In NIDDM, the increment in leucine oxidation (9.0 +/- 0.7 vs. 8.5 +/- 0.6 mumol.m-2.min-1) and nonoxidative leucine disposal (9.3 +/- 0.7 vs. 10.5 +/- 0.9 mumol.m-2.min-1) was similar to that observed in control subjects; the decrement in endogenous leucine flux (22.3 +/- 2.1 vs. 20.2 +/- 1.9 mumol.m-2.min-1) was comparable in both groups. We conclude that 1) insulin-mediated glucose disposal is significantly impaired in NIDDM and 2) the effect of insulin on endogenous leucine flux (protein degradation), nonoxidative leucine disposal (protein synthesis), and leucine oxidation is similar in NIDDM and control subjects. These results indicate a clear-cut dissociation between the effect of insulin on glucose and protein metabolism in NIDDM. C1 UNIV TEXAS,HLTH SCI CTR,DEPT INTERNAL MED,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP LUZI, L (reprint author), UNIV MILAN,S RAPHAEL SCI INST,DEPT MED,RADIOACT & STABLE ISOTOPES LAB,I-20132 MILAN,ITALY. RI Luzi, Livio/M-2696-2016 OI Luzi, Livio/0000-0003-3183-0552 FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 36 TC 62 Z9 63 U1 0 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD DEC PY 1993 VL 42 IS 12 BP 1868 EP 1877 DI 10.2337/diabetes.42.12.1868 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MJ775 UT WOS:A1993MJ77500023 PM 8243833 ER PT J AU LEUCHTER, AF COOK, IA NEWTON, TF DUNKIN, J WALTER, DO ROSENBERGTHOMPSON, S LACHENBRUCH, PA WEINER, H AF LEUCHTER, AF COOK, IA NEWTON, TF DUNKIN, J WALTER, DO ROSENBERGTHOMPSON, S LACHENBRUCH, PA WEINER, H TI REGIONAL DIFFERENCES IN BRAIN ELECTRICAL-ACTIVITY IN DEMENTIA - USE OF SPECTRAL POWER AND SPECTRAL RATIO MEASURES SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE QUANTITATIVE EEG; ALZHEIMERS DISEASE; MULTIINFARCT DEMENTIA; REGIONAL DIFFERENCES ID EMISSION COMPUTED-TOMOGRAPHY; MULTI-INFARCT DEMENTIA; ALZHEIMERS-DISEASE; SENILE DEMENTIA; VASCULAR DEMENTIA; DEPRESSED SUBJECTS; FREQUENCY-ANALYSIS; EEG ANALYSIS; DIAGNOSIS; DISTRIBUTIONS AB The pathologic changes in dementia of the Alzheimer's type (DAT) commonly affect selected brain regions. The cortical areas affected in multi-infarct dementia (MID) are less predictable and may be secondary to subcortical gray or white matter damage that is widespread in MID, We compared several types of quantitative EEG power measures (absolute and relative power, and ratios of power) to determine their regional distribution, and their association with changes in cognitive status and age. We examined 49 subjects with clinically diagnosed mild-to-moderate DAT, 29 with mild-to-moderate MID, and 38 elderly controls (CON). We used discriminant analysis to identify, for each parameter type, the brain region and frequency band where the parameter best distinguished between groups of subjects. The parameters showed regional differences in distinguishing between DAT and MID subjects, and in their association with age and cognitive status. All parameters were useful for detecting differences between normal and demented subjects and correctly identified comparable proportions of subjects as having dementia. Subjects who were abnormal on several parameters were much more likely to have dementia. The additive effects of these parameters in correct classification suggest that they may be monitoring different physiologic processes. Combinations of several types of parameters may be more useful than individual parameters for distinguishing demented from non-demented subjects. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT BIOSTAT,LOS ANGELES,CA 90024. RP LEUCHTER, AF (reprint author), UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,QUANTITAT EEG LAB,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. OI newton, thomas/0000-0002-3198-5901 FU NIMH NIH HHS [NIMH MH 00665, NIMH MH 17140, NIMH MH 40705] NR 45 TC 137 Z9 142 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD DEC PY 1993 VL 87 IS 6 BP 385 EP 393 DI 10.1016/0013-4694(93)90152-L PG 9 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA MR140 UT WOS:A1993MR14000006 PM 7508371 ER PT J AU WENZEL, SL GELBERG, L BAKHTIAR, L CASKEY, N HARDIE, E REDFORD, C SADLER, N AF WENZEL, SL GELBERG, L BAKHTIAR, L CASKEY, N HARDIE, E REDFORD, C SADLER, N TI INDICATORS OF CHRONIC HOMELESSNESS AMONG VETERANS SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID MENTAL-HEALTH; ADULTS; PROGRAM; SHELTER; OLDER; CITY AB Objective: This study sought to develop a set of indicators of chronic homelessness as a basis for better understanding and treatment of the homeless veteran population. Methods: Chi square analysis and the t test or Mann-Whitney U test were used to compare characteristics of veterans who reported long-term homelessness (more than 12 months total since age 18) with those of veterans who reported short-term homelessness (12 months or less). Subjects were 343 homeless male veterans receiving treatment for physical, mental, or substance abuse disorders at the West Los Angeles site of the Domiciliary Care for Homeless Veterans Program. Variables included history of homelessness, employment history, physical and mental health, substance abuse history, social and financial support, criminal history, age, ethnic group, education, military service, and program discharge status. Results: Veterans experiencing long-term homelessness were more likely to be white, to have had a longer period of recent homelessness and a greater number of homeless episodes, to have a poor employment history, to have symptoms of mental and substance abuse disorders, and to have weaker social support. Conclusions: Results show that variables besides duration of lifetime homelessness are important indicators of chronic homelessness. C1 W LOS ANGELES VET AFFAIRS MED CTR,DOMICILIARY CARE HOMELESS VET PROGRAM,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT SOCIOL,10833 LECONTE AVE,ROOM 50-071 CHS,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DIV FAMILY MED,LOS ANGELES,CA 90024. NR 42 TC 18 Z9 18 U1 2 U2 6 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD DEC PY 1993 VL 44 IS 12 BP 1172 EP 1176 PG 5 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA MK091 UT WOS:A1993MK09100009 PM 8132190 ER PT J AU BLAKE, DC RUSSELL, RG AF BLAKE, DC RUSSELL, RG TI DEMONSTRATION OF LIPOPOLYSACCHARIDE WITH O-POLYSACCHARIDE CHAINS AMONG DIFFERENT HEAT-STABLE SEROTYPES OF CAMPYLOBACTER-JEJUNI BY SILVER STAINING OF POLYACRYLAMIDE GELS SO INFECTION AND IMMUNITY LA English DT Note ID PASSIVE HEMAGGLUTINATION; PSEUDOMONAS-AERUGINOSA; NEISSERIA-MENINGITIDIS; THERMOSTABLE ANTIGENS; MACACA-NEMESTRINA; COLI; STRAINS; HETEROGENEITY AB Lipopolysaccharide (LPS) from three human and four monkey isolates of Campylobacter jejuni was extracted in high yields that revealed ladder-like structures in polyacrylamide gels by direct silver staining. These observations demonstrate that C. jejuni possesses LPS with O-chain repeating units typical of the family Enterobacteriaceae. The isolates showed differences in the number and electrophoretic mobility of bands in silver-stained gels. C1 US DEPT VET AFFAIRS,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,PROGRAM COMPARAT MED,BALTIMORE,MD 21201. FU NCRR NIH HHS [RR03123] NR 35 TC 9 Z9 9 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD DEC PY 1993 VL 61 IS 12 BP 5384 EP 5387 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MH823 UT WOS:A1993MH82300060 PM 7693600 ER PT J AU VENTURA, J GREEN, MF SHANER, A LIBERMAN, RP AF VENTURA, J GREEN, MF SHANER, A LIBERMAN, RP TI TRAINING AND QUALITY ASSURANCE WITH THE BRIEF PSYCHIATRIC RATING-SCALE - THE DRIFT BUSTERS SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH LA English DT Article DE BPRS; BPRS TRAINING; BPRS QUALITY ASSURANCE; PSYCHIATRIC SYMPTOM ASSESSMENT; BPRS RELIABILITY ID SCHIZOPHRENIA; RELIABILITY; SYMPTOMS AB Despite the prominence of the Brief Psychiatric Rating Scale (BPRS) in psychiatric research, relatively little has been published about training methods and procedures used to maintain consistency over time of interviewer style and inter-rater reliability. A training and quality assurance program, developed at the UCLA Clinical Research Center for Schizophrenia and Psychiatric Rehabilitation, has relied on an expanded manual with behavioral anchor points that are used when trainees view a series of videotaped BPRSs or conduct live BPRS interviews. Trainees with both advanced and predoctoral degrees were able to achieve and maintain high levels of reliability. RP VENTURA, J (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR, LOS ANGELES, CA 90073 USA. NR 30 TC 565 Z9 567 U1 2 U2 11 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1049-8931 J9 INT J METH PSYCH RES JI Int. J. Methods Psychiatr. Res. PD DEC PY 1993 VL 3 IS 4 BP 221 EP 244 PG 24 WC Psychiatry SC Psychiatry GA MX331 UT WOS:A1993MX33100003 ER PT J AU BENNETT, RL GILMAN, SC GEORGE, L GUZE, PA BENNETT, CL AF BENNETT, RL GILMAN, SC GEORGE, L GUZE, PA BENNETT, CL TI IMPROVED OUTCOMES IN INTENSIVE-CARE UNITS FOR AIDS-RELATED PNEUMOCYSTIS-CARINII PNEUMONIA - 1987-1991 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article DE PNEUMOCYSTIS-CARINII PNEUMONIA; INTENSIVE CARE UNIT; OUTCOME; SURVIVAL RATE ID ACQUIRED IMMUNODEFICIENCY SYNDROME; RESPIRATORY-FAILURE; SURVIVAL AB Respiratory failure due to Pneumocystis carinii pneumonia (PCP) is the most common complication requiring an intensive care unit (ICU) for persons with AIDS. In this study, we evaluated patterns of ICU use for ICU patients with first-episode PCP in 15 Veterans Administration Medical Centers from 1987 to 1991. Twelve percent of all patients with PCP received care in the ICU. The survival rates improved steadily during these years. Although there was little variation in the relative frequency of ICU use, the effectiveness of ICU use appeared to improve over time. In the more recent years, relatively more survivors and relatively fewer nonsurvivors received care in an ICU. Changes in medical practice such as adjunctive use of steroids for severe cases of PCP and more effective use of scarce resources may account for the improved survival rates for patients with PCP who are treated in an ICU. C1 DURHAM VET AFFAIRS, DIV HLTH SERV RES & DEV 152, 508 FULTON ST, DURHAM, NC 27705 USA. VET AFFAIRS WESTERN REG SPECIAL STUDIES GRP, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS HOSP, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. UNIV CALIF IRVINE, SCH MED, IRVINE, CA 92717 USA. DUKE UNIV, DURHAM, NC 27706 USA. FU AHRQ HHS [1R01HS06494-01] NR 12 TC 15 Z9 15 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD DEC PY 1993 VL 6 IS 12 BP 1319 EP 1321 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MM128 UT WOS:A1993MM12800006 PM 8254469 ER PT J AU MORALES, CF ANZUETO, A ANDRADE, F LEVINE, SM MAXWELL, LC LAWRENCE, RA JENKINSON, SG AF MORALES, CF ANZUETO, A ANDRADE, F LEVINE, SM MAXWELL, LC LAWRENCE, RA JENKINSON, SG TI DIETHYLMALEATE PRODUCES DIAPHRAGMATIC IMPAIRMENT AFTER RESISTIVE BREATHING SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE RESPIRATORY MUSCLES; DIAPHRAGM; FREE RADICALS; EXERTION; GLUTATHIONE; ANTIOXIDANT; MUSCLE FATIGUE; CONTRACTILE PROPERTIES; OXIDIZED GLUTATHIONE; GLUTATHIONE REDOX CYCLE ID EXHAUSTIVE EXERCISE; SKELETAL-MUSCLE; RAT DIAPHRAGM; GLUTATHIONE; METABOLISM; ACETYLCYSTEINE; PERFORMANCE; DAMAGE; CYCLE AB Formation of oxygen-derived free radicals and activation of the glutathione (GSH) redox cycle has been associated with impaired rat diaphragm performance. Diethylmaleate (DEM) given intraperitoneally irreversibly conjugates with GSH, resulting in marked decreases in tissue concentrations of GSH. We have investigated the effects of acute GSH depletion by DEM on diaphragmatic function during resistive breathing (RB) in the rat. The experimental groups were 1) control, 2) DEM alone, 3) RB, and 4) DEM with RB (DEM + RB). RB was obtained by inspiratory RB until the rats were unable to sustain 70% of maximum airway opening pressure. A portion of the diaphragm was frozen for biochemical assays, and the rest of the diaphragm was prepared for measurement of in vitro contractile properties, including maximum tetanic tension, twitch tension, force-frequency curves, and contraction times. DEM treatment produced a profound depletion of GSH in the DEM and DEM + RB groups. Neither DEM nor RB alone significantly altered diaphragm contractile properties. In DEM + RB rats, however, there was a significant decrease in maximum tetanic tension, twitch tension, and tetanic tension. These data reveal that DEM produced an acute depletion of GSH in the diaphragm without impairment of the muscle in nonstressed rats. In the presence of DEM-induced GSH depletion, RB did result in marked diaphragm impairment. The depletion of GSH and the subsequent impairment in diaphragm contractility after RB suggest that GSH may play an important role in protecting the diaphragm against oxidative stress associated with RB. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,SAN ANTONIO,TX 78236. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 FU NHLBI NIH HHS [HL-32824] NR 32 TC 21 Z9 21 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD DEC PY 1993 VL 75 IS 6 BP 2406 EP 2411 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA MN705 UT WOS:A1993MN70500010 PM 8125857 ER PT J AU HAFFNER, SM MYKKANEN, L VALDEZ, RA KATZ, MS AF HAFFNER, SM MYKKANEN, L VALDEZ, RA KATZ, MS TI RELATIONSHIP OF SEX-HORMONES TO LIPIDS AND LIPOPROTEINS IN NONDIABETIC MEN SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CARDIOVASCULAR RISK-FACTORS; HEPATIC TRIGLYCERIDE LIPASE; ANABOLIC-STEROID THERAPY; POST-MENOPAUSAL WOMEN; BODY-FAT DISTRIBUTION; HEALTHY ADULT MEN; BINDING GLOBULIN; DEHYDROEPIANDROSTERONE SULFATE; INSULIN-RESISTANCE; POSTMENOPAUSAL WOMEN AB Although many studies show that increased androgenicity is associated with increased triglyceride (TG) and decreased high density lipoprotein cholesterol in both pre- and postmenopausal women, relatively few data are available on the association of sex hormones to lipids and lipoproteins in men. We examined the association of sex hormone-binding globulin (SHBG), total and free testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), and estradiol with lipids and lipoproteins in 178 nondiabetic men from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. The TG concentration was significantly inversely related to SHBG (r = -0.22), free testosterone (r = -0.15), total testosterone (r = -0.22), and DHEA-SO4 (r = -0.16). High density lipoprotein (HDL) cholesterol was significantly positively correlated to SHBG (r = 0.21), free testosterone (r = 0.15), total testosterone (I = 0.17), and DHEA-SO4 (r = 0.16). Total testosterone was significantly related to total cholesterol (r = -0.17) and low density lipoprotein cholesterol (r = -0.15). After adjustment for age, body mass index, waist to hip ratio, and glucose and insulin concentrations, TG concentrations remained significantly related to SHBG (r = -0.20), free testosterone (r = -0.15), and DHEA-SO4 (r = -0.18), and HDL cholesterol remained significantly associated with SHBG (r = 0.17), free testosterone (r = 0.15), total testosterone (r = 0.14), and DHEA-SO4 (r = 0.16). In conclusion, we observed a less atherogenic lipid and lipoprotein profile with increased testosterone concentrations. This was not explained by differences in glucose or insulin concentrations. However, sex hormones explained only a small percentage of the variation in total TG and HDL cholesterol concentrations. These findings are in striking contrast to data from women, in whom increased androgenicity is strongly associated with increased TG and decreased HDL cholesterol levels. C1 AUDIE L MURPHY MEM VET ADM MED CTR, CTR GERIATR RES EDUC & CLIN, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV CLIN EPIDEMIOL, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV GERIATR & GERONTOL, SAN ANTONIO, TX 78284 USA. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU NHLBI NIH HHS [NHLBI R01-HL-24799, NHLBI R37-HL-36820] NR 50 TC 149 Z9 154 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD DEC PY 1993 VL 77 IS 6 BP 1610 EP 1615 DI 10.1210/jc.77.6.1610 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MM202 UT WOS:A1993MM20200031 PM 8263149 ER PT J AU GANZINI, L LEE, MA HEINTZ, RT BLOOM, JD AF GANZINI, L LEE, MA HEINTZ, RT BLOOM, JD TI DEPRESSION, SUICIDE, AND THE RIGHT TO REFUSE LIFE-SUSTAINING TREATMENT SO JOURNAL OF CLINICAL ETHICS LA English DT Note C1 OREGON HLTH SCI UNIV,DEPT PSYCHIAT,PORTLAND,OR 97201. DAMMASCH STATE HOSP,WILSONVILLE,OR. RP GANZINI, L (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR, USA. NR 12 TC 5 Z9 5 U1 0 U2 0 PU UNIV PUBL GROUP, INC PI FREDERICK PA 12 SOUTH MARKET ST, STE 301, FREDERICK, MD 21701 SN 1046-7890 J9 J CLIN ETHIC JI J. Clin. Ethics PD WIN PY 1993 VL 4 IS 4 BP 337 EP 340 PG 4 WC Ethics; Social Sciences, Biomedical SC Social Sciences - Other Topics; Biomedical Social Sciences GA MM314 UT WOS:A1993MM31400012 PM 7803833 ER PT J AU CAREY, K AF CAREY, K TI RESERVATION PRICE ANNOUNCEMENT IN SEALED BID AUCTIONS SO JOURNAL OF INDUSTRIAL ECONOMICS LA English DT Article AB This article compares the strategic announcement of a reservation price by a bid-taking buyer in a first-price sealed bid auction with the strategy of no announcement. Simulation results indicate that an operative ceiling price that is unknown to bidders will yield lower supply costs to the buyer than when the latter announces the reservation price truthfully. However, given enough bidders, the buyer can achieve an even lower expected cost of supply by announcing a falsely low reservation price. RP CAREY, K (reprint author), US DEPT VET AFFAIRS,MANAGEMENT SCI GRP,200 SPRINGS RD,BEDFORD,MA 01730, USA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0022-1821 J9 J IND ECON JI J. Indust. Econ. PD DEC PY 1993 VL 41 IS 4 BP 421 EP 429 DI 10.2307/2950601 PG 9 WC Business, Finance; Economics SC Business & Economics GA MJ198 UT WOS:A1993MJ19800006 ER PT J AU GORMAN, DG CUMMINGS, JL AF GORMAN, DG CUMMINGS, JL TI NEUROBEHAVIORAL PRESENTATIONS OF THE ANTIPHOSPHOLIPID ANTIBODY SYNDROME SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTICARDIOLIPIN ANTIBODIES; ANTICOAGULANT; DISEASE; PREVALENCE; DISORDERS; STANDARDIZATION; AUTOANTIBODIES; CARDIOLIPIN; COAGULATION AB Antiphospholipid antibodies, including lupus anticoagulant and anticardiolipin antibodies, are increasingly recognized as a cause of neurological morbidity. They may occur with or without evidence of systemic lupus erythematosus and have been associated with stroke, migraine, and confusional states. Their role as etiologic or contributing factors in neurobehavioral and neuro-psychiatric syndromes of obscure etiology has not been emphasized. The cases of 7 patients who were referred for evaluation of behavior abnormalities and had antiphospholipid antibodies are presented, and the potential relationships of the anti-phospholipid antibody syndrome to behavioral alterations are discussed. C1 W LOS ANGELES VAMC, PSYCHIAT SERV,BEHAV NEUROSCI SECT,NEUROBEHAV UNIT, BLDG 256B, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL & PSYCHIAT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT BIOBEHAV SCI, LOS ANGELES, CA USA. NR 28 TC 21 Z9 21 U1 0 U2 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD WIN PY 1993 VL 5 IS 1 BP 37 EP 42 PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KK041 UT WOS:A1993KK04100006 PM 8094019 ER PT J AU DEPAUL, R BROOKS, BR AF DEPAUL, R BROOKS, BR TI MULTIPLE OROFACIAL INDEXES IN AMYOTROPHIC-LATERAL-SCLEROSIS SO JOURNAL OF SPEECH AND HEARING RESEARCH LA English DT Article DE AMYOTROPHIC LATERAL SCLEROSIS (ALS); DYSARTHRIA; SPEECH; WEAKNESS; TONGUE; LIP; JAW ID PRIMARY MOTOR CORTEX; TRAINED TONGUE-PROTRUSION; FUNCTIONAL-PROPERTIES; SINGLE NEURONS; MOTONEURON INVOLVEMENT; SPEECH-INTELLIGIBILITY; CLINICAL-FEATURES; DYSARTHRIA; PERFORMANCE; DISEASE AB Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by significant speech and swallowing problems resulting from upper and lower motor neuron loss. Weakness is the primary ALS disease-related sign, and measures of muscle strength have revealed nonuniform patterns of muscle weakness in orofacial muscles. To a large extent, muscle strength measures in these studies have not been evaluated in terms of functional significance, and few researchers have addressed the relation between weakness and motor neuron loss. This study addressed whether multiple measures, including static isometric maximum voluntary contraction (MVC), a dynamic measure of the peak rate of change of force (PRCF), an upper motor neuron (UMN) index, and a functional disability score (FDS) might enhance understanding of speech dysfunction in ALS. Ten males diagnosed with sporadic ALS showing mild speech impairment and an equal number of matched controls were studied. Tongue MVC and PRCF were more impaired than those of the lip and jaw, irrespective of the time post onset and site of initial symptoms. Results also suggested that disproportionate tongue impairment may be related to UMN deficits. However, impairments in the rate of contraction did not appear to be related to UMN deficits. Tongue weakness and tongue and lower lip PRCF were related to the degree of speech severity, but none of the measures was related to speech intelligibility. The value of a functional outcome measure like speech intelligibility and its role in characterizing orofacial involvement in the early stages of ALS bulbar impairment are discussed. C1 UNIV WISCONSIN,WHITEWATER,WI 53190. WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV,MADISON,WI 53705. RP DEPAUL, R (reprint author), UNIV WISCONSIN,WAISMAN CTR,RM 579,1500 HIGHLAND AVE,MADISON,WI 53705, USA. FU NIDCD NIH HHS [R29DC00921-01] NR 87 TC 36 Z9 38 U1 0 U2 3 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE RD, ROCKVILLE, MD 20852-3279 SN 0022-4685 J9 J SPEECH HEAR RES JI J. Speech Hear. Res. PD DEC PY 1993 VL 36 IS 6 BP 1158 EP 1167 PG 10 WC Language & Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA MK809 UT WOS:A1993MK80900005 PM 8114482 ER PT J AU GERETY, MB CORNELL, JE PLICHTA, DT EIMER, M AF GERETY, MB CORNELL, JE PLICHTA, DT EIMER, M TI ADVERSE EVENTS RELATED TO DRUGS AND DRUG-WITHDRAWAL IN NURSING-HOME RESIDENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ELDERLY POPULATION; HIP FRACTURE; LONG; SERVICES; ILLNESS; THERAPY; TRIAL; RISK AB Objective: To (1) develop and standardize explicit criteria to link clinical adverse events to drug withdrawal, (2) determine the incidence and severity of Adverse Drug Events (ADEs) and Adverse Drug Withdrawal Events (ADWEs) in a nursing home population, and (3) establish the contribution of demographic, clinical, and functional characteristics to ADEs and ADWEs. Design: Retrospective record review of an admission cohort. Setting and Subjects: Consecutive admissions of residents of an academic Veterans Affairs nursing home with available records and lengths of stay >30 days (n = 175). Subjects were 96% men, aged 70 +/- 12 years, and took 7.0 +/- 3.4 medications. Methods: We applied standardized algorithms to determine incidence, probability, and severity of ADEs and ADWEs. Multiple regression techniques were used to identify factors associated with frequency and risk of events. Results: Ninety five residents experienced 201 ADEs. Twelve required hospitalization or prolonged hospitalization, and one resident died. Sixty two persons had 94 ADWEs. None were associated with death and one with hospitalization. The four most commonly prescribed drug classes accounted for 72% of ADEs and 80% of ADWEs. Results of multivariate analyses showed common risk factors for both ADEs and ADWEs: number of diagnoses, number of medications, and hospitalization during the nursing home stay. Conclusions: ADEs and ADWEs were common in nursing home residents in this Veteran's Affairs setting. Explicit criteria developed and applied in this study should be applied prospectively in other settings, both to further define risk of drug discontinuation and to assist in development of specific drug discontinuation guidelines. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. RP GERETY, MB (reprint author), AUDIE L MURPHY VET MEM HOSP,GRECC 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 39 TC 64 Z9 64 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD DEC PY 1993 VL 41 IS 12 BP 1326 EP 1332 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA MK559 UT WOS:A1993MK55900007 PM 8227915 ER PT J AU COHEN, SN HOBSON, RW WEISS, DG CHIMOWITZ, M JARRETT, F RILES, T CALLIGARO, K THIELE, BL SCHECHTER, DC SMITH, RB AMMONS, J GIANNETTI, R VOLLMAN, RW JOHNSON, W BUTLER, R KASE, C HAMILTON, J WALKER, N GAGE, A POWELL, CS SORIA, E OLSZEWSKI, WA GUTIERREZ, I YOUNG, DE BURCH, K LYNCH, TG PADBERG, F SHANAWANI, S JOHNSON, DA ROGERS, C HIRATZKA, LF CORSON, J TALMAN, WT MARTIN, C GRIMTH, VB YUTZY, J LUTES, B THOMPSON, BW MORGAN, D MCDONALD, C BAKER, JD METTER, EJ RABEY, N DIX, D TOWNE, JB BANDYK, D SAXENA, VK NAVINE, J CATAROZOLI, K LANZA, D PARSON, P KRUPSKI, WC RAPP, J SHARP, F PEREZ, S GOLDSTONE, J BERNHARD, V LABADIE, E NASH, M PHELPS, B VANCE, J ANDERSON, G ZIERLER, RE STABILE, B WILSON, S EMMA, L HUBBERT, C HAAKENSON, CI TOUSSAINT, D YOUNG, L COLLING, C FIELDS, WS MOORE, WS WRIGHT, CB ROSSOS, S GEORGE, A CALLOW, AD FLORA, RE GROTTA, JC IMPARATO, A CRIGLER, C BEARD, W CAESAR, SL COVI, L GAUVEY, SK LIPMAN, RS KURZ, R BLOCK, K LEVITON, SP RASKIN, A MOORE, M SAFER, D FELDBUSH, MW PEREZ, E WEISS, R ARTHUR, MM HOBBINS, TE SONG, IS CAPLAN, LR WRIGHT, C KLETT, CJ COLLINS, JF JACKSON, P MORSON, D CARTER, BD MCMULLEN, B KUHN, R MILLER, B LEE, M PRESTON, D DAVIS, D LINZY, L LUCAS, C DEYKIN, D GOLD, J HUANG, P AF COHEN, SN HOBSON, RW WEISS, DG CHIMOWITZ, M JARRETT, F RILES, T CALLIGARO, K THIELE, BL SCHECHTER, DC SMITH, RB AMMONS, J GIANNETTI, R VOLLMAN, RW JOHNSON, W BUTLER, R KASE, C HAMILTON, J WALKER, N GAGE, A POWELL, CS SORIA, E OLSZEWSKI, WA GUTIERREZ, I YOUNG, DE BURCH, K LYNCH, TG PADBERG, F SHANAWANI, S JOHNSON, DA ROGERS, C HIRATZKA, LF CORSON, J TALMAN, WT MARTIN, C GRIMTH, VB YUTZY, J LUTES, B THOMPSON, BW MORGAN, D MCDONALD, C BAKER, JD METTER, EJ RABEY, N DIX, D TOWNE, JB BANDYK, D SAXENA, VK NAVINE, J CATAROZOLI, K LANZA, D PARSON, P KRUPSKI, WC RAPP, J SHARP, F PEREZ, S GOLDSTONE, J BERNHARD, V LABADIE, E NASH, M PHELPS, B VANCE, J ANDERSON, G ZIERLER, RE STABILE, B WILSON, S EMMA, L HUBBERT, C HAAKENSON, CI TOUSSAINT, D YOUNG, L COLLING, C FIELDS, WS MOORE, WS WRIGHT, CB ROSSOS, S GEORGE, A CALLOW, AD FLORA, RE GROTTA, JC IMPARATO, A CRIGLER, C BEARD, W CAESAR, SL COVI, L GAUVEY, SK LIPMAN, RS KURZ, R BLOCK, K LEVITON, SP RASKIN, A MOORE, M SAFER, D FELDBUSH, MW PEREZ, E WEISS, R ARTHUR, MM HOBBINS, TE SONG, IS CAPLAN, LR WRIGHT, C KLETT, CJ COLLINS, JF JACKSON, P MORSON, D CARTER, BD MCMULLEN, B KUHN, R MILLER, B LEE, M PRESTON, D DAVIS, D LINZY, L LUCAS, C DEYKIN, D GOLD, J HUANG, P TI DEATH ASSOCIATED WITH ASYMPTOMATIC CAROTID-ARTERY STENOSIS - LONG-TERM CLINICAL-EVALUATION SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID ENDARTERECTOMY; BRUIT; MANAGEMENT AB Purpose: As part of a prospective clinical trial on the efficacy of carotid endarterectomy in patients with asymptomatic carotid artery stenosis, we studied the risk factors for death in 444 male patients. Methods: At entry to the trial, patients were judged to be healthy enough to be randomized to operative intervention and were judged to be free of any disease that would preclude a minimal 5-year life expectancy after randomization. Results: Patients were treated with aspirin and optimal medical care and were monitored for an average of 4 years. Combined mortality rate was 37% (9% per year) for the medical group (38%) and surgical group (35%). Eight factors were identified that were significantly associated with increased mortality rates: coronary artery disease (p = 0.044), history of angina (p = 0.047), congestive heart failure (CHP) (P = 0.012), abnormal electrocardiography results at entry (p = 0.005), peripheral vascular disease (p = 0.019), claudication (p = 0.044), diabetes (p = 0.008), and history of hypertension (p = 0.044). The increase in risk indicated by the odds ratios (OR) were moderate (OR < 2.00) for each of the clinical risk factors except for CHP. Sixteen of 27 patients (59%) with a history of CHF at entry to the study died during follow-up (OR = 2.67). Arteriographic predictors of increased mortality rates included bilateral carotid artery stenosis and intracranial vascular disease (ICVD). With bilateral stenosis, 42% (80 of 190 patients) died compared with 33% (83 of 252 patients) with unilateral stenosis (p = 0.062). With ICVD, 43% (56 of 130 patients) died compared with 34% (107 of 314 patients) of those without ICVD (p = 0.073). Multivariate analysis demonstrated that three risk factors were significantly associated with an increased risk of death: diabetes, abnormal electrocardiography results, and claudication. Patients with two or three of these risk factors demonstrated annual mortality rates of 11.3% and 13%, respectively. This was significantly higher than patients with none of these risks (OR = 2.95 and OR = 4.06, respectively). Conclusion: Adult male patients with high-grade asymptomatic carotid artery stenosis demonstrate a mortality rate of 37% at a mean follow-up of 4 years. Although age was not a risk for increased mortality rates in this population, diabetes, abnormal electrocardiography results, and claudication were significant. Patients with two or three of these risk factors were at high risk of death and may require aggressive treatment of their concurrent medical diseases. C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. E ORANGE VET AFFAIRS MED CTR, NEWARK, NJ USA. UNIV MED & DENT NEW JERSEY, NEWARK, NJ USA. US DEPT VET AFFAIRS, COOPERAT STUDIES PROGRAM, PERRY POINT, MD USA. UNIV MICHIGAN, ANN ARBOR, MI 48109 USA. VET AFFAIRS MED CTR, ANN ARBOR, MI USA. RP COHEN, SN (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, NEUROL SERV W127, LOS ANGELES, CA 90073 USA. NR 26 TC 27 Z9 27 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD DEC PY 1993 VL 18 IS 6 BP 1002 EP 1011 PG 10 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MM412 UT WOS:A1993MM41200013 PM 8264028 ER PT J AU HELTON, RA HARRISON, WA KELLEY, K KANE, MA AF HELTON, RA HARRISON, WA KELLEY, K KANE, MA TI MELATONIN INTERACTIONS WITH CULTURED MURINE B16 MELANOMA-CELLS SO MELANOMA RESEARCH LA English DT Article DE CANCER; MELANOMA; MELATONIN; RECEPTOR; TAMOXIFEN AB Both in vitro and in vivo observations have suggested that melatonin modulates malignant cell growth. The present studies aimed to characterize the interactions of melatonin with cultured murine B16 melanoma cells. Time- and temperature-dependent specific melatonin accumulation by B16 murine melanoma cells was observed. B16 cells possessed a high affinity binding site (K-D = 1.4 nM) which exhibited structural specificity in its affinity for analogues of melatonin (melatonin > 6-hydroxymelatonin = N-acetyl-5-hydroxytryptamine > 5-methoxytryptamine >> 5-hydroxytryptamine). Evidence for a lower affinity uptake system without structural specificity was also observed. Ninety-five per cent of the specific cell-associated melatonin in B16 cells was present in the soluble subcellular fraction of lysed cells; more than 97% of the cell-associated radioactivity was authentic melatonin. When the solubilized cell extracts from the binding assay were analysed by gel filtration Immediately, all of the bound counts eluted at the void volume. Continuous exposure to melatonin for 48-120 h did not affect B16 cell proliferation as determined by cell counts, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay or [H-3]thymidine incorporation. After 8-h pulse exposures to melatonin daily for 3 days, a 15% stimulation of B16 cell proliferation (p < 0.02) was observed at melatonin concentrations of 0.1 and 1 nM. The anti-oestrogen, tamoxifen, Inhibited B16 cell growth and increased specific melatonin accumulation by B16 cells at 1 x 10(-6) M (p < 0.02). Cultured 816 murine melanoma cells possessed a specific, high affinity uptake system for melatonin which appeared to be altered by anti-oestrogen exposure. C1 DENVER VET AFFAIRS MED CTR,MED ONCOL SECT,DENVER,CO 80220. NR 0 TC 20 Z9 20 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0960-8931 J9 MELANOMA RES JI Melanoma Res. PD DEC PY 1993 VL 3 IS 6 BP 403 EP 413 DI 10.1097/00008390-199311000-00003 PG 11 WC Oncology; Dermatology; Medicine, Research & Experimental SC Oncology; Dermatology; Research & Experimental Medicine GA MU244 UT WOS:A1993MU24400003 PM 8161880 ER PT J AU HALEYZITLIN, V RICHARDSON, A AF HALEYZITLIN, V RICHARDSON, A TI EFFECT OF DIETARY RESTRICTION ON DNA-REPAIR AND DNA-DAMAGE SO MUTATION RESEARCH LA English DT Article DE DNA REPAIR; DIETARY RESTRICTION; DNA DAMAGE ID DRUG-METABOLIZING-ENZYMES; CALORIC RESTRICTION; FEED RESTRICTION; RATS; RODENTS; MICE; AGE; LONGEVITY; KIDNEY; CANCER AB Dietary restriction is the only experimental manipulation known to extend lifespan and retard aging in mammals. Therefore, it is a powerful tool for identifying cellular processes that are involved in aging and senescence. Recently, several laboratories have begun to examine the effects of dietary restriction on the integrity of the genome and the ability of cells to repair DNA. In most studies, it was found that the repair of DNA damage, as measured by unscheduled DNA synthesis, was significantly higher in cells isolated from rodents fed calorie-restricted diets compared to cells isolated from rodents fed ad libitum. Dietary restriction also was observed to be associated with a reduction of the levels of certain types of DNA damage; however, preliminary experiments suggest that the effect of dietary restriction on the age-related accumulation of DNA damage depends on the type of DNA damage studied. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG-0188, AG-0548] NR 32 TC 39 Z9 40 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD DEC PY 1993 VL 295 IS 4-6 BP 237 EP 245 DI 10.1016/0921-8734(93)90023-V PG 9 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA MV034 UT WOS:A1993MV03400008 PM 7507560 ER PT J AU MEYER, JS OBARA, K MURAMATSU, K AF MEYER, JS OBARA, K MURAMATSU, K TI DIASCHISIS SO NEUROLOGICAL RESEARCH LA English DT Review DE DIASCHISIS; STROKE; CEREBRAL BLOOD FLOW; METABOLISM; NEUROLOGICAL RECOVERY ID CROSSED CEREBELLAR DIASCHISIS; EMISSION COMPUTED-TOMOGRAPHY; TEMPORARY BALLOON OCCLUSION; CEREBRAL BLOOD-FLOW; CORTICAL DIASCHISIS; STROKE; INFARCTION; METABOLISM; LESIONS; HUMANS AB Following acute, localized lesions of the central nervous system, arising from any cause, there are immediate depressions of neuronal synaptic functions in other areas of the central nervous system remote from the lesion. These remote effects result from deafferentation, a phenomenon known as ''diaschisis''. After an interval of time, which will vary directly with the severity of the lesion, functional recovery occurs due to synaptic reactivation of neurones. This is favourably influenced by rehabilitation. Diaschisis most commonly manifests itself by such neurological signs as impaired consciousness or cognitive impairments including dementia, dyspraxias, dystaxias, dysphasias, incoordination and sensory neglect. The nature of diaschisis has been demonstrated by widespread depressions of local cerebral blood flow and metabolism extending far beyond the anatomical lesion. Recovery of function is associated with recovery of local perfusion and metabolism. C1 BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. RP MEYER, JS (reprint author), BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBROVASC RES LAB,BLDG 100,ROOM 225,HOUSTON,TX 77030, USA. NR 41 TC 84 Z9 84 U1 1 U2 3 PU FOREFRONT PUBL GROUP PI LONDON PA MONOMARK HOUSE 27 OLD GLOUCESTER STREET, LONDON, ENGLAND WC1N 3XX SN 0161-6412 J9 NEUROL RES JI Neurol. Res. PD DEC PY 1993 VL 15 IS 6 BP 362 EP 366 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MK401 UT WOS:A1993MK40100001 PM 7907401 ER PT J AU SANDERS, MH KERN, NB COSTANTINO, JP STILLER, RA STUDNICKI, K COATES, J ORRIS, S SCHIMERMAN, S AF SANDERS, MH KERN, NB COSTANTINO, JP STILLER, RA STUDNICKI, K COATES, J ORRIS, S SCHIMERMAN, S TI PRESCRIPTION OF POSITIVE AIRWAY PRESSURE FOR SLEEP-APNEA ON THE BASIS OF A PARTIAL-NIGHT TRIAL SO SLEEP LA English DT Article; Proceedings Paper CT 3rd International Conference on Sleep and Breathing CY AUG 31-SEP 03, 1992 CL PALM COVE, AUSTRALIA SP AMER SLEEP DISORDERS ASSOC, SLEEP RES SOC, EUROPEAN SLEEP RES SOC, LATIN AMER SLEEP RES SOC, JAPANESE SLEEP RES SOC C1 US DEPT VET AFFAIRS,DEPT MED,OAKLAND,PA. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT BIOSTAT,PITTSBURGH,PA 15261. RP SANDERS, MH (reprint author), UNIV PITTSBURGH,SCH MED,DEPT MED,DIV PULM ALLERGY & CRIT CARE MED,PITTSBURGH,PA, USA. FU NHLBI NIH HHS [NHLBI 5T32HL07563-07] NR 2 TC 4 Z9 4 U1 0 U2 0 PU AMER SLEEP DISORDERS ASSOC PI ROCHESTER PA 1610 14TH STREET NW SUITE 300, ROCHESTER, MN 55806 SN 0161-8105 J9 SLEEP JI Sleep PD DEC PY 1993 VL 16 IS 8 SU S BP S106 EP S107 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MW457 UT WOS:A1993MW45700038 PM 8177993 ER PT J AU HERSHMAN, JM AF HERSHMAN, JM TI UNTITLED SO THYROID LA English DT Editorial Material RP HERSHMAN, JM (reprint author), W LOS ANGELES VA MED CTR, BLDG 114, ROOM 200, WILSHIRE & SAWTELLE BLVDS, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1050-7256 J9 THYROID JI Thyroid PD WIN PY 1993 VL 3 IS 4 BP 267 EP 267 DI 10.1089/thy.1993.3.267 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ061 UT WOS:A1993MQ06100001 ER PT J AU PANG, XP YOSHIMURA, M HERSHMAN, JM AF PANG, XP YOSHIMURA, M HERSHMAN, JM TI SUPPRESSION OF RAT THYROTROPH AND THYROID-CELL FUNCTION BY TUMOR-NECROSIS-FACTOR-ALPHA SO THYROID LA English DT Note ID FACTOR-KAPPA-B; GAMMA-INTERFERON; FRTL5 CELLS; CACHECTIN; ACTIVATION; ILLNESS; HORMONE; GROWTH; INTERLEUKIN-1; RECEPTORS AB We studied the effect of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interferon-gamma (IFN-gamma) on the function of thyroid cells and pituitary thyrotrophs. In FRTL-5 rat thyroid cells, both human and murine TNF-alpha inhibited basal and TSH-stimulated [I-125]iodide transport. IL-1 shared this action with TNF-alpha, but was less potent. IL-1 and IFN-gamma did not cause a further reduction of TNF-alpha-induced inhibition of [I-125]iodide transport. TNF-alpha, phorbol ester 12-myristate 13-acetate (PMA), and calcium ionophore (CI) A23817 all inhibited [I-125]iodide transport, but high doses of PMA and CI also blocked the inhibitory action of TNF-alpha on [I-125]iodide transport. Inhibition of protein kinase A and protein kinase C by H7 or HA inhibited TSH-stimulated iodide transport, but did not block the TNF-alpha action, suggesting that the mechanism of TNF-alpha action on thyroid cells is independent of protein kinase A and C. In pituitary cells, both human and murine TNF-alpha did not affect basal TSH secretion, but TNF-alpha reduced TRH-stimulated TSH secretion. This study provides further in vitro evidence that TNF-alpha inhibits the function of the hypothalamus-pituitary-thyroid axis acting directly on both the pituitary and thyroid glands. C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. RP PANG, XP (reprint author), W LOS ANGELES DEPT VET AFFAIRS MED CTR, DIV ENDOCRINOL W111D, ENDOCRINE RES LAB, LOS ANGELES, CA 90073 USA. NR 29 TC 34 Z9 36 U1 0 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1050-7256 J9 THYROID JI Thyroid PD WIN PY 1993 VL 3 IS 4 BP 325 EP 330 DI 10.1089/thy.1993.3.325 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ061 UT WOS:A1993MQ06100013 PM 8118227 ER PT J AU PAYTON, M HU, H SPARROW, D YOUNG, JB LANDSBERG, L WEISS, ST AF PAYTON, M HU, H SPARROW, D YOUNG, JB LANDSBERG, L WEISS, ST TI RELATION BETWEEN BLOOD LEAD AND URINARY BIOGENIC-AMINES IN COMMUNITY-EXPOSED MEN SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE AGE FACTORS; BIOGENIC AMINES; BODY WEIGHT; CREATININE; LEAD; SMOKING ID CATECHOLAMINE METABOLITES; BRAIN CATECHOLAMINES; RENAL-FUNCTION; DOPAMINE; RAT; SEROTONIN; EXCRETION; PRESSURE; SYSTEM; AGE AB The cross-sectional relation between levels of urinary biogenic amines (dopamine, epinephrine, norepinephrine, and serotonin) and levels of blood lead was examined in a study of 645 male participants from a longitudinal study of aging. This stable population of men had initially been recruited from communities in and around Boston, Massachusetts, and had not been selected with regard to lead exposure. Blood lead samples and 24-hour and 2-hour urine specimens were collected during regularly scheduled clinic visits. In multivariate linear regression step-forward models, 24-hour epinephrine excretion was significantly and positively associated with blood lead (beta = 0.101 mu g(mu g/dl)(-1) blood lead, SE (standard error) (beta) = 0.045, p = 0.026). Twenty-four-hour norepinephrine excretion was positively associated with blood lead (beta = 0.023 mu g(mu g/dl)(-1) blood lead, SE(beta) = 0.029, p = 0.425), and both 24-hour dopamine (beta = -4.35 mu g(mu g/dl)(-1) blood lead, SE(beta) = 6.90, p = 0.529) and 2-hour serotonin (beta = -0.348 mu g(mu g/dl)(-1) blood lead, SE(beta) = 0.277, p = 0.210) excretion were negatively associated with blood lead; however, these relations did not achieve statistical significance. An increase of 10 mu g/dl in blood lead was associated with an increase in epinephrine excretion of 11 mu g/24 hours. These results support the hypothesis that epinephrine metabolism is influenced by low levels of lead exposure. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA. US DEPT VET AFFAIRS,OUTPATIENT CLIN,NORMAT AGING STUDY,BOSTON,MA. NORTHWESTERN UNIV,MEM HOSP,DEPT MED,CHICAGO,IL. RP PAYTON, M (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,180 LONGWOOD AVE,BOSTON,MA 02115, USA. OI Hu, Howard/0000-0002-3676-2707 FU NHLBI NIH HHS [HL37871]; NIEHS NIH HHS [NIEHS 2 P30 ES 00002, NIEHS ES05257-01A1] NR 63 TC 5 Z9 6 U1 1 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD NOV 15 PY 1993 VL 138 IS 10 BP 815 EP 825 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA ML239 UT WOS:A1993ML23900005 PM 8237970 ER PT J AU BALDWIN, GC CHUNG, GY HUANG, M WANG, J DUBINETT, SM AF BALDWIN, GC CHUNG, GY HUANG, M WANG, J DUBINETT, SM TI RECOMBINANT INTERLEUKIN-7 INDUCES FUNCTIONAL ACTIVATION OF CULTURED HUMAN MACROPHAGES BY DOWN-REGULATING BOTH TGF-BETA EXPRESSION AND TGF-BETA PROTEIN-PRODUCTION SO BLOOD LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DIV HEMATOL ONCOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DIV PULM MED,LOS ANGELES,CA 90024. W LOS ANGELES VET ADM,LOS ANGELES,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A24 EP A24 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200084 ER PT J AU FREYTES, CO SALZMAN, DE BACHIER, C BOLDT, DH ROODMAN, GD CRAIG, F CASTRO, J LEMAISTRE, CF AF FREYTES, CO SALZMAN, DE BACHIER, C BOLDT, DH ROODMAN, GD CRAIG, F CASTRO, J LEMAISTRE, CF TI HIGH-DOSE CHEMOTHERAPY WITH STEM-CELL RESCUE IN OLDER PATIENTS SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A173 EP A173 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200675 ER PT J AU GALLICCHIO, VS TSE, KF HUGHES, NK GUIGON, M AF GALLICCHIO, VS TSE, KF HUGHES, NK GUIGON, M TI REDUCED ZIDOVUDINE (AZT) MURINE HEMATOPOIETIC TOXICITY IN-VIVO WITH THE TETRAPEPTIDE ACSERASPLYSPRO (ACSDKP, SERASPENIDE) SO BLOOD LA English DT Meeting Abstract C1 UNIV KENTUCKY,MED CTR,LEXINGTON,KY 40506. US DEPT VET AFFAIRS,LEXINGTON,KY. UNIV PARIS 06,HEMATOL LAB,F-75571 PARIS 12,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A103 EP A103 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200396 ER PT J AU GRELLIER, P YEE, D GONZALEZ, M ABBOUD, S AF GRELLIER, P YEE, D GONZALEZ, M ABBOUD, S TI CHARACTERIZATION OF INSULIN-LIKE GROWTH-FACTOR (IGF) BINDING-PROTEINS IN BONE-MARROW STROMAL CELLS SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A498 EP A498 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201975 ER PT J AU RAN, JY DOU, P WANG, LY YUAN, RX HAO, JM ZHANG, H JIN, SY LI, ZP QIN, Y HERBERT, V AF RAN, JY DOU, P WANG, LY YUAN, RX HAO, JM ZHANG, H JIN, SY LI, ZP QIN, Y HERBERT, V TI IN A HIGH-FREQUENCY ESOPHAGEAL-CARCINOMA (EC) AREA, FOLATE AND B12 DEFICIENT SUBJECTS WITH ESOPHAGEAL DYSPLASIA (ED) IMPROVE WITH ADDED FOLATE AND B12 SO BLOOD LA English DT Meeting Abstract C1 SHANXI MED COLL,TAIYUAN,PEOPLES R CHINA. BRONX VET AFFAIRS MED CTR,BRONX,NY. MT SINAI MED CTR,NEW YORK,NY 10029. NR 1 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A532 EP A532 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68202110 ER PT J AU RAN, JY DOU, P WANG, LY QIN, Y JIN, SY LI, XF HERBERT, V AF RAN, JY DOU, P WANG, LY QIN, Y JIN, SY LI, XF HERBERT, V TI CORRELATION OF LOW SERUM FOLATE AND TOTAL B12 WITH HIGH-INCIDENCE OF ESOPHAGEAL-CARCINOMA (EC) IN SHANXI, CHINA SO BLOOD LA English DT Meeting Abstract C1 SHANXI MED COLL,TAIYUAN,PEOPLES R CHINA. BRONX VET AFFAIRS MED CTR,BRONX,NY. MT SINAI MED CTR,NEW YORK,NY 10029. NR 1 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A532 EP A532 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68202109 ER PT J AU REDDY, SV ALCANTARA, O ROODMAN, GD BOLDT, DH AF REDDY, SV ALCANTARA, O ROODMAN, GD BOLDT, DH TI TRANSCRIPTIONAL INHIBITION OF THE TARTRATE-RESISTANT ACID-PHOSPHATASE (TRAP) GENE BY HEMIN SO BLOOD LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A43 EP A43 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200160 ER PT J AU TAKAHASHI, S GOLDRING, S ROODMAN, GD AF TAKAHASHI, S GOLDRING, S ROODMAN, GD TI REGULATION OF CALCITONIN RECEPTOR (CTR) MESSENGER-RNA EXPRESSION IN OSTEOCLASTS (OCL) AND THEIR PRECURSORS SO BLOOD LA English DT Meeting Abstract C1 VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A492 EP A492 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201951 ER PT J AU YEOMAN, H GRESS, RE BARE, CV LEARY, AG BOYSE, EA BARD, J SHULTZ, LD HARRIS, DT DELUCA, D AF YEOMAN, H GRESS, RE BARE, CV LEARY, AG BOYSE, EA BARD, J SHULTZ, LD HARRIS, DT DELUCA, D TI HUMAN BONE-MARROW AND UMBILICAL-CORD BLOOD-CELLS GENERATE CD4+ AND CD8+ SINGLE-POSITIVE T-CELLS IN MURINE FETAL THYMUS ORGAN-CULTURE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID THYMOCYTES; INVITRO; DIFFERENTIATION; EXPRESSION; INVIVO AB Murine fetal thymus lobes isolated from both normal and scid/scid mice can be colonized by donor cells from either human bone marrow or human umbilical cord blood in vitro. Subsequent organ culture results in a transient production of a few CD4+ CD8+ (double-positive) cells and then the accumulation of CD4+ or CD8+ (single-positive) T cells. A significant number of immature T-cell intermediates (e.g., CD8low, CD3-/low cells) were present in early organ cultures, suggesting that these were progenitors of the mature CD3+/high single-positive T cells that dominated late cultures. Depletion of mature T cells from the donor-cell populations did not affect their ability to colonize thymus lobes. However, colonization depended on the presence of CD7+ progenitor T cells. Limiting dilution experiments using mature T-cell populations (human peripheral blood leukocytes, human bone marrow cells, and human umbilical cord blood cells) suggested that thymic organ culture supports the growth of progenitor T cells but does not support the growth of mature human T cells. Each of these donor populations produced single-positive populations with different CD4/CD8 ratios, suggesting that precursor cells from different sources differ qualitatively in their capacity to differentiate into T cells. C1 UNIV ARIZONA,DEPT MICROBIOL & IMMUNOL,TUCSON,AZ 85721. NCI,BETHESDA,MD 20892. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29403. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29403. JACKSON LAB,BAR HARBOR,ME 04609. FU NCI NIH HHS [CA 39827]; NIAID NIH HHS [AI 30389, AI/GM 29407] NR 22 TC 50 Z9 51 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 15 PY 1993 VL 90 IS 22 BP 10778 EP 10782 DI 10.1073/pnas.90.22.10778 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MH322 UT WOS:A1993MH32200076 PM 7902570 ER PT J AU BUSH, RK AF BUSH, RK TI FUNGAL EXTRACTS IN CLINICAL-PRACTICE SO ALLERGY PROCEEDINGS LA English DT Article AB Sensitivity to fungi is a common clinical problem. Although many commercial extracts for diagnosis and treatment of fungal sensitivity are available, there is a lack of standardized materials. New research into the isolation and purification of fungal allergens may improve upon this situation. Controlled immunotherapy trials with fungal extracts have identified selected populations who may benefit from this type of therapy. RP BUSH, RK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 0 TC 16 Z9 17 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 SN 1046-9354 J9 ALLERGY PROC JI Allergy Proc. PD NOV-DEC PY 1993 VL 14 IS 6 BP 385 EP 390 DI 10.2500/108854193778792803 PG 6 WC Allergy SC Allergy GA MR585 UT WOS:A1993MR58500001 PM 8157160 ER PT J AU CHOUDHURY, GG BISWAS, P GRANDALIANO, G ABBOUD, HE AF CHOUDHURY, GG BISWAS, P GRANDALIANO, G ABBOUD, HE TI INVOLVEMENT OF PKC-ALPHA IN PDGF-MEDIATED MITOGENIC SIGNALING IN HUMAN MESANGIAL CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE KIDNEY; GROWTH FACTORS; SIGNAL TRANSDUCTION ID PROTEIN-KINASE-C; GROWTH-FACTOR; TYROSINE PHOSPHORYLATION; PHOSPHOLIPASE-C; MESSENGER-RNAS; RECEPTOR; EPSILON; RAT; EXPRESSION; ACTIVATION AB Platelet-derived growth factor (PDGF) is a potent mitogen for a variety of cells. The calcium/phospholipid-dependent protein kinase C (PKC) represents a major signal transduction pathway for many growth stimuli including PDGF. Various isoforms of PKC are differentially expressed in the same or in different cells and tissues, and diverse stimuli may selectively activate one or more PKC isoforms. We studied the effect of PDGF on DNA synthesis and on the activity of PKC in human mesangial cells and vascular pericytes in the glomerular microvascular bed. PKC activity was measured as the amount of phosphorylated myelin basic protein-derived peptide substrate in the absence and presence of an inhibitor, a peptide spanning the pseudosubstrate region of PKC. PDGF (15 ng/ml) stimulated PKC activity within 5 min, and the effect was sustained for 60 min. Pretreatment of mesangial cells with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), an inhibitor of PKC, abolished the stimulation of PKC and DNA synthesis in response to PDGF. This effect of H-7 was specific, because H-7 did not inhibit the tyrosine phosphorylation of the PDGF receptor in vivo when added to the cells or the in vitro kinase activity in the PDGF beta-receptor immunoprecipitates. Utilizing isotype-specific antibodies against PKC-alpha, -beta, or -gamma for immunoprecipitation of PDGF-treated mesangial cell extracts, followed by assay of PKC activity, we demonstrated the activation of PKC-alpha only. Northern blot analysis of mRNA prepared from mesangial cells also revealed two transcripts, 3.7 kb and 1.8 kb, that hybridized with cDNA specific for PKC-alpha. Moreover, specific ribonuclease (RNase) protection assay using cRNAs specific for PKC-alpha, -beta, and -gamma as probes revealed predominantly the presence of PKC-alpha in mesangial cells. These studies demonstrate that in mesangial cells stimulation of DNA synthesis in response to PDGF is dependent on activation of PKC and that the alpha-isoform of this kinase may mediate the mitogenic effect of PDGF. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP CHOUDHURY, GG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK-33665, DK-43988] NR 30 TC 39 Z9 39 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD NOV PY 1993 VL 265 IS 5 BP F634 EP F642 PN 2 PG 9 WC Physiology SC Physiology GA MJ168 UT WOS:A1993MJ16800087 PM 8238543 ER PT J AU CONHAIM, RL ROSENFELD, DJ SCHREIBER, MA BAASKE, DM HARMS, BA AF CONHAIM, RL ROSENFELD, DJ SCHREIBER, MA BAASKE, DM HARMS, BA TI EFFECTS OF INTRAVENOUS PENTAFRACTION ON LUNG AND SOFT-TISSUE LIQUID EXCHANGE IN HYPOPROTEINEMIC SHEEP SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PLASMA PROTEIN DEPLETION; PLASMA VOLUME EXPANDERS; MICROVASCULAR FILTRATION; LYMPH FLOW; PLASMA OSMOTIC PRESSURE ID TRANS-VASCULAR FLUID; AWAKE SHEEP; PROTEIN FLUX; LYMPH; FILTRATION; PERMEABILITY; COAGULATION; MUSCLE; FLOW AB Effects of infusing pentafraction (Pen), a synthetic hydroxyethyl starch plasma volume expander, on lung and soft tissue lymph flux were compared in nonanesthetized sheep that were protein depleted by batch plasmapheresis. Pen (5%) was infused to raise pulmonary arterial wedge pressure by 5 mmHg for 2 h (1.8 +/- 0.3 1). Pen raised plasma osmotic pressure from plasmapheresis baseline (10.7 +/- 2.2 mmHg; preplasmapheresis baseline, 19.6 +/- 0.6 mmHg) to 16.6 +/- 2.4 mmHg. After Pen, lung lymph flows peaked at 3.9 +/- 2.0 times a preplasmapheresis baseline value of 1.0 (plasmapheresis baseline, 2.7 +/- 0.7), but soft tissue lymph flows rose insignificantly. Plasma Pen concentrations were 2.3 +/- 1.0% postinfusion and 1.6 +/- 0.3% at 12 h. Pen mean molecular masses at these times, measured by high-performance liquid chromatography, were 160 +/- 44 and 129 +/- 23 kDa, respectively. In lung lymph, Pen concentrations were 0.8 +/- 0.6% postinfusion and 0.7 +/- 0.2% at 12 h, with mean molecular masses of 125 +/- 44 and 112 +/- 18 kDa, respectively. In soft tissue lymph Pen was nearly undetectable postinfusion, but at 12 h concentrations averaged 0.3 +/- 0.2% with a mean molecular mass of 80 +/- 10 kDa. The osmotic effectiveness of Pen may be related to its molecular mass, which was large enough to restrict filtration so that the plasma-to-lung lymph osmotic pressure gradient widened. Pen remained effective in the circulation for at least 24 h. C1 UNIV WISCONSIN,DEPT SURG,MADISON,WI 53705. DUPONT MERCK PHARMACEUT CO,WILMINGTON,DE 19880. RP CONHAIM, RL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT SURG,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 26 TC 9 Z9 9 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD NOV PY 1993 VL 265 IS 5 BP H1536 EP H1543 PN 2 PG 8 WC Physiology SC Physiology GA MJ168 UT WOS:A1993MJ16800010 ER PT J AU PICOU, MA ANTONOVIC, R HOLDEN, WE AF PICOU, MA ANTONOVIC, R HOLDEN, WE TI POSITION-DEPENDENT MEDIASTINAL MASS - ANEURYSM OF THE SUPERIOR VENA-CAVA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP PICOU, MA (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97201, USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1993 VL 161 IS 5 BP 1110 EP 1111 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MD368 UT WOS:A1993MD36800048 PM 8273622 ER PT J AU KABUS, D SIDHU, GS WIECZOREK, RL CHOI, HSH AF KABUS, D SIDHU, GS WIECZOREK, RL CHOI, HSH TI METASTATIC MENINGIOMA - HEMANGIOPERICYTOMA OR ANGIOBLASTIC MENINGIOMA SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE MENINGIOMA; HEMANGIOPERICYTOMA; ANGIOBLASTIC MENINGIOMA ID MENINGEAL HEMANGIOPERICYTOMA; ELECTRON-MICROSCOPY; CULTURE; TISSUE AB The question of whether meningeal hemangiopericytoma is a variant of meningioma (''angioblastic meningioma'') or a nosologically distinct entity remains controversial. We present the case histories of an intracranial meningioma and of a meningeal hemangiopericytoma, both of which developed extracranial metastases. The metastatic lesions in both cases were studied by electron microscopy, which demonstrated pericytomatous differentiation in one instance and meningothelial differentiation in the other. This report supports the opinion that meningeal hemangiopericytomas and meningiomas of the CNS are distinct pathological entities. C1 VET AFFAIRS MED CTR,DEPT PATHOL,LAB SERV,NEW YORK,NY 10010. BRONX VET AFFAIRS MED CTR,DEPT PATHOL,NEW YORK,NY. NYU,SCH MED,DEPT PATHOL,NEW YORK,NY. NR 26 TC 23 Z9 25 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 1993 VL 17 IS 11 BP 1144 EP 1150 DI 10.1097/00000478-199311000-00007 PG 7 WC Pathology; Surgery SC Pathology; Surgery GA ME250 UT WOS:A1993ME25000007 PM 8214259 ER PT J AU ASHTON, CM WU, L AF ASHTON, CM WU, L TI SLEEP-APNEA AND THE RISK FOR PERIOPERATIVE MYOCARDIAL-INFARCTION - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP ASHTON, CM (reprint author), DEPT VET AFFAIRS MED CTR,HOUSTON,TX 77030, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD NOV 1 PY 1993 VL 119 IS 9 BP 953 EP 953 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MD711 UT WOS:A1993MD71100021 ER PT J AU WEINBERG, JM ROOK, AH LESSIN, SR AF WEINBERG, JM ROOK, AH LESSIN, SR TI MOLECULAR DIAGNOSIS OF LYMPHOCYTIC INFILTRATES OF THE SKIN SO ARCHIVES OF DERMATOLOGY LA English DT Article ID T-CELL RECEPTOR; GENE REARRANGEMENT ANALYSIS; REGRESSING ATYPICAL HISTIOCYTOSIS; CUTANEOUS LYMPHOID HYPERPLASIA; POLYMERASE CHAIN-REACTION; SOUTHERN BLOT ANALYSIS; MYCOSIS-FUNGOIDES; LYMPHOMATOID PAPULOSIS; B-CELL; PERIPHERAL-BLOOD AB Background: Advances in our understanding of the molecular genetics of lymphocyte antigen receptors (B-cell immunoglobulin and T-cell antigen receptor), have led to the application of molecular biologic techniques to molecularly characterize lymphocytic infiltrates of the skin. Molecular diagnosis refers to the application of these techniques as a diagnostic aid in the clinicopathologic evaluation of cutaneous lymphocytic infiltrates. Observation: Molecular studies have clinical application in the determination of lineage and detection of retroviruses in cutaneous lymphoid neoplasms, distinguishing between lymphoproliferative and reactive infiltrates, and staging and monitoring response to therapy in cutaneous T-cell lymphoma. Southern blot analysis of immunoglobulin and T-cell antigen receptor gene rearrangements may fail to aid the clinician in establishing a diagnosis of a cutaneous malignancy due to the limits of detection sensitivity in minimally infiltrated lesions (eg, parapsoriasis and patch-stage mycosis fungoides) or the still uncertain prognostic significance of clonality in benign cutaneous diseases (eg, follicular mucinosis, pityriasis lichenoides et varioliformis acuta, lymphomatoid papulosis, and cutaneous lymphoid hyperplasia). Conclusions: Molecular studies have enormous research value, providing new means to explore the pathogenesis and clonal evolution of lymphoproliferative skin diseases. Presently, however, they have limited applications as an independent diagnostic tool. As our understanding of the clinical and biologic significance of the molecular detection of clonal lymphocyte populations in the skin expands and as the application of polymerase chain reaction amplification provides us with greater detection sensitivity and specificity, the clinical utility of molecular diagnosis of lymphocytic infiltrates of the skin will be enhanced. C1 UNIV PENN, DEPT DERMATOL, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. FU NCI NIH HHS [R29 CA-55017] NR 97 TC 31 Z9 31 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-987X EI 1538-3652 J9 ARCH DERMATOL JI Arch. Dermatol. PD NOV PY 1993 VL 129 IS 11 BP 1491 EP 1500 DI 10.1001/archderm.129.11.1491 PG 10 WC Dermatology SC Dermatology GA MG677 UT WOS:A1993MG67700015 PM 8239706 ER PT J AU GULLEY, ML RAABTRAUB, N AF GULLEY, ML RAABTRAUB, N TI DETECTION OF EPSTEIN-BARR-VIRUS IN HUMAN TISSUES BY MOLECULAR-GENETIC TECHNIQUES SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID POLYMERASE CHAIN-REACTION; INSITU HYBRIDIZATION; HODGKINS-DISEASE; NASOPHARYNGEAL CARCINOMA; VIRAL-DNA; CELL LINES; LYMPHOPROLIFERATIVE DISORDERS; REACTION AMPLIFICATION; TRANSPLANT RECIPIENTS; EPITHELIAL-CELLS AB In the past few years, there has been an explosion of new data on the association of Epstein-Barr virus (EBV) with human disease. Many of these discoveries have come as a direct result of the application of DNA technology. The nucleic acid hybridization techniques most commonly used to detect EBV in human tissues include Southern blot analysis, in situ hybridization to viral DNA or RNA, and polymerase chain reaction. An advantage of Southern blotting is the ability to distinguish latent from infectious EBV and to determine the clonality of infected tumors with respect to the structure of the viral terminal repeat sequences. In situ hybridization has the advantage of precise localization of the virus in infected tissues or tumors. Polymerase chain reaction is exquisitely sensitive in detecting viral DNA, perhaps too sensitive for disease-specific purposes given the ubiquitous nature of EBV. Each of these molecular genetic methods of EBV analysis is currently used in research laboratories, while some methods have found their way into routine diagnostic pathology because they are faster, more sensitive, or more informative than previous assays. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. UNIV N CAROLINA, DEPT MICROBIOL IMMUNOL, CHAPEL HILL, NC 27514 USA. RP UNIV TEXAS, HLTH SCI CTR, DEPT PATHOL, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. FU NCI NIH HHS [K08-CA01615, R01-CA32979] NR 58 TC 27 Z9 27 U1 0 U2 0 PU COLL AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA SN 0003-9985 EI 1543-2165 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD NOV PY 1993 VL 117 IS 11 BP 1115 EP 1120 PG 6 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MF095 UT WOS:A1993MF09500012 PM 8239932 ER PT J AU MARCINIAK, CM HEINEMANN, AW MONGA, T AF MARCINIAK, CM HEINEMANN, AW MONGA, T TI CHANGES IN MEDICAL STABILITY UPON ADMISSION TO A REHABILITATION UNIT SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article ID CARE C1 NORTHWESTERN UNIV,SCH MED,DEPT REHABIL MED,CHICAGO,IL 60611. BAYLOR COLL MED,HOUSTON VET ADM MED CTR,DEPT PM&R,DEPT RMS,HOUSTON,TX 77030. RI Heinemann, Allen /K-6283-2012 OI Heinemann, Allen /0000-0003-2782-7326; Marciniak, Christina/0000-0003-3300-0050 NR 6 TC 5 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD NOV PY 1993 VL 74 IS 11 BP 1157 EP 1160 PG 4 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA MD088 UT WOS:A1993MD08800006 PM 8239953 ER PT J AU ADKINS, D ENCARNACION, C SALZMAN, D BOLDT, D FREYTES, C VONHOFF, DD LEMAISTRE, CF AF ADKINS, D ENCARNACION, C SALZMAN, D BOLDT, D FREYTES, C VONHOFF, DD LEMAISTRE, CF TI DURABLE COMPLETE REMISSION IN A PATIENT WITH REFRACTORY MEDIASTINAL NONSEMINOMATOUS GERM-CELL TUMOR AFTER TANDEM HIGH-DOSE CHEMOTHERAPY AND AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO BONE MARROW TRANSPLANTATION LA English DT Note ID CANCER; CARBOPLATIN; IFOSFAMIDE; CISPLATIN; ETOPOSIDE; VP-16; PLUS AB The prognosis of patients with relapsed or refractory mediastinal germ cell tumors is uniformly poor. There have been no reports of long-term disease-free survivors using any currently available salvage regimen. We describe a patient with primary mediastinal non-seminomatous germ cell tumor refractory to initial and salvage chemotherapy, who entered his first complete remission after surgical resection and tandem autologous bone marrow transplantation. The patient remains without evidence of disease 19 months after the first BMT. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 15 TC 4 Z9 4 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD NOV PY 1993 VL 12 IS 5 BP 541 EP 546 PG 6 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA MG557 UT WOS:A1993MG55700019 PM 7507767 ER PT J AU KROENKE, K LAWRENCE, VA THEROUX, JF TULEY, MR HILSENBECK, S AF KROENKE, K LAWRENCE, VA THEROUX, JF TULEY, MR HILSENBECK, S TI POSTOPERATIVE COMPLICATIONS AFTER THORACIC AND MAJOR ABDOMINAL-SURGERY IN PATIENTS WITH AND WITHOUT OBSTRUCTIVE LUNG-DISEASE SO CHEST LA English DT Article ID PREOPERATIVE PULMONARY EVALUATION; SURGICAL PROCEDURES; RISK; SPIROMETRY; ANESTHESIA; PREDICTION AB Study objective: To determine the risk of thoracic and major abdominal surgery in patients with chronic obstructive pulmonary disease (COPD). Design: Retrospective cohort study with controls. Setting: A 692-bed teaching hospital. Patients: A cohort of 26 patients with severe COPD (FEV1 < 50 percent predicted) undergoing thoracic and major abdominal surgery was matched by age and type of operation to 52 patients with mild-moderate COPD and 52 patients with no COPD. Measurements and results: The 26 patients with severe COPD had rates of cardiac, vascular, and minor pulmonary complications similar to patients with mild-moderate COPD and without COPD, but experienced higher rates of serious pulmonary complications (23 percent vs 10 percent vs 4 percent, p = 0.03) and death (19 percent vs 4 percent vs 2 percent, p = 0.02). All deaths and instances of ventilatory failure in the patients with severe COPD occurred in the subset undergoing coronary artery bypass surgery. Logistic regression revealed that increased age, higher American Society of Anesthesiologists class, an abnormal chest radiograph, and perioperative bronchodilator administration were associated with higher cardiac or serious pulmonary complication rates. Spirometry was not an independent predictor of postoperative complications. Conclusions: Clinical variables appear better than preoperative spirometry in predicting postoperative cardiopulmonary complications. The utility of preoperative spirometry as well as the benefits of perioperative bronchodilators in patients in stable condition remain to be determined. C1 WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. RP KROENKE, K (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814, USA. NR 38 TC 100 Z9 107 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD NOV PY 1993 VL 104 IS 5 BP 1445 EP 1451 DI 10.1378/chest.104.5.1445 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MF615 UT WOS:A1993MF61500031 PM 8222804 ER PT J AU CASALE, LM SIEGEL, RE AF CASALE, LM SIEGEL, RE TI NEUROMUSCULAR BLOCKADE IN THE ICU SO CHEST LA English DT Letter RP CASALE, LM (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PULM & CRIT CARE MED,BRONX,NY, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD NOV PY 1993 VL 104 IS 5 BP 1639 EP 1640 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MF615 UT WOS:A1993MF61500084 PM 8222855 ER PT J AU KNAPP, RG SCHREINER, PJ SUTHERLAND, SE KEIL, JE GILBERT, GE KLEIN, RL HAMES, C TYROLER, HA AF KNAPP, RG SCHREINER, PJ SUTHERLAND, SE KEIL, JE GILBERT, GE KLEIN, RL HAMES, C TYROLER, HA TI SERUM LIPOPROTEIN(A) LEVELS IN ELDERLY BLACK-AND-WHITE MEN IN THE CHARLESTON HEART-STUDY SO CLINICAL GENETICS LA English DT Article DE AGING; ETHNICITY; LIPOPROTEIN(A); LIPOPROTEINS ID LP(A) LIPOPROTEIN; MYOCARDIAL-INFARCTION; RISK FACTOR; DISEASE; PLASMA; CHILDREN; DENSITY AB Lipoprotein(a) [Lp(a)l is an important genetic trait associated with cardiovascular disease. While Lp(a) levels have been demonstrated to be approximately twice as high in black adults and children compared with whites, this relationship:has not been assessed in the elderly. During the 1987 recall of the Charleston Heart Study cohort, plasma Lp(a) [mg/dl] was measured on 113 white men and 83 black men. The average age of those having Lp(a) measurements was 71 years (+/-6) for white men and 72 years (+/-9) for black men. The distribution of Lp(a) was skewed in both whites (mean = 14.8, median = 8.2 mg/dl) and blacks (mean = 18.1, median = 12.8 mg/dl). The skewed distribution in elderly black men was in contrast to the bell-shaped distribution commonly reported for younger blacks. The Charleston Heart Study data suggest a shift to lower values among elderly as compared to younger men, with the greatest shift occurring among the black men. For black men who have survived to the 7th, 8th, and 9th decades of life, Lp(a) levels appear to be approaching the lower levels of white men. Despite this shift in distribution among black men, there remained a statistically significant difference in Lp(a) between racial groups. C1 UNIV N CAROLINA,DEPT EPIDEMIOL,CHAPEL HILL,NC. RALPH H JOHNSON VET ADM MED CTR,CHARLESTON,SC. CURTIS HAMES CLIN,CLAXTON,GA. RP KNAPP, RG (reprint author), MED UNIV S CAROLINA,DEPT BIOSTAT EPIDEMIOL & SYST SCI,CHARLESTON,SC 29425, USA. RI Gilbert, Gregory/C-7735-2016 OI Gilbert, Gregory/0000-0003-0879-5496 FU NHLBI NIH HHS [HL 31397] NR 33 TC 12 Z9 12 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD NOV PY 1993 VL 44 IS 5 BP 225 EP 231 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA MM211 UT WOS:A1993MM21100001 PM 8313620 ER PT J AU DEKEYSER, F TAKEI, M DANG, H DEKEYSER, H ISENBERG, DA TALAL, N AF DEKEYSER, F TAKEI, M DANG, H DEKEYSER, H ISENBERG, DA TALAL, N TI CHARACTERIZATION OF A CROSS-REACTIVE IDIOTYPE ON 2 HUMAN AUTOANTIBODIES ASSOCIATED WITH SYSTEMIC AUTOIMMUNE-DISEASE SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID ANTI-SM AUTOANTIBODY; LUPUS-ERYTHEMATOSUS; INTERSPECIES IDIOTYPE; RETROVIRAL PROTEINS; ANTIBODIES; SLE; IDIOTOPES; SEQUENCE; HEAVY; SERA C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. BLOOMSBURY RHEUMATOL UNIT,LONDON,ENGLAND. FU NIDCR NIH HHS [DE-09311] NR 23 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD NOV PY 1993 VL 69 IS 2 BP 155 EP 160 DI 10.1006/clin.1993.1164 PG 6 WC Immunology; Pathology SC Immunology; Pathology GA MC285 UT WOS:A1993MC28500005 PM 7691456 ER PT J AU ACHIM, CL MINERS, DK BURROLA, PG MARTIN, FC WILEY, CA AF ACHIM, CL MINERS, DK BURROLA, PG MARTIN, FC WILEY, CA TI IN-VIVO MODEL OF HIV-INFECTION OF THE HUMAN BRAIN SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE CENTRAL NERVOUS SYSTEM, FETAL; HIV, IN VIVO; MACROPHAGE; SCID MICE ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY-SYNDROME; AIDS DEMENTIA COMPLEX; DISEASE; NEUROPATHOLOGY; MACROPHAGES; PATHOLOGY AB Approximately one quarter of the AIDS patients have severe HIV encephalitis with diffuse neuronal damage that may be mediated by immune factors secreted by CNS macrophages. Based on an in vitro brain microsphere model, we developed an in vivo system in which human embryonic brain tissue survives for several months in the interscapular fat pad of SCID mice. Coculture of human brain tissue with macrophages prior to transplantation resulted in infiltration of the microspheres by activated macrophages. When the macrophages were infected in vitro with a neurotropic HIV strain, viral particles were detected in vivo up to 3 months after transplantation. HIV-infected transplants contained multinucleated giant cells similar to those seen in HIV encephalitis. However, the neuroglial component degenerated in the fat pad of SCID mice. The absence of synaptogenesis in the human transplants suggests that the murine fat pad lacks adequate stimuli or support for human neuronal differentiation. To study neurologic damage associated with HIV infection, sites of implantation that stimulate synaptogenesis (e.g. murine CNS) will need to be explored. Based on these findings we conclude that transplantation of brain microspheres with HIV-infected macrophages into SCID mice may be an achievable model of HIV encephalitis. C1 UNIV PITTSBURGH,MED CTR,DIV NEUROPATHOL,PITTSBURGH,PA. UNIV CALIF SAN DIEGO,DEPT PATHOL,LA JOLLA,CA 92093. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. FU NIMH NIH HHS [MH43298, MH45294]; NINDS NIH HHS [NS-2578] NR 18 TC 9 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PD NOV-DEC PY 1993 VL 15 IS 6 BP 423 EP 432 DI 10.1159/000111368 PG 10 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA PM203 UT WOS:A1993PM20300006 PM 7835248 ER PT J AU DEMULDER, A TAKAHASHI, S SINGER, FR HOSKING, DJ ROODMAN, GD AF DEMULDER, A TAKAHASHI, S SINGER, FR HOSKING, DJ ROODMAN, GD TI ABNORMALITIES IN OSTEOCLAST PRECURSORS AND MARROW ACCESSORY CELLS IN PAGETS-DISEASE SO ENDOCRINOLOGY LA English DT Article ID MULTINUCLEATED CELLS; PROGENITOR CELLS; BONE-MARROW; CULTURES; INTERLEUKIN-6 AB Paget's disease of bone is characterized by increased numbers of abnormal osteoclasts. To determine if osteoclast precursors were increased or abnormal in this disease, we examined CFU-GM, the committed granulocyte-macrophage progenitor and the most likely precursor for osteoclasts. In cultures of unfractionated marrow mononuclear cells, CFU-GM colony formation was significantly increased in Paget's marrow cultures compared to that in normal cells (356 +/- 44 vs. 271 +/- 15/10(5) cells; P < 0.05). However, when we enriched hematopoietic precursors from Paget's and normal marrow samples using an antibody that recognizes the CD34 antigen present on most hematopoietic precursors, we found that similar numbers of CFU-GM colonies were formed (87 +/- 13/10(4) cells plated vs. 83 +/- 13). Coculture experiments with highly purified hematopoietic precursors (CD34+ cells) and non-hematopoietic marrow accessory cells (CD34- cells) revealed that the growth of Paget's precursors was significantly enhanced above expected levels by normal or Pagetic CD34- cells (P < 0.05). CFU-GM colony formation was also significantly enhanced when normal CD34+ cells were cocultured with Pagetic, but not with normal, CD34- cells. In addition, CFU-GM colony-derived cells from Paget's patients were hyperresponsive to 1,25-dihydroxyvitamin D3 and could form osteoclast-like multinucleated cells with 1,25-dihydroxyvitamin D3 concentrations one tenth of that required for normal multinucleated formation (10(-11) vs. 10(-10) m). These data suggest that osteoclast precursors may be abnormal in Paget's disease, and other cells in the Pagetic marrow microenvironment may further enhance the growth and differentiation of these abnormal precursors. C1 VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. CEDARS SINAI MED CTR,LOS ANGELES,CA 90404. CITY HOSP NOTTINGHAM,NOTTINGHAM NG5 1PD,ENGLAND. FU NCI NIH HHS [NCI CA-40035]; NIADDK NIH HHS [NIDDK AM-35188]; NIAMS NIH HHS [NIDDK AR39539] NR 13 TC 49 Z9 49 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1993 VL 133 IS 5 BP 1978 EP 1982 DI 10.1210/en.133.5.1978 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ME080 UT WOS:A1993ME08000009 PM 7691583 ER PT J AU GULATI, S DHAUNSI, GS SINGH, AK ORAK, JK SINGH, I AF GULATI, S DHAUNSI, GS SINGH, AK ORAK, JK SINGH, I TI EFFECT OF CIPROFIBRATE ON PEROXISOMAL ANTIOXIDANT-ENZYME SYSTEM IN RAT-LIVER SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,CHARLESTON,SC 29403. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 505 EP 505 DI 10.1016/0891-5849(93)90316-M PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700132 ER PT J AU SINGH, AK GULATI, S SINGH, I AF SINGH, AK GULATI, S SINGH, I TI ISCHEMIA-REPERFUSION ALTERATIONS IN THE STRUCTURE-FUNCTION OF PEROXISOMES SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,DEPT PATHOL,CHARLESTON,SC 29403. NR 0 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 522 EP 522 DI 10.1016/0891-5849(93)90380-D PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700194 ER PT J AU SINGH, I DHAUNSI, GS ORAK, JK SINGH, AK AF SINGH, I DHAUNSI, GS ORAK, JK SINGH, AK TI ANTIOXIDANT ENZYME-SYSTEM IN PEROXISOMES SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,DEPT PATHOL,CHARLESTON,SC 29403. NR 1 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 536 EP 536 DI 10.1016/0891-5849(93)90429-X PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700245 ER PT J AU GULATI, S SINGH, I ORAK, JK SINGH, AK AF GULATI, S SINGH, I ORAK, JK SINGH, AK TI EXPRESSION OF ANTIOXIDANT ENZYMES IN RAT-KIDNEY DURING ISCHEMIA-REPERFUSION INJURY SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VA MED CTR,DEPT PATHOL,CHARLESTON,SC 29403. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD NOV PY 1993 VL 15 IS 5 BP 545 EP 545 DI 10.1016/0891-5849(93)90462-4 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA MD267 UT WOS:A1993MD26700277 ER PT J AU BJORNSDOTTIR, US BUSH, RK AF BJORNSDOTTIR, US BUSH, RK TI LEUKOTRIENE ANTAGONISTS AND INHIBITORS SO IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA LA English DT Review ID ARACHIDONIC-ACID METABOLISM; EXERCISE-INDUCED BRONCHOCONSTRICTION; ASPIRIN-INDUCED ASTHMA; LUNG MAST-CELLS; RECEPTOR ANTAGONIST; GUINEA-PIG; URINARY LEUKOTRIENE-E4; AIRWAY RESPONSIVENESS; POLYMORPHONUCLEAR LEUKOCYTES; BRONCHIAL-ASTHMA C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. NR 121 TC 5 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8561 J9 IMMUNOL ALLERGY CLIN JI Immunol. Allerg. Clin. North Am. PD NOV PY 1993 VL 13 IS 4 BP 861 EP 890 PG 30 WC Allergy; Immunology SC Allergy; Immunology GA ME137 UT WOS:A1993ME13700009 ER PT J AU SORKNESS, CA BUSH, RK AF SORKNESS, CA BUSH, RK TI ALTERNATIVES TO CORTICOSTEROIDS IN THE TREATMENT OF ASTHMA SO IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA LA English DT Article ID STEROID-DEPENDENT ASTHMA; INTRAVENOUS IMMUNE GLOBULIN; DOUBLE-BLIND; RHEUMATOID-ARTHRITIS; BRONCHIAL-ASTHMA; GAMMA-GLOBULIN; GOLD SALT; METHOTREXATE; AURANOFIN; TRIAL C1 UNIV WISCONSIN,SCH MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP SORKNESS, CA (reprint author), UNIV WISCONSIN,SCH PHARM,425 N CHARTER ST,MADISON,WI 53706, USA. NR 55 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8561 J9 IMMUNOL ALLERGY CLIN JI Immunol. Allerg. Clin. North Am. PD NOV PY 1993 VL 13 IS 4 BP 917 EP 938 PG 22 WC Allergy; Immunology SC Allergy; Immunology GA ME137 UT WOS:A1993ME13700012 ER PT J AU MOUNTZ, JD TALAL, N AF MOUNTZ, JD TALAL, N TI RETROVIRUSES, APOPTOSIS AND AUTOGENES SO IMMUNOLOGY TODAY LA English DT Editorial Material ID ENDOGENOUS RETROVIRUSES; AUTOIMMUNE-DISEASE; ELEMENT ETN; MICE; TRANSPOSON; INFECTION; INSERTION; PROTEINS; SEQUENCE; GENE AB Autoimmunity and autoimmune disease are not the same. Autoimmunity is a normal consequence of aging, potentially reversible and possibly physiological. Autoimmune disease is dependent on genetic, viral, hormonal and psychoneuroimmunological factors. Aside from the apparently normal regulation of autoimmune responses by immune response genes, little is known about other genetic factors. Here, Norman Talal and John Mountz propose the term autogene to describe non-MHC genes which directly or indirectly interfere with important immunoregulatory actions. When mutated or otherwise genetically altered (e.g. by retrotransposon insertion), these genes predispose to immune dysregulation, lymphoproliferation and autoimmunity. C1 UNIV ALABAMA,SCH MED,DEPT MED,DIV CLIN IMMUNOL & RHEUMATOL,BIRMINGHAM,AL 35294. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP MOUNTZ, JD (reprint author), BIRMINGHAM VET HOSP,BIRMINGHAM,AL 35294, USA. NR 36 TC 52 Z9 54 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD NOV PY 1993 VL 14 IS 11 BP 532 EP 536 DI 10.1016/0167-5699(93)90182-K PG 5 WC Immunology SC Immunology GA MF709 UT WOS:A1993MF70900004 PM 8274195 ER PT J AU KAHN, RS DAVIDSON, M AF KAHN, RS DAVIDSON, M TI SEROTONIN RECEPTOR RESPONSIVITY IN SCHIZOPHRENIA SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT International Scientific Symposium on Advances in the Pharmacology and Clinical Applications of Serotonin CY JAN 07-09, 1993 CL HI ID META-CHLOROPHENYLPIPERAZINE; NEUROLEPTIC TREATMENT; NEURO-ENDOCRINE; CLOZAPINE; MCPP; 5-HT1C C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY. RP KAHN, RS (reprint author), UNIV HOSP UTRECHT,DEPT PSYCHIAT,HEIDELBERGLAAN 100,3584 CX UTRECHT,NETHERLANDS. FU NIMH NIH HHS [NIMH R01 MH46957-01] NR 23 TC 10 Z9 10 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0268-1315 J9 INT CLIN PSYCHOPHARM JI Int. Clin. Psychopharmacol. PD NOV PY 1993 VL 8 SU 2 BP 47 EP 51 DI 10.1097/00004850-199311002-00007 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA MU110 UT WOS:A1993MU11000007 PM 7911140 ER PT J AU HAFFNER, SM VALDEZ, RA STERN, MP KATZ, MS AF HAFFNER, SM VALDEZ, RA STERN, MP KATZ, MS TI OBESITY, BODY-FAT DISTRIBUTION AND SEX-HORMONES IN MEN SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE BODY FAT DISTRIBUTION; OBESITY; TESTOSTERONE; SEX HORMONE BINDING GLOBULIN; ESTRADIOL; DHEA-SO4; SEX HORMONES; AGE ID ADIPOSE-TISSUE DISTRIBUTION; BINDING-GLOBULIN; POSTMENOPAUSAL WOMEN; DIABETES-MELLITUS; DEHYDROEPIANDROSTERONE SULFATE; CARDIOVASCULAR-DISEASE; CENTRALIZED ADIPOSITY; PREMENOPAUSAL WOMEN; ABDOMINAL ADIPOSITY; MEXICAN-AMERICANS AB An unfavourable body fat distribution may cause metabolic abnormalities including diabetes and dyslipidemia. These effects may be mediated by alterations in sex hormones. In women the available data suggest that upper body adiposity is related to increased androgenicity (especially as indicated by low concentrations of sex hormone binding globulin). Few data, however, are available on these relationships in men. We therefore examined the association of total testosterone, free testosterone, oestradiol, dehydroepiandrosterone sulphate (DHEA-SO4) and sex hormone binding globulin (SHBG) to waist-to-hip ratio (WHR) and conicity index in 178 men from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. The conicity index is equal to the abdominal circumference divided by 0.109 x the square root of (weight/ height). The conicity index and WHR were significantly inversely related to DHEA-SO4 and free testosterone. SHBG was only weakly associated with body mass index (r= -0.18, P< 0.05). After adjustment for age and body mass index, DHEA-SO, remained inversely correlated with WHR (r = -0.22, P < 0.01) and conicity index (r = -0.31, P < 0.001) and free testosterone remained inversely associated with conicity index (r = -0.21, P < 0.01). Thus, in men, the association between unfavourable body fat distribution and increased androgenicity is inverse in contrast to the situation in women. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIAT & GERONTOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU NHLBI NIH HHS [R01HL-24799, R37HL-36820] NR 53 TC 154 Z9 157 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD NOV PY 1993 VL 17 IS 11 BP 643 EP 649 PG 7 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA MF383 UT WOS:A1993MF38300005 PM 8281222 ER PT J AU GLASS, WF KREISBERG, JI AF GLASS, WF KREISBERG, JI TI REGULATION OF INTEGRIN-MEDIATED ADHESION AT FOCAL CONTACTS BY CYCLIC-AMP SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID CULTURED MESANGIAL CELLS; DEPENDENT PROTEIN-KINASE; EXTRACELLULAR-MATRIX; PLASMINOGEN-ACTIVATOR; VITRONECTIN; FIBROBLASTS; FIBRONECTIN; MORPHOLOGY; ACTIN; SHAPE AB Cyclic AMP (cAMP) elevation causes diverse types of cultured cells to round partially and develop arborized cell processes. Renal glomerular mesangial cells are smooth, muscle-like cells and in culture contain abundant actin microfilament cables that insert into substratum focal contacts. cAMP elevation causes adhesion loss, microfilament cable fragmentation, and shape change in cultured mesangial cells. We investigated the roles of the classical vitronectin (alphaVbeta3 integrin) and fibronectin (alpha5beta1 integrin) receptors in these changes. Mesangial cells on vitronectin-rich substrata contained microfilament cables that terminated in focal contacts that stained with antibodies to vitronectin receptor. cAMP elevation caused loss of focal contact and associated vitronectin receptor. Both fibronectin and its receptor stained in a fibrillary pattern at the cell surface under control conditions but appeared aggregated along the cell processes after cAMP elevation. This suggested that cAMP elevation caused loss of adhesion mediated by vitronectin receptor but not by fibronectin receptor. We plated cells onto fibronectin-coated slides to test the effect of ligand immobilization on the cellular response to cAMP. On fibronectin-coated slides fibronectin receptor was observed in peripheral focal contacts where actin filaments terminated, as seen with vitronectin receptor on vitronectin-coated substrata, and in abundant linear arrays distributed along microfilaments as well. Substratum contacts mediated by fibronectin receptor along the length of actin filaments have been termed fibronexus contacts. After cAMP elevation, microfilaments fragmented and fibronectin receptor disappeared from peripheral focal contacts, but the more central contacts along residual microfilament fragments appeared intact. Also, substratum adhesion was maintained after cAMP elevation on fibronectin-but not on vitronectin-coated surfaces. Although other types of extracellular matrix receptors may also be involved, our observations suggest that cAMP regulates adhesion at focal contacts but not at fibronexus-type extracellular matrix contacts. (C) 1993 Wiley-Liss, Inc. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL,CHARLOTTESVILLE,VA 22908. RP GLASS, WF (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK29787] NR 32 TC 50 Z9 50 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD NOV PY 1993 VL 157 IS 2 BP 296 EP 306 PG 11 WC Cell Biology; Physiology SC Cell Biology; Physiology GA ME671 UT WOS:A1993ME67100011 PM 7693723 ER PT J AU LAWRENCE, VA GAFNI, A KROENKE, K AF LAWRENCE, VA GAFNI, A KROENKE, K TI PREOPERATIVE HIV TESTING - IS IT LESS EXPENSIVE THAN UNIVERSAL PRECAUTIONS SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE MEDICAL ECONOMICS; PREOPERATIVE CARE; SURGICAL (OPERATIVE); HIV INFECTION, TRANSMISSION, PREVENTION AND CONTROL; OCCUPATIONAL DISEASES; RISK FACTORS ID UNITED-STATES HOSPITALS; HEALTH-CARE WORKERS; GLOVE PERFORATIONS; SURGERY; RISK; AIDS; INFECTION; BLOOD; TRANSMISSION; PHYSICIANS AB Universal precautions are officially recommended to prevent HIV transmission in health care settings but for elective surgery some advocate routine preoperative HIV testing. These strategies have not been tested in clinical trials but universal precautions are very expensive and not cost-effective. Thus, for elective surgery, routine testing might save resources by permitting selective use of additional barrier precautions. We performed an economic evaluation to compare both strategies, using a simple approach to determine if routine testing (RT) is less expensive than universal precautions (UP). Conservatively assuming equal effectiveness in preventing HIV transmission, we compared a minimized estimate for the average cost of RT with a maximized estimate for the average cost of UP per elective operation. The minimized estimate for RT (US$57) was greater than the maximized estimate for UP (US$36) per procedure. Results were stable or strengthened by sensitivity analysis. Routine HIV testing is not a valid economic alternative to UP for elective surgery. The simple methodology used in this study can be a preliminary strategy to review other strategies for preventing HIV transmission. This method is particularly useful when data are inadequate for a formal economic evaluation to determine the utility of collecting the detailed information necessary for a full comparison. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. MCMASTER UNIV,HLTH SCI CTR,CTR HLTH ECON & POLICY ANAL,HAMILTON,ON,CANADA. MCMASTER UNIV,HLTH SCI CTR,DEPT CLIN EPIDEMIOL & BIOSTAT,HAMILTON,ON,CANADA. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. RP LAWRENCE, VA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 40 TC 14 Z9 14 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD NOV PY 1993 VL 46 IS 11 BP 1219 EP 1227 DI 10.1016/0895-4356(93)90084-E PG 9 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA MG589 UT WOS:A1993MG58900001 PM 8229097 ER PT J AU LAWRENCE, VA GAFNI, A KROENKE, K AF LAWRENCE, VA GAFNI, A KROENKE, K TI EVIDENCE-BASED VS EMOTION-BASED MEDICAL DECISION-MAKING - ROUTINE PREOPERATIVE HIV TESTING VS UNIVERSAL PRECAUTIONS SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; RISK; AIDS C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. MCMASTER UNIV,HLTH SCI CTR,DEPT CLIN EPIDEMIOL & BIOSTAT,HAMILTON,ON,CANADA. MCMASTER UNIV,HLTH SCI CTR,CTR HLTH ECON & POLICY ANAL,HAMILTON,ON,CANADA. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. RP LAWRENCE, VA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284, USA. NR 8 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD NOV PY 1993 VL 46 IS 11 BP 1233 EP 1236 DI 10.1016/0895-4356(93)90086-G PG 4 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA MG589 UT WOS:A1993MG58900003 PM 8229099 ER PT J AU EBBINGHAUS, SW GEE, JE RODU, B MAYFIELD, CA SANDERS, G MILLER, DM AF EBBINGHAUS, SW GEE, JE RODU, B MAYFIELD, CA SANDERS, G MILLER, DM TI TRIPLEX FORMATION INHIBITS HER-2 NEU TRANSCRIPTION IN-VITRO SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE FOOTPRINT; GEL SHIFT; SEQUENCE DNA; ONCOGENE; GENE EXPRESSION ID DIHYDROFOLATE-REDUCTASE PROMOTER; HELIX FORMATION; C-ERBB-2 PROTOONCOGENE; ONCOGENIC ACTIVATION; POINT MUTATION; PROTO-ONCOGENE; HUMAN-BREAST; RECEPTOR; BINDING; DNA AB Triplex-forming oligonucleotides (TFOs) have been shown to bind to target DNA sequences in several human gene promoters such as the c-myc oncogene, the epidermal growth factor receptor, and the dihydrofolate reductase genes. TFOs have been shown to inhibit transcription in vitro and gene expression in cell culture of the c-myc and other genes. The HER-2/neu oncogene, which is overexpressed in breast cancer and other human malignancies, contains a purine-rich sequence in its promoter, which is favorable for purine:purine:pyrimidine (R:R:Y) triplex formation. Although its function in the HER-2/neu promoter is unknown, this purine-rich site is homologous to a protein-binding sequence in the promoter of the epidermal growth factor receptor that is necessary for efficient transcription of this gene. We have shown that this sequence is a site for nuclear protein binding by incubation with a crude nuclear extract. We describe the formation of an interstrand triplex using a purine-rich oligonucleotide antiparallel to this purine-rich target sequence of the HER-2 / neu promoter. Triplex formation by the oligonucleotide prevents protein binding to the target site in the HER-2/neu promoter in vitro. We have shown that this oligonucleotide is a potent and specific inhibitor of HER-2 / neu transcription in an in vitro assay. The triplex target site contains a single pyrimidine base that does not conform to the R:R:Y triplex motif. In an attempt to abrogate the potentially destabilizing effects of this pyrimidine base on triplex formation, we have substituted an abasic linker for the pyrimidine residue in the triplex forming oligonucleotide. Triplex formation with the modified oligonucleotide appears to occur with approximately equivalent binding affinity. Triplex formation in the HER-2/neu oncogene promoter prevents transcription in vitro and may represent a future modality for specific inhibition of this gene in vivo. C1 BIRMINGHAM VET AFFAIRS MED CTR, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT MED, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT ORAL PATHOL, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT BIOCHEM, BIRMINGHAM, AL 35294 USA. FU NCI NIH HHS [R01 CA 42337, CA 09467-08, CA42664] NR 32 TC 76 Z9 76 U1 1 U2 4 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 EI 1558-8238 J9 J CLIN INVEST JI J. Clin. Invest. PD NOV PY 1993 VL 92 IS 5 BP 2433 EP 2439 DI 10.1172/JCI116850 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MF291 UT WOS:A1993MF29100045 PM 7901237 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R AF SILVA, JA LEONG, GB WEINSTOCK, R TI THE PSYCHOTIC PATIENT AS SECURITY GUARD SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; PSYCHOTIC DISORDERS; DANGEROUSNESS; PUBLIC SAFETY; SECURITY GUARDS AB The job of the security guard is generally regarded as stressful because of the potential for violent or other hostile confrontation. Although the public assumes that only mentally healthy individuals who possess the capability to handle stressful situations become employed as security guards, this may not be the case. A series of 15 individuals who suffered from psychotic disorders while working as security guards is studied and discussed in terms of the issues of dangerousness and public safety. One case is described in detail in order to highlight important issues resulting from being psychotic while working as a security guard. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD NOV PY 1993 VL 38 IS 6 BP 1436 EP 1440 PG 5 WC Medicine, Legal SC Legal Medicine GA MH369 UT WOS:A1993MH36900026 PM 8263486 ER PT J AU HARDIN, TC KOELLER, JM KUHN, JG ROODMAN, D VONHOFF, DD AF HARDIN, TC KOELLER, JM KUHN, JG ROODMAN, D VONHOFF, DD TI NUTRITIONAL PARAMETERS OBSERVED DURING 28-DAY INFUSION OF RECOMBINANT HUMAN TUMOR-NECROSIS-FACTOR-ALPHA SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID CACHECTIN; CACHEXIA; METABOLISM; RAT; INTERLEUKIN-1; RABBITS; INJURY AB In conjunction with a Phase I investigation of the antineoplastic activity of recombinant human tumor necrosis factor-alpha (TNF-alpha), administered as a 28-day continuous infusion, selected nutritional parameters were evaluated to identify any effect that might be attributed to the TNF infusion. Seven clinically stable men with a variety of tumor types were studied. None had clinical or laboratory evidence of significant malnutrition before entry into the study. Five patients received 10 mug of recombinant human TNF-alpha per square meter per day and two patients received 25 mug/m2 per day. Indirect calorimetry assessment of resting energy expenditure, body weight, serum TNF concentration, and laboratory analysis of common nutritional markers (albumin, prealbumin, and triglycerides) were performed at baseline, day 14, day 28, and 2 weeks (day 42) after completion of the infusion. There were no statistically significant differences by analysis of variance observed in any parameter during the study period compared with baseline values and values on day 42. Also, there were no differences between any parameters when stratified by dose administered, although the number of patients studied was small. Measured serum TNF concentrations ranged from 0.02 to 1.56 ng/mL and did not correlate with study day or dose of TNF infused. No correlation was observed between serum TNF concentrations and resting energy expenditure. Although others have reported significant metabolic changes associated with acute administration of TNF in humans and animals, our experience does not support a hypermetabolic state in patients receiving low daily dose, long-term (28-day) continuous infusion of recombinant human TNF-alpha, a state that may be consistent with many neoplastic conditions. C1 UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78285. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. RP HARDIN, TC (reprint author), UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT PHARMACOL,PHARM SERV 119,SAN ANTONIO,TX 78284, USA. FU NCI NIH HHS [NCI CM-07305] NR 31 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD NOV-DEC PY 1993 VL 17 IS 6 BP 541 EP 545 DI 10.1177/0148607193017006541 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MH740 UT WOS:A1993MH74000010 PM 8301809 ER PT J AU SEARLES, JS ALTERMAN, AI MILLER, SM AF SEARLES, JS ALTERMAN, AI MILLER, SM TI COMPARABILITY OF SELF-REPORT OF FAMILIAL ALCOHOLISM AMONG MALE AND FEMALE COLLEGE-STUDENTS SO JOURNAL OF STUDIES ON ALCOHOL LA English DT Article AB There is a general impression in the literature that women are more accurate reporters of familial psychiatric history. In this regard, this study presents data from a large cohort of young men (n = 427) and women (n = 607) who in answering a questionnaire self-reported alcohol abuse symptoms for various biological relatives. No significant gender differences emerged for any of the family history comparisons including reports for father, mother, either parent, any first- or second-degree relatives, or men or women relatives. The findings are discussed in the context of the existing literature. C1 UNIV VERMONT,DEPT PSYCHIAT,BURLINGTON,VT 05405. UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA. TEMPLE UNIV,DEPT PSYCHOL,PHILADELPHIA,PA 19122. RP SEARLES, JS (reprint author), VERMONT ALCOHOL RES CTR,2000 MT VIEW DR,COLCHESTER,VT 05446, USA. FU NIAAA NIH HHS [5-RO1-AA07361] NR 4 TC 7 Z9 7 U1 0 U2 0 PU ALCOHOL RES DOCUMENTATION INC CENT ALCOHOL STUD RUTGERS UNIV PI PISCATAWAY PA PO BOX 969, PISCATAWAY, NJ 08855-0969 SN 0096-882X J9 J STUD ALCOHOL JI J. Stud. Alcohol PD NOV PY 1993 VL 54 IS 6 BP 730 EP 732 PG 3 WC Substance Abuse; Psychology SC Substance Abuse; Psychology GA ME009 UT WOS:A1993ME00900011 PM 8271809 ER PT J AU BALLARD, J SOKOLOV, Y YUAN, WL KAGAN, BL TWETEN, RK AF BALLARD, J SOKOLOV, Y YUAN, WL KAGAN, BL TWETEN, RK TI ACTIVATION AND MECHANISM OF CLOSTRIDIUM-SEPTICUM ALPHA-TOXIN SO MOLECULAR MICROBIOLOGY LA English DT Article ID PHOSPHOLIPID-BILAYER MEMBRANES; ESCHERICHIA-COLI HEMOLYSIN; PERFRINGENS THETA-TOXIN; FORMING TOXIN; AEROLYSIN; AGGREGATION; CHANNELS; ERYTHROCYTES; FRAGMENT; DIVALENT AB Clostridium septicum produces a single lethal factor, alpha toxin (AT), which is a cytolytic protein with a molecular mass of approximately 48 kDa. The 48 kDa toxin was found to be an inactive protoxin (AT(pro)) which could be activated via a carboxy-terminal cleavage with trypsin. The cleavage site was located approximately 4 kDa from the carboxy-terminus. Proteolytically activated AT(pro) had a specific activity of approximately 1.5 x 10(6) haemolytic units mg-1. The trypsin-activated toxin (AT(act)) was haemolytic, stimulated a prelytic release of potassium ions from erythrocytes which was followed by haemoglobin release, induced channel formation in planar membranes and aggregated into a complex of M(r) > 210 000 on erythrocyte membranes. AT(pro) did not exhibit these properties. AT(act) formed pores with a diameter of at least 1.3-1.6 nm. We suggest that pore formation on target cell membranes is responsible for the cytolytic activity of alpha toxin. C1 UNIV OKLAHOMA HLTH SCI CTR, HLTH SCI CTR, DEPT MICROBIOL & IMMUNOL, OKLAHOMA CITY, OK 73190 USA. UNIV CALIF LOS ANGELES, INST NEUROPSYCHIAT, DEPT PSYCHIAT, LOS ANGELES, CA 90024 USA. W LOS ANGELES DEPT VET AFFAIRS MED CTR, LOS ANGELES, CA 90024 USA. FU NIAID NIH HHS [AI32097, AI28697]; NIMH NIH HHS [MH43433] NR 26 TC 62 Z9 63 U1 0 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD NOV PY 1993 VL 10 IS 3 BP 627 EP 634 DI 10.1111/j.1365-2958.1993.tb00934.x PG 8 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA MF565 UT WOS:A1993MF56500018 PM 7968539 ER PT J AU VANDENBARK, AA BOURDETTE, DN WHITHAM, R CHOU, YK HASHIM, GA OFFNER, H AF VANDENBARK, AA BOURDETTE, DN WHITHAM, R CHOU, YK HASHIM, GA OFFNER, H TI EPISODIC CHANGES IN T-CELL FREQUENCIES TO MYELIN BASIC-PROTEIN IN PATIENTS WITH MULTIPLE-SCLEROSIS SO NEUROLOGY LA English DT Note C1 OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MICROBIOL & IMMUNOL,PORTLAND,OR 97201. COUNCIL TOBACCO RES,NEW YORK,NY. RP VANDENBARK, AA (reprint author), PORTLAND VET AFFAIRS MED CTR,NEUROIMMUNOL RES 151-D,3710 SW US VET HOSP RD,PORTLAND,OR 97201, USA. FU NINDS NIH HHS [NS23221, NS23444] NR 7 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1993 VL 43 IS 11 BP 2416 EP 2417 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA MH652 UT WOS:A1993MH65200059 PM 7694188 ER PT J AU MANZO, CB DICKERSON, RN SETTLE, RG RAJTER, JJ AF MANZO, CB DICKERSON, RN SETTLE, RG RAJTER, JJ TI INSULIN-LIKE GROWTH FACTOR-I AND ENDOTOXIN-MEDIATED KIDNEY DYSFUNCTION IN CRITICALLY ILL, PARENTERALLY FED RATS SO NUTRITION LA English DT Article DE INSULIN-LIKE GROWTH FACTOR-I; ACUTE KIDNEY FAILURE; LIPOPOLYSACCHARIDE; GLOMERULAR FILTRATION RATE; SOMATOMEDIN-C; CREATININE CLEARANCE ID PLATELET-ACTIVATING FACTOR; GLOMERULAR-FILTRATION RATE; ACUTE RENAL-FAILURE; FACTOR-I; PLASMA-FLOW; NECROSIS; HORMONE; HUMANS AB Endotoxemia is an important contributor to the pathogenesis of acute kidney failure in sepsis. Data suggest insulinlike growth factor 1 (IGF-1) can increase creatinine clearance in healthy humans. The influence of recombinant human IGF-1 on kidney function in endotoxemia was investigated in 34 male Sprague-Dawley rats. After venous cannulation and postoperative parenteral nutrition (PN), the animals were randomly assigned to receive PN only, PN plus Escherichia coli lipopolysaccharide (LPS), or PN plus LPS plus IGF-1. Urine output was significantly higher for the IGF-1 and control groups compared with the LPS group (18.9 +/- 5.7, 13.0 +/- 3.8, and 17.7 +/- 3.1 ml/day for control, LPS, and IGF-1 groups, respectively, analysis of variance, p < 0.05). Creatinine clearance was significantly higher in the IGF-1 group than the LPS group and exceeded the control group (0.49 +/- 0.27, 0.36 +/- 0.14, and 0.65 +/- 0.27 ml min-1 100(-1) g body wt) for control, LPS, and IGF-1, respectively (analysis of variance, p < 0.05). IGF-1 ameliorates the effects of endotoxin on kidney function as measured by creatinine clearance and urine output in endotoxemic parenterally fed rats. C1 UNIV TENNESSEE CTR HLTH SCI,DEPT CLIN PHARM,MEMPHIS,TN 38163. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. PHILADELPHIA COLL PHARM & SCI,PHILADELPHIA,PA 19104. RI Dickerson, Roland/C-5185-2008 FU NIDDK NIH HHS [1R15DK46545-01] NR 26 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0899-9007 J9 NUTRITION JI Nutrition PD NOV-DEC PY 1993 VL 9 IS 6 BP 528 EP 531 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MM144 UT WOS:A1993MM14400007 PM 8111143 ER PT J AU WOLFSON, M AF WOLFSON, M TI SEVERE MALNUTRITION .1. SO SEMINARS IN DIALYSIS LA English DT Article AB A.Y. is a 56-year-old retired male airline pilot who presented with rapidly progressive renal failure in a single functioning (right) kidney. His left kidney had been obstructed by stones for several years and at presentation he had a left kidney double-J stent. His creatinine had. increased from 1.9 to 7.0 over the previous eight months. Physical examination revealed a well-developed, well-nourished male who had a blood pressure of 150/95, pulse 80 and regular, and respirations of 12/min. The rest of the physical exam was within normal limits. Laboratory studies revealed a blood urea nitrogen (BUN) of 70 mg/dl, creatinine of 7.2 mg/dl, glucose of 95 mg/dl, and normal liver function tests with a normal serum albumin. His complete blood count (CBC) was remarkable for a hematocrit of 33%. Serum iron and total iron binding capacity (TIBC) were also normal. The underlying cause of his renal insufficiency was never delineated. He was initially begun on hemodialysis, but underwent placement of a continuous ambulatory peritoneal dialysis (CAPD) catheter and was to begin training in this procedure. He was given 1 g of ceftriaxone at the time of catheter placement to prevent catheter infection and subsequently developed severe diarrhea, secondary to C. dificil infection. Despite this, the patient completed his dialysis training and hemodialysis was discontinued. Soon after he began CAPD, he also developed severe nausea and vomiting and was unable to eat. He was hospitalized and treated with intravenous fluids. His diarrhea resolved as did his nausea and vomiting. He was discharged from the hospital. At home he began vomiting again. He refused initially to be hospitalized, but awoke 72 hr after discharge with sudden blindness in both eyes. At presentation to the emergency room he was diagnosed with bilateral retinal artery emboli or thromboses. Vasculitis was ruled out, although he was given a short course of high dose prednisone therapy. The patient also was begun on subcutaneous heparin therapy. Hemodialysis was again instituted and CAPD discontinued. He continued to have severe nausea whenever food was offered. Complete gastroenterologic evaluation failed to reveal an anatomical cause for the vomiting. His course was also complicated by the development of pericarditis, refractory to treatment, and the patient underwent surgery for a pericardial window. The patient developed severe malnutrition over the course of these events with marked weight loss, serum albumin of 2.1, and serum prealbumin of 7.0. While initially reluctant, he subsequently agreed to placement of a nasoenteric feeding tube and was started on tube feedings daily. During his hemodialysis procedures, an attempt was made to provide intradialytic parenteral nutrition (IDPN). However, this resulted in severe hypophosphatemia. He initially did well with the nasoenteral tube feedings and was able to return home. However, he developed severe esophagitis and the tube was removed. Since he was still unable to eat because of continued nausea and vomiting, a feeding jejunostomy tube was placed. The patient did very well. His esophagitis improved, his albumin increased over three to four months to 3.9 g/dl and his prealbumin increased to 37. His appetite gradually improved and he began eating while continuing the jejunal feedings. After approximately one year, the jejunostomy tube was successfully removed:The patient is able to eat normally and his malnutrition is now resolved. RP WOLFSON, M (reprint author), PORTLAND VET AFFAIRS MED CTR,NEPHROL SECT 111C,3710 SW US VET HOSP RD,POB 1034,PORTLAND,OR 97201, USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0894-0959 J9 SEMIN DIALYSIS JI Semin. Dial. PD NOV-DEC PY 1993 VL 6 IS 6 BP 361 EP 362 DI 10.1111/j.1525-139X.1993.tb00175.x PG 2 WC Urology & Nephrology SC Urology & Nephrology GA MH463 UT WOS:A1993MH46300010 ER PT J AU DRINKA, PJ VOEKS, S BAUWENS, S BINKLEY, N AF DRINKA, PJ VOEKS, S BAUWENS, S BINKLEY, N TI SENSITIVITY AND POSITIVE PREDICTIVE VALUE OF CLINICAL SIGNS OF HYPOGONADISM IN ELDERLY MEN SO SOUTHERN MEDICAL JOURNAL LA English DT Article AB One hundred three ambulatory elderly men had serum free testosterone (FT) assessed as part of a study of bone loss. The FT was analyzed using radioimmunoassay. Each participant was questioned regarding the presence of erections adequate for sexual activity and the presence of sexual desire. Each was examined for decreased axillary and pubic hair. h FT of less than 9.0 pg/mL was found in eight subjects. The sensitivity of the clinical predictors as an indicator of a low FT value ranged from 4.3% to 86%, while positive predictive value ranged from 12% to 19%. The abnormal clinical signs and symptoms investigated in this study obviously have mechanisms in addition to hypogonadism. A history of adequate erections ruled out a low FT value in all but 1 of 44 cases. C1 MANAGED CARE RESOURCES INC,CHESAPEAKE,VA. WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIATR SECT,MADISON,WI 53705. RP DRINKA, PJ (reprint author), WISCONSIN VET HOME,KING,WI 54946, USA. NR 7 TC 6 Z9 6 U1 0 U2 0 PU SOUTHERN MEDICAL ASSN PI BIRMINGHAM PA 35 LAKESHORE DR PO BOX 190088, BIRMINGHAM, AL 35219 SN 0038-4348 J9 SOUTHERN MED J JI South.Med.J. PD NOV PY 1993 VL 86 IS 11 BP 1264 EP 1265 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MH676 UT WOS:A1993MH67600017 PM 8235781 ER PT J AU HAMMOND, TG MORRE, DJ HARRIS, HW ZEIDEL, ML AF HAMMOND, TG MORRE, DJ HARRIS, HW ZEIDEL, ML TI ISOLATION OF HIGHLY PURIFIED, FUNCTIONAL ENDOSOMES FROM TOAD URINARY-BLADDER SO BIOCHEMICAL JOURNAL LA English DT Article ID ANTIDIURETIC-HORMONE; MEMBRANE-VESICLES; WATER; TRANSPORT; PROTON AB Endosomes are difficult to isolate as they share size and density properties with much more abundant cellular organelles such as mitochondria. In cultured cell lines the tandem use of charge-dependent isolation techniques and differential centrifugation is necessary to isolate endosomes. Endosomal populations of the toad urinary bladder are of special interest because they are thought to contain a water channel. Understanding of the molecular structure of the water channel has been constrained. as there is currently no practical method to isolate functional water-channel-containing vesicles. This study reports the tandem use of charge-dependent techniques and centrifugation to isolate populations of endosomes from the toad urinary bladder. To purify water-channel-containing vesicles aqueous two-phase partition was utilized to fractionate a preparation partially purified by differential centrifugation. Populations of endosomes were analysed by small-particle flow cytometry techniques. A 5-fold enrichment in endosomes, achieved with aqueous two-phase partition, allowed us to identify two populations of endosomes of diverse size in a toad bladder endosomal fraction. Pre-enrichment also improved the efficiency of flow cytometry sorting, allowing isolation of the two endosomal populations in sufficient quantities for secondary analysis. A population of larger endosomes had very high water permeability. indicating the presence of water channels. The two populations had different SDS/PAGE fingerprints. Electron micrographs of the flow-sorted material shows a uniform population of membrane vesicles devoid of mitochondria and other identifiable cellular organelles. Hence. aqueous two-phase partition and flow cytometry allow identification of two populations of endosomes in the toad urinary bladder which have diverse structural and functional properties. Isolation of functional water-channel-containing vesicles allows co-localization of water-channel function with candidate water-channel proteins. C1 BROCKTON W ROXBURY DEPT VET AFFAIRS MED CTR,MED SERV,RENAL SECT,BOSTON,MA. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. PURDUE UNIV,DEPT MED CHEM & PHARMACOGNOSY,W LAFAYETTE,IN 47907. CHILDRENS HOSP MED CTR,DIV RENAL,BOSTON,MA 02115. RP HAMMOND, TG (reprint author), UNIV WISCONSIN HOSP & CLIN,MADISON,WI, USA. FU NIDDK NIH HHS [DK46117, DK38744, R01 DK43955] NR 20 TC 7 Z9 7 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD OCT 15 PY 1993 VL 295 BP 471 EP 476 PN 2 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA ME516 UT WOS:A1993ME51600019 PM 8240245 ER PT J AU KATAYAMA, N SHIH, JP NISHIKAWA, S KINA, T CLARK, SC OGAWA, M AF KATAYAMA, N SHIH, JP NISHIKAWA, S KINA, T CLARK, SC OGAWA, M TI STAGE-SPECIFIC EXPRESSION OF C-KIT PROTEIN BY MURINE HEMATOPOIETIC PROGENITORS SO BLOOD LA English DT Article ID STEM-CELL FACTOR; COLONY FORMATION; GROWTH-FACTOR; W-LOCUS; MONOCLONAL-ANTIBODY; MARROW-CELLS; LIGAND; MOUSE; DIFFERENTIATION; CULTURE C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. KUMAMOTO UNIV,SCH MED,INST MOLEC EMBRYOL & GENET,KUMAMOTO 860,JAPAN. KYOTO UNIV,CHEST DIS RES INST,DEPT MOLEC PATHOL,KYOTO 606,JAPAN. GENET INST INC,CAMBRIDGE,MA. FU NIDDK NIH HHS [DK32294] NR 34 TC 115 Z9 116 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1993 VL 82 IS 8 BP 2353 EP 2360 PG 8 WC Hematology SC Hematology GA MC276 UT WOS:A1993MC27600013 PM 7691257 ER PT J AU HERBERT, V AF HERBERT, V TI HEALTH QUACKERY - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 BRONX VET AFFAIRS MED CTR,BRONX,NY 10468. RP HERBERT, V (reprint author), MT SINAI MED CTR,NEW YORK,NY 10029, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 14 PY 1993 VL 329 IS 16 BP 1204 EP 1204 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MA667 UT WOS:A1993MA66700029 ER PT J AU MATSUYAMA, SS JARVIK, LF AF MATSUYAMA, SS JARVIK, LF TI ABNORMAL FIBROBLAST MICROTUBULE RESPONSE IN FAMILIAL ALZHEIMER-DISEASE SO AGE LA English DT Article ID PAIRED HELICAL FILAMENTS; PROTEIN-TAU TAU; AMYLOID PRECURSOR; PHILOTHERMAL RESPONSE; TRANSPORT INVIVO; SKIN FIBROBLASTS; GENE-MUTATIONS; DEMENTIA; LINKAGE; BRAIN AB There is increasing evidence that cytoskeletal changes, in particular perturbation of the microtubule (MT) system, play a role in the pathogenesis of Alzheimer disease (AD). The reappearance of the cytoplasmic MT network following treatment with the MT disrupting agent colchicine was investigated in commercially available (Human Genetic Cell Repository, Camden, NJ) fibroblasts derived from 11 patients with familial AD and 11 controls. The AD cells revealed a significant delay in the reappearance of that network following release from treatment with colchicine. Further research with larger samples is needed to determine the sensitivity and specificity of this finding for AD as well as research into the underlying bases for the observed differences. C1 W LOS ANGELES VA MED CTR,PSYCHOGERIATR UNIT & LAB,BRENTWOOD DIV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. NR 47 TC 3 Z9 3 U1 1 U2 1 PU AMER AGING ASSOC PI CHESTER PA 2129 PROVIDENCE AVENUE, CHESTER, PA 19013 SN 0161-9152 J9 AGE JI Age PD OCT PY 1993 VL 16 IS 4 BP 152 EP 158 DI 10.1007/BF02434992 PG 7 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA NA507 UT WOS:A1993NA50700003 ER PT J AU SIMON, JA AF SIMON, JA TI SERUM CERULOPLASMIN LEVEL AND THE RISK OF MYOCARDIAL-INFARCTION AND STROKE SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter ID VITAMIN-C; DISEASE RP SIMON, JA (reprint author), SAN FRANCISCO VET AFFAIRS MED CTR,GEN INTERNAL MED SECT,SAN FRANCISCO,CA 94121, USA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD OCT 1 PY 1993 VL 138 IS 7 BP 550 EP 550 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MC311 UT WOS:A1993MC31100009 PM 8213759 ER PT J AU RABENECK, L CRANE, MM RISSER, JMH LACKE, CE WRAY, NP AF RABENECK, L CRANE, MM RISSER, JMH LACKE, CE WRAY, NP TI EFFECT OF HIV TRANSMISSION CATEGORY AND CD4 COUNT ON THE OCCURRENCE OF DIARRHEA IN HIV-INFECTED PATIENTS SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; HOMOSEXUAL MEN; INTESTINAL INFECTIONS; RECTAL MUCOSA; SYNDROME AIDS; MANIFESTATIONS; PREDICTORS; COHORT; VIRUS AB This study was designed to assess the relative contributions of HIV transmission category and immunodeficiency to the risk of HIV-related diarrhea. We reviewed the medical records of 169 HIV-infected non-AIDS patients seen between 1986 and 1990 at the Houston VA Special Medicine Clinic. The prevalence of diarrhea at any given clinic visit ranged from 3% to 7%. Diarrhea was three times more common in homosexual/bisexual men [odds ratio = 3.0 (1.01-9.53)], and this pattern persisted when stratified by CD4 count. Previous studies have focused mainly on the detection of enteric organisms in patients with HIV-related diarrhea. Studies of the temporal relationships between sexual practices, enteric pathogens, diarrhea, and immunodeficiency are needed to clarify the pathogenesis of HIV-related diarrhea. C1 UNIV TEXAS,SCH PUBL HLTH,EPIDEMIOL DISCIPLINE,HOUSTON,TX 77025. RP RABENECK, L (reprint author), VET ADM MED CTR 111D,BAYLOR COLL MED,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 16 TC 14 Z9 14 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD OCT PY 1993 VL 88 IS 10 BP 1720 EP 1723 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MB687 UT WOS:A1993MB68700012 PM 8105679 ER PT J AU TARI, A YAMAMOTO, G SUMII, K SUMII, M TAKEHARA, Y HARUMA, K KAJIYAMA, G WU, V SACHS, G WALSH, JH AF TARI, A YAMAMOTO, G SUMII, K SUMII, M TAKEHARA, Y HARUMA, K KAJIYAMA, G WU, V SACHS, G WALSH, JH TI ROLE OF HISTAMINE(2) RECEPTOR IN INCREASED EXPRESSION OF RAT GASTRIC H+-K+-ATPASE ALPHA-SUBUNIT INDUCED BY OMEPRAZOLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GASTRIC ADENOSINE-TRIPHOSPHATASE; ACID SECRETION; GASTRIN; FAMOTIDINE ID PARIETAL-CELLS; MESSENGER-RNA; BETA-SUBUNIT; MEMBRANES; CLONING; STOMACH; MUCOSA; GENE AB Omeprazole is a specific inhibitor in vivo of the functioning gastric acid pump, the H+-K+-adenosinetriphosphatase (ATPase), in the secretory canaliculus of the parietal cell. It has been shown previously that omeprazole in rats led to an increase in the mRNA for the alpha-subunit of the H+-K+-ATPase. Omeprazole causes a marked increase in circulating gastrin in this species, which in turn stimulates release of histamine from the enterochromaffin-like cell. The possible role of this pathway was investigated by the in vivo administration of famotidine, a potent H-2 receptor antagonist. A single intraperitoneal dose of famotidine, 200 mg/kg, produced a transient hypergastrinemia peaking at 3 h and normalizing at 12 h, inhibition of secretion that lasted for 12 h, but no change in the level of the alpha-subunit mRNA or of beta-actin mRNA. In contrast, a single dose of omeprazole, 100 mg/kg, inhibited acid secretion and produced hypergastrinemia, peaking at 12 h, both effects lasting for the 24-h observation period. Omeprazole elevated the alpha-subunit mRNA transiently by more than threefold at 3 h, with normal levels being restored at 24 h. The administration of famotidine 1 h after omeprazole did not change the effects of omeprazole on acid secretion but elevated the gastrin levels further. There was now no elevation of the alpha-subunit mRNA for the first 6 h, but a small increase at 12 h and a further increase to approximately 2.5-fold at 24 h. Hence the acute effect of omeprazole on alpha-subunit mRNA transcription appears to require activation of the H-2 receptor on the parietal cell, probably resulting from the histamine release induced by hypergastrinemia. C1 W LOS ANGELES VET AFFAIRS MED CTR,BLDG 115,RM 115,LOS ANGELES,CA 90073. HIROSHIMA UNIV,SCH MED,DEPT INTERNAL MED 1,HIROSHIMA 734,JAPAN. UNIV CALIF LOS ANGELES,CTR ULCER RES & EDUC,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PHYSIOL,LOS ANGELES,CA 90024. FU NIDDK NIH HHS [DK-17294, DK-41301] NR 28 TC 22 Z9 22 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD OCT PY 1993 VL 265 IS 4 BP G752 EP G758 PN 1 PG 7 WC Physiology SC Physiology GA ME480 UT WOS:A1993ME48000075 PM 8238359 ER PT J AU MULLIGAN, LJ ESCOBEDO, D FREEMAN, GL AF MULLIGAN, LJ ESCOBEDO, D FREEMAN, GL TI MECHANICAL DETERMINANTS OF CORONARY BLOOD-FLOW DURING DYNAMIC ALTERATIONS IN MYOCARDIAL-CONTRACTILITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PULSUS ALTERNANS; ELASTANCE; MYOCARDIAL BLOOD FLOW ID CLOSED-CHEST DOGS; ANESTHETIZED GOAT; VARYING ELASTANCE; END-EJECTION; HEART-RATE; PRESSURE; IMPEDIMENT; VENTRICLE AB Recently it has been proposed that the decrease in coronary blood flow (CBF) resulting from cardiac contraction referred to as systolic flow impediment (SFI) is dependent on the level of left ventricular elastance (E(es)) The average rate of LV relaxation (R(avg)) has been shown to be major determinant of diastolic flow development (DFD). We tested these hypotheses using the unique hemodynamic condition of pulsus alternans (PA) where end-systolic LV pressure and instantaneous E(es) vary on beat-to-beat basis. In six mongrel dogs instrumented with LV and aortic manometers, ultrasonic dimension crystals, and Doppler coronary flow probes we measured phasic CBF and E(es) during PA and control conditions. Maximal pressure development over time (dP/dt(max)) and SFI were significantly different between weak (WB) and strong beats (SB) as were R(avg) and DFD. Minimum CBF (Q(min)) was not different between SB and WB; however, Q(min) and peak E(es) occurred nearly simultaneously in the WB. Q(min) occurred much earlier than peak E(es) in the strong and control beats. Plots of instantaneous LV elastance and CBF showed that for control beats and for the strong beats of PA CBF was similar during systole and diastole, suggesting elastance is a unique determinant of CBF. This was quantified as CBF at the time in either systole or diastole when elastance was half-maximal for that beat (E50). During the WB of PA, however, CBF at E50 was significantly higher during systole than during diastole. We conclude that while SFI and DFD are highly dependent on the dP/dt and R(avg), E(es) is not a unique determinant of CBF under all conditions. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED & CARDIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 19 TC 6 Z9 6 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD OCT PY 1993 VL 265 IS 4 BP H1112 EP H1118 PN 2 PG 7 WC Physiology SC Physiology GA ME481 UT WOS:A1993ME48100011 ER PT J AU PRABHU, SD FREEMAN, GL AF PRABHU, SD FREEMAN, GL TI LEFT-VENTRICULAR ENERGETICS IN CLOSED-CHEST DOGS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE OXYGEN CONSUMPTION; MYOCARDIAL MECHANICS; CONTRACTILITY ID PRESSURE-VOLUME AREA; MYOCARDIAL OXYGEN-CONSUMPTION; CONSCIOUS DOGS; HEART-RATE; CONTRACTILITY; TACHYCARDIA; MUSCLE; PERFORMANCE; DYSFUNCTION; AFTERLOAD AB Studies of ventricular energetics using the relation between myocardial O2 consumption (MVo2) and pressure-volume area (PVA) have been performed extensively in the isolated heart, but not in the intact animal. We characterized the MVo2-PVA relation and its response to heart rate (HR) in eight closed-chest dogs instrumented with high-fidelity micromanometers, piezoelectric crystals, coronary flow probes, and coronary sinus oximetric catheters. The effect of dobutamine was studied in five dogs. MVo2 is linearly related to PVA with lower MVo2 required for the generation of smaller PVAs. Baseline contractile efficiency (EFF) was 25.6 +/- 2.8%. High pacing rates reduced EFF (25.7 +/- 3.2% at a HR of 107 +/- 3 beats/min vs. 16.3 +/- 2.4% at a HR of 194 +/- 5 beats/min, P < 0.0167) and load-independent MVo2 per beat (0.562 +/- 0.119 vs. 0.377 +/- 0.074 J.beat-1.100 g LV-1, P < 0.0167) while increasing end-systolic elastance (E(es)) (9.4 +/- 1.3 vs. 18.6 +/- 3.1 mmHg/ml, P < 0.0167). Dobutamine administration increased load-independent MVo2 per beat (0.392 +/- 0.108 vs. 0.607 +/- 0.083 J.beat-1.100 g LV-1, P < 0.05) and contractility (E(es) 10.1 +/- 1.5 vs. 32.0 +/- 7.6 mmHg/ml, P < 0.05) without changing EFF (28.8 +/- 3.8 vs. 30.3 +/- 3.8%, P = NS). Thus the intact animal displays loss of EFF at high heart rates but maintains EFF during dobutamine stimulation. Both interventions increased load-independent MVo2 per minute, indicating increased O2 requirements for excitation-contraction coupling. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Prabhu, Sumanth/D-5223-2009 NR 45 TC 7 Z9 8 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD OCT PY 1993 VL 265 IS 4 BP H1048 EP H1055 PN 2 PG 8 WC Physiology SC Physiology GA ME481 UT WOS:A1993ME48100003 ER PT J AU JENNINGS, TS HARDIN, TC AF JENNINGS, TS HARDIN, TC TI TREATMENT OF ASPERGILLOSIS WITH ITRACONAZOLE SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; INVASIVE ASPERGILLOSIS; PULMONARY ASPERGILLOSIS; THERAPY; ANTIFUNGAL; MYCOSES AB OBJECTIVE: To review the role of itraconazole as oral therapy for the major infections caused by Aspergillus spp.: allergic bronchopulmonary aspergillosis, aspergilloma, and invasive aspergillosis. DATA SOURCES: A MEDLINE search of articles published in the English language between 1986 and 1993 was used to identify relevant citations, including review articles. In addition, a search of die published abstracts of the past two Interscience Conferences on Antimicrobial Agents and Chemotherapy (ICAAC) was performed. STUDY SELECTION: Clinical trials that evaluated itraconazole therapy in either allergic bronchopulmonary aspergillosis, aspergilloma, or invasive aspergillosis were critically reviewed. Trials were evaluated based upon entry criteria for die diagnosis of each type of aspergillosis, risk factors for the development of aspergillosis (neutropenia, transplant recipient, hematologic malignancy), prior antifungal chemotherapy, and dose and duration of itraconazole therapy. DATA SYNTHESIS: Overall, the clinical trials of itraconazole therapy for aspergillosis are limited and of variable quality. In the treatment of allergic bronchopulmonary aspergillosis, itraconazole has been reported to prompt a reduction in corticosteroid dosage in selected patients. There have been no controlled trials of itraconazole as treatment for aspergilloma, but data from several open-label trials suggest that this agent may be of clinical benefit in aspergilloma, primarily as an alternative to surgery. The use of itraconazole for invasive aspergillosis has been evaluated in several trials, most often in patients who were intolerant to amphotericin B treatment. Response to oral itraconazole has generally been promising. CONCLUSIONS: Although itraconazole offers promise for oral therapy against infections caused by Aspergillus spp., it should not presently be regarded as primary therapy for any of these diseases. Amphotericin B, in doses ranging from 1 to 1.5 mg/kg to a total dose of 1.5-4.0 g, should remain the treatment of choice in both aspergilloma and invasive aspergillosis. Itraconazole use should be restricted to patients who experience severe toxicity with amphotericin B therapy. Corticosteroids continue to be first-line therapy for allergic bronchopulmonary aspergillosis, with the use of itraconazole reserved for those patients who would benefit from a reduction in corticosteroid dose. C1 UNIV TEXAS, COLL PHARM, AUSTIN, TX 78712 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT PHARMACOL, SAN ANTONIO, TX 78284 USA. RP JENNINGS, TS (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR, PHARM SERV, 7400 MERTON MINTER BLVD, SAN ANTONIO, TX 78284 USA. NR 25 TC 32 Z9 32 U1 1 U2 2 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD OCT PY 1993 VL 27 IS 10 BP 1206 EP 1211 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MC459 UT WOS:A1993MC45900013 PM 8251691 ER PT J AU TAKAHASHI, LK RUBIN, WW AF TAKAHASHI, LK RUBIN, WW TI CORTICOSTEROID INDUCTION OF THREAT-INDUCED BEHAVIORAL-INHIBITION IN PREWEANLING RATS SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID 2-WEEK-OLD RATS; MINERALOCORTICOID RECEPTORS; ULTRASONIC VOCALIZATION; SEXUAL-DIFFERENTIATION; EARLY ADRENALECTOMY; RATTUS-NORVEGICUS; BRAIN GROWTH; GLUCOCORTICOIDS; RESPONSES; ONTOGENY AB Termination of ongoing behavior and assumption of defensive postures when threatened are adaptive characteristics of vertebrates. Altricial rat pups develop these characteristics by 14 days of age. At this time, pups inhibit their ultrasonic vocalizations and freeze when threatened. This emergence of behavioral inhibition is impaired when rats are adrenalectomized (ADX) at 10 days of age. That is, 14-day-old ADX pups exhibit deficits in freezing and continue to emit ultrasounds when confronted by an adult male rat. Studies also showed that removal of adrenal hormones does not potentiate vocalizations or render pups incapable of reducing their ultrasounds. More important, 3.0 mg/kg of corticosterone (CORT), but not lower doses, administered daily to ADX pups restored freezing, with lesser effects on ultrasound inhibition. Disrupting the developmental action of endogenous CORT appears to impair the ontogenetic expression of behavioral inhibition. C1 DUKE UNIV,DEPT NEUROBIOL,DURHAM,NC 27706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [MH-43986] NR 54 TC 52 Z9 52 U1 0 U2 1 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD OCT PY 1993 VL 107 IS 5 BP 860 EP 866 DI 10.1037//0735-7044.107.5.860 PG 7 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA MG763 UT WOS:A1993MG76300013 PM 8280395 ER PT J AU SWIERGIEL, AH TAKAHASHI, LK KALIN, NH AF SWIERGIEL, AH TAKAHASHI, LK KALIN, NH TI ATTENUATION OF STRESS-INDUCED BEHAVIOR BY ANTAGONISM OF CORTICOTROPIN-RELEASING FACTOR RECEPTORS IN THE CENTRAL AMYGDALA IN THE RAT SO BRAIN RESEARCH LA English DT Article DE AMYGDALA; CORTICOTROPIN-RELEASING FACTOR; STRESS; DEFENSIVE BEHAVIOR; FREEZING ID LOCUS-CERULEUS; IMMUNOREACTIVE NEURONS; EXPLORATORY-BEHAVIOR; CENTRAL NUCLEUS; BRAIN; CRF; HYPOTHALAMUS; ORGANIZATION; PROJECTIONS; INJECTIONS AB Research suggests that endogenous corticotropin-releasing factor (CRF) in the amygdala plays a role in the expression of stress-induced behavior. This study examined in rats whether antagonism of CRF receptors in the central amygdala (CA) region using alpha-helical CRF9-41, a CRF antagonist, was effective in attenuating the occurrence of stress-induced freezing. Bilateral infusions of 50, 100, or 200 ng of the CRF antagonist were made in the CA region using 33-gauge cannula immediately prior to testing. Freezing was measured in two test conditions. In one condition, the effects of the CRF antagonist on freezing was assessed immediately after exposure to electric foot shock. In the other condition, freezing was examined in shock-experienced rats that were re-exposed to the shock environment. Results suggested that 50 and 100 ng of the CRF antagonist were effective in reducing the duration of freezing in the immediate post-shock period. In addition, the 100 ng dose produced a significant reduction in freezing duration after rats were re-exposed to the shock environment. Collectively, data suggest that antagonizing the action of endogenous CRF in the CA region contributes to a general alleviation of stress-induced freezing. C1 UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NIMH NIH HHS [NIMH MH-40855] NR 34 TC 173 Z9 175 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 1 PY 1993 VL 623 IS 2 BP 229 EP 234 DI 10.1016/0006-8993(93)91432-R PG 6 WC Neurosciences SC Neurosciences & Neurology GA LY947 UT WOS:A1993LY94700008 PM 8221104 ER PT J AU WILLIAMS, AJ AF WILLIAMS, AJ TI THE NOSE AND OBSTRUCTIVE SLEEP-APNEA SO CHEST LA English DT Editorial Material ID NASAL RESISTANCE; FLOW C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. RP WILLIAMS, AJ (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VA MED CTR, CTR SLEEP DISORDERS, LOS ANGELES, CA USA. NR 11 TC 3 Z9 3 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1993 VL 104 IS 4 BP 993 EP 993 PG 1 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA MC283 UT WOS:A1993MC28300004 PM 8404236 ER PT J AU LAUDE, D GOLDMAN, M ESCOURROU, P ELGHOZI, JL AF LAUDE, D GOLDMAN, M ESCOURROU, P ELGHOZI, JL TI EFFECT OF BREATHING PATTERN ON BLOOD-PRESSURE AND HEART-RATE OSCILLATIONS IN HUMANS SO CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY LA English DT Article DE BLOOD PRESSURE; FINGER BLOOD PRESSURE; HEART RATE; PARADOXICAL PULSE; RESPIRATION; RESPIRATORY SINUS ARRHYTHMIA; SYSTOLIC BLOOD PRESSURE; TIDAL VOLUME; VARIABILITY ID RESPIRATORY SINUS ARRHYTHMIA; RATE-VARIABILITY; SPECTRAL-ANALYSIS; ORTHOSTATIC LOAD; FLUCTUATIONS AB 1. The relationships of respiratory sinus arrhythmia (RSA) and respiratory changes in systolic blood pressure (SBP) to tidal volume (V(T)) and breathing frequency (BF), were quantified during voluntary control of V(T) and BF in healthy subjects. 2. Respiration was measured non-invasively with a respiratory inductive plethysmograph, which was calibrated prior to each study while breathing through a pneumotachygraph. Finger arterial blood pressure was measured non-invasively by the Finapres. 3. Heart rate (HR) increased during inspiration, with a nearly fixed time delay for most V(T) and BF approximating 0.9 s. The magnitude of RSA increased with increases in V(T) and with decreases in BF. SBP decreased during inspiration, with a time delay which increased as BF decreased, resulting in a phase delay approximating 160-degrees. The magnitude of the inspiratory fall in SBP increased with increases in V(T). Increased amplitudes of RSA and SBP variation occurred at the lowest BF, consistent with the possibility of interactions between respiratory-related influences and those due to slow waves' of vasomotor tone. 4. The present results are consistent with the conclusion that respiratory effects on SBP are caused by a mechanism other that simply changes in HR. C1 W LOS ANGELES VA MED CTR,PULM SECT,LOS ANGELES,CA. HOP ANTOINE BECLERE,SERV EXPLORAT FONCT,CLAMART,FRANCE. RP LAUDE, D (reprint author), FAC MED NECKER ENFANTS MALAD,PHARMACOL LAB,CNRS,URA 1482,156 RUE VAUGIRARD,F-75015 PARIS,FRANCE. NR 30 TC 49 Z9 50 U1 2 U2 6 PU BLACKWELL SCIENCE PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON VICTORIA 3053, AUSTRALIA SN 0305-1870 J9 CLIN EXP PHARMACOL P JI Clin. Exp. Pharmacol. Physiol. PD OCT PY 1993 VL 20 IS 10 BP 619 EP 626 DI 10.1111/j.1440-1681.1993.tb01643.x PG 8 WC Pharmacology & Pharmacy; Physiology SC Pharmacology & Pharmacy; Physiology GA MD396 UT WOS:A1993MD39600002 PM 8261656 ER PT J AU FLICK, MR WEBSTER, RO HOEFFEL, JM JULIEN, M MILLIGAN, SA KENT, B LESSER, M AF FLICK, MR WEBSTER, RO HOEFFEL, JM JULIEN, M MILLIGAN, SA KENT, B LESSER, M TI EFFECT OF PHENYTOIN ON ACUTE LUNG INJURIES IN UNANESTHETIZED SHEEP SO CRITICAL CARE MEDICINE LA English DT Article DE ADULT RESPIRATORY DISTRESS SYNDROME; ENDOTOXIN; PHENYTOIN; EMBOLISM, AIR; OLEIC ACID; SEPTICEMIA; NEUTROPHILS; LUNGS; LYMPH; ESCHERICHIA-COLI ID RESPIRATORY-DISTRESS SYNDROME; MICRO-VASCULAR PERMEABILITY; MEDIASTINAL LYMPH-NODE; SEPTIC SHOCK; AIR EMBOLI; ANESTHETIZED SHEEP; N-ACETYLCYSTEINE; PULMONARY-EDEMA; DOUBLE-BLIND; ENDOTOXIN AB Objective. To determine if the intravenous administration of phenytoin attenuates or prevents acute experimental lung injury. Design: Placebo-controlled, longitudinal animal investigative study. Setting. University research laboratory. Subjects: Sixteen yearling female lambs weighing 30 +/- 3 kg. Intervention: After administration of anesthesia, the animals were endotracheally intubated and mechanically ventilated. Using sterile techniques, four thoracotomies were performed. Through the left fourth intercostal space, cannulas for pressure measurements were inserted directly into the main pulmonary artery and left atrium. An ultrasound flow cuff for determination of cardiac output was placed around the main pulmonary artery. Through the left tenth intercostal space, the diaphragmatic and mediastinal parietal pleura were widely cauterized. Through the right tenth intercostal space, the caudal mediastinal lymph node was identified and divided at the caudal margin of the right pulmonary ligament, and a 1- to 2-cm portion of the node distal to the ligament was resected. The diaphragmatic and mediastinal parietal pleura were widely cauterized. Through the right sixth intercostal space, the efferent duct (or ducts) was identified, ligated at the site of entry into the thoracic duct, and cannulated. The lymph cannula was brought to the outside of the thorax through a separate stab wound. Measurements and Main Results: Unanesthetized sheep were studied 7 to 10 days after surgery. Hemodynamic, lung fluid balance, and arterial blood variables were measured in uninjured sheep and in sheep injured by intravenous infusions of Escherichia coli endotoxin (1 mug/kg iv over 30 mins), air bubbles (0.056 to 0.074 mL/kg/min over 4 hrs), or oleic acid (0.06 mL/kg over 1 hr). The sheep were studied when untreated and after pretreatment with phenytoin. We found that the expected increase in protein-rich lung lymph flow with injuries, resulting from increased microvascular permeability in the lungs, was attenuated by phenytoin when the lungs were injured by endotoxin or air bubbles. In contrast, phenytoin had no effect on oleic acid-induced lung injury or on uninjured lungs. Conclusions. Phenytoin attenuates acute lung injuries in sheep that are thought to be caused by stimulation of host inflammatory responses (e.g., endotoxin and air bubbles), but has no effect on direct injuries to the lungs (e.g., oleic acid). A plausible mechanism for this finding is phenytoin inhibition of polymorphonuclear leukocyte function. C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,MED CTR,ROSALIND RUSSELL ARTHRITIS RES LAB,SAN FRANCISCO,CA 94110. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94143. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT SURG,NEW YORK,NY 10029. BRONX VET ADM MED CTR,NEW YORK,NY. RP FLICK, MR (reprint author), UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,MED CTR,MED SERV,SAN FRANCISCO,CA 94110, USA. FU NHLBI NIH HHS [HL-26913, HL-19155] NR 45 TC 2 Z9 2 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD OCT PY 1993 VL 21 IS 10 BP 1563 EP 1571 DI 10.1097/00003246-199310000-00027 PG 9 WC Critical Care Medicine SC General & Internal Medicine GA MB228 UT WOS:A1993MB22800027 PM 8403968 ER PT J AU PUGH, JA MEDINA, R RAMIREZ, M AF PUGH, JA MEDINA, R RAMIREZ, M TI COMPARISON OF THE COURSE TO END-STAGE RENAL-DISEASE OF TYPE-1 (INSULIN-DEPENDENT) AND TYPE-2 (NON-INSULIN-DEPENDENT) DIABETIC NEPHROPATHY SO DIABETOLOGIA LA English DT Article; Proceedings Paper CT SYMP ON DIABETIC RENAL DISEASE IN TYPE-2 DIABETIC PATIENT : A MAJOR WORLDWIDE HEALTH PROBLEM CY SEP 07, 1992 CL PRAGUE, CZECHOSLOVAKIA SP HOECHST AKTIENGESELL DE END-STAGE RENAL DISEASE; TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS; TYPE-1 (INSULIN-DEPENDENT) DIABETES ID MELLITUS; ONSET; PRESSURE; FAILURE; KIDNEY AB Is the course leading to diabetic end-stage renal disease similar for Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus? We identified all diabetic end-stage renal disease patients starting renal replacement therapy from 1989 to 1991 in two urban counties in Texas. Three ethnic/racial groups were enrolled: Mexican Americans, non-Hispanic Whites, African Americans. Patients were interviewed and their medical records, both inpatient and out-patient, were abstracted for relevant diagnostic and therapeutic information. We attempted to obtain records as far back as the onset of diabetes or hypertension and from all physicians who had cared for the patient. An historical algorithm was used to determine diabetic type. Of the patients enrolled, 91 were Type 1 and 438 were Type 2 diabetic patients. Type 1 diabetic patients had higher mean glucose levels in the first 10 years of diabetes (16.3 vs 11.4 mmol/l) but lower systolic blood pressures (148 vs 157 mm Hg). The duration of diabetes prior to end-stage renal disease was longer for Type 1 than Type 2 patients (22 vs 17 years). Type 1 diabetic patients were more likely to have other microvascular complications (retinopathy, neuropathy, gastroparesis), less likely to have coronary disease (myocardial infarction and congestive heart failure), and had similar rates of stroke and vascular surgery procedures (carotid endarterectomy, coronary artery bypass surgery, aorto-femoral bypass). Type 1 and Type 2 diabetic patients were just as likely to have a first degree relative with hypertension (60.5 vs 65.5 %). The late manifestations of end-stage renal disease were similar between the two groups (kidney size, proteinuria, slope of the inverse of creatinine, laboratory data prior to end-stage renal disease, reasons for starting dialysis). The course to end-stage renal disease may be different for Type 1 and Type 2 diabetes, with hyperglycaemia playing a more dominant role in Type 1 and hypertension playing a more dominant role for Type 2. The Type 1/Type 2 differences in patterns of other diabetic complications add weight to this hypothesis. However, the late course of the renal disease and the end result on the kidney is very similar. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. MEXICAN AMER MED TREATMENT EFFECTIVENESS CTR,SAN ANTONIO,TX. RP PUGH, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,AMBULATORY CARE 11C6,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. OI Pugh, Jacqueline/0000-0003-4933-141X FU AHRQ HHS [1-U01-HS07397-01]; NIDDK NIH HHS [DK38392] NR 19 TC 46 Z9 46 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD OCT PY 1993 VL 36 IS 10 BP 1094 EP 1098 DI 10.1007/BF02374504 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LZ223 UT WOS:A1993LZ22300039 PM 8243860 ER PT J AU NOBLE, EP BLUM, K KHALSA, ME RITCHIE, T MONTGOMERY, A WOOD, RC FITCH, RJ OZKARAGOZ, T SHERIDAN, PJ ANGLIN, MD PAREDES, A TREIMAN, LJ SPARKES, RS AF NOBLE, EP BLUM, K KHALSA, ME RITCHIE, T MONTGOMERY, A WOOD, RC FITCH, RJ OZKARAGOZ, T SHERIDAN, PJ ANGLIN, MD PAREDES, A TREIMAN, LJ SPARKES, RS TI ALLELIC ASSOCIATION OF THE D(2) DOPAMINE-RECEPTOR GENE WITH COCAINE DEPENDENCE SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE D(2) DOPAMINE RECEPTOR GENE; COCAINE DEPENDENCE; TAQ1-A AND TAQ1-B ALLELES; FAMILY HISTORY OF ALCOHOLISM; DEVIANT BEHAVIORS ID DRUG-ABUSE; D2-DOPAMINE RECEPTOR; ALCOHOLISM; FAMILY; MECHANISMS; ADDICTION; DISORDER; LOCUS AB The objective of the present study was to examine allelic prevalence of the D2 dopamine receptor (DRD2) gene in male cocaine-dependent (CD) Caucasian (non-Hispanic) subjects and to determine the relationship of DRD2 alleles to family history and selected behavioral measures. The prevalence of the A1 allele in CD subjects (n = 53) was 50.9%. It was significantly higher than either the 16.0% prevalence (P < 10(-4)) in non-substance abusing controls (n = 100) or the 30.9% prevalence (P < 10(-2)) in population controls (n = 265) wherein substance abusers were not excluded. Similarly, a significantly higher prevalence (p < 10(-2)) of the B1 allele was found in CD subjects (n = 52) compared with non-substance abusing controls (n = 53); 38.5% vs. 13.2%. Logistic regression analysis of CD subjects identified potent routes of cocaine use and the interaction of early deviant behaviors and parental alcoholism as significant risk factors associated with the A1 allele. The cumulative number of these three risk factors in CD subjects was positively and significantly (P < 10(-3)) related to A1 allelic prevalence. The data showing a strong association of the minor alleles (A1 and B1) of the DRD2 with cocaine dependence suggest that a gene, located on the q22-q23 region of chromosome 11, confers susceptibility to this drug disorder. C1 UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, ALCOHOL RES CTR, INST NEUROPSYCHIAT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, DRUG ABUSE RES CTR, LOS ANGELES, CA USA. UTHSC, DEPT CELLULAR & STRUCT BIOL, SAN ANTONIO, TX USA. UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA USA. UNIV TEXAS, HLTH SCI CTR,DEPT PHARMACOL,DIV ADDICT DIS, PHARMACOGENET LAB, SAN ANTONIO, TX 78284 USA. UTHSC, DEPT COMP RESOURCES, SAN ANTONIO, TX USA. RP NOBLE, EP (reprint author), UNIV CALIF LOS ANGELES, DEPT PSYCHIAT & BEHAV SCI, LOS ANGELES, CA 90024 USA. FU NIDA NIH HHS [NIDA DA04268, NIDA DA00146, NIDA DA06250] NR 66 TC 181 Z9 182 U1 0 U2 3 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0376-8716 EI 1879-0046 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD OCT PY 1993 VL 33 IS 3 BP 271 EP 285 DI 10.1016/0376-8716(93)90113-5 PG 15 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA MD306 UT WOS:A1993MD30600006 PM 8261891 ER PT J AU ELLIOTT, ME GOODFRIEND, TL JEFCOATE, CR AF ELLIOTT, ME GOODFRIEND, TL JEFCOATE, CR TI BOVINE ADRENAL GLOMERULOSA AND FASCICULATA CELLS EXHIBIT 28.5-KILODALTON PROTEINS SENSITIVE TO ANGIOTENSIN, OTHER AGONISTS, AND ATRIAL-NATRIURETIC-PEPTIDE SO ENDOCRINOLOGY LA English DT Article ID STIMULATED ALDOSTERONE SYNTHESIS; LEYDIG TUMOR-CELLS; CORPUS-LUTEUM; RAPID ACCUMULATION; CORTEX CELLS; STEROIDOGENESIS; PHOSPHOPROTEIN; BIOSYNTHESIS; SECRETION; CAMP AB Protein synthesis by bovine adrenal glomerulosa and fasciculata cells in response to various modulators of steroid synthesis was examined using [S-35]methionine labeling and two-dimensional gel electrophoresis. Both cell types responded to steroidogenic stimuli with rapid changes in a family of 28- to 30-kilodalton (kDa) proteins similar to those described in rat fasciculata by Epstein and Orme-Johnson. In glomerulosa, angiotensin-II (AII), potassium, and (Bu)2cAMP stimulated the appearance of two 28.5-kDa proteins (no. 3 and 4) with pI values of 6.44 and 6.33 and decreased labeling of two other 28.5-kDa proteins (no. 1 and 2) with pI values of 6.9 and 6.59. The rank order of potency on aldosterone synthesis and that on proteins 1-4 were the same: (Bu)2cAMP > AII > potassium. Atrial natriuretic peptide blocked the effects of AII on all four proteins and on aldosterone synthesis. Adrenal secretagogues also affected labeling of four slightly larger (30 kDa) proteins (no. 5-8). Corresponding proteins in each quartet are separated by the same difference in isoelectric points. These eight proteins may represent a core protein systematically modified in a number of ways. Aldosterone synthesis in glomerulosa, like glucocorticoid synthesis in fasciculata, requires ongoing protein synthesis. The 28- to 30-kDa proteins increased by steroidogenic stimuli in both cells and decreased by atrial natriuretic peptide in glomerulosa may be the proteins whose synthesis is crucial to acute control of steroidogenesis. Our results indicate that these proteins are made in response to calcium- or calcium/phosphoinositide-dependent mechanisms as well as by cAMP. C1 UNIV WISCONSIN, SCH MED, DEPT MED, MADISON, WI 53705 USA. UNIV WISCONSIN, SCH MED, DEPT PHARMACOL, MADISON, WI 53705 USA. RP ELLIOTT, ME (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR, HYPERTENS RES LAB, ROOM C4114, 2500 OVERLOOK TERRACE, MADISON, WI 53705 USA. FU NIDDK NIH HHS [DK-18585] NR 32 TC 50 Z9 50 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD OCT PY 1993 VL 133 IS 4 BP 1669 EP 1677 DI 10.1210/en.133.4.1669 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MA411 UT WOS:A1993MA41100025 PM 8404608 ER PT J AU REDDY, SV SCARCEZ, T WINDLE, JJ LEACH, RJ HUNDLEY, JE CHIRGWIN, JM CHOU, JY ROODMAN, GD AF REDDY, SV SCARCEZ, T WINDLE, JJ LEACH, RJ HUNDLEY, JE CHIRGWIN, JM CHOU, JY ROODMAN, GD TI CLONING AND CHARACTERIZATION OF THE 5'-FLANKING REGION OF THE MOUSE TARTRATE-RESISTANT ACID-PHOSPHATASE GENE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID MULTINUCLEATED CELLS; OSTEOCLAST PHENOTYPE; BONE-RESORPTION; SEQUENCE; PROMOTER; TYPE-5; TRANSCRIPTION; UTEROFERRIN; EXPRESSION; PROTEIN AB Little information is available on the molecular mechanisms controlling osteoclastic bone resorption. We used tartrate-resistant acid phosphatase (TRAP) to begin to investigate the regulation of bone resorption at the molecular level. TRAP is expressed at high levels in osteoclasts and may play an important role in the bone resorptive process. Therefore, we isolated the murine TRAP gene from a mouse spleen genomic library and characterized its promoter. A restriction map was generated for the 17 kb TRAP insert. A 2 kb SmaI fragment, containing the 5'-flanking region, was subcloned and the nucleotide sequence determined. Sequence analysis of the SmaI fragment revealed the presence of numerous candidate transcription factor binding sequences, including those for AP1 and H-APF-1. The H-APF-1 site matches the consensus sequence for the IL-6-regulated transcription factor. An intron was identified at -1 to -393 bp relative to the ATG. The presence of an intron was confirmed by PCR analysis of RNA isolated from murine osteoclasts. Primer extension analysis indicated the presence of a transcription initiation site at -552 bp from the ATG. The region from -1846 to 2 bp relative to the ATG initiation codon drove the transient expression of a luciferase reporter gene when transfected into HRE H9 rabbit endometrial cells. PMA treatment of HRE H9 cells enhanced luciferase transcription approximately threefold. These data suggest that the TRAP promoter is complex and contains multiple regulatory elements. The availability of the TRAP promoter may also permit production of transgenic mice, which can be used to develop previously unavailable osteoclast cell lines. C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT HEMATOL,SAN ANTONIO,TX 78284. CANC THERAPY & RES CTR S TEXAS,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT,SAN ANTONIO,TX 78284. NICHHD,BETHESDA,MD 20892. OI Windle, Jolene/0000-0001-6690-385X FU NIADDK NIH HHS [AM 35188]; NIAMS NIH HHS [AR 41336, AR 39539] NR 30 TC 28 Z9 29 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD OCT PY 1993 VL 8 IS 10 BP 1263 EP 1270 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LY890 UT WOS:A1993LY89000014 PM 8256664 ER PT J AU KLASSEN, D GOODFRIEND, TL SCHUNA, AA YOUNG, DY PETERSON, CA AF KLASSEN, D GOODFRIEND, TL SCHUNA, AA YOUNG, DY PETERSON, CA TI ASSESSMENT OF BLOOD-PRESSURE DURING TREATMENT WITH NAPROXEN OR IBUPROFEN IN HYPERTENSIVE PATIENTS TREATED WITH HYDROCHLOROTHIAZIDE SO JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Article ID ANTI-INFLAMMATORY DRUGS; INDOMETHACIN; DIURETICS; PROSTAGLANDINS; PROPRANOLOL; CAPTOPRIL; SULINDAC; ASPIRIN; AGENTS AB This study determined the effect of nonsteroidal anti-inflammatory drug (NSAID) administration on blood pressure in hypertensive patients taking hydrochlorothiazide (HCTZ). Ninety-seven patients with mild essential hypertension and a musculoskeletal indication for NSAID use were studied in a three-phase, multi-center, double-blind, randomized, parallel study based in 15 academic and community clinics. Patients served as their own controls. Patients with stable hypertension, not taking antihypertensive or NSAID medications, were treated with HCTZ 50 mg/day. After 4 to 5 weeks of treatment and documented stable blood pressure, naproxen 375 mg twice a day or ibuprofen 800 mg three times a day was added. Blood pressure was measured at 2 and 4 weeks of NSAID therapy. The average diastolic blood pressure was 97.5 +/- 2.4 mm Hg and the average of the mean arterial pressure (MAP) was 116.8 +/- 6.04 before treatment with HCTZ. Hydrochlorothiazide treatment decreased diastolic blood pressure to 83.1 +/- 5.6 mm Hg, and MAP to 101. 1 +/- 6.5 mm Hg. With naproxen or ibuprofen treatments, mean diastolic blood pressure increased less than 3 mm Hg. At 2 weeks, ibuprofen increased diastolic blood pressure by 2.6 mm Hg (P = .004) and naproxen increased diastolic blood pressure 0.7 mm Hg (P = .40). Both ibuprofen and naproxen significantly increased diastolic pressure at 4 weeks (2.1 mm Hg, P = .042; and 1.8 mm Hg, P = .043, respectively). There was no correlation between the pre-NSAID blood pressure and the magnitude of change after 2 or 4 weeks of treatment. Changes in MAP reflected a pattern similar to diastolic pressure. Ibuprofen increased MAP 3.6 mm Hg (P < .001) and 2.7 mm Hg (P = .019) at 2 and 4 weeks, respectively. Naproxen increased MAP 1.1 mmHg(P = .29)and 1.5 mmHg(P = .16)at2 and 4 weeks, respectively. Patient weight increased 1.0 kg (P <.001) and 0.9 kg (P <.001) with ibuprofen and 0.3 kg (P = .24) and .5 (P = .12) with naproxen at 2 and 4 weeks, respectively. Comparing naproxen and ibuprofen treatments, there were no significant differences in blood pressure or body weight changes. In patients with mild essential hypertension controlled with a thiazide diuretic, the concurrent use of either naproxen or ibuprofen resulted in small but statistically significant increases in blood pressure. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. SYNTEX LABS INC,DIV MED AFFAIRS,DEPT CLIN INVEST,PALO ALTO,CA. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. SYNTEX LABS INC,DIV MED AFFAIRS,DEPT BIOSTAT,PALO ALTO,CA. RP KLASSEN, D (reprint author), UNIV MARYLAND,SCH MED,DEPT MED,DIV NEPHROL,22 S GREENE ST,BALTIMORE,MD 21201, USA. NR 29 TC 15 Z9 15 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0091-2700 J9 J CLIN PHARMACOL JI J. Clin. Pharmacol. PD OCT PY 1993 VL 33 IS 10 BP 971 EP 978 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MA786 UT WOS:A1993MA78600014 PM 8227469 ER PT J AU SELLERS, EM CIRAULO, DA DUPONT, RL GRIFFITHS, RR KOSTEN, TR ROMACH, MK WOODY, GE SHADER, RI SHEAR GREENBLATT, DJ BALLENGER, JC SCHATZBERG BARBEE, JG AF SELLERS, EM CIRAULO, DA DUPONT, RL GRIFFITHS, RR KOSTEN, TR ROMACH, MK WOODY, GE SHADER, RI SHEAR GREENBLATT, DJ BALLENGER, JC SCHATZBERG BARBEE, JG TI ALPRAZOLAM AND BENZODIAZEPINE DEPENDENCE SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on Issues in the Clinical Use of Alprazolam CY MAR 13, 1993 CL WASHINGTON, DC ID DISCRIMINATIVE STIMULUS PROPERTIES; ABUSE LIABILITY; PANIC DISORDER; ALCOHOL WITHDRAWAL; DRUG-USE; ANXIETY DISORDERS; MULTICENTER TRIAL; RELATIVE ABUSE; SELF-INJECTION; DIAZEPAM AB The incidence of nonmedical use of alprazolam is very low relative to its widespread legitimate medical use; in fact, given the millions of patients who have received this medication, the incidence is remarkably small. In particular, among patients with anxiety disorders, dependence does not appear to be a clinically important problem. Alprazolam abuse and dependence represent only a small fraction of the large and serious nonmedical use problem in the United States, and when they occur, are among individuals who abuse other drugs. For example, a serious problem of alprazolam abuse may exist among patients in methadone maintenance treatment. A similar problem exists with diazepam. Alcohol abusers and alcohol-dependent individuals are another group among whom concern about benzodiazepine and alprazolam abuse exists. However, more and better information about the extent and nature of this use is needed. Many patients with alcohol or drug abuse also have anxiety disorders for whom effective pharmacotherapy may be needed. In the interim, caution but not prohibition to use should prevail in prescribing alprazolam to such patients. To the extent that nonmedical alprazolam use exists, evidence suggests that the vast majority of such use is the consequence of the inappropriate prescribing of the medication by a small number of physicians. One way to reduce the inappropriate use of benzodiazepines in methadone programs is to drug test the methadone-maintenance patients and to link positive urine tests to contingency-management strategies. The available data provide some support to the idea that alprazolam and diazepam have more abuse liability than other benzodiazepines. C1 UNIV TORONTO,DEPT PHARMACOL,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT MED,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT PSYCHIAT,TORONTO M5S 1A1,ONTARIO,CANADA. TUFTS UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02111. DEPT VET AFFAIRS OUTPATIENT CLIN,BOSTON,MA. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20057. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06510. UNIV PENN,PHILADELPHIA VET AFFAIRS MED CTR,SUBST ABUSE TREATMENT & RES CTR,PHILADELPHIA,PA 19104. MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC 29425. LOUISIANA STATE UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,NEW ORLEANS,LA 70112. RP SELLERS, EM (reprint author), ADDICT RES FDN,33 RUSSELL ST,TORONTO M5S 2S1,ONTARIO,CANADA. OI Shader, Richard/0000-0002-1888-7565 NR 93 TC 46 Z9 47 U1 2 U2 3 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1993 VL 54 SU S BP 64 EP 77 PG 14 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA MQ072 UT WOS:A1993MQ07200006 PM 8262891 ER PT J AU BOWDEN, CL SCHATZBERG, AF ROSENBAUM, A CONTRERAS, SA SAMSON, JA DESSAIN, E SAYLER, M AF BOWDEN, CL SCHATZBERG, AF ROSENBAUM, A CONTRERAS, SA SAMSON, JA DESSAIN, E SAYLER, M TI FLUOXETINE AND DESIPRAMINE IN MAJOR DEPRESSIVE DISORDER SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID CLINICAL-TRIAL; OUTPATIENTS; AMITRIPTYLINE; CLOMIPRAMINE; IMIPRAMINE AB The efficacy and safety of fluoxetine and desipramine were compared in a 6-week double-blind, parallel group study of patients with major depression. Twenty-five were studied while hospitalized for treatment, and 33 were studied as outpatients. Improvement on the Hamilton Rating Scale for Depression was significant for both treatments from week 1 through the end of the study and did not differ between the two treatments at any week. Overall, 64% of fluoxetine-treated patients and 68% of desipramine-treated patients had at least a 50% reduction in Hamilton Depression score. We assessed whether improvement relatively early in treatment was predictive of categorical response at 6 weeks. Among fluoxetine-treated patients, but not desipramine-treated patients, the week 3 change in the Hamilton Depression mood item was significantly predictive of the response at 6 weeks. Patients treated with fluoxetine had significantly fewer side effects than those treated with desipramine. Desipramine, but not fluoxetine, caused a persistent increase in heart rate. The results suggest that early signs of response to fluoxetine are not dependent on achieving steady-state levels of the drug. C1 MASSACHUSETTS MENTAL HLTH CTR,NEUROPSYCHOPHARMACOL LAB,BOSTON,MA 02115. STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. HARPER GRACE HOSP,DETROIT,MI 48201. TEXAS TECH UNIV,HLTH SCI CTR,LUBBOCK,TX 79430. MCLEAN HOSP,AFFECT DIS PROGRAM,BELMONT,MA 02178. RP BOWDEN, CL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 17 TC 67 Z9 67 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD OCT PY 1993 VL 13 IS 5 BP 305 EP 310 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LZ737 UT WOS:A1993LZ73700002 PM 8227488 ER PT J AU FRYE, MA WIRSHING, WC AMES, D AF FRYE, MA WIRSHING, WC AMES, D TI CLOZAPINE AS A DIAGNOSTIC-TOOL FOR A PSYCHOTIC PARKINSONIAN PATIENT SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter RP FRYE, MA (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA 90073 USA. NR 10 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD OCT PY 1993 VL 13 IS 5 BP 359 EP 360 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LZ737 UT WOS:A1993LZ73700010 PM 7901246 ER PT J AU SUBRAMANIAN, R VOLOVSEK, A HO, YS AF SUBRAMANIAN, R VOLOVSEK, A HO, YS TI LACK OF CHANGE IN MNSOD DURING ISCHEMIA-REPERFUSION OF ISOLATED RAT-HEART SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE ISCHEMIA; REPERFUSION; SUPEROXIDE DISMUTASE; MYOCARDIUM; RAT; CARDIAC OUTPUT; LACTATE; LACTIC DEHYDROGENASE ID MITOCHONDRIAL SUPEROXIDE-DISMUTASE; FREE-RADICAL GENERATION; MYOCARDIAL ISCHEMIA; INJURY; OXYGEN; PROTEINS; NITRONE; DAMAGE C1 UNIV WISCONSIN, DEPT PATHOL, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, LAB SERV, MADISON, WI USA. DUKE UNIV, MED CTR, DEPT PULM MED, DURHAM, NC 27710 USA. FU NHLBI NIH HHS [HL-39585] NR 30 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD OCT PY 1993 VL 25 IS 10 BP 1179 EP 1186 DI 10.1006/jmcc.1993.1131 PG 8 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA ME936 UT WOS:A1993ME93600006 PM 8263952 ER PT J AU CIRESI, KF ANTHONY, JP HOFFMAN, WY BOWERSOX, JC REILLY, LM RAPP, JH AF CIRESI, KF ANTHONY, JP HOFFMAN, WY BOWERSOX, JC REILLY, LM RAPP, JH TI LIMB SALVAGE AND WOUND COVERAGE IN PATIENTS WITH LARGE ISCHEMIC ULCERS - A MULTIDISCIPLINARY APPROACH WITH REVASCULARIZATION AND FREE TISSUE TRANSFER SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID RANDOM-PATTERN FLAPS; LOWER-EXTREMITY; DISTAL REVASCULARIZATION; MAJOR AMPUTATIONS; MUSCLE FLAP; BYPASS; RECONSTRUCTION; PERONEAL; FOOT AB Purpose: Large ischemic wounds, particularly with exposed bone or tendons, may not heal even after successful revascularization. We have taken an aggressive approach for limb salvage that uses autogenous vein grafting and simultaneous microvascular free tissue transfer. Methods: In the past year, seven patients (average age 67 years; range 56 to 79) with ischemic disease and distal ulceration underwent revascularization for limb salvage and free tissue transfer. Each had a nonhealing wound (average size 80 cm2), present for 8.6 months (range 2 to 24 months). Simultaneous vein bypass and free tissue transfer was performed in four (57%) of the seven patients. Results: All flaps were initially viable; however, one was lost on day 4 because of hypotension and congestive heart failure. One patient with a successful flap died at 1 month of pneumonia. Minor wound complications were seen in four (57%) of seven patients. Five of the seven patients had the wounds heal completely and are ambulatory at an average follow up of 10 months. Conclusions: Our aggressive approach was successful in preserving limb length and function in 71% of our patients. We perform simultaneous procedures whenever possible to minimize operative and hospitalization times. We believe that this combined approach optimizes the treatment of ischemic limbs with large ulcers. C1 UNIV CALIF SAN FRANCISCO, SAN FRANCISCO VET AFFAIRS MED CTR, DIV PLAST & RECONSTRUCT SURG, SAN FRANCISCO, CA 94143 USA. UNIV CALIF SAN FRANCISCO, SAN FRANCISCO VET AFFAIRS MED CTR, DIV VASC SURG, SAN FRANCISCO, CA 94143 USA. NR 24 TC 32 Z9 32 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD OCT PY 1993 VL 18 IS 4 BP 648 EP 655 PG 8 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MB165 UT WOS:A1993MB16500012 PM 8411472 ER PT J AU SHERRY, B LI, XY TYLER, KL CULLEN, JM VIRGIN, HW AF SHERRY, B LI, XY TYLER, KL CULLEN, JM VIRGIN, HW TI LYMPHOCYTES PROTECT AGAINST AND ARE NOT REQUIRED FOR REOVIRUS-INDUCED MYOCARDITIS SO JOURNAL OF VIROLOGY LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; NATURAL-KILLER CELLS; MONOCLONAL-ANTIBODIES; VIRAL MYOCARDITIS; T-CELLS; MICE; VIRUS; PATHOGENESIS; COXSACKIEVIRUS-B3; INFECTION AB Many studies suggest that host lymphocytes are damaging, rather than protective, in virally induced myocarditis. We have investigated the role of lymphocyte-based immunity in murine myocarditis by using a myocarditic reovirus (reovirus serotype 3 8B), nonmyocarditic reoviruses, adoptive transfer experiments, and mice with severe combined immunodeficiency (SCID mice). Prior to infection, passive transfer of monoclonal antibodies specific for 8B capsid proteins protected neonatal mice against 8B-induced myocarditis, indicating that humoral immunity can protect against myocarditis. Some monoclonal antibodies acted by blocking viral spread to and/or replication in the heart. Passive transfer of reovirus-immune, but not naive, spleen cells prior to infection protected neonatal mice from 8B-induced myocarditis. Depletion of either CD4 or CD8 T cells resulted in increased viral titer in the heart but did not abrogate immune cell-mediated protection against myocardial injury. This shows that both CD4 and CD8 T cells can act independently to protect myocardial tissue from reovirus infection. In addition, reovirus 8B caused extensive myocarditis in SCID mice. This confirms a prior report (B. Sherry, F. J. Schoen, E. Wenske, and B. N. Fields, J. Virol. 63:4840-4849, 1989) that T cells are not required for reovirus-induced myocarditis and demonstrates for the first time that B cells are not required for reovirus-induced myocarditis. We used SCID mice and a panel of reoviruses to assess (i) the relationship between growth in the heart and myocardial damage and (ii) the possibility that nonmyocarditic reoviruses exhibit a myocarditic phenotype in the absence of functional lymphocytes. Growth in the heart was not the sole determinant of myocarditic potential in SCID mice. Although 8B induced myocarditis in SCID mice, no or minimal myocarditis was found in SCID mice infected with four reovirus strains previously shown (B. Sherry and B. N. Fields J. Virol. 63:4850-4856, 1989) to be nonmyocarditic or poorly myocarditic in normal neonatal mice. We conclude that (i) humoral immunity and cellular immunity are protective against, and not required for, reovirus-induced myocarditis and (ii) the potential to induce cardiac damage is a property of the virus independent of lymphocyte-based immunity. C1 DENVER VET AFFAIRS MED CTR,DEPT NEUROL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT NEUROL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT MICROBIOL IMMUNOL,DENVER,CO 80262. WASHINGTON UNIV,SCH MED,DEPT MED,DIV INFECT DIS,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PATHOL,DIV INFECT DIS,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT MOLEC MICROBIOL,DIV INFECT DIS,ST LOUIS,MO 63110. RP SHERRY, B (reprint author), N CAROLINA STATE UNIV,COLL VET MED,DEPT MICROBIOL PATHOL & PARASITOL,4700 HILLSBOROUGH ST,RALEIGH,NC 27606, USA. OI Tyler, Kenneth/0000-0003-3294-5888 FU NIAID NIH HHS [AI31250]; NINDS NIH HHS [2 P50 NS16998] NR 33 TC 48 Z9 52 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD OCT PY 1993 VL 67 IS 10 BP 6119 EP 6124 PG 6 WC Virology SC Virology GA LX120 UT WOS:A1993LX12000048 PM 8396673 ER PT J AU MCENTEE, CM CANTWELL, R RAHMAN, MU HUDSON, AP AF MCENTEE, CM CANTWELL, R RAHMAN, MU HUDSON, AP TI TRANSCRIPTION OF THE YEAST MITOCHONDRIAL GENOME REQUIRES CYCLIC-AMP SO MOLECULAR & GENERAL GENETICS LA English DT Article DE SACCHAROMYCES-CEREVISIAE; MITOCHONDRIA; TRANSCRIPTIONAL REGULATION; PROTEIN PHOSPHORYLATION; STRINGENT RESPONSE ID DEPENDENT PROTEIN-KINASE; CAMP-BINDING PROTEIN; SACCHAROMYCES-CEREVISIAE; ADENYLATE-CYCLASE; RAS PROTEINS; CATABOLITE REPRESSION; REGULATORY SUBUNIT; STRINGENT RESPONSE; RECEPTOR PROTEIN; GLUCOSE REPRESSION AB Using various mutant strains and nutritional manipulations, we investigated a potential role for cyclic AMP (cAMP) in the regulation of mitochondrial (mt) gene expression in the yeast Saccharomyces cerevisiae. In RAS mutants known to have either abnormally low or high cellular levels of this nucleotide, we show that both mt transcription rate and overall mt transcript levels vary directly with cellular cAMP levels. We further show that nutritional downshift of actively growing cells causes a severe, rapid fall in cAMP levels, and that this fall is concomitant with the stringent mt transcriptional curtailment that we and others have previously shown to follow this nutritional manipulation. In in vitro mt transcription assays using intact organelles from downshifted and actively growing cells, stringently curtailed mt gene expression can be restored to 75% of control levels by addition of cAMP to the assay mix. Consistent with these observations a RAS2vall9 mutant strain, which cannot adjust cAMP levels in response to external stimuli, shows no mt stringent response following nutritional downshift. We also demonstrate a significant but transient increase in both mt transcript levels and mt transcription rate following shift of actively respiring wild-type cells to glucose-based medium, a manipulation known to cause a short-lived pulse of cAMP in yeast; similar manipulation of the RAS2vall9 mutant strain generates no such response. Taken together all these observations indicate that cellular cAMP levels are involved in the regulation of mt transcription in yeast. Moreover, the lack of a mt stringent transcriptional response following downshift in a strain in which the BCY1 gene had been insertionally inactivated suggests that cAMP may influence mt transcription via a mt cAMP-dependent protein kinase. These results link mt gene expression with mechanisms governing growth control and nutrient adaptation in yeast, and they provide a means by which mt gene expression might be coordinated with that of related nuclear genes. C1 DEPT VET AFFAIRS MED CTR,RES SERV,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. NR 67 TC 22 Z9 22 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD OCT PY 1993 VL 241 IS 1-2 BP 213 EP 224 DI 10.1007/BF00280219 PG 12 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MB252 UT WOS:A1993MB25200026 PM 8232206 ER PT J AU GORMAN, DG READ, S CUMMINGS, JL AF GORMAN, DG READ, S CUMMINGS, JL TI CHOLINERGIC THERAPY OF BEHAVIORAL DISTURBANCES IN ALZHEIMERS-DISEASE SO NEUROPSYCHIATRY NEUROPSYCHOLOGY AND BEHAVIORAL NEUROLOGY LA English DT Article DE PHYSOSTIGMINE; HALOPERIDOL; CHOLINERGIC; NEUROLEPTIC; ALZHEIMERS DISEASE; PSYCHOSIS ID ACETYLTRANSFERASE ACTIVITY; SENILE DEMENTIA; HALOPERIDOL; SYMPTOMS; ABNORMALITIES; DIAGNOSIS; PSYCHOSIS; SEVERITY AB Cholinergic dysfunction in Alzheimer's disease (AD) may contribute to the behavioral disturbances exhibited by many AD patients, and cholinergic replacement therapy may diminish these behaviors. We compared physostigmine, an anticholinesterase agent, with haloperidol, a commonly used treatment for the delusions and hallucinations of AD, in a double-blind, crossover trial in a group of behaviorally disturbed patients with advanced AD. Both agents reduced the behavioral problems of AD, supporting a role for cholinergic dysfunction in the psychotic manifestations of AD. A high frequency of adverse side effects were produced by haloperidol. C1 UNIV CALIF LOS ANGELES, SCH MED, REED NEUROL RES CTR, DEPT NEUROL, LOS ANGELES, CA 90024 USA. JOHN DOUGLAS FRENCH CTR ALZHEIMERS DIS, LOS ALAMITOS, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHIAT SERV, BEHAV NEUROSCI SECT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. NR 32 TC 38 Z9 38 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0894-878X J9 NEUROPSY NEUROPSY BE JI Neuropsychiatr. Neuropsychol. Behav. Neurol. PD OCT PY 1993 VL 6 IS 4 BP 229 EP 234 PG 6 WC Clinical Neurology; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA MK018 UT WOS:A1993MK01800004 ER PT J AU ROYALL, DR MAHURIN, RK CORNELL, J GRAY, KF AF ROYALL, DR MAHURIN, RK CORNELL, J GRAY, KF TI BEDSIDE ASSESSMENT OF DEMENTIA TYPE USING THE QUALITATIVE EVALUATION OF DEMENTIA SO NEUROPSYCHIATRY NEUROPSYCHOLOGY AND BEHAVIORAL NEUROLOGY LA English DT Article DE QED; CORTICAL AND SUBCORTICAL DEMENTIAS; RATING SCALE ID CLINICAL DIAGNOSTIC-CRITERIA; ADRDA WORK GROUP; ALZHEIMERS-DISEASE; SUBCORTICAL DEMENTIA; DIFFERENTIAL-DIAGNOSIS; COGNITIVE IMPAIRMENT; ILLNESS; SCALE AB Problem: We present a novel dementia assessment instrument, the Qualitative Evaluation of Dementia (QED), designed to discriminate dementia type at the bedside. The QED is a brief, clinically based checklist which operationalizes the approach of a geriatric psychiatrist to the qualitative assessment of dementing illnesses. Scores range from 0 = pure ''subcortical'' illness, to 30 = pure ''cortical'' disease. Internal consistency (Chronbach's alpha = .69) and interrater reliability (r = .93) are acceptable. Blinded raters agree on dementia type in > 90% of cases. When QED scores are mapped against measures of general cognitive function a qualitative picture of dementia typology emerges. Method: The QED's ability to discriminate NINCDS ''Probable'' Alzheimer's disease (AD) from those with ''no dementia'' and ''dementia without cortical features'' was assessed in a cross-sectional sample of 118 consecutive patients presenting to a multidisciplinary geriatric assessment clinic and consultation service. Results: The QED accurately discriminated air three study groups. When combined with the Executive Interview (EXIT), 87.7% of subjects were correctly classified. Misclassification rates ranged from 11.8% for ''Probable'' AD to 13% for ''no dementia.'' Substituting the Mini-Mental State Examination (MMSE) correctly classified 74% of subjects, with misclassification rates ranging from 11.8% for ''Probable'' AD to 40.0% for ''dementia with no cortical features.'' The EXIT was more sensitive than the MMSE to mild cognitive impairment, and subcortical dementia. Conclusions: These results suggest that dementia subtypes can be accurately and reliably assessed using a combination of the QED and either the EXIT or the MMSE. This evaluation can be completed in 20 minutes, and requires no access to brood or laboratory work. The use of the EXIT in this assessment reduces misclassification rates and improves sensitivity in early stages. The implications of this technique for clinical assessment, subject recruitment, and the conceptualization of dementia are discussed. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT PSYCHIAT,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT MED,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 34 TC 26 Z9 26 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0894-878X J9 NEUROPSY NEUROPSY BE JI Neuropsychiatr. Neuropsychol. Behav. Neurol. PD OCT PY 1993 VL 6 IS 4 BP 235 EP 244 PG 10 WC Clinical Neurology; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA MK018 UT WOS:A1993MK01800005 ER PT J AU BAKER, DG SCHUMACHER, HR AF BAKER, DG SCHUMACHER, HR TI CURRENT CONCEPTS - ACUTE MONOARTHRITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; SEPTIC ARTHRITIS; SYNOVIAL-FLUID; GONOCOCCAL-INFECTION; BACTERIAL ARTHRITIS; MYCOBACTERIUM-AVIUM; VIRUS-INFECTION; CRYSTALS; DISEASE; OSTEOMYELITIS C1 PHILADELPHIA VET AFFAIRS MED CTR, CTR RHEUMATOL IMMUNOL, UNIV & WOODLAND AVE, PHILADELPHIA, PA 19104 USA. MED COLL PENN, PHILADELPHIA, PA 19129 USA. UNIV PENN, PHILADELPHIA, PA 19104 USA. NR 60 TC 78 Z9 80 U1 0 U2 3 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD SEP 30 PY 1993 VL 329 IS 14 BP 1013 EP 1020 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA LY587 UT WOS:A1993LY58700007 PM 8366902 ER PT J AU SONG, CS HER, S SLOMCZYNSKA, M CHOI, SJ JUNG, MH ROY, AK CHATTERJEE, B AF SONG, CS HER, S SLOMCZYNSKA, M CHOI, SJ JUNG, MH ROY, AK CHATTERJEE, B TI A DISTAL ACTIVATION DOMAIN IS CRITICAL IN THE REGULATION OF THE RAT ANDROGEN RECEPTOR GENE PROMOTER SO BIOCHEMICAL JOURNAL LA English DT Article ID HUMAN GLUCOCORTICOID RECEPTOR; TRANSCRIPTION FACTOR; DNA; SUPERFAMILY; BINDING; PROTEIN; RNA; PURIFICATION; CLONING; ELEMENT AB The far upstream region of the rat androgen receptor (AR) gene has been cloned, and the nucleotide sequence up to -2656 bp established. Nested deletion mutants of rat AR 5' flanking sequences were ligated to the luciferase reporter gene, and their promoter activities were examined in transfected COS1 cells. Results show a critical cis-acting domain located between positions -960 and -940. Deletion of this cis element resulted in a greater than 90 % decrease in the promoter activity. A nuclear protein that specifically binds to this 21-nucleotide sequence was identified by gel mobility shift analysis. The -960/-940 cis element has no identity to the binding sequence of any known transcription factor. Furthermore, the cognate binding protein is present in both rat and human (HeLa) cell nuclear extracts. We conclude that a novel trans-activator interacting at the -960/ -940 region plays a critical role in the regulation of AR gene expression. C1 UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIA NIH HHS [P01-AG06872, R01-AG03527]; NIDDK NIH HHS [R37-DK14744] NR 38 TC 29 Z9 29 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD SEP 15 PY 1993 VL 294 BP 779 EP 784 PN 3 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LY645 UT WOS:A1993LY64500024 PM 8379933 ER PT J AU TRESTMAN, RL COCCARO, EF MITROPOULOU, V GABRIEL, SM HORVATH, T SIEVER, LJ AF TRESTMAN, RL COCCARO, EF MITROPOULOU, V GABRIEL, SM HORVATH, T SIEVER, LJ TI THE CORTISOL RESPONSE TO CLONIDINE IN ACUTE AND REMITTED DEPRESSED MEN SO BIOLOGICAL PSYCHIATRY LA English DT Article DE DEPRESSION; CLONIDINE; CORTISOL ID CORTICOTROPIN-RELEASING FACTOR; GROWTH-HORMONE; PLASMA-CORTISOL; BLOOD-PRESSURE; ENDOGENOUS-DEPRESSION; NORADRENERGIC NEURONS; LOCUS COERULEUS; SECRETION; ACTH; NORADRENALINE AB To assess the relationship between the hypothalamo-pituitary-adrenal (HPA) axis and the noradrenergic system in patients with major depression, 26 normal controls, 32 acutely depressed patients, and 21 patients with remitted depression, all men, were administered intravenous clonidine (2 mug/kg) or placebo. Acute, but not remitted, depressed patients had a greater plasma cortisol baseline than did normal controls (t = 2.0, p < 0.03). Only acutely depressed patients had a greater decrease in plasma cortisol in response to clonidine than to placebo (t = 2.5, p < 0.02). Statistically controlling for both diurnal variation and baseline cortisol, acute, but not remitted, depressed patients had a greater decrease in plasma cortisol in response to clonidine than did the controls (analysis of covariance: F[1,35] = 4.26, p < 0.05). These results support a state-dependent noradrenergic-HPA axis regulatory disturbance in depressed patients, suggesting that clonidine inhibits the elevated plasma cortisol in acute depression but not the normal concentrations observed in remitted depression or healthy controls. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. MED COLL PENN,PHILADELPHIA,PA 19129. RP TRESTMAN, RL (reprint author), BRONX VET ADM MED CTR,PSYCHIAT SERV,116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NCRR NIH HHS [RR00071]; NIMH NIH HHS [R01-MH41131] NR 43 TC 11 Z9 11 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD SEP 15 PY 1993 VL 34 IS 6 BP 373 EP 379 DI 10.1016/0006-3223(93)90181-C PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MA800 UT WOS:A1993MA80000005 PM 8218604 ER PT J AU CHRISTAKIS, NA ASCH, DA AF CHRISTAKIS, NA ASCH, DA TI BIASES IN HOW PHYSICIANS CHOOSE TO WITHDRAW LIFE-SUPPORT SO LANCET LA English DT Article ID SUSTAINING TREATMENT; ADVANCE DIRECTIVES; DECISION-MAKING; CRITICALLY ILL; CARE; PREFERENCES; EUTHANASIA; ATTITUDES AB We have investigated biases in physicians' decisions regarding the form of life support to withdraw from critically ill patients in whom the decision to withdraw has already been made. Using a specially designed instrument that solicited both self-reported preferences and also responses to experimentally varied clinical vignettes, we surveyed 862 American internists, of whom 481 (56%) responded. Physicians do have preferences about the form of life support withdrawn. From most likely to least likely the order is: blood products, haemodialysis, intravenous vasopressors, total parenteral nutrition, antibiotics, mechanical ventilation, tube feedings, and intravenous fluids. Four biases in decision making were also identified. Physicians prefer to withdraw forms of therapy supporting organs that failed for natural rather than iatrogenic reasons, to withdraw recently instituted rather than longstanding interventions, to withdraw forms of therapy resulting in immediate death rather than delayed death, and to withdraw forms of therapy resulting in delayed death when confronted with diagnostic uncertainty. Because these biases may have clinical, social, and ethical consequences counter to patient goals, and because they may affect the underlying decision whether to withdraw life support at all, they may represent impediments to rational and compassionate decision making in critical care. C1 UNIV PENN, LEONARD DAVIS INST HLTH ECON, PHILADELPHIA, PA 19104 USA. UNIV PENN, SCH MED, DIV FISIOL VEGETAL, PHILADELPHIA, PA 19104 USA. UNIV PENN, DEPT SOCIOL, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. RI Christakis, Nicholas/B-6690-2008; Christakis, Nicholas/C-3205-2009 NR 30 TC 126 Z9 128 U1 1 U2 7 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0140-6736 EI 1474-547X J9 LANCET JI Lancet PD SEP 11 PY 1993 VL 342 IS 8872 BP 642 EP 646 DI 10.1016/0140-6736(93)91759-F PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA LX272 UT WOS:A1993LX27200010 PM 8103146 ER PT J AU WILLIAMS, JW SIMEL, DL AF WILLIAMS, JW SIMEL, DL TI DOES THIS PATIENT HAVE SINUSITIS - DIAGNOSING ACUTE SINUSITIS BY HISTORY AND PHYSICAL-EXAMINATION SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ACUTE MAXILLARY SINUSITIS; CHILDREN; NASAL; RADIOGRAPHY; ULTRASONOGRAPHY; INFECTIONS; ULTRASOUND; ETIOLOGY; SYMPTOMS; SINUSES C1 UNIV TEXAS,HLTH SCI CTR,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284. VET AFFAIRS MED CTR,AMBULATORY CARE SERV,DURHAM,NC. VET AFFAIRS MED CTR,CTR HLTH SERV RES PRIMARY CARE,DURHAM,NC. DUKE UNIV,MED CTR,DIV GEN INTERNAL MED,DURHAM,NC 27710. RP WILLIAMS, JW (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,AMBULATORY CARE SERV,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 37 TC 112 Z9 113 U1 0 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 SEP 8 PY 1993 VL 270 IS 10 BP 1242 EP 1246 DI 10.1001/jama.270.10.1242 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA LV649 UT WOS:A1993LV64900032 PM 8355389 ER PT J AU LIEBER, CS AF LIEBER, CS TI HERMAN AWARD LECTURE, 1993 - A PERSONAL PERSPECTIVE ON ALCOHOL, NUTRITION, AND THE LIVER SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE 2E1; ACETALDEHYDE; GLUTATHIONE; COLLAGEN; S-ADENOSYL-L-METHIONINE; DILINOLEOYLPHOSPHATIDYLCHOLINE; LIPIDS; FIBROSIS ID CHRONIC ETHANOL-CONSUMPTION; HEPATIC VITAMIN-A; INDUCED LIPID-PEROXIDATION; 1ST PASS METABOLISM; FAT-STORING CELLS; RAT-LIVER; DEHYDROGENASE-ACTIVITY; ACETALDEHYDE ADDUCTS; 1ST-PASS METABOLISM; ACETAMINOPHEN HEPATOTOXICITY AB Alcohol causes primary malnutrition by displacing nutrients in the diet and secondary malnutrition via malabsorption and cellular injury through direct cytotoxicity. Hepatotoxicity results from metabolic disturbances associated with the oxidation of ethanol via liver alcohol dehydrogenase (ADH) and the redox changes produced by the generated NADH (the reduced form of nicotinamide adenine dinucleotide), which in turn affects the metabolism of lipids, carbohydrates, proteins, and purines. Ethanol is also oxidized in liver microsomes by an ethanol-inducible cytochrome P450, which contributes to the alcoholic's tolerance and his increased vulnerability to the toxicity of industrial solvents, anesthetics, commonly prescribed drugs, over-the-counter analgesics, chemical carcinogens, and retinoids. Increased acetaldehyde generation, with formation of protein adducts, results in antibody production, enzyme inactivation, decreased DNA repair, impaired utilization of oxygen, glutathione depletion, free radical-mediated toxicity, lipid peroxidation, and increased collagen synthesis. Therapy may eventually improve with the use of supernutrients such as S-adenosyl-L-methionine, which replenishes glutathione, restores methylation, and attenuates liver injury, as well as dilinolcoyl-phosphatidylcholine, which prevents cirrhosis. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,LIVER DIS & NUTR SECT,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIAAA NIH HHS [AA 03508, AA 05934]; NIDDK NIH HHS [DK 32810] NR 199 TC 45 Z9 48 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD SEP PY 1993 VL 58 IS 3 BP 430 EP 442 PG 13 WC Nutrition & Dietetics SC Nutrition & Dietetics GA LV751 UT WOS:A1993LV75100019 PM 8237856 ER PT J AU MACKINNEY, AA CLARK, SS BORCHERDING, W FIZZOTTI, M HONG, R AF MACKINNEY, AA CLARK, SS BORCHERDING, W FIZZOTTI, M HONG, R TI SIMULTANEOUS DEMONSTRATION OF THE PHILADELPHIA-CHROMOSOME IN T-CELLS, B-CELLS, AND MYELOID CELLS SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Note DE T-CELL LYMPHOMA; FLOW CYTOMETRY; CYTOGENETICS; STEM CELL ID CHRONIC MYELOGENOUS LEUKEMIA; CHRONIC MYELOCYTIC-LEUKEMIA; BREAKPOINT CLUSTER REGION; ACUTE LYMPHOBLASTIC-LEUKEMIA; BLAST CRISIS; MALIGNANT-LYMPHOMA; MULTIPLE-MYELOMA; BONE-MARROW; REARRANGEMENT; PATIENT AB A patient presented with lymphoblastic lymphoma in lymph-nodes and chronic myelogenous leukemia (CML) in marrow and peripheral blood. All marrow and unstimulated peripheral blood cells contained the Philadelphia chromosome{t(9:22)}. Lymphoma cells were analyzed by flow cytometry and were identified as T cells (CD2+CD5+CD7+CD34+). All fresh lymphoma cells contained the t(9:22) translocation. Cultures of purified peripheral blood T and B cells and specifically stimulated NK cells revealed that 59% of the B cells, 10% of the NK cells, and none of the normal T cells contained the translocation. The lack of translocation in normal peripheral T cells is attributed to their long lifespan. No rearrangement of immunoglobulin or T cell receptor beta or gamma genes was found in either the leukemia or lymphoma cells. Analysis of the DNA from cryopreserved lymphoma biopsy showed clonal rearrangement within the common breakpoint cluster region of the bcr gene identical to the bcr rearrangement in DNA from leukemia blood cells. The data support the concept that T and B cells originate in the patient's totipotent stem cell from which the CML is also derived. (C) 1993 Wiley-Liss, Inc. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. NR 41 TC 15 Z9 17 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 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD SEP PY 1993 VL 44 IS 1 BP 48 EP 52 DI 10.1002/ajh.2830440110 PG 5 WC Hematology SC Hematology GA LP906 UT WOS:A1993LP90600009 PM 7688179 ER PT J AU SHARKEYMATHIS, PK KAUFFMAN, CA GRAYBILL, JR STEVENS, DA HOSTETLER, JS CLOUD, G DISMUKES, WE BENNETT, J BRADSHER, RW CHAPMAN, SW FISHER, JF KERKERING, TM MEDOFF, G PERFECT, JR PANKEY, GA REX, JH SAAG, MS AF SHARKEYMATHIS, PK KAUFFMAN, CA GRAYBILL, JR STEVENS, DA HOSTETLER, JS CLOUD, G DISMUKES, WE BENNETT, J BRADSHER, RW CHAPMAN, SW FISHER, JF KERKERING, TM MEDOFF, G PERFECT, JR PANKEY, GA REX, JH SAAG, MS TI TREATMENT OF SPOROTRICHOSIS WITH ITRACONAZOLE SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID PRIMARY PULMONARY SPOROTRICHOSIS; HIGH-DOSE KETOCONAZOLE; SPOROTHRIX-SCHENCKII; CUTANEOUS SPOROTRICHOSIS; SYSTEMIC SPOROTRICHOSIS; FUNGAL-INFECTIONS; AMPHOTERICIN-B; THERAPY; ARTHRITIS; EMPHASIS AB PURPOSE: To describe the clinical presentation and outcomes of treatment with itraconazole in patients with sporotrichosis. METHODS: A culture for Sporothrix schenckii or compatible histopathology was required for inclusion in the study. Patients with both cutaneous and systemic sporotrichosis were treated. Patients received from 100 to 600 mg of itraconazole daily for 3 to 18 months. Patients were classified as responders or nonresponders. Responders were further classified as remaining on treatment, relapsed, or free of disease. Nonresponders included patients who failed to respond or progressed during treatment with itraconazole. RESULTS: Twenty-seven patients (mean age: 53 years) were treated with 30 courses of itraconazole. Diabetes mellitus and alcoholism were present in eight and seven patients, respectively. Sites of involvement included lymphocutaneous alone in 9 patients, articular/osseous in 15 (multifocal in 3), and lung in 3. Prior therapy was unsuccessful in 11 patients. Among the 30 courses, there were 25 responders and 5 nonresponders. All 5 nonresponders received at least 200 mg daily of itraconazole for durations that ranged from 6 to 18 months. Of the 25 responders, 7 relapsed 1 to 7 months after treatment durations of 6 to 18 months. Of the 7 who relapsed, 2 are responding to a second course. One responder was lost to follow-up after 10 months of treatment with itraconazole. Of the re 17 responders, 3 remain on treatment, and 14 are free of disease over follow-up durations of 6 to 42 months (mean: 17.6 months). Itraconazole was well tolerated with few side effects noted. CONCLUSIONS: These results document the efficacy of itraconazole in the treatment of cutaneous and systemic sporotrichosis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. DEPT VET AFFAIRS MED CTR,ANN ARBOR,MI. UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48104. SANTA CLARA VALLEY MED CTR,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,SAN JOSE,CA. UNIV ALABAMA,BIRMINGHAM,AL 35294. NIAID,MYCOSES STUDY GRP,BETHESDA,MD 20892. UNIV ARKANSAS MED SCI HOSP,LITTLE ROCK,AR 72205. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. MED COLL GEORGIA,AUGUSTA,GA 30912. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. DUKE UNIV,MED CTR,DURHAM,NC 27710. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121. RP SHARKEYMATHIS, PK (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [N01-AI-52562] NR 36 TC 87 Z9 88 U1 1 U2 2 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 SEP PY 1993 VL 95 IS 3 BP 279 EP 285 DI 10.1016/0002-9343(93)90280-3 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LX046 UT WOS:A1993LX04600007 PM 8396321 ER PT J AU KAYSEN, GA AF KAYSEN, GA TI THE NEPHROTIC SYNDROME - PATHOGENESIS AND CONSEQUENCES - THE HOMEOSTATIC AND PATHOGENIC CONSEQUENCES OF PROTEINURIA - INTRODUCTION SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Editorial Material C1 UNIV CALIF DAVIS,SCH MED,DEPT MED,DIV NEPHROL,RENAL BIOCHEM LAB,DAVIS,CA. US DEPT VET AFFAIRS,NO CALIF SYST CLIN,PLEASANT HILL,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PD SEP-OCT PY 1993 VL 13 IS 5 BP 309 EP 310 DI 10.1159/000168644 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA MR955 UT WOS:A1993MR95500001 PM 8116682 ER PT J AU HUTCHISON, FN AF HUTCHISON, FN TI HORMONAL MODULATION OF PROTEINURIA IN THE NEPHROTIC SYNDROME SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Article DE PROTEINURIA; NEPHROTIC SYNDROME; RENIN; ANGIOTENSIN; PROSTAGLANDINS; THROMBOXANE; KALLIKREIN; BRADYKININ; DIETARY PROTEIN; CONVERTING ENZYME INHIBITOR ID CONVERTING-ENZYME-INHIBITION; PASSIVE HEYMANN NEPHRITIS; DIETARY-PROTEIN; RENAL HEMODYNAMICS; ALBUMIN SYNTHESIS; ANGIOTENSIN-II; AMINONUCLEOSIDE NEPHROSIS; DIABETIC GLOMERULOPATHY; THROMBOXANE SYNTHESIS; RECEPTOR ANTAGONIST AB Proteinuria is the primary manifestation of a variety of glomerular diseases which are characterized clinically by the nephrotic syndrome. In many cases there is little effective treatment for the primary disease process. However, reduction of proteinuria can frequently improve the hypoalbuminemia, hyperlipidemia and edema which are responsible for the morbidity of the nephrotic syndrome. Proteinuria can be reduced in nephrotic humans and experimental animal models by restriction of dietary protein intake, nonsteroidal anti-inflammatory drug, and by angiotensin-converting enzyme inhibitors. Each of these therapies modifies the activity of locally acting glomerular hormones, autocoids, suggesting that there is a component of proteinuria which is hormonally mediated. The effects of dietary protein, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors on nephrotic proteinuria and their potential hormonal mechanisms of action is the subject of this review. C1 MED UNIV S CAROLINA,DEPT INTERNAL MED,DIV NEPHROL,CHARLESTON,SC. RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC. FU NIDDK NIH HHS [DK43186] NR 80 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PD SEP-OCT PY 1993 VL 13 IS 5 BP 337 EP 346 DI 10.1159/000168648 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA MR955 UT WOS:A1993MR95500005 PM 8116686 ER PT J AU KAYSEN, GA AF KAYSEN, GA TI PLASMA COMPOSITION IN THE NEPHROTIC SYNDROME SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Review DE ONCOTIC PRESSURE; ALBUMIN; TRANSFERRIN; LIPOPROTEINS; ANALBUMINEMIA; FIBRINOGEN; PROTEIN SYNTHESIS ID LOW-DENSITY LIPOPROTEIN; COLLOID OSMOTIC-PRESSURE; APOLIPOPROTEIN GENE-EXPRESSION; MOLECULAR-WEIGHT PROTEINS; RENAL-VEIN THROMBOSIS; MINIMAL-CHANGE; ANALBUMINEMIC RATS; ALBUMIN SYNTHESIS; DIETARY-PROTEIN; HEYMANN NEPHRITIS AB The nephrotic syndrome is a consequence of urinary loss of intermediate sized plasma proteins and the resulting homeostatic responses to those losses. Plasma protein composition is changed greatly. Intermediate sized proteins, including albumin, transferrin, IgG, hormone binding proteins, and low molecular weight inhibitors of the clotting cascade, are lost in the urine and their concentration in plasma reduced. Synthesis of many proteins secreted by the liver is increased either at the level of transcription or posttranscriptionally. Synthesis of several liver-derived proteins is increased in the absence of their urinary loss, suggesting that hypoalbuminemia or reduced plasma oncotic pressure (pi) stimulates the production or reduces the rate of catabolism of these proteins. Their plasma levels, including those of lipoproteins and elements of the coagulation cascade, are increased. Plasma pi falls and plasma viscosity increases because of the replacement of intermediate sized plasma proteins by larger ones. The plasma concentration of several proteins lost in the urine but not secreted by the liver, such as erythropoietin and IgG, are not defended by increased synthesis, suggesting that increased synthesis of plasma proteins is primarily confined to the liver. Loss of both liver-derived and nonliver-derived proteins may cause reduced immunity, anemia, and deficiency syndromes. Urinary loss of albumin alone is not responsible for decreased plasma pi. The relationship between plasma protein concentration and pi is greatly disturbed in nephrotic rats. In contrast, the relationship between pi and plasma protein concentration is nearly the same in rats with hereditary analbuminemia (NAR) and normal rats, despite the absence of albumin from the plasma of NAR. When proteinuria is induced in NAR the relationship between plasma protein concentration and pi becomes identical to that in nephrotic animals, although no albumin was lost in the urine of NAR. C1 UNIV CALIF DAVIS,SCH MED,DEPT MED,DIV NEPHROL,RENAL BIOCHEM LAB,DAVIS,CA. US DEPT VET AFFAIRS,NO CALIF SYST CLIN,PLEASANT HILL,CA. FU NIDDK NIH HHS [R01 DK 42297] NR 147 TC 36 Z9 38 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PD SEP-OCT PY 1993 VL 13 IS 5 BP 347 EP 359 DI 10.1159/000168649 PG 13 WC Urology & Nephrology SC Urology & Nephrology GA MR955 UT WOS:A1993MR95500006 PM 8116687 ER PT J AU MARKOWITZ, AJ WU, GD BIRKENMEIER, EH TRABER, PG AF MARKOWITZ, AJ WU, GD BIRKENMEIER, EH TRABER, PG TI THE HUMAN SUCRASE-ISOMALTASE GENE DIRECTS COMPLEX PATTERNS OF GENE-EXPRESSION IN TRANSGENIC MICE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE TRANSCRIPTION; DIFFERENTIATION; INTESTINE; COLON ID MOUSE SMALL-INTESTINE; EPITHELIAL-CELL TYPES; HORMONE FUSION GENES; CRYPT-VILLUS AXIS; ACID-BINDING-PROTEIN; RAT SMALL-INTESTINE; MESSENGER-RNA; PANETH CELLS; DIFFERENTIATION; ORIGIN AB Sucrase-isomaltase (SI) is an enterocyte-specific gene that is expressed in complex developmental and spatial patterns. In this study, we examine the ability of regulatory elements within the human SI (hSI) gene to direct appropriate cell lineage and spatial patterns of expression in transgenic mice. Transgenic mouse lines were established using a construct containing bases -3424 to +54 of the hSI gene linked to the human growth hormone (hGH) structural gene. In each transgenic line, hGH mRNA and protein were expressed only in the small intestine and colon. In contrast to the endogenous mouse SI (mSI) gene, which was expressed along the entire length of the small intestine, hGH mRNA expression was predominantly found in the distal jejunum and ileum, with very low levels in more proximal portions of the small intestine. However, the pattern of transgene expression along the small intestinal crypt-villus axis was identical to the pattern of the endogenous mSI gene. These results suggest that regulatory elements necessary for intestine-specific transcription and differential expression along the intestinal crypt-villus axis are included in the 5'-flanking region of the hSI gene. Furthermore, these data suggest that different DNA regulatory regions regulate transcription along the horizontal intestinal axis. In the colon, there was aberrant expression of hGH in a subpopulation of enteroendocrine cells that contained peptide tyrosine tyrosine (PYY). This suggests that there are DNA regulatory elements, missing in the transgene construct, which normally suppress expression of the endogenous mSI gene in these cells. Taken together, these findings define the SI gene as a useful model for studies of differentiation, cell lineage determination, and mechanisms of complex spatial gene expression in the intestine. C1 UNIV PENN,SCH MED,DEPT INTERNAL MED,DIV GASTROENTEROL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. JACKSON LAB,BAR HARBOR,ME 04609. FU NIDDK NIH HHS [DK-41393, DK-44621] NR 36 TC 63 Z9 63 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 SEP PY 1993 VL 265 IS 3 BP G526 EP G539 PN 1 PG 14 WC Physiology SC Physiology GA MA184 UT WOS:A1993MA18400070 PM 8214074 ER PT J AU WHEATLEY, JR MEZZANOTTE, WS TANGEL, DJ WHITE, DP AF WHEATLEY, JR MEZZANOTTE, WS TANGEL, DJ WHITE, DP TI INFLUENCE OF SLEEP ON GENIOGLOSSUS MUSCLE ACTIVATION BY NEGATIVE-PRESSURE IN NORMAL MEN SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID UPPER AIRWAY PRESSURE; RESPIRATORY ACTIVITY; RESPONSES; REFLEX; APNEA; OCCLUSION; NASAL; WAKEFULNESS; MECHANISM; PATTERN AB An important mechanism controlling genioglossus (GG) muscle activity is the reflex response to negative airway pressure. We hypothesize that this reflex response may be lost during sleep and believe that this loss may be important in the pathogenesis of airway collapse during sleep. Thus, we determined the effect of non-rapid eye movement (NREM) sleep on the GG electromyogram (EMG) response to brief (0.2 to 0.6 s) episodes of negative pressure generation (NPG) in the upper airway of six normal subjects. Up to 100 NPGs (mean 58 +/- 12) were recorded both awake and during stable NREM sleep. During wakefulness, the change in GG moving time average EMG from basal to peak levels (during NPG) was 17.1 +/- 2.5 au (a 154 +/- 22% increase above basal levels). This response was markedly reduced during NREM sleep (2.7 +/- 1.2 au; p < 0.01). The latency of the GG EMG response was 53.8 +/- 11.5 ms during wakefulness (n = 6), but much longer during sleep (132.7 +/- 24.5 ms; n = 3; p < 0.03). We conclude that in normal subjects (1) the GG muscle responds to negative airway pressure by reflex activation during wakefulness, and (2) this reflex activation is reduced or lost during NREM sleep. We speculate that loss of this mechanism during sleep may contribute to pharyngeal collapse in obstructive apnea patients. C1 NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80262. RP WHEATLEY, JR (reprint author), DENVER VA MED CTR,DIV PULM,1055 CLERMONT ST,DENVER,CO 80220, USA. NR 38 TC 139 Z9 140 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 SEP PY 1993 VL 148 IS 3 BP 597 EP 605 PG 9 WC Respiratory System SC Respiratory System GA LW465 UT WOS:A1993LW46500009 PM 8368629 ER PT J AU KASINATH, BS AF KASINATH, BS TI GLOMERULAR ENDOTHELIAL-CELL PROTEOGLYCANS - REGULATION BY TGF-BETA-1 SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID TRANSFORMING GROWTH-FACTOR; HEPARAN-SULFATE PROTEOGLYCANS; SMOOTH-MUSCLE CELLS; FACTOR-BETA; BASEMENT-MEMBRANE; EPITHELIAL-CELLS; MESANGIAL CELLS; RENAL GLOMERULUS; TISSUE-REPAIR; MATRIX RP KASINATH, BS (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET ADM HOSP,DEPT MED,DIV NEPHROL,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK41517] NR 50 TC 27 Z9 27 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 SEP PY 1993 VL 305 IS 2 BP 370 EP 377 DI 10.1006/abbi.1993.1434 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LY022 UT WOS:A1993LY02200022 PM 8373175 ER PT J AU ORTIZBRAVO, E SIECK, MS SCHUMACHER, HR AF ORTIZBRAVO, E SIECK, MS SCHUMACHER, HR TI CHANGES IN THE PROTEINS COATING MONOSODIUM URATE CRYSTALS DURING ACTIVE AND SUBSIDING INFLAMMATION - IMMUNOGOLD STUDIES OF SYNOVIAL-FLUID FROM PATIENTS WITH GOUT AND OF FLUID OBTAINED USING THE RAT SUBCUTANEOUS AIR POUCH MODEL SO ARTHRITIS AND RHEUMATISM LA English DT Article ID CALCIUM PYROPHOSPHATE DIHYDRATE; LOW-DENSITY LIPOPROTEIN; SERUM-PROTEINS; KNEE JOINTS; BINDING; MONOHYDRATE; IMMUNOGLOBULIN; NEUTROPHILS; ADSORPTION; RECEPTOR AB Objective. In this in vivo study, we investigated changes in the proteins that coat monosodium urate (MSU) crystals in human synovial fluid samples and rat air pouch fluid samples obtained sequentially during periods of active and resolving inflammation, in order to evaluate whether in vivo findings are consistent with hypotheses on roles of protein coating based on in vitro findings. Methods. Crystals from patients with gout were isolated from joint fluids with acute inflammation, and subsequently from the same joints at the time inflammation was resolving. Crystals were also obtained using the rat subcutaneous air pouch model. Immunogold was used to label proteins coating MSU crystals, for light microscopy (LM) and transmission electron microscopy (TEM) studies. Results. Dense immunogold-silver labeling for IgG was observed under LM on crystals from fluid with acute inflammation, whereas other proteins (apolipoproteins [Apo], fibronectin, fibrinogen, albumin) were not labeled significantly. Apo B became strongly positive on crystals as the inflammation subsided, whereas other proteins were only weakly positive and IgG became absent or weakly positive. Quantitative TEM evaluation confirmed the LM observations. Conclusion. This study provides the first in vivo evidence supporting the notion derived from previous in vitro studies that proteins coating MSU crystals change as inflammation evolves. Protein coatings may play an important role in the self-limited nature of gouty inflammation. IgG coating MSU crystals may enhance the inflammation. As the inflammation subsides, Apo B could displace the IgG by competitively coating sites on crystals and could contribute in part to the resolution of the acute gouty arthritis. C1 VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL 151-K,WOODLAND & UNIV AVE,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. NR 40 TC 51 Z9 51 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 BP 1274 EP 1285 DI 10.1002/art.1780360912 PG 12 WC Rheumatology SC Rheumatology GA MB211 UT WOS:A1993MB21100011 PM 8216421 ER PT J AU BAUTISTA, BB SCHUMACHER, HR AF BAUTISTA, BB SCHUMACHER, HR TI INFLAMMATORY MONOARTHRITIS OF LESS-THAN 6 WEEKS DURATION - CAUSES, COURSES AND PREDICTIVE FACTORS SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S204 EP S204 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600976 ER PT J AU BRIDGES, AJ LORDEN, T AF BRIDGES, AJ LORDEN, T TI SICCA SYNDROME IN WOMEN WITH SILICONE IMPLANTS - ABSENCE OF SERUM AUTOANTIBODIES SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53792. MIDDLETON VET ADM HOSP,MADISON,WI 53705. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S70 EP S70 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600190 ER PT J AU JIAN, YC ZHOU, T WU, JG MOUNTZ, JD AF JIAN, YC ZHOU, T WU, JG MOUNTZ, JD TI THE FAS-LIGAND AND APOPTOSIS IN LPR AND GLD MICE SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S52 EP S52 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600079 ER PT J AU SANZ, I MENESES, G FISCHBACH, M AF SANZ, I MENESES, G FISCHBACH, M TI GENETIC-CHARACTERIZATION OF HUMAN-IMMUNOGLOBULIN HEAVY-CHAIN DIR GENES SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S240 EP S240 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81601187 ER PT J AU VEDDER, C HEFENEIDER, SH FREED, AC KHAW, K HAN, SY BAKKE, AC MCCOY, SL BENNETT, RM AF VEDDER, C HEFENEIDER, SH FREED, AC KHAW, K HAN, SY BAKKE, AC MCCOY, SL BENNETT, RM TI PARTIAL CLONING AND EXPRESSION OF A CELL-SURFACE GLYCOPROTEIN HAVING AN IDIOTYPIC CONNECTIVITY WITH ANTI-DNA ANTIBODIES SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S102 EP S102 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600375 ER PT J AU ZHOU, T JIAN, YC WU, JG MOUNTZ, JD AF ZHOU, T JIAN, YC WU, JG MOUNTZ, JD TI FAS+ COS CELLS AND ANTI-FAS ANTIBODY FOR IN-VIVO LOCALIZATION OF FAS/FAS LIGAND-BINDING AND APOPTOSIS SITES IN AUTOIMMUNE LPR AND GLD MICE SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. 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 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S52 EP S52 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600080 ER PT J AU TREVINO, RJ HOROWITZ, PM CHIRGWIN, JM AF TREVINO, RJ HOROWITZ, PM CHIRGWIN, JM TI ELIMINATION OF GLYCEROL ARTIFACTS IN CYCLE SEQUENCING SO BIOTECHNIQUES LA English DT Note ID DNA-POLYMERASE C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV ENDOCRINOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIGMS NIH HHS [GM 25177] NR 8 TC 3 Z9 3 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD SEP PY 1993 VL 15 IS 3 BP 366 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LW417 UT WOS:A1993LW41700003 PM 8217140 ER PT J AU REDDY, SV TAKAHASHI, S HAIPEK, C CHIRGWIN, JM ROODMAN, GD AF REDDY, SV TAKAHASHI, S HAIPEK, C CHIRGWIN, JM ROODMAN, GD TI TARTRATE-RESISTANT ACID-PHOSPHATASE GENE-EXPRESSION AS A FACILE REPORTER GENE FOR SCREENING TRANSFECTION EFFICIENCY IN MAMMALIAN-CELL CULTURES SO BIOTECHNIQUES LA English DT Note ID TYPE-5 AB The efficiency of DNA transfection into mammalian cell cultures has been monitored using a variety of reporter assays. However the common procedures are expensive, time-consuming and usually cannot identify the transfected cell population directly. In the present communication we describe a simple, inexpensive and efficient method to directly identify DNA transfection in mammalian cells using tartrate-resistant acid phosphatase (TRAP) gene expression. The method involves the transfection of a plasmid (pCT3), which contains TRAP cDNA driven by a CMV promoter into mammalian cells. The cells can then be stained for TRAP activity, and the transfection efficiency can be determined by simply counting the positively transfected cells in a defined area with a microscope. This method permits screening of mammalian cells for transfection efficiency in multi-well plates. After waiting 30-40 minutes to allow the TRAP assay to saturate, wells can be scored in 1-2 minutes with little difficulty in detecting the transfected cells. C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED HEMATOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED ENDOCRINOL,SAN ANTONIO,TX 78284. FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM35188]; NIAMS NIH HHS [AR39539] NR 11 TC 8 Z9 8 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD SEP PY 1993 VL 15 IS 3 BP 444 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LW417 UT WOS:A1993LW41700022 PM 7692895 ER PT J AU WARD, TT THOMAS, RG FYE, CL ARBEIT, R COLTMAN, CA CRAIG, W DANA, BW FINEGOLD, SM LENTINO, J PENN, RL WEINBERG, JB CHOW, B OCHI, S WEBER, JH LAYARD, MW CHANG, P GREENBERG, P RIMLAND, D BALDIWIN, V MIREAULT, K LAWRENCE, W STANKO, S HOBBS, E OLMSTEAD, C INGRAMDRAKE, L NEILL, HB DISNEY, C YU, V HAMILTON, R LYMAN, GH LYMAN, C GALGIANI, J KIZZIER, F AMON, M GRINICH, K SEWELL, D BASSETT, R JACOBSON, I JAMES, KE FETTER, R MONTANO, L HICKS, R SATHER, MR YOUNG, LM WEBER, JH AF WARD, TT THOMAS, RG FYE, CL ARBEIT, R COLTMAN, CA CRAIG, W DANA, BW FINEGOLD, SM LENTINO, J PENN, RL WEINBERG, JB CHOW, B OCHI, S WEBER, JH LAYARD, MW CHANG, P GREENBERG, P RIMLAND, D BALDIWIN, V MIREAULT, K LAWRENCE, W STANKO, S HOBBS, E OLMSTEAD, C INGRAMDRAKE, L NEILL, HB DISNEY, C YU, V HAMILTON, R LYMAN, GH LYMAN, C GALGIANI, J KIZZIER, F AMON, M GRINICH, K SEWELL, D BASSETT, R JACOBSON, I JAMES, KE FETTER, R MONTANO, L HICKS, R SATHER, MR YOUNG, LM WEBER, JH TI TRIMETHOPRIM-SULFAMETHOXAZOLE PROPHYLAXIS IN GRANULOCYTOPENIC PATIENTS WITH ACUTE-LEUKEMIA - EVALUATION OF SERUM ANTIBIOTIC LEVELS IN A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED DEPARTMENT-OF-VETERANS-AFFAIRS COOPERATIVE STUDY SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID CONTROLLED TRIAL; INFECTION PROPHYLAXIS; CANCER-PATIENTS; CO-TRIMOXAZOLE; SELECTIVE DECONTAMINATION; NEUTROPENIC PATIENTS; BACTERIAL-INFECTION; PREVENTION; CHEMOTHERAPY; CHILDREN AB Despite widespread use of trimethoprim-sulfamethoxazole (TMP-SMZ) for prophylaxis in neutropenic patients, questions remain regarding its efficacy, toxicity, the risk of selection of resistant isolates, and the relation of its activity to selective decolonization vs. the attainment of direct inhibitory levels within blood and tissues. We evaluated the effect of TMP-SMZ (160/800 mg orally every 12 hours) in 42 adult granulocytopenic patients (<100 absolute neutrophils/mm3, mean duration 13.3 days) undergoing chemotherapy for acute leukemia at 11 participating Veterans Administration Medical Centers in a randomized, double-blind, placebo-controlled trial. No significant differences in survival, frequency of bacteremia, overall infections, use of systemic antimicrobial therapy, or adverse effects, including myelosuppression, were observed between patients receiving TMP-SMZ vs. those receiving placebo. All patients acquired trimethoprim-resistant organisms. Concentrations of trimethoprim in serum were significantly lower before febrile episodes than when patients were afebrile. These results suggest that the purported activity of TMP-SMZ may be related to the serum concentration achieved. Moreover, the results highlight the need for additional study of the value of antibiotic prophylaxis in neutropenic patients. C1 DEPT VET AFFAIRS MED CTR,PALO ALTO,CA. DEPT VET AFFAIRS MED CTR,W LOS ANGELES,LA. DEPT VET AFFAIRS MED CTR,ALBUQUERQUE,NM. DEPT VET AFFAIRS MED CTR,BOSTON,MA. DEPT VET AFFAIRS MED CTR,SAN ANTONIO,TX. DEPT VET AFFAIRS MED CTR,MADISON,WI. DEPT VET AFFAIRS MED CTR,HINES,IL. DEPT VET AFFAIRS MED CTR,SHREVEPORT,LA. DEPT VET AFFAIRS MED CTR,DURHAM,NC. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. RP WARD, TT (reprint author), DEPT VET AFFAIRS MED CTR,INFECT DIS SECT 111F,3710 US VET RD,PORTLAND,OR 97207, USA. NR 35 TC 23 Z9 23 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 SEP PY 1993 VL 17 IS 3 BP 323 EP 332 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LW237 UT WOS:A1993LW23700002 PM 8218671 ER PT J AU JOHN, JF GRIESHOP, TJ ATKINS, LM PLATT, CG AF JOHN, JF GRIESHOP, TJ ATKINS, LM PLATT, CG TI WIDESPREAD COLONIZATION OF PERSONNEL AT A VETERANS AFFAIRS MEDICAL-CENTER BY METHICILLIN-RESISTANT, COAGULASE-NEGATIVE STAPHYLOCOCCUS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID PROSTHETIC VALVE ENDOCARDITIS; CARDIAC-SURGERY; RIBOSOMAL-RNA; MOLECULAR EPIDEMIOLOGY; GENTAMICIN-RESISTANCE; HOSPITALIZED-PATIENTS; RESTRICTION PATTERNS; GEL-ELECTROPHORESIS; EPIDERMIDIS; BACTEREMIA AB A serial prospective survey of nasal colonization of hospital personnel by methicillin-resistant coagulase-negative staphylococci (MRCNS) was conducted at a Veterans Affairs medical center on three occasions over a 16-month period. The epidemiological typing systems used to assess relatedness included antimicrobial susceptibility profiles; biotyping; phage typing; plasmid profiles; restriction fragment length polymorphism (RFLP) analysis with ribosomal RNA; and plasmid hybridization with a 1.68-MD plasmid as the DNA probe. Forty-three percent of all personnel and 62% of all nurses were colonized with MRCNS. Nurses on the wards (72%) and in the intensive care unit (73%) were significantly more likely to be colonized with MRCNS than nurses who had less contact with patients or those who worked in the operating room. The molecular epidemiological typing systems indicated some degree of relatedness among the strains. Specifically, riboprobe analysis revealed a Dice coefficient of >90%. However, each typing system detected dissimilarity among strains. Further studies are needed to determine the role that such human reservoirs of MRCNS serve in horizontal transmission to and subsequent infection of hospitalized patients. C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,CHARLESTON,SC 29425. NR 59 TC 22 Z9 22 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 SEP PY 1993 VL 17 IS 3 BP 380 EP 388 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LW237 UT WOS:A1993LW23700010 PM 8105982 ER PT J AU WU, GD BEER, DG MOORE, JH ORRINGER, MB APPELMAN, HD TRABER, PG AF WU, GD BEER, DG MOORE, JH ORRINGER, MB APPELMAN, HD TRABER, PG TI SUCRASE-ISOMALTASE GENE-EXPRESSION IN BARRETT-ESOPHAGUS AND ADENOCARCINOMA SO GASTROENTEROLOGY LA English DT Article ID INTESTINAL METAPLASIA; EPITHELIUM; CANCER; CRYPT; CELLS; TRANSCRIPTION; CHEMOTHERAPY; CARCINOMAS; ENTEROCYTE; DYSPLASIA C1 UNIV PENN, SCH MED, DEPT INTERNAL MED, DIV GASTROENTEROL, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. UNIV MICHIGAN, SCH MED, DEPT SURG, ANN ARBOR, MI 48104 USA. UNIV MICHIGAN, SCH MED, DEPT PATHOL, ANN ARBOR, MI 48104 USA. FU NCI NIH HHS [CA 46592]; NIDDK NIH HHS [DK44621, DK41393] NR 51 TC 40 Z9 40 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 SEP PY 1993 VL 105 IS 3 BP 837 EP 844 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LV382 UT WOS:A1993LV38200024 PM 8359653 ER PT J AU DEVI, BG HENDERSON, GI FROSTO, TA SCHENKER, S AF DEVI, BG HENDERSON, GI FROSTO, TA SCHENKER, S TI EFFECT OF ETHANOL ON RAT FETAL HEPATOCYTES - STUDIES ON CELL REPLICATION, LIPID-PEROXIDATION AND GLUTATHIONE SO HEPATOLOGY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; ALCOHOLIC LIVER-DISEASE; VITAMIN-E; REDUCED GLUTATHIONE; OXYGEN RADICALS; ENZYMES; METABOLISM; GROWTH; INJURY; DEPLETION AB Studies have shown that ethanol at moderate concentrations inhibits epidermal growth factor-dependent replication of fetal rat hepatocytes in culture. This may account for the growth/development impairment associated with fetal alcohol syndrome and decreased liver regeneration in alcoholic liver disease. In this study, we further define the mechanism(s) of the negative impact of ethanol on fetal rat hepatocytes and provide evidence that ethanol-induced injury to these cells is associated with membrane damage caused by lipid peroxidation, altered cell glutathione homeostasis and deranged mitochondrial structure and function. Exposure of fetal rat hepatocyte replication to ethanol (2 mg/ml) promptly resulted in blockade of replication, as indicated by a 40% reduction in DNA synthesis (p < 0.05). Assessment of cell injury on the basis of lactate dehydrogenase and ALT leakage indicated a statistically significant but not appreciable effect, whereas Cr-51 leakage was more substantially increased (p < 0.05). Within 6 hr of ethanol exposure, superoxide radical levels increased more than twofold (P < 0.05). We noted a 56% increase in levels of diene conjugates, a 131% increase in malonaldehyde concentration and a 66% increase in fluorescent products of lipid peroxidation (all p < 0.05). Glutathione levels were decreased to 47% below control values (p < 0.05). Electron microscopic studies illustrated a slight disruption of mitochondrial structure (enlargement of mitochondria and dilation of cristae). This disruption was accompanied by mitochondrial swelling (increased permeability), altered mitochondrial membrane potential (a 16% decrease in rhodamine uptake), a 28% decrease in succinate dehydrogenase activity and a 30% decrease in cellular ATP level (p < 0.05). Pretreatment of fetal rat hepatocytes with 0.1 mmol/L N-acetylcysteine or S-adenosylmethionine for 24 hr Prevented the ethanol-induced reduction of ATP and glutathione levels, essentially restored cell replication, ameliorated Cr-51 leakage and decreased malonaldehyde and diene conjugate levels to 41% to 65% and 25% above control values, respectively. Pretreatment with 0.1 mmol/L vitamin E fully normalized malonaldehyde and diene conjugate levels and Cr-51 leakage but failed to improve ATP levels or to increase significantly cell replication and glutathione levels. Concomitant administration of glutathione precursors with ethanol, rather than pretreatment, did not alter the impaired cell replication. Thus our data underscore the importance of cellular glutathione and ATP in preventing ethanol-induced decreases in fetal cell replication and suggest that alleviation of cellular lipid peroxidation alone is not sufficient to prevent this abnormality in fetal rat hepatocyte function. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL & NUTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIAAA NIH HHS [R01 AA07514, KO2 AA00121] NR 77 TC 79 Z9 82 U1 0 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD SEP PY 1993 VL 18 IS 3 BP 648 EP 659 DI 10.1016/0270-9139(93)90367-V PG 12 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LV018 UT WOS:A1993LV01800024 PM 8359806 ER PT J AU YOSHIKAWA, TT NORMAN, DC AF YOSHIKAWA, TT NORMAN, DC TI ANTIBIOTIC-THERAPY - WHAT TO CONSIDER WHEN TREATING GERIATRIC-PATIENTS SO HOSPITAL FORMULARY LA English DT Review AB The epidemiology, etiology, clinical manifestations, diagnostic approach, and therapeutic choices may be quite different for infections that occur in elderly patients compared with those that occur in younger adults. Given these variables, it is essential for clinicians who care for older patients to understand how to prescribe antibiotics appropriately for this population. This article examines the unique characteristics of infections in the elderly as well as provides recommendations on the use of specific antibiotic agents commonly used to treat infections in geriatric patients. RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE 114,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 SN 0098-6909 J9 HOSP FORMUL PD SEP PY 1993 VL 28 IS 9 BP 754 EP & PG 0 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LZ519 UT WOS:A1993LZ51900003 PM 10128820 ER PT J AU BELL, NH YERGEY, AL VIEIRA, NE OEXMANN, MJ SHARY, JR AF BELL, NH YERGEY, AL VIEIRA, NE OEXMANN, MJ SHARY, JR TI DEMONSTRATION OF A DIFFERENCE IN URINARY CALCIUM, NOT CALCIUM-ABSORPTION, IN BLACK-AND-WHITE ADOLESCENTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID D-ENDOCRINE SYSTEM; VITAMIN-D; DIETARY CALCIUM; 1,25-DIHYDROXYVITAMIN-D; CHROMATOGRAPHY; CHILDREN; ASSAY; AGE AB Bone mineral density (BMD) of the forearm, lumbar spine, and femoral neck is greater in black than in white children. Studies were performed to determine whether differences in intestinal absorption of calcium or urinary calcium or both account for an assumed more positive calcium balance and greater bone mass in black children. Normal black and white boys and girls were admitted to a metabolic ward and given a constant daily diet containing 1000 mg calcium, 60% as calcium carbonate, for 2 1/2 days (study 1) or 3 1/2 days (study II). Fasting blood and 24 h urine collections were obtained, and in study II, unidirectional fractional absorption of calcium (alpha) was determined with stable isotopes of calcium. It was found that (1) serum 25-hydroxyvitamin D (25-OHD) and urinary calcium were lower and serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] was higher in black than in white children, and (2) alpha was higher in boys than in girls with no racial difference, and (3) there were significant positive correlations between alpha and urinary calcium in the blacks and in the black and white children together. It is concluded that (1) alpha is higher in boys than in girls and (2) a lower urinary calcium, not increased intestinal absorption of calcium, is the means for a more positive calcium balance in blacks that accounts for the racial difference in BMD. C1 MED UNIV SO CAROLINA,DEPT MED,CHARLESTON,SC 29401. MED UNIV SO CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29401. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. RP BELL, NH (reprint author), MED UNIV SO CAROLINA,RALPH H JOHNSON VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. FU NCRR NIH HHS [MO1 RR0170]; NIAMS NIH HHS [R01 AR36066] NR 20 TC 71 Z9 71 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD SEP PY 1993 VL 8 IS 9 BP 1111 EP 1115 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LU336 UT WOS:A1993LU33600011 PM 8237481 ER PT J AU WAGNER, CR MORRIS, TE SHIPLEY, GD HOSENPUD, JD AF WAGNER, CR MORRIS, TE SHIPLEY, GD HOSENPUD, JD TI REGULATION OF HUMAN AORTIC ENDOTHELIAL CELL-DERIVED MESENCHYMAL GROWTH-FACTORS BY ALLOGENEIC LYMPHOCYTES IN-VITRO - A POTENTIAL MECHANISM FOR CARDIAC ALLOGRAFT VASCULOPATHY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE TRANSPLANTATION IMMUNOLOGY; VASCULAR SMOOTH MUSCLE; CORONARY DISEASE; LYMPHOCYTES; CHRONIC REJECTION ID SMOOTH-MUSCLE CELLS; CORONARY-ARTERY DISEASE; MONOCLONAL-ANTIBODY; TRANSPLANTATION; ATHEROSCLEROSIS; PROTEIN; ARTERIOSCLEROSIS; REJECTION; INFECTION; ACTIN AB Cardiac allograft vasculopathy is thought to be triggered by an alloreactive response to the donor coronary vasculature, resulting in smooth muscle cell proliferation and ultimate occlusion of the donor coronary arteries. To determine whether allogeneic lymphocytes are capable of regulating endothelial-derived smooth muscle cell (SMC) growth factors, human aortic endothelial cells (HAECs) were exposed to allogeneic lymphocytes. The HAEC-lymphocyte co-cultures were assessed for (a) lymphocyte proliferation in response to the allogeneic HAECs; (b) release of soluble factors that stimulate human aortic SMC proliferation; and (c) alteration of HAEC mRNA levels for a panel of known SMC growth factors. Co-culture conditioned medium increased SMC proliferation, compared to medium conditioned by HAECs alone. HAECs exposed to allogeneic lymphocytes increased their expression of mRNA for basic fibroblast growth factor, transforming growth factors alpha and beta, and platelet derived growth factor A and B chains. These results demonstrate that allogeneic lymphocytes are capable of inducing HAECs to increase mRNA levels for several mesenchymal growth factors and to release bioactive products capable of stimulating SMC cell proliferation in vitro. Additionally, the data support the hypothesis that alloreactive lymphocytes can stimulate allogeneic donor endothelial cells to produce growth factors that may contribute to the intimal thickening seen in cardiac allograft vasculopathy. C1 PORTLAND VET AFFAIRS MED CTR,IMMUNOL RES LAB,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED,OREGON CARDIAC TRANSPLANT PROGRAM,IMMUNOBIOL RES LAB,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT CELL BIOL,OREGON CARDIAC TRANSPLANT PROGRAM,IMMUNOBIOL LAB,PORTLAND,OR 97201. FU NHLBI NIH HHS [HL-43369] NR 32 TC 27 Z9 27 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 SEP PY 1993 VL 92 IS 3 BP 1269 EP 1277 DI 10.1172/JCI116699 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LX770 UT WOS:A1993LX77000023 PM 8376585 ER PT J AU CLEVELAND, M AF CLEVELAND, M TI EXERCISE GUIDELINES SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Letter RP CLEVELAND, M (reprint author), PORTLAND VET AFFAIRS MED CTR,INTERNAL MED & SPORTS,PORTLAND,OR 97207, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD SEP PY 1993 VL 8 IS 9 BP 522 EP 522 DI 10.1007/BF02600119 PG 1 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA LZ337 UT WOS:A1993LZ33700012 PM 8410428 ER PT J AU COUPAYEGERARD, B KLEYMAN, TR AF COUPAYEGERARD, B KLEYMAN, TR TI DIFFERENTIAL ARRIVAL OF NEWLY SYNTHESIZED APICAL AND BASOLATERAL PLASMA-MEMBRANE PROTEINS IN THE EPITHELIAL-CELL LINE A6 SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE EPITHELIAL POLARITY; A6-CELLS; BIOTIN; PROTEIN TRAFFICKING; PROTEIN SYNTHESIS ID ENDOPLASMIC-RETICULUM; BIOGENETIC PATHWAYS; MDCK CELLS; BULK FLOW; SURFACE; CACO-2; GLYCOPROTEINS; TRANSPORT; RATES; NA+ AB The labeling of specific cell surface proteins with biotin was used to examine both protein distribution and delivery of newly synthesized proteins to the apical and basolateral cell surface in A6 cells. Steady-state metabolic labeling with [S-35]methionine followed by specific cell surface biotinylation demonstrated polarization of membrane proteins. The delivery of newly synthesized proteins to the apical or basolateral cell surface was examined by metabolic labeling with [S-35]methionine using a pulse-chase protocol in combination with specific cell surface biotinylation. Newly synthesized biotinylated proteins at the apical cell surface reached a maximum after a 5 min chase, and then fell over the remainder of a 2 hr chase. The bulk flow of newly synthesized proteins to the basolateral membrane slowly rose to a maximum after 90 min. The detergent Triton X-114 was used to examine delivery of hydrophilic and hydrophobic proteins to the cell surface. Delivery of both hydrophilic and hydrophobic proteins to the apical cell surface reached a maximum 5 to 10 min into the chase period. The arrival of hydrophilic proteins at the basolateral surface showed early delivery and a maximum peak delivery at 120 min into the chase period. In contrast, only an early peak of delivery of newly synthesized hydrophobic proteins to the basolateral membrane was observed. C1 VET AFFAIRS MED CTR,DEPT MED & PHYSIOL,PHILADELPHIA,PA 19104. RP COUPAYEGERARD, B (reprint author), UNIV PENN,DEPT MED & PHYSIOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 25 TC 4 Z9 4 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD SEP PY 1993 VL 135 IS 3 BP 225 EP 235 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA LZ363 UT WOS:A1993LZ36300004 PM 8271262 ER PT J AU ALTERMAN, AI MCLELLAN, AT SHIFMAN, RB AF ALTERMAN, AI MCLELLAN, AT SHIFMAN, RB TI DO SUBSTANCE-ABUSE PATIENTS WITH MORE PSYCHOPATHOLOGY RECEIVE MORE TREATMENT SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID ADDICTION SEVERITY INDEX; ANTISOCIAL PERSONALITY-DISORDER; ALCOHOLICS; DIAGNOSIS; VALIDITY AB The association between psychopathology at treatment entry and the amount of treatment services received was evaluated in 104 alcohol-dependent and 100 cocaine-dependent male veterans treated for 1 month in either a day hospital or inpatient program Measures of psychopathology included the Addiction Severity Index psychiatric composite score, the presence or absence of an antisocial personality disorder diagnosis, and the total number of additional lifetime or current psychiatric diagnoses. Patients with higher admission Addiction Severity Index psychiatric composite scores received more medical, alcohol, family/social, and psychiatric services. There was also preliminary evidence that patients who received more treatment showed greater improvement 7 months after admission. The relationships between the other measures of psychopathology and treatment services failed to achieve overall statistical significance, although significant relationships were found in several individual areas. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA. TEMPLE UNIV,DEPT PSYCHOL,PHILADELPHIA,PA 19122. RP ALTERMAN, AI (reprint author), UNIV PENN,SCH MED,TREATMENT RES CTR,PHILADELPHIA,PA 19104, USA. NR 28 TC 48 Z9 48 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD SEP PY 1993 VL 181 IS 9 BP 576 EP 582 DI 10.1097/00005053-199309000-00009 PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LX800 UT WOS:A1993LX80000009 PM 8245927 ER PT J AU ANDERSON, RC CARNES, M CLARK, A DEPROSSE, CA HORBACH, N MORLEY, J OUSLANDER, J RAPPAPORT, S SAND, P STONE, AR VENABLE, DD ZIRKER, W AF ANDERSON, RC CARNES, M CLARK, A DEPROSSE, CA HORBACH, N MORLEY, J OUSLANDER, J RAPPAPORT, S SAND, P STONE, AR VENABLE, DD ZIRKER, W TI EFFECTS OF TERODILINE ON URINARY-INCONTINENCE AMONG OLDER NONINSTITUTIONALIZED WOMEN SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID MOTOR URGE INCONTINENCE; NURSING-HOME PATIENTS; DOUBLE-BLIND; DETRUSOR INSTABILITY; GERIATRIC-PATIENTS; ELDERLY WOMEN; CROSSOVER; DYSFUNCTION; MANAGEMENT; OXYBUTYNIN AB Objective: To determine the effectiveness of terodiline, a drug with calcium antagonist and anticholinergic properties, on the frequency of incontinence in older non-institutionalized women. Design: Randomized, placebo-controlled, parallel-group, double-blind trial. Setting: Twelve outpatient clinics across the United States affiliated with programs in either geriatrics, gynecology, or urology. Participants: Ninety-eight women, age 60 or older, with symptoms of urge incontinence and self-reported frequency of incontinence four or more times per week and involuntary bladder contractions on dual-channel water cystometry. Main Outcome Measures: Self-reported urinary frequency urgency number of incontinence episodes, and number of heavily soaked pads. Results: Eighty-one women, average age 71, completed the trial, 40 in the active drug group, 41 in the placebo group. Incontinence frequency and the number of heavily soaked pads were reduced in the active drug group by 64% and 55%, respectively, and by 21% (P = 0.002) and 9% (P = 0.04) in the placebo group. No patients dropped out due to adverse effects. An intention-to-treat analysis of all 98 patients yielded the same conclusion. Conclusion: Terodiline is highly effective in reducing incontinence in older, noninstitutionalized women with urge incontinence. Because of its potential association with polymorphic ventricular tachycardia (torsades de pointes), terodiline must undergo further testing to define its safety before it can be recommended for clinical use in the incontinent geriatric population. C1 WOMENS UROL CTR, SEATTLE, WA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI USA. OREGON HLTH SCI UNIV, PORTLAND, OR 97201 USA. UNIV IOWA HOSP & CLIN, IOWA CITY, IA 52242 USA. GEORGE WASHINGTON UNIV, MED CTR, WASHINGTON, DC 20037 USA. ST LOUIS UNIV, MED CTR, ST LOUIS, MO 63103 USA. METHODIST HOSP INDIANA, INDIANAPOLIS, IN 46202 USA. EVANSTON HOSP CORP, EVANSTON, IL 60201 USA. UNIV CALIF DAVIS, SACRAMENTO MED CTR, MED CTR, SACRAMENTO, CA 95817 USA. LOUISIANA STATE UNIV, MED CTR, SHREVEPORT, LA 71105 USA. VET ADM MED CTR, NORTHPORT, NY 11768 USA. NR 36 TC 2 Z9 2 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0002-8614 EI 1532-5415 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD SEP PY 1993 VL 41 IS 9 BP 915 EP 922 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA LW378 UT WOS:A1993LW37800003 ER PT J AU GERETY, MB CHIODO, LK KANTEN, DN TULEY, MR CORNELL, JE AF GERETY, MB CHIODO, LK KANTEN, DN TULEY, MR CORNELL, JE TI MEDICAL-TREATMENT PREFERENCES OF NURSING-HOME RESIDENTS - RELATIONSHIP TO FUNCTION AND CONCORDANCE WITH SURROGATE DECISION-MAKERS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID LONG-TERM CARE; LIFE-SUSTAINING TREATMENTS; CARDIOPULMONARY RESUSCITATION; HEALTH-STATUS; DEPRESSION; PATIENT; PREDICTIONS; PHYSICIANS; ATTITUDES; CAPACITY AB Objective: To describe treatment preferences of nursing home residents, concordance with decisions by self-selected proxies and to establish the relationship of sociodemographic and functional measures to decisions. Setting and Subjects: 52 patient-proxy pairs at a Veterans Affairs nursing home. Methods: Treatment preferences were elicited from residents and proxies regarding cardiopulmonary resuscitation, mechanical ventilation, and intensive care unit care. Hospitalization, intravenous antibiotics, intravenous fluid administration, and tube feeding were presented in three separate health scenarios. Concordance was determined for the entire interview and separately for each scenario. Treatment-seeking intensity and decision-making consistency were scored and used to explore associations with sociodemographic variables and function. Results: Subjects were predominantly male (97%) and non-Hispanic white (74%); average age was 70 +/- 12 years, with 4 +/- 2.9 diagnoses. Residents accepted 70% of all treatments. The proportion of subjects accepting interventions declined parallel to health status in each scenario. Only 7/52 (13%) subjects made inconsistent decisions. Resident treatment acceptance was inversely associated with GDS scores but not associated with any other sociodemographic or functional measure. Concordance with proxies was no greater than chance. Proxies' decisions were not systematically biased against resident preferences or influenced by patient characteristics. Conclusions: Veterans desired most treatments, but adjusted preferences according to health status and were not inconsistent. Depressive symptoms should be addressed prior to advance directive selection. The patient remains the best source of information, but proxies' decisions exhibit no bias and are not affected by patient status. C1 UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. RP GERETY, MB (reprint author), AUDIE L MURPHY VET MEM HOSP,GRECC 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 38 TC 68 Z9 68 U1 3 U2 6 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD SEP PY 1993 VL 41 IS 9 BP 953 EP 960 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA LW378 UT WOS:A1993LW37800009 PM 8204138 ER PT J AU GRANDALIANO, G BISWAS, P CHOUDHURY, GG ABBOUD, HE AF GRANDALIANO, G BISWAS, P CHOUDHURY, GG ABBOUD, HE TI SIMVASTATIN INHIBITS PDGF-INDUCED DNA-SYNTHESIS IN HUMAN GLOMERULAR MESANGIAL CELLS SO KIDNEY INTERNATIONAL LA English DT Article ID GROWTH-FACTOR PDGF; PROTEIN-KINASE-C; MEVALONATE; EXPRESSION; INJURY; RAT; GLOMERULOSCLEROSIS; MICROINJECTION; PROLIFERATION; NIH-3T3-CELLS AB Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase ameliorate glomerular pathology and renal dysfunction in different models of glomerular disease. This effect has generally been attributed to a decrease in the circulating levels of cholesterol. Focal or diffuse mesangial cell proliferation is a common feature of glomerular pathology. There is now evidence from studies in vitro and in vivo that platelet-derived growth factor (PDGF) is an important mediator of glomerular hypercellularity. The activity of HMGCoA reductase has previously been shown to be a requirement for cell growth. In the present study, we examined the effect of simvastatin, an HMGCoA reductase inhibitor, on PDGF-induced DNA synthesis and PDGF B chain gene expression in human glomerular mesangial cells. In addition, we investigated the effect of simvastatin on phospholipase C (PLC) and protein kinase C (PKC) activation stimulated by PDGF. We demonstrate that treatment of the cells with simvastatin completely inhibits PDGF-induced DNA synthesis. This inhibition is reversed by mevalonate but not by cholesterol or farnesol, two major metabolites of the mevalonate pathway. On the other hand inhibition of HMGCoA reductase does not influence PDGF-induced activation of PLC and PKC, or PDGF B chain gene expression. These data suggest that simvastatin acts at a late step in the PDGF mitogenic pathway without interfering with other early cellular responses elicited by this growth factor. These studies also raise the possibility that the ameliorative effect of HMGCoA reductase inhibitors on glomerular pathology may be mediated, at least in part, by a direct cellular effect. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK 33665, DK 43988] NR 34 TC 102 Z9 103 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD SEP PY 1993 VL 44 IS 3 BP 503 EP 508 DI 10.1038/ki.1993.274 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA LT428 UT WOS:A1993LT42800004 PM 8231022 ER PT J AU WAYS, DK QIN, WX COOK, P PARKER, PJ MENKE, JB HAO, EH SMITH, AM JONES, C HERSHMAN, JM GEFFNER, ME SU, F SAMUELS, HH USALA, SJ AF WAYS, DK QIN, WX COOK, P PARKER, PJ MENKE, JB HAO, EH SMITH, AM JONES, C HERSHMAN, JM GEFFNER, ME SU, F SAMUELS, HH USALA, SJ TI DOMINANT AND NONDOMINANT NEGATIVE C-ERBA-BETA-1 RECEPTORS ASSOCIATED WITH THYROID-HORMONE RESISTANCE SYNDROMES AUGMENT 12-O-TETRADECANOYL-PHORBOL-13-ACETATE INDUCTION OF THE COLLAGENASE PROMOTER AND EXHIBIT DEFECTIVE 3,5,3'-TRIIODOTHYRONINE-MEDIATED REPRESSION SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID PROTEIN-KINASE-C; TRANSCRIPTION FACTOR AP-1; LIGAND-BINDING DOMAIN; RETINOIC ACID RECEPTORS; GENERALIZED RESISTANCE; DNA-BINDING; MOLECULAR HETEROGENEITY; FUNCTIONAL-PROPERTIES; RESPONSE ELEMENTS; PHORBOL ESTERS AB C-erbA receptors and v-erbA have been shown to functionally interact with 12-0-tetradecanoyl-phorbol-13-acetate (TPA)-inducible gene expression. These proteins enhance trans-activation by c-jun, and the c-erbA receptors in the presence of thyroid hormone repress TPA and c-jun induction of transcription. Also, v-erbA can abrogate T3-mediated repression. We have examined how dominant negative (S and CL) and nondominant negative (G-H) receptors cloned from various patients with thyroid hormone resistance syndromes affect expression of the collagenase promoter induced with TPA. The CL receptor (ARG315HIS mutation) has a 2-fold reduction in T3-binding affinity compared with human c-erbAbeta1 wild-type (WT) receptor, whereas the G-H receptor (ARG311HIS) and S receptor (deletion, THR codon 332) have T3-binding affinities reduced by 100-fold and greater than 100-fold, respectively. These mutant receptors were cotransfected with a collagenase promoter (-1200 to +63 base pairs) chloramphenicol acetyltransferase reporter gene (Col-CAT) into COS-7 cells. Levels of CAT reporter gene expression after transient transfection were determined in the presence or absence of 3-10 nM T3 and the presence or absence of 100 nM TPA. Unoccupied CL receptor and G-H and S receptors stimulated TPA-induced Col-CAT expression 1.5- to 9-fold. The CL receptor with thyroid hormone totally repressed TPA induction of the collagenase receptor. In the presence of thyroid hormone, the enhancing effects by S and G-H receptors on TPA-induced Col-CAT expression were unaffected and minimally diminished, respectively. However, when WT receptor was cotransfected with G-H or S receptors at 1:1 molar ratios in the presence of T3, the transcriptional enhancement was completely abrogated. Similar results with WT and mutant receptors on Col-CAT activity were seen in cells transiently transfected with a constitutively active protein kinase C construct corresponding to the catalytic domain of protein kinase C-alpha and grown in the absence of TPA. We conclude that human mutant c-erbAbeta1 receptors, dominant and nondominant negative, have functional properties similar to v-erbA in terms of effects on a TPA-inducible promoter. The transcriptional enhancement of a TPA-inducible gene by the human mutants can be overcome by T3-activated WT receptor. This effect of WT on mutant receptor function may diminish a potential neoplastic effect of the human mutant receptors. C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. IMPERIAL CANC RES FUND, PROT PHOSPHORYLAT LAB, LONDON WC2A 3PX, ENGLAND. E CAROLINA UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, GREENVILLE, NC 27858 USA. NYU MED CTR, DEPT MED, DIV MOLEC ENDOCRINOL, NEW YORK, NY 10016 USA. UNIV CALIF LOS ANGELES, LOS ANGELES MED CTR, DEPT PEDIAT, LOS ANGELES, CA 90024 USA. NYU MED CTR, DEPT PHARMACOL, NEW YORK, NY 10016 USA. RP WAYS, DK (reprint author), E CAROLINA UNIV, SCH MED, DEPT MED, ENDOCRINOL SECT, GREENVILLE, NC 27858 USA. RI Parker, Peter/D-5192-2013 FU NCI NIH HHS [CA-43823]; NIDDK NIH HHS [DK-16636, DK-42807] NR 59 TC 12 Z9 12 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 SEP PY 1993 VL 7 IS 9 BP 1112 EP 1120 DI 10.1210/me.7.9.1112 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LZ180 UT WOS:A1993LZ18000002 PM 8247013 ER PT J AU AMES, D WIRSHING, WC MARDER, SR YUWILER, A BRAMMER, GL MIDHA, KK VANPUTTEN, T AF AMES, D WIRSHING, WC MARDER, SR YUWILER, A BRAMMER, GL MIDHA, KK VANPUTTEN, T TI ADJUNCTIVE FLUOXETINE IN HALOPERIDOL-STABILIZED SCHIZOPHRENICS SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD SEP PY 1993 VL 9 IS 2 SU S BP S116 EP S116 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV408 UT WOS:A1993LV40800252 ER PT J AU WIRSHING, WC WEST, LJ AF WIRSHING, WC WEST, LJ TI IMPACT OF PUBLIC-OPINION AND NEWS MEDIA ON PSYCHOPHARMACOLOGY IN THE 1990S SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD SEP PY 1993 VL 9 IS 2 SU S BP S57 EP S58 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV408 UT WOS:A1993LV40800120 ER PT J AU TYAN, ML AF TYAN, ML TI MURINE FETAL DEVELOPMENT ENHANCED BY DIETARY VITAMIN-A, CORN-OIL, AND INOSITOL SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID PLACENTAL-LACTOGEN RELEASE; HUMAN TROPHOBLASTIC CELLS; CONGENIC MICE; RETINOIC ACID; REPRODUCTIVE-PERFORMANCE; PHOSPHATE PRODUCTION; GROWTH-FACTORS; H-2; RATS; SUPPLEMENTATION AB Previous work on the effects of dietary vitamin A on craniofacial anomalies in mice revealed that 18-day-old fetuses from dams given 200 IU of vitamin A in corn oil daily in their diet weighed approximately 10% more than fetuses from mothers fed the unsupplemented standard mouse diet, Purina 5001. In the experiments reported here, it has been found that water-soluble vitamin A (200 IU/day) and myo-inositol (5 mg/day) added separately to the diets of pregnant mice increased the weight of 11-day gestations by approximately 25% and enhanced development of the eyes by the equivalent of 0.5-1.0 day without significantly affecting development of the liver or hind limbs. Corn oil alone (0.2 ml/day) had a similar effect on weight and eye development of 11-day fetuses and, in addition, growth of the hind limbs was enhanced modestly. The addition to the diet of vitamin A (200 IU/day) dissolved in corn oil (0.2 ml/day) resulted in a 25% increase in the weight of the 11-day fetuses and enhanced development of the eyes and hind limbs by the equivalent of about 1 day of gestation, suggesting that corn oil contains a factor(s) that interacts with vitamin A to accelerate limb development. Corn oil contains very small quantities of beta-carotene or retinol (<1.0 IU vitamin A/ml); however, it is a rich source of the essential growth factors linoleic and linolenic acids and of inositol esters. The data suggest that the growth-promoting actions of dietary corn oil are due in part to the inositol esters. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90073. RP TYAN, ML (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 42 TC 3 Z9 3 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD SEP PY 1993 VL 203 IS 4 BP 485 EP 489 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA PC069 UT WOS:A1993PC06900013 PM 8351289 ER PT J AU LANSKY, MR AF LANSKY, MR TI FAMILY GENESIS OF AGGRESSION SO PSYCHIATRIC ANNALS LA English DT Article C1 W LOS ANGELES VA MED CTR, BRENTWOOD DIV, FAMILY TREATMENT PROGRAM, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, MED SCH FAC, LOS ANGELES PSYCHOANALYT INST, LOS ANGELES, CA USA. NR 13 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD SEP PY 1993 VL 23 IS 9 BP 494 EP 499 PG 6 WC Psychiatry SC Psychiatry GA LX368 UT WOS:A1993LX36800003 ER PT J AU WOLFSON, M AF WOLFSON, M TI VALUE OF INTRADIALYTIC PARENTERAL-NUTRITION - COMMENT SO SEMINARS IN DIALYSIS LA English DT Letter RP WOLFSON, M (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0894-0959 J9 SEMIN DIALYSIS JI Semin. Dial. PD SEP-OCT PY 1993 VL 6 IS 5 BP 324 EP 324 DI 10.1111/j.1525-139X.1993.tb00505.x PG 1 WC Urology & Nephrology SC Urology & Nephrology GA LY139 UT WOS:A1993LY13900012 ER PT J AU DRINKA, PJ SIEBERS, M VOEKS, SK AF DRINKA, PJ SIEBERS, M VOEKS, SK TI POOR POSITIVE PREDICTIVE VALUE OF LOW SENSITIVE THYROTROPIN ASSAY LEVELS FOR HYPERTHYROIDISM IN NURSING-HOME RESIDENTS SO SOUTHERN MEDICAL JOURNAL LA English DT Article ID THYROID-STIMULATING HORMONE; SERUM THYROTROPIN; MULTINODULAR GOITER AB We assessed the positive predictive value of a low thyrotropin (TSH) level on sensitive TSH (STSH) assay as an indicator of hyperthyroidism. In 742 determinations on nursing home residents who were not taking thyroid hormone, we identified 15 with low TSH levels. None of the residents had a completely suppressed (undetectable) TSH level upon initial testing or an elevated total triiodothyronine (T3) or thyroxine (T4) level. Half the patients in whom total T3 was measured had low levels. Of 11 surviving residents, four subsequently had a normal TSH level and six others had a normal free T4 level. Only one patient had a slight elevation of the free T4 level. None of the residents were diagnosed as having hyperthyroidism. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. UNIV WISCONSIN,DEPT INTERNAL MED,MADISON,WI 53706. RP DRINKA, PJ (reprint author), WISCONSIN VET HOME,KING,WI 54946, USA. NR 8 TC 4 Z9 5 U1 0 U2 0 PU SOUTHERN MEDICAL ASSN PI BIRMINGHAM PA 35 LAKESHORE DR PO BOX 190088, BIRMINGHAM, AL 35219 SN 0038-4348 J9 SOUTHERN MED J JI South.Med.J. PD SEP PY 1993 VL 86 IS 9 BP 1004 EP 1007 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA LX611 UT WOS:A1993LX61100006 PM 8367743 ER PT J AU SAMUELS, MH HENRY, P LUTHER, M RIDGWAY, EC AF SAMUELS, MH HENRY, P LUTHER, M RIDGWAY, EC TI PULSATILE TSH SECRETION DURING 48-HOUR CONTINUOUS TRH INFUSIONS SO THYROID LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; HYPOTHYROID RATS; GROWTH-HORMONE; PROLACTIN SECRETION; SERUM THYROTROPIN; PITUITARY-TUMORS; LONG-TERM; RESPONSES; MEN; SOMATOSTATIN AB Thyroid-stimulating hormone (TSH), like other anterior pituitary hormones, is normally secreted in a series of pulses over 24 h. However, the factors that control TSH pulse generation are unknown. We investigated the potential role of thyrotropin-releasing hormone (TRH) in TSH pulse generation by measuring TSH pulses during constant TRH infusions. Two groups of subjects were studied: five healthy subjects and five subjects with treated primary hypothyroidism and normal TSH levels. Each subject underwent four separate studies: (1) TSH levels were measured every 15 min over 24 h (baseline study). (2) TSH levels were measured every 15 min over 48 h during TRH infusions at 0.1 mug/min (low dose TRH study). (3) TSH levels were measured every 15 min over 48 h during TRH infusions at 0.5 mug/min (medium dose TRH study). (4) TSH levels were measured every 15 min over 48 h during TRH infusions at 1.0 mug/min (high dose TRH study). TSH pulses were located by cluster analysis. We found that constant TRH infusions at any of the doses utilized did not alter TSH pulse frequency in normal or treated hypothyroid subjects, although pulse amplitude increased. Normal subjects had lower TSH pulse amplitude than treated hypothyroid subjects at all TRH doses, perhaps due to slightly higher serum T3 levels. This suggests that, at least acutely, pulsatile input of TRH to the pituitary gland does not determine pulsatile TSH release. However, TRH may modulate TSH pulse amplitude. C1 UNIV COLORADO,HLTH SCI CTR,DIV ENDOCRINOL,DENVER,CO 80262. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP SAMUELS, MH (reprint author), OREGON HLTH SCI UNIV,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. FU NCRR NIH HHS [M01-RR-00051, M01-RR-01-346] NR 29 TC 16 Z9 17 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 1993 VL 3 IS 3 BP 201 EP 206 DI 10.1089/thy.1993.3.201 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MA711 UT WOS:A1993MA71100005 PM 8257859 ER PT J AU PAUL, RV WACKYM, PS BUDISAVLJEVIC, M EVERETT, E NORRIS, JS AF PAUL, RV WACKYM, PS BUDISAVLJEVIC, M EVERETT, E NORRIS, JS TI REGULATION OF ATRIAL-NATRIURETIC-PEPTIDE CLEARANCE RECEPTORS IN MESANGIAL CELLS BY GROWTH-FACTORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SMOOTH-MUSCLE CELLS; ANGIOTENSIN-II; ENDOTHELIAL-CELLS; PROLIFERATIVE NEPHRITIS; GUANYLATE-CYCLASE; C-RECEPTORS; CYCLIC-GMP; RAT; PDGF; EXPRESSION AB Rat mesangial cells can express both 130-kDa guanylyl cyclase-coupled and 66-kDa non-coupled atrial natriuretic peptide (ANP) receptors (ANPR-A and ANPR-C, respectively). Exposure of mesangial cells, grown in 20% fetal calf serum, to 0.1% serum for 24 h increased total ANP receptor density more than 2-fold (B(max) = 87 versus 37 fmol/mg of cell protein) without changing binding affinity (K(d) = 94 versus 88 pM). Radioligand binding and cross-linking studies demonstrated that up-regulation of ANP binding after serum deprivation was entirely due to an increase in ANPR-C, with little or no change in ANPR-A. Inhibition of protein synthesis with cycloheximide blocked up-regulation after serum deprivation. Steady-state ANPR-C mRNA level was increased 15-fold by serum deprivation, as judged by Northern blotting. There was no change in ANPR-A mRNA. Platelet-derived growth factor and phorbol myristate acetate, when added to low serum medium, blocked or reversed the effect of serum deprivation on ANPR-C. We conclude that synthesis and expression of ANPR-C but not ANPR-A is suppressed by serum, platelet-derived growth factor, and phorbol myristate acetate. Suppression of ANPR-C in vivo could contribute to mesangial cell proliferative responses to growth factors. C1 MED UNIV S CAROLINA,DEPT BIOCHEM & MOLEC BIOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. VET AFFAIRS MED CTR,RALPH H JOHNSON DEPT,DIV NEPHROL,CHARLESTON,SC. FU NCI NIH HHS [R01-CA-49949] NR 47 TC 25 Z9 25 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 1993 VL 268 IS 24 BP 18205 EP 18212 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LT743 UT WOS:A1993LT74300083 PM 8349696 ER PT J AU TALAL, N AF TALAL, N TI LESSONS FROM AUTOIMMUNITY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID INTERSPECIES IDIOTYPE; INDUCTION; NETWORK; MICE C1 UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. RP TALAL, N (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR, CLIN IMMUNOL SECT, SAN ANTONIO, TX 78284 USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD AUG 12 PY 1993 VL 690 BP 19 EP 23 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX021 UT WOS:A1993LX02100004 ER PT J AU DATTA, AK TAKAYAMA, K AF DATTA, AK TAKAYAMA, K TI BIOSYNTHESIS OF A NOVEL 3-OXO-2-TETRADECYLOCTADECANOATE-CONTAINING PHOSPHOLIPID BY A CELL-FREE-EXTRACT OF CORYNEBACTERIUM-DIPHTHERIAE SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE CORYNOMYCOLIC ACID; PHOSPHOLIPID; (CORYNEBACTERIUM) ID BACTERIONEMA-MATRUCHOTII; MYCOLIC ACIDS; FREE SYSTEM; TREHALOSE AB We have isolated, purified, and identified by chemical analyses and mass spectrometry, a novel 3-oxo-2-tetradecyloctadecanoate (dehydrocorynomycolate)-containing phospholipid (PL-1) from the chloroform-methanol extract of Corynebacterium diphtheriae. This phospholipid was separated from all of the other known dehydrocorynomycolate and 3-hydroxy-2-tetradecyloctadecanoate (corynomycolate)-containing lipids and found to be unstable even at -20-degrees-C. It was present in trace amounts as a homologous series (molecular weights of 1400 and 1404 as the methyl esters) and composed of a dehydrocorynomycolate, a phosphate group, a diacylglycerol, and an unidentified amine-containing component. Because of the complexity of these phospholipids, their complete structural determination is yet to be completed. A cell-free extract of C diphtheriae catalyzed the incorporation of radiolabel from [C-14]palmitic acid into PL-1. This incorporation was ATP-dependent, and the rate was linear with respect to both time and protein concentration. The radiolabel was incorporated primarily into the dehydrocorynomycoloyl moiety of PL-1. While avidin did not show any significant effect, cerulenin showed a marked inhibition of this reaction. Based on these results, we suggest that this dehydrocorynomycolate-containing PL-1 may be the long-sought acyl carrier-containing product of a Claisen-type condensation. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,2500 OVERLOOK TERR,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NIGMS NIH HHS [GM-36054] NR 27 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD AUG 11 PY 1993 VL 1169 IS 2 BP 135 EP 145 DI 10.1016/0005-2760(93)90198-I PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LT360 UT WOS:A1993LT36000003 PM 8343537 ER PT J AU BAGBY, SP KIRK, EA MITCHELL, LH OREILLY, MM HOLDEN, WE STENBERG, PE BAKKE, AC AF BAGBY, SP KIRK, EA MITCHELL, LH OREILLY, MM HOLDEN, WE STENBERG, PE BAKKE, AC TI PROLIFERATIVE SYNERGY OF ANG-II AND EGF IN PORCINE AORTIC VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HYPERTROPHY; HYPERPLASIA; FLOW CYTOMETRY; CELL CYCLE ANALYSIS; PROTEIN SYNTHESIS; DEOXYRIBONUCLEIC ACID SYNTHESIS; CELL SIZE; HYDROGEN-3-LABELED THYMIDINE INCORPORATION; SULFUR-35-LABELED METHIONINE INCORPORATION; VASCULAR GROWTH; INDOMETHACIN; LOSARTAN ID EPIDERMAL GROWTH-FACTOR; ANGIOTENSIN-II; DNA-SYNTHESIS; FLOW-CYTOMETRY; C-MYC; RAT; HYPERTROPHY; HYPERTENSION; STIMULATION; RECEPTORS AB To test growth effects of angiotensin II (ANG II) in porcine vascular smooth muscle cells (VSMC) and potential ANG II synergy with epidermal growth factor (EGF), we exposed subconfluent, near-quiescent porcine aortic VSMC to ANG II, EGF, or ANG II + EGF (each 10(-9) M) in Dulbecco's modified Eagle's-Ham's F-12 medium with insulin + 0.4% fetal calf serum (FCS) selected for minimal ANG II-degrading capacity. Cell number and DNA and protein synthesis (by [H-3]thymidine and [S-35]methionine incorporation, respectively) were determined serially over 1-6 days. ANG II alone induced an early 20% increase and then a plateau in cell number over the 0.4% FCS control (P < 0.01; n = 8), thus without sustained increase in proliferation rate. Yet ANG II alone did not increase fractional DNA or protein synthesis (each as cpm/10(3) cells) and, by flow cytometry, reduced S phase fraction without increase in cell size. EGF alone induced brisk DNA synthesis yet minimal cell division over days 0-4, thus late-cycle arrest. ANG II + EGF, despite no increase in fractional DNA or protein synthesis rates over EGF alone, induced significant indomethacin-resistant dose-dependent (P < 0.001) increase in cell proliferation rate over EGF alone with a median effective dose of 5 x 10(-10) M ANG II, thus proliferative synergy. We propose that 1) ANG II induces a subpopulation of cells arrested in or beyond S phase to proceed through mitosis but does not influence G1 traversal or S phase entry and 2) ANG II + EGF achieve proliferative synergy by complementary actions at sequential cell cycle loci, with EGF supporting progression from G0/G1 to S phase and ANG II inducing completion of mitosis by cells already in or beyond S phase (''late-cycle completion''). C1 PORTLAND VET AFFAIRS MED CTR,DEPT MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,DEPT PATHOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NR 30 TC 25 Z9 26 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD AUG PY 1993 VL 265 IS 2 BP F239 EP F249 PN 2 PG 11 WC Physiology SC Physiology GA LW032 UT WOS:A1993LW03200087 PM 8368333 ER PT J AU IVESTER, CT KENT, RL TAGAWA, H TSUTSUI, H IMAMURA, T COOPER, G MCDERMOTT, PJ AF IVESTER, CT KENT, RL TAGAWA, H TSUTSUI, H IMAMURA, T COOPER, G MCDERMOTT, PJ TI ELECTRICALLY STIMULATED CONTRACTION ACCELERATES PROTEIN-SYNTHESIS RATES IN ADULT FELINE CARDIOCYTES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MYOSIN HEAVY CHAIN; 2,3-BUTANEDIONE MONOXIME; TRANSLATION; HYPERTROPHY ID HEART-CELLS; 2,3-BUTANEDIONE MONOXIME; CARDIAC MYOCYTES; VENTRICULAR MYOCYTES; MAMMALIAN MYOCARDIUM; THYROID-HORMONE; GENE-EXPRESSION; LOAD REGULATION; BREAST MUSCLE; HYPERTROPHY AB Cardiocytes were induced to contract via electrical field stimulation with an 8 V/cm electrical square-wave pulse of 5 ms at 0.125-2.0 Hz for up to 6 h. Protein synthesis rates were measured as rate of incorporation of [H-3]-phenylalanine into total cell protein. Rates of protein synthesis were accelerated 43 +/- 4%, P < 0.001, by 4 h. The acceleration of total protein synthesis showed a frequency dependence between 0.125 and 0.5 Hz. In addition to accelerating rates of total protein synthesis, electrical stimulation of contraction accelerated fractional rates of synthesis of myosin heavy chain by 42 +/-8%, P < 0.05. Protein synthesis rates were not accelerated upon electrical stimulation using subthreshold voltages. Addition of 100 ng/ml of actinomycin D had no effect on the ability of electrical stimulation of contraction to accelerate protein synthesis. To uncouple excitation-contraction coupling, 2,3-butanedione monoxime (BDM) was used to block actin-myosin cross-bridge interactions. BDM significantly decreased the ability of electrical stimulation to accelerate protein synthesis rates. C1 MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT MED,CHARLESTON,SC 29401. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT CELL BIOL & ANAT,CHARLESTON,SC 29401. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT PHARMACOL,CHARLESTON,SC 29401. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT PHYSIOL,CHARLESTON,SC 29401. MED UNIV S CAROLINA,RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. RI Tsutsui, Hiroyuki/A-4070-2012 NR 44 TC 49 Z9 49 U1 2 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD AUG PY 1993 VL 265 IS 2 BP H666 EP H674 PN 2 PG 9 WC Physiology SC Physiology GA LW032 UT WOS:A1993LW03200033 PM 8368369 ER PT J AU BERNSTEIN, DP COHEN, P VELEZ, CN SCHWABSTONE, M SIEVER, LJ SHINSATO, L AF BERNSTEIN, DP COHEN, P VELEZ, CN SCHWABSTONE, M SIEVER, LJ SHINSATO, L TI PREVALENCE AND STABILITY OF THE DSM-III-R PERSONALITY-DISORDERS IN A COMMUNITY-BASED SURVEY OF ADOLESCENTS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DISTURBANCE; DYSFUNCTION AB Objective: The purpose of this study was to estimate the prevalence, concurrent validity, and stability of DSM-III-R personality disorders in a large community-based sample of adolescents. Method: A randomly selected community sample of 733 youths ranging in age from 9 to 19 years was followed over a 2-year period. The protocol consisted of structured interviews with the adolescents and their mothers and self-report questionnaires. Algorithms for 1 0 DSM-III-R axis II disorders were developed to produce diagnoses at two levels of severity; these were validated against multiple indicators of distress and functional impairment. Results: The overall prevalence of personality disorders peaked at age 12 in boys and at age 13 in girls and declined thereafter. Obsessive-compulsive personality disorder was the most prevalent moderate axis II disorder, narcissistic personality disorder the most prevalent severe disorder, and schizotypal personality disorder the least prevalent axis II disorder, based on both moderate and severe diagnostic thresholds. All moderate axis II disorders were associated with significantly greater odds for at least five of 12 diagnostic validators. Longitudinal follow-up revealed that although most axis II disorders did not persist over a 2-year period, subjects with disorders identified earlier remained at elevated risk for receiving a diagnosis again at follow-up. Conclusions: These findings suggest that a substantial minority of adolescents who are not in treatment qualify for DSM-III-R personality disorder diagnoses and that these diagnoses are associated with increased risk of psychological distress and functional impairment. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT PSYCHIAT,NEW YORK,NY 10032. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT EPIDEMIOL,NEW YORK,NY 10032. RP BERNSTEIN, DP (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,PSYCHIAT SERV 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIDA NIH HHS [DA-03188]; NIMH NIH HHS [NIMH MH-36971] NR 20 TC 245 Z9 250 U1 1 U2 12 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD AUG PY 1993 VL 150 IS 8 BP 1237 EP 1243 PG 7 WC Psychiatry SC Psychiatry GA LP806 UT WOS:A1993LP80600018 PM 8328570 ER PT J AU SILVERSTEIN, JH SILVA, DA IBERTI, TJ AF SILVERSTEIN, JH SILVA, DA IBERTI, TJ TI OPIOID ADDICTION IN ANESTHESIOLOGY SO ANESTHESIOLOGY LA English DT Review DE NARCOTIC DEPENDENCE; PHYSICIAN IMPAIRMENT; SUBSTANCE ABUSE ID SUBSTANCE-ABUSE; IMPAIRED PHYSICIANS; TRAINING-PROGRAMS; DRUG-ABUSE; LEGAL ISSUES; ALCOHOLISM; URINE; NALTREXONE; ADULTERANTS; EXCRETION C1 CUNY MT SINAI SCH MED,DEPT ANESTHESIOL,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT SURG,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. RP SILVERSTEIN, JH (reprint author), BRONX VET AFFAIRS MED CTR,ANESTHESIA SECT,BOX 112A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 94 TC 17 Z9 21 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD AUG PY 1993 VL 79 IS 2 BP 354 EP 375 DI 10.1097/00000542-199308000-00022 PG 22 WC Anesthesiology SC Anesthesiology GA LP761 UT WOS:A1993LP76100021 PM 8267716 ER PT J AU CUMMINGS, JL AF CUMMINGS, JL TI FRONTAL-SUBCORTICAL CIRCUITS AND HUMAN-BEHAVIOR SO ARCHIVES OF NEUROLOGY LA English DT Review ID PARAMEDIAN THALAMIC INFARCTION; OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; MOOD DISORDERS; BLOOD-FLOW; LESIONS; LOBE; DEMENTIA AB objective.-This synthetic review was performed to demonstrate the utility of frontal-subcortical circuits in the explanation of a wide range of human behavioral disorders. Data Sources.-Reports of patients with degenerative disorders or focal lesions involving frontal lobe or linked subcortical structures were chosen from the English literature. Individual case reports and group investigations from peer-reviewed journals were evaluated. Study Selection.-Studies were included if they described patient behavior in detail or reported pertinent neuropsychological findings and had compelling evidence of a disorder affecting frontal-subcortical circuits. Data Extraction.-Information was used if the report from which it was taken met study selection criteria. Data Synthesis.-Five parallel segregated circuits link the frontal lobe and subcortical structures. Clinical syndromes observed with frontal lobe injury are recapitulated with lesions of subcortical member structures of the circuits. Each prefrontal circuit has a signature behavioral syndrome: executive function deficits occur with lesions of the dorsolateral prefrontal circuit, disinhibition with lesions of the orbito-frontal circuit, and apathy with injury to the anterior cingulate circuit. Depression, mania, and obsessive-compulsive disorder may also be mediated by frontal-subcortical circuits. Movement disorders identify involvement of the basal ganglia component of frontal-subcortical circuits. Conclusions.-Frontal-subcortical circuits mediate many aspects of human behavior. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. RP CUMMINGS, JL (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, NEUROBEHAV UNIT, BEHAV NEUROSCI SECT, BLDG 256B 691B116AF, LOS ANGELES, CA 90073 USA. RI Frank, David/E-8213-2012 NR 71 TC 1470 Z9 1496 U1 4 U2 48 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD AUG PY 1993 VL 50 IS 8 BP 873 EP 880 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA LR028 UT WOS:A1993LR02800018 PM 8352676 ER PT J AU MILLER, AL MAAS, JW CONTRERAS, S SELESHI, E TRUE, JE BOWDEN, C CASTIGLIONI, J AF MILLER, AL MAAS, JW CONTRERAS, S SELESHI, E TRUE, JE BOWDEN, C CASTIGLIONI, J TI ACUTE EFFECTS OF NEUROLEPTICS ON UNMEDICATED SCHIZOPHRENIC-PATIENTS AND CONTROLS SO BIOLOGICAL PSYCHIATRY LA English DT Article DE METHOXYHYDROXYPHENYLGLYCOL; HOMOVANILLIC ACID; SCHIZOPHRENIA; HALOPERIDOL CHALLENGE; NEUROLEPTIC; DEBRISOQUIN ID PLASMA HOMOVANILLIC-ACID; BRAIN DOPAMINE METABOLISM; CHRONIC HALOPERIDOL TREATMENT; CEREBROSPINAL-FLUID; ENDOGENOUS DOPAMINE; CLONIDINE TREATMENT; DEBRISOQUIN; NEURONS; NOREPINEPHRINE; APOMORPHINE AB Acute administration of haloperidol (0.2 mg/kg) produced many more side effects in normal controls than in unmedicated schizophrenic patients. Prior to the neuroleptic challenge, both groups were on the peripheral monoamine oxidase inhibitor, debrisoquin, for at least 1 week, in order to enhance the relative contribution of CNS catecholamine metabolites to those measured in both plasma and urine. The patient group had higher plasma levels of methoxyhydroxyphenylglycol (MHPG) and homovanillic acid (HVA) and higher urinary MHPG output than controls, but there were no effects of haloperidol challenge, compared to placebo challenge. In both groups there were significant declines in plasma HVA levels from 8:30 AM to 12 NOON. These declines were unaffected by the haloperidol challenge. Explanations for the marked differences in behavioral effects of haloperidol on patients and controls include the possibility that dopamine receptor numbers were increased in the brains of the schizophrenic patients. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP MILLER, AL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NCRR NIH HHS [MO1-RR01346]; NIMH NIH HHS [MH40935] NR 81 TC 23 Z9 23 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD AUG 1 PY 1993 VL 34 IS 3 BP 178 EP 187 DI 10.1016/0006-3223(93)90389-U PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LT691 UT WOS:A1993LT69100010 PM 8104509 ER PT J AU WEISS, JN VENKATESH, N AF WEISS, JN VENKATESH, N TI METABOLIC-REGULATION OF CARDIAC ATP-SENSITIVE K+ CHANNELS SO CARDIOVASCULAR DRUGS AND THERAPY LA English DT Article DE ATP-SENSITIVE POTASSIUM CHANNELS; MYOCARDIAL ISCHEMIA; HYPOXIA; METABOLIC INHIBITION; GLYCOLYSIS; ACTION POTENTIAL DURATION; POTASSIUM ACCUMULATION; POTASSIUM LOSS ID RAT VENTRICULAR MYOCYTES; EXTRACELLULAR POTASSIUM; MYOCARDIAL ISCHEMIA; ARRHYTHMIAS; HEART; ACCUMULATION; GLYCOLYSIS; INFARCTION; MODULATION; MUSCLE AB Activation of ATP-sensitive K+ (K(ATP)) channels has been implicated as a cause of increased cellular K+ efflux and action potential duration (APD) shortening during myocardial ischemia, hypoxia, and selective glycolytic inhibition, since selective K(ATP) channel antagonists partially or completely block increased cellular K+ efflux and APD shortening under these conditions. During substrate-free hypoxia or myocardial ischemia in intact rabbit ventricle, unidirectional K+ efflux rate during systole approximately doubled and APD decreased by almost-equal-to 40% after 10 minutes. In patch-clamped guinea pig ventricular myocytes, similar changes could be produced by activation of <0.5% of the maximal K(ATP) channel conductance. Furthermore, from studying the desensitizing effects of ADP(i) on the ATP sensitivity of K(ATP) channels in excised inside-out patches, it was estimated that the rapid changes in the cytosolic ATP/ADP ratio during ischemia and hypoxia were of sufficient magnitude to activate K(ATP) channels to this degree. During selective glycolytic inhibition, however, the global cytosolic ATP/ADP ratio in intact heart remained normal despite an increase in cellular K+ efflux comparable to ischemia and hypoxia. In patch-clamped saponin-permeabilized ventricular myocytes. K(ATP) channels were preferentially suppressed by glycolytic ATP production compared to ATP generated by mitochondria or by the creatinine kinase reaction, and functional glycolytic enzymes were found to be associated with K(ATP) channels in excised membrane patches. We hypothesize that sarcolemma-associated glycolytic enzymes may be important in maintaining a high local cytosolic ATP/ADP ratio in the vicinity of K(ATP) channels, where sarcolemmal ATPases are tending to depress the local ATP/ADP ratio. C1 UNIV CALIF LOS ANGELES, DEPT MED CARDIOL, CARDIOVASC RES LAB, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, W LOS ANGELES VA MED CTR, LOS ANGELES, CA USA. FU NHLBI NIH HHS [1K04 HL01890, 1R01 HL36729, 1R29 HL38366] NR 19 TC 71 Z9 71 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-3206 J9 CARDIOVASC DRUG THER JI Cardiovasc. Drugs Ther. PD AUG PY 1993 VL 7 SU 3 BP 499 EP 505 DI 10.1007/BF00877614 PG 7 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA MB806 UT WOS:A1993MB80600004 PM 8251419 ER PT J AU CARNES, M GOODMAN, BM LENT, SJ VO, H AF CARNES, M GOODMAN, BM LENT, SJ VO, H TI HIGH-INTENSITY VENOUS SAMPLING REVEALS SUBTLE ALTERATIONS IN PLASMA ADRENOCORTICOTROPIN PATTERNS IN OLD RATS SO ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; DIMINISHED DIURNAL SECRETION; ULTRADIAN RHYTHMS; SPECTRAL-ANALYSIS; PULSE FREQUENCY; ACTH; CORTICOSTERONE; PULSATILE; PITUITARY; CORTISOL AB Dysregulation of the hypothalamic-pituitary-adrenocortical axis has been theoretically linked to the processes of aging for decades. To investigate the effect of age on high frequency rhythms of plasma ACTH at the time of circadian activation, integrated 2-min blood samples were collected over 4 h in 10 young and 14 old rats with simultaneous plasma volume replacement. Plasma ACTH time series were analyzed in the time and frequency domains. Relative to young rats, old rats had a significantly later onset of the diurnal surge, more spectral power (R2) at lower frequencies, a lack of correlation between the slope of the spectral background continuum and the R2 at periods less than approximately 11 min, a stretching of the time scale in the composite spectra by 18.5%, and an amplitude reduction of the major composite spectral peak by 31%. These findings support the existence of subtle, but significant, alterations in the pattern of plasma ACTH with age and a delayed response of the hypothalamic-pituitary-adrenocortical axis to circadian activation. The differences in spectra suggest a weaker coupling with age between the high frequency signal input (that may reflect depolarization of groups of corticotrophs) and the system response, which could account for the delay in onset of the diurnal surge seen in the time domain. C1 UNIV WISCONSIN, DEPT MED, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT BIOSTAT, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT SPACE SCI, MADISON, WI 53705 USA. UNIV WISCONSIN, CTR ENGN, MADISON, WI 53705 USA. RP CARNES, M (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR, CTR GERIATR RES EDUC & CLIN, 2500 OVERLOOK TERRACE, MADISON, WI 53705 USA. FU NIDDK NIH HHS [DK-40759] NR 52 TC 11 Z9 11 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD AUG PY 1993 VL 133 IS 2 BP 608 EP 616 DI 10.1210/en.133.2.608 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LQ846 UT WOS:A1993LQ84600027 PM 8393770 ER PT J AU MARKESICH, DC ELZAATARI, FAK GRAHAM, DY AF MARKESICH, DC ELZAATARI, FAK GRAHAM, DY TI ACTIVITY OF CLARITHROMYCIN AGAINST INTRACELLULAR MYCOBACTERIUM-PARATUBERCULOSIS - PUTATIVE AGENT OF CROHNS-DISEASE SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY LA English DT Article DE MYCOBACTERIUM-PARATUBERCULOSIS; CROHNS DISEASE; SUSCEPTIBILITY; CLARITHROMYCIN; MYCOBACTERIA AB Objective: To test whether Mycobacterium paratuberculosis, the putative etiologic agent of Crohn's disease, was senisitive to clarithromycin. Design: To test the susceptibility of two mycobactin-dependent mycobacteria, M. paratuberculosis and M. avium subsp. silvaticum, to clarithromycin grown in mouse monocyte/macrophage cell line J774A.1. Results: Clarithromycin, 2 and 4 mug/ml, inhibited M. paratuberculosis (80 and 25% of control, respectively) but was less effective against M. avium subsp. silvaticum (80 and 82% of control, respectively) growing intracellularly in the murine macrophage cell line J-774A.1. Conclusions: Clarithromycin shows promise for use in double-blind controlled trials for testing the hypothesis that M. paratuberculosis is etiologically related to Crohn's disease. C1 VET AFFAIRS MED CTR 111D,INFLAMMATORY BOWEL DIS LAB,2002 HOLCOMBE BLVD,HOUSTON,TX 77030. NR 0 TC 7 Z9 7 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-691X J9 EUR J GASTROEN HEPAT JI Eur. J. Gastroenterol. Hepatol. PD AUG PY 1993 VL 5 IS 8 BP 613 EP 615 DI 10.1097/00042737-199308000-00010 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LV086 UT WOS:A1993LV08600010 ER PT J AU MANTHEY, CL PERERA, PY QURESHI, N STUTZ, PL HAMILTON, TA VOGEL, SN AF MANTHEY, CL PERERA, PY QURESHI, N STUTZ, PL HAMILTON, TA VOGEL, SN TI MODULATION OF LIPOPOLYSACCHARIDE-INDUCED MACROPHAGE GENE-EXPRESSION BY RHODOBACTER-SPHAEROIDES LIPID-A AND SDZ-880.431 SO INFECTION AND IMMUNITY LA English DT Article ID TUMOR-NECROSIS-FACTOR; MURINE PERITONEAL-MACROPHAGES; RHODOPSEUDOMONAS-SPHAEROIDES; MESSENGER-RNA; HUMAN-NEUTROPHILS; INDUCIBLE GENES; BINDING-PROTEIN; HUMAN MONOCYTES; LPS BINDING; IFN-GAMMA AB Rhodobacter sphaeroides lipid A (RsDPLA) and SDZ 880.431 (3-aza-lipid X4-phosphate) are prototypic lipopolysaccharide (LPS) antagonists. Herein, we examined the ability of these structures to regulate murine macrophage tumor necrosis factor (TNF) secretion and LPS-inducible gene expression (tumor necrosis factor alpha [TNF-alpha], interleukin-1beta [IL-1beta], IP-10, type 2 TNF receptor [TNFR-2], D3, and D8 genes). We report that RsDPLA alone (> 1 mug/ml) induced low levels of TNF-alpha secretion and a selective pattern of gene expression in peritoneal exudate macrophages; SDZ 880.431 alone was completely inactive. When LPS was present at a low concentration (1 ng/ml), RxDPLA and SDZ 880.431 blocked TNF secretion and gene induction in a concentration-dependent fashion. In general, gene induction was measurably reduced by 10 to 30 ng of RsDPLA per ml or 300 ng of SDZ 880.431 per ml, but inhibition could be uniformly overridden by increasing the concentration of LPS. Although induction of all six genes by LPS was suppressed by either inhibitor, effective inhibitor concentrations depended on the gene of interest. Induction of TNFR-2 by LPS was relatively resistant to inhibition by RxDPLA, and induction of TNFR-2 and D3 was relatively resistant to inhibition by SDZ 880.431. When LPS was present at greater-than-or-equal-to 100 ng/ml, correspondingly high concentrations (greater-than-or-equal-to 20 mug/ml) of either inhibitor influenced gene expression in a bidirectional manner. Under these conditions, LPS-induced expression of IP-10, D3, and D8 was suppressed regardless of the LPS concentration used (concentrations tested up to 50 mug/ml), while expression of TNF-alpha mRNA was enhanced about fourfold. In toto, RsDPIA and SDZ 880.431, when present at low concentrations, act in a manner consistent with competitive inhibition of LPS, while at higher concentrations, these structures inhibit certain LPS responses noncompetitively and synergize with LPS for other responses. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL,4301 JONES BRIDGE RD,BETHESDA,MD 20814. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. CLEVELAND CLIN EDUC FDN,RES INST,DEPT IMMUNOL,CLEVELAND,OH 44106. FU NIAID NIH HHS [AI 08451] NR 46 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 AUG PY 1993 VL 61 IS 8 BP 3518 EP 3526 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LP357 UT WOS:A1993LP35700056 PM 8335383 ER PT J AU WILLIAMS, DM GRUBBS, BG SCHACHTER, J MAGEE, DM AF WILLIAMS, DM GRUBBS, BG SCHACHTER, J MAGEE, DM TI GAMMA-INTERFERON LEVELS DURING CHLAMYDIA-TRACHOMATIS PNEUMONIA IN MICE SO INFECTION AND IMMUNITY LA English DT Note ID TUMOR NECROSIS FACTOR; DELTA-T-CELLS; ROLE INVIVO; IFN-GAMMA; MOUSE; INFECTION; IMMUNITY; ACTIVATION; ALPHA; AGENT AB Host defense against murine Chlamydia trachomatis (mouse pneumonitis agent [MoPn]) in a murine model was investigated. Gamma interferon (IFN-gamma) was produced in the lungs by both MoPn-susceptible nude athymic (nu/nu) and MoPn-resistant heterozygous (nu/+) mice. In vivo depletion of IFN-gamma in nu/nu mice led to exacerbation of infection. Fluorescence-activated cell sorter analysis disclosed induction of GL3 antibody-positive cells (putatively gamma/delta+ T cells) in nu/nu mouse lung during infection with MoPn. Treatment of nu/nu mice in vivo with antibody to NK cells (anti-asialo GM1 antibody) or to gamma/delta cells (UC7-13D5) did not significantly decrease IFN-gamma production in the lung. However, treatment of severe combined immunodeficiency mice (which lack gamma/delta cells) with antibody to NK cells significantly reduced lung IFN-gamma levels. C1 STATE CHEST HOSP,DEPT IMMUNOL,SAN ANTONIO,TX 78223. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV CALIF SAN FRANCISCO,DEPT CARDIOL,SAN FRANCISCO,CA 94143. RP WILLIAMS, DM (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DIV INFECT DIS,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [AI 22380] NR 25 TC 24 Z9 25 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 1993 VL 61 IS 8 BP 3556 EP 3558 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LP357 UT WOS:A1993LP35700065 PM 8335389 ER PT J AU WHEATLEY, JR TANGEL, DJ MEZZANOTTE, WS WHITE, DP AF WHEATLEY, JR TANGEL, DJ MEZZANOTTE, WS WHITE, DP TI INFLUENCE OF SLEEP ON ALAE-NASI EMG AND NASAL RESISTANCE IN NORMAL MEN SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE UPPER AIRWAY PHYSIOLOGY; NON-RAPID-EYE-MOVEMENT SLEEP; AIR-WAY PATENCY ID UPPER AIRWAY; MUSCLE RESPONSES; NORMAL HUMANS; FLOW; PRESSURE; WAKEFULNESS; ACTIVATION AB The influence of sleep on the upper airway musculature varies considerably, with some muscles maintaining their activity at waking levels and others falling substantially. The influence of sleep on the alae nasi (AN), a dilator muscle of the nasal airway, has been minimally studied to date. Thus we determined the effect of non-rapid-eye-movement (NREM) sleep on the AN electromyogram and its relationship to nasal resistance (Rn) in nine normal supine males. Phasic inspiratory AN activity decreased from 20 +/- 6 arbitrary units during wakefulness to 5 +/- 1 arbitrary units (P < 0.001) at the onset of stage 2 NREM sleep and remained unchanged for two subsequent hours of NREM sleep. However, the Rn at the onset of NREM sleep remained similar to awake values (5.7 +/- 0.9 cmH2O . l-1 . s) and increased only after 1 h of NREM sleep (8.6 +/- 1.7 cmH2O . l-1 . s, P < 0.05), thus demonstrating little relationship to AN activity. We conclude that Rn increases slightly after 1 h of sleep, whereas AN activity decreases at stage 2 sleep onset. Thus AN activity has little influence on Rn during sleep. C1 DENVER VET AFFAIRS MED CTR,NATL JEWISH CTR IMMUNOL & RESP MED,DIV PULM,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80220. NR 29 TC 12 Z9 12 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD AUG PY 1993 VL 75 IS 2 BP 626 EP 632 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA LT582 UT WOS:A1993LT58200021 PM 8226461 ER PT J AU CONHAIM, RL HARMS, BA AF CONHAIM, RL HARMS, BA TI PERFUSION OF ALVEOLAR SEPTA IN ISOLATED RAT LUNGS IN ZONE-1 SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE ZONE-1 LUNGS; FLUORESCENCE MICROSCOPY; RAPID FREEZING; PULMONARY MICROCIRCULATION; ALVEOLAR VESSELS; EXTRA-ALVEOLAR VESSELS; PULMONARY MICROVASCULAR FILTRATION; PULMONARY INTERSTITIUM ID INSITU DOG LUNGS; INTERSTITIAL COMPLIANCE; FILTRATION COEFFICIENT; PULMONARY-EDEMA; RABBIT LUNGS; PERMEABILITY; PRESSURE; VESSELS; VOLUME; FLUID AB The combination of high inflation and low vascular pressures in zone 1 lungs is assumed to collapse alveolar vessels, making them inaccessible to vascular liquid. To test this assumption, we perfused isolated rat lungs in zone 1 (n = 5) with fluorescent albumin solution (inflation pressure = 25 cmH2O, pulmonary arterial pressure = 10 cmH2O, left atrial pressure = 0 cmH2O; flow = 0.11 +/- 0.06 ml . 100 g body wt-1 . min-1) and rapidly froze them. Histologically, 33 +/- 19% (SD) of alveolar septa fluoresced, demonstrating that the perfusate had not been excluded. However, we could not resolve whether the fluorescence originated in the septal microvascular lumen or in the adjacent perimicrovascular interstitial space. To address this issue, we perfused an additional lung with horseradish peroxidase (HRP) and examined it by transmission electron microscopy. HRP filled interstitial spaces around septal vessels and extraseptal alveolar comer vessels, but because the septal vascular lumina were too compressed, we were unable to determine whether they also contained HRP. Therefore we perfused two additional lungs with particles of colloidal gold (0.05 mum diam). Using transmission electron microscopy, we found gold particles in 15-25% of septal vascular lumina, demonstrating that septal vessels were at least partially accessible in zone 1. Our interpretation is that filtration in zone 1 may occur from septal vessels and extraseptal alveolar vessels. Furthermore, results of the HRP study suggest that the perimicrovascular interstitial space is less compressible than the septal vascular lumen. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT SURG,MADISON,WI 53706. NR 31 TC 11 Z9 11 U1 0 U2 5 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD AUG PY 1993 VL 75 IS 2 BP 704 EP 711 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA LT582 UT WOS:A1993LT58200032 PM 8226472 ER PT J AU BERGMAN, RJ TRUONG, TC HAHN, TJ AF BERGMAN, RJ TRUONG, TC HAHN, TJ TI OSTEOPROGENITOR CELL DEFECTS IN AGE-RELATED OSTEOPOROSIS IN THE MOUSE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VAMC, CTR GERIATR RES EDUC & CLIN, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S364 EP S364 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500990 ER PT J AU BOYCE, BE WINDLE, JJ REDDY, SV WRIGHT, K LEACH, RJ ROODMAN, GD AF BOYCE, BE WINDLE, JJ REDDY, SV WRIGHT, K LEACH, RJ ROODMAN, GD TI TARGETING SV40 T-ANTIGEN TO THE OSTEOCLAST IN TRANSGENIC MICE CAUSES OSTEOPETROSIS, TRANSFORMATION AND APOPTOSIS OF OSTEOCLASTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 CANC THERAPY RES CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S118 EP S118 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500005 ER PT J AU REDDY, SV TAKAHASHI, S CHIRGWIN, JM ROODMAN, GD AF REDDY, SV TAKAHASHI, S CHIRGWIN, JM ROODMAN, GD TI MOLECULAR-CLONING AND INITIAL CHARACTERIZATION OF AN AUTOCRINE STIMULATORY FACTOR (SF) THAT INCREASES HUMAN OSTEOCLAST-LIKE CELL-FORMATION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0884-0431 EI 1523-4681 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S166 EP S166 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500199 ER PT J AU TAKAHASHI, S SINGER, FR ROODMAN, GD AF TAKAHASHI, S SINGER, FR ROODMAN, GD TI PAGETIC MARROW STROMAL CELL-LINES ENHANCE CFU-GM AND OSTEOCLAST-LIKE CELL-FORMATION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. ST JOHNS HOSP, CTR BONE, LOS ANGELES, CA 90404 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0884-0431 EI 1523-4681 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S285 EP S285 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500672 ER PT J AU TAKAHASHI, S GOLDRING, S ROODMAN, GD AF TAKAHASHI, S GOLDRING, S ROODMAN, GD TI DETECTION OF CALCITONIN RECEPTOR (CTR) MESSENGER-RNA AT MULTIPLE STAGES IN THE OSTEOCLAST (OCL) LINEAGE BY THE POLYMERASE CHAIN-REACTION (PCR) SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0884-0431 EI 1523-4681 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S381 EP S381 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20501058 ER PT J AU UY, HL DALLAS, M WRIGHT, K BOYCE, B ROODMAN, GD MUNDY, GR AF UY, HL DALLAS, M WRIGHT, K BOYCE, B ROODMAN, GD MUNDY, GR TI MULTIPOTENT HEMATOPOIETIC OSTEOCLAST PRECURSORS ARE INCREASED BY INTERLEUKIN-1 IN-VIVO 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 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S388 EP S388 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20501083 ER PT J AU SAMUELS, MH VELDHUIS, J CAWLEY, C URBAN, RJ LUTHER, M BAUER, R MUNDY, G AF SAMUELS, MH VELDHUIS, J CAWLEY, C URBAN, RJ LUTHER, M BAUER, R MUNDY, G TI PULSATILE SECRETION OF PARATHYROID-HORMONE IN NORMAL YOUNG SUBJECTS - ASSESSMENT BY DECONVOLUTION ANALYSIS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID LUTEINIZING-HORMONE; GROWTH-HORMONE; IMMUNORADIOMETRIC ASSAY; FREQUENCY-MODULATION; PITUITARY INVITRO; TRABECULAR BONE; DOWN-REGULATION; PLASMA; RELEASE; FRAGMENT AB Preliminary reports suggest that PTH is secrete in a pulastile fashion. However, available studies have not attempted to calculate actual PTH secretion rates in healthy individuals. To accurately characterize PTH secretory dynamics in healthy subjects, we studied seven young women and six young men, all of whom had hip and spine bone densities by dual photon densitometry in the upper tertile for age-matched control subjects. PTH concentrations were measured by immunoradiometric assay in blood sampled every 2 min over 6 h. Ionized calcium levels were obtained during the second and third hours of the study. Plasma PTH profiles were subjected to deconvolution analysis, which resolves measured hormone levels into secretion and clearance components. Cross-correlation analysis was performed to assess direct or inverse correlations between serum PTH and ionized calcium concentrations at various time lags. In these subjects, PTH was secreted in a dual fashion, with significant basal (tonic) secretion and PTH pulses approximately every 20 min. Pulsatile PTH secretion accounted for approximately 25% of the total secreted PTH. There were no differences in PTH secretory parameters between men and women, nor were there any significant correlations between PTH and ionized calcium concentrations. We conclude that in normal subjects, the predominant mode of PTH secretion is tonic, with superimposed PTH pulses of small amplitude but high frequency. The clinical significance of this complex physiological pattern of secretion awaits further study. C1 UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. UNIV TEXAS MED BRANCH, GALVESTON, TX 77555 USA. UNIV VIRGINIA, HLTH SCI CTR, CHARLOTTESVILLE, VA 22908 USA. FU NCRR NIH HHS [M01-RR-01-346]; NICHD NIH HHS [NICHHD LK04-HD-00634] NR 33 TC 22 Z9 23 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD AUG PY 1993 VL 77 IS 2 BP 399 EP 403 DI 10.1210/jc.77.2.399 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR719 UT WOS:A1993LR71900021 PM 8345044 ER PT J AU MANTHEY, CL QURESHI, N STUTZ, PL VOGEL, SN AF MANTHEY, CL QURESHI, N STUTZ, PL VOGEL, SN TI LIPOPOLYSACCHARIDE ANTAGONISTS BLOCK TAXOL-INDUCED SIGNALING IN MURINE MACROPHAGES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TUMOR-NECROSIS-FACTOR; DIPHOSPHORYL-LIPID-A; RHODOPSEUDOMONAS-SPHAEROIDES; BINDING-PROTEIN; EXPRESSION; ENDOTOXIN; LPS; NEUTROPHILS; DERIVATIVES; RECEPTORS AB Taxol is the prototype of a new class of microtubule stabilizing agents with promising anticancer activity. Several studies show that taxol mimics the actions of lipopolysaccharide (LPS) on murine macrophages. To investigate the mechanism of taxol-induced macrophage stimulation, we evaluated the ability of Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA) and SDZ 880.431 to block taxol-induced effects. RsDPLA and SDZ 880.431 are lipid A analogues that lack LPS-like activity, but inhibit the actions of LPS, presumably by blocking critical cellular binding sites. We report that RsDPLA and SDZ 880.431 potently inhibited taxol-induced TNF secretion, gene activation, and protein-tyrosine phosphorylation. The role of microtubules in taxol signaling was investigated. Taxol-induced microtubule bundling in primary and transformed RAW 264.7 macrophages was not blocked by RsDPLA or SDZ 880.431. Taxotere, a semisynthetic taxoid, was more potent than taxol as an inducer of microtubule bundling, but did not induce tumor necrosis factor alpha secretion and gene activation. These data dissociate the microtubule effects of taxol from macrophage stimulation and suggest that taxol stimulates macrophages through an LPS receptor-dependent mechanism. The results underscore the potential of taxol as a tool for studying LPS receptor activation and provide insights into possible therapeutic actions of this new class of drugs. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL,4301 JONES BRIDGE RD,BETHESDA,MD 20814. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,SCH AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. FU NIAID NIH HHS [AI-08451, AI-18797] NR 41 TC 108 Z9 108 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD AUG 1 PY 1993 VL 178 IS 2 BP 695 EP 702 DI 10.1084/jem.178.2.695 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA LP830 UT WOS:A1993LP83000035 PM 8101863 ER PT J AU VELEZ, JD ALLENDOERFER, R LUTHER, M RINALDI, MG GRAYBILL, JR AF VELEZ, JD ALLENDOERFER, R LUTHER, M RINALDI, MG GRAYBILL, JR TI CORRELATION OF IN-VITRO AZOLE SUSCEPTIBILITY WITH IN-VIVO RESPONSE IN A MURINE MODEL OF CRYPTOCOCCAL MENINGITIS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; AMPHOTERICIN-B; CONTROLLED TRIAL; FLUCONAZOLE AB Correlations between in vitro susceptibility and in vivo responses to fluconazole were sought in a mouse model of cryptococcal meningitis. Twenty clinical isolates were used. Two distinct populations were noted. Eight high-virulence isolates had an LD50 of less-than-or-equal-to 252 cfu of Cryptococcus neoformans. Twelve low-virulence isolates had an LD50 of >252 cfu. For 7 low-virulence isolates, the LD50 was >20,000 cfu. C. neoformans also had a broad range of in vitro susceptibilities (MICs of 1.25 to >80 mug/mL) at 24 h. A correlation was found between the MIC and the minimum effective dose of fluconazole in mice. This was observed with both survival and tissue counts as parameters of efficacy. This study documents for the first time the in vivo relevance of in vitro susceptibility to an azole antifungal for C. neoformans. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RP VELEZ, JD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,DIV INFECT DIS,MAIL CODE 111,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 10 TC 55 Z9 55 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD AUG PY 1993 VL 168 IS 2 BP 508 EP 510 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LN813 UT WOS:A1993LN81300043 PM 8335995 ER PT J AU TYAN, ML AF TYAN, ML TI EFFECT OF PROMETHAZINE ON LUMBAR VERTEBRAL BONE MASS IN POSTMENOPAUSAL WOMEN SO JOURNAL OF INTERNAL MEDICINE LA English DT Article DE CALCIUM; ESTROGEN; OSTEOPENIA; PROMETHAZINE; POSTMENOPAUSAL ID AGE-RELATED OSTEOPENIA; OSTEOPOROSIS; CELLS; MOUSE AB Objectives. Work in mice suggests that the age-related loss of bone mineral noted in that species is caused by an intrinsic defect in a haematopoietic cell population which results directly or indirectly in increased bone resorption. This age-related loss of bone mineral is prevented or reversed by well-tolerated doses of promethazine HCL. The present study was undertaken to determine if promethazine would retard or reverse bone loss in postmenopausal women. Design. Postmenopausal women whose spine (L2 to L4) bone mineral content (BMC) was two standard deviations below young normal values were assigned randomly to receive calcium or promethazine and calcium daily. Subjects who had been taking oral oestrogen for more than 4 years also were assigned randomly but independently to the calcium or promethazine groups. Setting. AU subjects were seen in the out-patient clinic of the Department of Medicine, School of Medicine, University of California, Los Angeles. Subjects. Healthy, ambulatory postmenopausal females were recruited by word of mouth and by advertisement from the local community. Fifty-four subjects completed the first 6 months of the study and 43 completed 30 months. Interventions. The subjects were assigned randomly to receive 1 000 mg calcium daily or promethazine 50 mg and calcium 1000 mg daily throughout the period of the study. Main outcome measures. Bone mineral content of the lumbar vertebrae (L2 to L4) was determined by dual photon densitometry every 6 months. Dorsolumbar spine X-rays were obtained yearly and at the completion of the study to detect new compression fractures. Results. In the groups not taking oestrogen, BMC decreased at the rate of 1.53% year-1 in the group given only calcium; in contrast, BMC increased at 3.22% year-1 in the group given promethazine and calcium (P < 0.001). Among the women taking oestrogen, increases in mean BMC were noted in both groups, but those taking promethazine and calcium had a greater rate of increase than observed in the group taking only calcium (5.62% vs. 1.97% per year-1, P < 0.001). Conclusions. These results suggest that promethazine can induce a modest increase in vertebral BMC in postmenopausal women who are not taking oestrogen and greater increases in those who are. C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. RP TYAN, ML (reprint author), W LOS ANGELES VAMC, W111M, WILSHIRE & SAWTELLE BLVD, LOS ANGELES, CA 90073 USA. FU FDA HHS [FD-R-00296] NR 18 TC 13 Z9 13 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0954-6820 J9 J INTERN MED JI J. Intern. Med. PD AUG PY 1993 VL 234 IS 2 BP 143 EP 148 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA LQ918 UT WOS:A1993LQ91800006 PM 8340736 ER PT J AU HUTCHISON, FN AF HUTCHISON, FN TI ENDOTHELIN - A NEW ROLE FOR AN OLD FRIEND SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Editorial Material ID INDUCED DIABETIC RATS; IMMUNOREACTIVITY C1 RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC. RP HUTCHISON, FN (reprint author), MED UNIV S CAROLINA,CHARLESTON,SC 29425, USA. NR 12 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD AUG PY 1993 VL 122 IS 2 BP 126 EP 127 PG 2 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA LR502 UT WOS:A1993LR50200001 PM 8340696 ER PT J AU CHAMBERLAIN, J OFFORD, SJ WOLFE, BB TYAU, LS WANG, HL FRAZER, A AF CHAMBERLAIN, J OFFORD, SJ WOLFE, BB TYAU, LS WANG, HL FRAZER, A TI POTENCY OF 5-HYDROXYTRYPTAMINE(1A) AGONISTS TO INHIBIT ADENYLYL-CYCLASE ACTIVITY IS A FUNCTION OF AFFINITY FOR THE LOW-AFFINITY STATE OF [H-3] 8-HYDROXY-N,N-DIPROPYLAMINOTETRALIN ([H-3]8-OH-DPAT) BINDING SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID RAT HIPPOCAMPAL MEMBRANES; BETA-ADRENERGIC-RECEPTOR; PHARMACOLOGICAL AGONISM; 5-HT1A RECEPTOR; MULTIPLE STATES; FRONTAL-CORTEX; G-PROTEINS; GTP; CELLS; SITES AB In this study, the radiolabeled 5-hydroxytryptamine1A agonist, [H-3]8-hydroxy-N,N-dipropylamino tetralin ([H-3]B-OH-DPAT), was shown to have both a high (K(d), 0.7 +/- 0.2 nM) and a low (K(d), 17 +/- 4 nM) affinity binding component in rat hippocampal homogenate preparations in the absence of guanine nucleotides. The high-affinity binding component was markedly reduced by the elimination of Mg++ from the incubation medium and the addition of both the nonhydrolyzable guanine nucleotide guanylylimidodiphosphate (Gpp(NH)p) (100 muM) and 1.0 mM EDTA to the incubation medium. Under these latter conditions, a single binding affinity component was observed with a K(d) of 11 +/- 1 nM, a value in good agreement with the value for the low-affinity component measured in the absence of Gpp(NH)p. Further, the B(max) value for the single low-affinity binding component measured in the presence of Gpp(NH)p was essentially equivalent to the total of the two B(max) values found in the absence of Gpp(NH)p. A binding assay was developed using 15 nM [H-3]8-OH-DPAT to determine the affinities of serotonergic drugs for the low-affinity component of [H-3]8-OH-DPAT binding and these values were compared with their affinities for the high-affinity binding component as well as their potencies in a hippocampal adenylyl cyclase assay. For agonists, the K(i) value for the high-affinity binding component was always less than the low-affinity K(i) value, whereas the antagonist spiperone had similar values for both the high-affinity and low-affinity binding components. Furthermore, when K(i) values of the agonists for the high-affinity [H-3]8-OH-DPAT binding component were compared to their EC50 values for inhibition of forskolin-stimulated adenylyl cyclase activity, K(i)/EC50 ratios were 1 5-1 00. By contrast, the ratio of the K(i) values for the low-affinity component to the EC50 values were near unity for these drugs. It appears that the potency of agonists to elicit 5-hydroxytryptamine1A-Mediated responses is quantitatively better related to their affinity for the low-affinity state of [H-3]8-OH-DPAT binding than for the high-affinity state. C1 UNIV PENN,SCH MED,DEPT VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20057. FU NIMH NIH HHS [MH 14654, MH 48125] NR 46 TC 27 Z9 27 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD AUG PY 1993 VL 266 IS 2 BP 618 EP 625 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LT482 UT WOS:A1993LT48200020 PM 8355195 ER PT J AU SANDERS, R BISSADA, NK BIELSKY, S AF SANDERS, R BISSADA, NK BIELSKY, S TI URETEROENTERIC ANASTOMOTIC STRICTURES - TREATMENT WITH PALMAZ PERMANENT INDWELLING STENTS SO JOURNAL OF UROLOGY LA English DT Note DE URETER; URETERAL OBSTRUCTION; URINARY DIVERSION; STENTS; ANASTOMOSIS, SURGICAL ID IMPLANTED URETHRAL STENT; MANAGEMENT AB A 70-year-old man with bilateral ureteroenteric anastomotic strictures and recurrent urinary tract sepsis that continued despite bilateral Double-J dagger ureteral stents and nephrostomy tubes was successfully treated with bilateral Palmaz double dagger indwelling permanent stents. C1 MED UNIV S CAROLINA,DIV UROL ONCOL,171 ASHLEY AVE,CHARLESTON,SC 29425. RALPH JOHNSON MED CTR,CHARLESTON,SC. NR 12 TC 19 Z9 20 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 1993 VL 150 IS 2 BP 469 EP 470 PN 1 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA LM765 UT WOS:A1993LM76500060 PM 8326581 ER PT J AU WARPINSKI, JR FOLGERT, J VOSS, M BUSH, RK AF WARPINSKI, JR FOLGERT, J VOSS, M BUSH, RK TI FISH SURFACE MUCIN HYPERSENSITIVITY SO JOURNAL OF WILDERNESS MEDICINE LA English DT Article DE FISH; MUCIN; HYPERSENSITIVITY AB Most reports of allergy to fish describe systemic symptoms upon ingestion of fish muscle or contact urticaria in commercial fish handlers. We report three recreational fishermen with symptoms of asthma, angioedema, rhinitis and urticaria upon exposure to surface mucin from bluegills (Lepomis machrochirus). All three had symptoms upon handling bluegills. Subsequently, two of them experienced wheezing and/or angioedema while in proximity to contaminated fishing clothing. One of them later developed symptoms upon eating bluegills. Prick skin testing was positive to crude bluegill surface mucin in all three individuals and to bluegill and cod muscle in one. Bluegill surface mucin was defatted in ether and acetone and extracted in phosphate buffered saline. Sodium dodecyl-polyacrylamide gel electrophoresis (SDS-PAGE) showed at least 20 distinct protein bands by Coomassie Blue staining. Many of these were glycoproteins by periodic acid schiff (PAS) staining. Immunoblotting showed at least seven IgE binding protein bands with molecular weights between 10 and 100 kDa. Radioallergosorbent (RAST) assay using a bluegill surface-mucin solid phase demonstrated that serum IgE binding in the three individuals was 4-25 times that of pooled serum from nonatopic controls. IgE binding using a serum pool from the three allergic patients was inhibited by extracts of bluegill mucin and muscle and cod muscle but not by tuna, crab or peanut. Our results demonstrate that bluegill surface mucin contains specific glycoproteins which bind IgE in sensitive individuals. Hypersensitivity to these surface proteins may cause systemic allergic symptoms. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0953-9859 J9 J WILDERNESS MED PD AUG PY 1993 VL 4 IS 3 BP 261 EP 269 DI 10.1580/0953-9859-4.3.261 PG 9 WC Medicine, General & Internal; Physiology SC General & Internal Medicine; Physiology GA LQ272 UT WOS:A1993LQ27200005 ER PT J AU LIVINGSTON, EH AF LIVINGSTON, EH TI THE STOMACH AS A SYSTEM AND THE PATHOGENESIS OF EXPERIMENTAL ULCER SO MEDICAL HYPOTHESES LA English DT Article ID GASTRIC-MUCOSAL MICROCIRCULATION; ACID; RAT AB The stomach is prone to ulceration because of the hostile environment that exists within its lumen. The most important etiologic factor remains a topic of debate. We have considered the stomach as a system to lend insight into which pathophysiologic mechanisms might be most important. Systems are described by their content, hierarchy, entropy and interactions. The states of health, disease and death (i.e. ulceration) are represented by progressively increasing levels of entropy. It is argued that many of the purported causes of ulcer disease, such as acid back-diffusion or alcohol related necrosis, represent alterations in the system that affect small groups of cells that are low in the hierarchy and cause the tissue to enter the diseased state. We hypothesize that because blood flow is high within the hierarchy it represents the major homeostatic mechanism. If blood flow responds appropriately the system may return to the healthy state. If it does not the death of the system results in ulceration. Experimental evidence to support these contentions is presented. C1 UNIV CALIF LOS ANGELES, SCH MED, W LOS ANGELES VAMC, RES SERV, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, W LOS ANGELES VAMC, SURG SERV, LOS ANGELES, CA 90073 USA. FU NIADDK NIH HHS [AM 25891] NR 4 TC 1 Z9 1 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD AUG PY 1993 VL 41 IS 2 BP 173 EP 176 DI 10.1016/0306-9877(93)90065-X PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LT972 UT WOS:A1993LT97200014 PM 8231998 ER PT J AU WEINRIEB, RM OBRIEN, CP AF WEINRIEB, RM OBRIEN, CP TI PERSISTENT COGNITIVE DEFICITS ATTRIBUTED TO SUBSTANCE-ABUSE SO NEUROLOGIC CLINICS LA English DT Article ID CHRONIC COCAINE ABUSERS; NEUROPSYCHOLOGICAL IMPAIRMENT; FOLLOW-UP; CANNABIS USE; PERFORMANCE; DRUGS; HYPNOTICS; MARIJUANA; SEQUELAE; MEMORY C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP WEINRIEB, RM (reprint author), UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104, USA. NR 62 TC 9 Z9 9 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD AUG PY 1993 VL 11 IS 3 BP 663 EP 691 PG 29 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA LT632 UT WOS:A1993LT63200013 PM 8377749 ER PT J AU PAVEZA, GJ AF PAVEZA, GJ TI SOCIAL-SERVICES AND THE ALZHEIMERS-DISEASE PATIENT - AN OVERVIEW SO NEUROLOGY LA English DT Article ID DEMENTIA PATIENTS; SENILE DEMENTIA; FAMILY MEMBERS; CAREGIVERS; DEPRESSION; PREDICTORS; CARE; INTERVENTIONS; IMPAIRMENT AB With the number of patients and families affected by Alzheimer's disease increasing, many physicians will find themselves having to refer these patients and family members to social services. Many physicians, however, lack of understanding of the available social services. This article provides a contextual framework for the social service system, discussing social services according to three principal domains: assessment, counseling, and behavioral management. From the information presented, physicians will be able to assess the level of services provided by different social workers and refer patients and families to the social worker most likely to meet their needs. RP PAVEZA, GJ (reprint author), US DEPT VET AFFAIRS,CTR LONG TERM MENTAL HLTH EVALUAT,GREAT LAKES HLTH SERV,ANN ARBOR,MI 48113, USA. NR 48 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD AUG PY 1993 VL 43 IS 8 SU 4 BP S11 EP S15 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA LV411 UT WOS:A1993LV41100003 ER PT J AU LIBERMAN, RP CORRIGAN, PW AF LIBERMAN, RP CORRIGAN, PW TI DESIGNING NEW PSYCHOSOCIAL TREATMENTS FOR SCHIZOPHRENIA SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article ID SOCIAL SKILLS; PSYCHIATRIC-INPATIENTS; DEVELOPMENTAL COURSE; MANAGEMENT; DYSFUNCTIONS; DISORDERS; STRESS; TRIAL; LIFE AB SCHIZOPHRENIA is a disease characterized by cognitive, psychophysiological, and interpersonal deficits that result in a marked vulnerability to stress (Dawson and Nuechterlein 1984; Nuechterlein 1977; Strauss et al. 1987). Episodes of illness occur in vulnerable individuals who experience stressful life events (G. W. Brown and Rutter 1966; Lukoff et al. 1984) or stressful interactions with family members (G. W. Brown et al. 1972; Imber Mintz et al. 1987; Leff and Vaughn 1985). Similarly, overstimulating therapeutic environments have been shown to exacerbate psychosis (Drake and Sederer 1986; Liberman 1982; Linn et al. 1980; Van Putten 1976). A full understanding of disease-specific deficits resulting from stress and vulnerability is necessary for developing psychosocial treatment programs that augment pharmacotherapies in significantly ameliorating the symptoms and disabilities of schizophrenia. RP LIBERMAN, RP (reprint author), UNIV CALIF LOS ANGELES, CAMARILLO CLIN RES CTR SCHIZOPHRENIA & PSYCHIAT RE, W LOS ANGELES VA MED CTR, LOS ANGELES, CA 90073 USA. NR 56 TC 40 Z9 40 U1 2 U2 4 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 USA SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD AUG PY 1993 VL 56 IS 3 BP 238 EP 249 PG 12 WC Psychiatry SC Psychiatry GA LT868 UT WOS:A1993LT86800002 PM 8416005 ER PT J AU KASPER, CE MCNULTY, AL OTTO, AJ THOMAS, DP AF KASPER, CE MCNULTY, AL OTTO, AJ THOMAS, DP TI ALTERATIONS IN SKELETAL-MUSCLE RELATED TO IMPAIRED PHYSICAL MOBILITY - AN EMPIRICAL-MODEL SO RESEARCH IN NURSING & HEALTH LA English DT Article ID HINDLIMB SUSPENSION; CONTRACTILE PROPERTIES; LIMB IMMOBILIZATION; PROTEIN-TURNOVER; SOLEUS MUSCLE; TIME COURSE; RAT; HYPOKINESIA; ATROPHY; RECOVERY AB The objective of this investigation was to study impaired physical mobility and the resulting skeletal muscle atrophy. An animal model was used to study morphological adaptations of the soleus and plantaris muscles to decreased loading induced by hindlimb suspension of an adult rat for 7, 14, and 28 consecutive days. Alterations in weight, skeletal muscle growth, and changes in fiber type composition were studied in synergistic plantar flexors of the rat hindlimb. Body weight and the soleus muscle mass to body mass ratio demonstrated significant progressive atrophy over th 28-day experimental period with the most significant changes occurring in the first 7 days of hindlimb suspension. Hindlimb suspension produced atrophy of Type I and Type IIa muscle fibers as demonstrated by significant decreases in fiber cross-sectional area (mum2). These latter changes account for the loss of contractile force production reported in the rat following hindlimb unloading. When compared to traditional models of hindlimb suspension and immobilization, the ISC model produces a less severe atrophy while maintaining animal mobility and health. We conclude that it is the preferred animal model to address nursing questions of impaired physical mobility. (C) 1993 John Wiley & Sons, Inc. C1 UNIV WISCONSIN,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. UNIV WYOMING,COLL HLTH SCI,HUMAN ENERGY RES LAB,LARAMIE,WY 82071. RP KASPER, CE (reprint author), UNIV CALIF LOS ANGELES,SCH NURSING,10833 LE CONTE AVE,LOS ANGELES,CA 90024, USA. FU DRS NIH HHS [BRSG2507]; NINR NIH HHS [NR05866, NR02204] NR 34 TC 18 Z9 21 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0160-6891 J9 RES NURS HEALTH JI Res. Nurs. Health PD AUG PY 1993 VL 16 IS 4 BP 265 EP 273 DI 10.1002/nur.4770160405 PG 9 WC Nursing SC Nursing GA LM486 UT WOS:A1993LM48600004 PM 8378556 ER PT J AU GRAHAM, DY GO, MF LEW, GM GENTA, RM REHFELD, JF AF GRAHAM, DY GO, MF LEW, GM GENTA, RM REHFELD, JF TI HELICOBACTER-PYLORI INFECTION AND EXAGGERATED GASTRIN-RELEASE - EFFECTS OF INFLAMMATION AND PROGASTRIN PROCESSING SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY LA English DT Article DE AMMONIUM; BIOPSY; CLINICAL TRIAL; GASTRIN PROCESSING; GASTRIN, REGULATION; HELICOBACTER-PYLORI; PROGASTRIN; TRIPLE THERAPY; UREA ID DUODENAL-ULCER PATIENTS; PLASMA GASTRIN; HYPERGASTRINEMIA; ERADICATION; CHILDREN; INFUSION AB Helicobacter pylori infection is associated with exaggerated gastrin release. We investigated whether this abnormality was due to the bacteria or the immune response. Fasting and meal-stimulated 'total' and amidated gastrin were measured in 10 H. pylori-infected volunteers before eradication therapy, after 2 and 14 days of therapy, and 4 weeks after completion of therapy. The exaggerated meal-stimulated gastrin concentration remained unchanged after 2 days of therapy, although the polymorphonuclear cell infiltrate and H. pylori bacteria were no longer evident. The expected fall in gastrin concentration after 14 days of therapy was associated with a reduction in the density of mucosal mononuclear cells, suggesting exaggerated gastrin release was related to chronic inflammation or to H. pylori or its products. The effect of H. pylori on normal progastrin processing was also assessed; 2 control groups were included: 10 H. pylori-uninfected volunteers and 13 patients with H. pylori peptic ulcers. There was a significant difference in the proportion of circulating gastrins that were biologically active amidated gastrins between ulcer patients and uninfected controls (56,7 +/- 4% versus 33.8 +/- 4%, p < 0.001). The proportion of amidated to total gastrins did not increase after successful eradication. C1 UNIV COPENHAGEN,RIGSHOSP,DEPT CLIN BIOCHEM,DK-2100 COPENHAGEN,DENMARK. BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MED,DIV MOLEC VIROL,HOUSTON,TX 77030. RP GRAHAM, DY (reprint author), VET AFFAIRS MED CTR 111D,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NIDDK NIH HHS [DK 39919] NR 27 TC 62 Z9 63 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5521 J9 SCAND J GASTROENTERO JI Scand. J. Gastroenterol. PD AUG PY 1993 VL 28 IS 8 BP 690 EP 694 DI 10.3109/00365529309098274 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LT598 UT WOS:A1993LT59800008 PM 8210984 ER PT J AU STERN, RG KAHN, RS HARVEY, PD AMIN, F APTER, SH HIRSCHOWITZ, J AF STERN, RG KAHN, RS HARVEY, PD AMIN, F APTER, SH HIRSCHOWITZ, J TI EARLY RESPONSE TO HALOPERIDOL TREATMENT IN CHRONIC-SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Article DE HALOPERIDOL; EARLY TREATMENT RESPONSE; RESPONSE PREDICTION; (SCHIZOPHRENIA) ID PLASMA HOMOVANILLIC-ACID; NEUROLEPTIC TREATMENT; PREDICTION; SYMPTOMS; INPATIENTS; REGIMENS; MODEL AB This study examined the time-course of treatment response to haloperidol in chronic schizophrenia. Furthermore the predictive value of baseline psychopathology and early therapeutic changes for the identification of the eventual treatment outcome was examined. After a two-week drug-free period forty-three chronic schizophrenic patients were treated with haloperidol for five weeks. Psychopathology was assessed on the last drug-free day and on the third and eighth day from the initiation of treatment, and then at weekly intervals. At the end of the study based on a priori criteria patients were classified as responders or non-responders to haloperidol. Seventeen patients met criteria for treatment response at the end of five weeks of treatment, while 26 did not. Already by the third day of treatment, in the responders there was a significant decrease in total BPRS and in the subscales scores for psychosis, tension and anergia, but not for hostility-suspiciousness and depression. These decreases represented approximately half of the eventual improvement obtained by the end of the study. Discriminant function analysis showed that severity of symptoms at baseline and improvement by day 3 correctly classified overall outcome in 72% of the cases. RP STERN, RG (reprint author), BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,1 GUSTAVE LEVY PL,NEW YORK,NY 10029, USA. FU NIMH NIH HHS [NIMH RO1 37922-07] NR 31 TC 27 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD AUG PY 1993 VL 10 IS 2 BP 165 EP 171 DI 10.1016/0920-9964(93)90052-K PG 7 WC Psychiatry SC Psychiatry GA LU408 UT WOS:A1993LU40800010 PM 8398949 ER PT J AU REYES, H SIMON, FR AF REYES, H SIMON, FR TI INTRAHEPATIC CHOLESTASIS OF PREGNANCY - AN ESTROGEN-RELATED DISEASE SO SEMINARS IN LIVER DISEASE LA English DT Review ID ADENOSYL-L-METHIONINE; INTRA-HEPATIC CHOLESTASIS; PLASMA-MEMBRANE FLUIDITY; ESTRADIOL-INDUCED CHOLESTASIS; ORGANIC ANION TRANSPORT; ATP-DEPENDENT TRANSPORT; BILE SECRETORY FAILURE; D-RING GLUCURONIDES; MUTANT TR RATS; ETHINYL ESTRADIOL C1 UNIV COLORADO,SCH MED,HEPATOBILIARY RES CTR,CAMPUS BOX B-145,4200 E 9TH AVE,DENVER,CO 80262. UNIV CHILE,HOSP SALVADOR,SCH MED,DEPT MED,SANTIAGO,CHILE. DENVER VET AFFAIRS MED CTR,DENVER,CO. UNIV COLORADO,SCH MED,DEPT MED,DENVER,CO 80262. UNIV CHILE,HOSP SALVADOR,SCH MED,DEPT EXPTL MED,SANTIAGO,CHILE. FU NIDDK NIH HHS [P30-DK-34914, DK-15851] NR 138 TC 108 Z9 118 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 1993 VL 13 IS 3 BP 289 EP 301 DI 10.1055/s-2007-1007357 PG 13 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LZ816 UT WOS:A1993LZ81600007 PM 8235718 ER PT J AU GREGERMAN, RI AF GREGERMAN, RI TI SOLITARY THYROID-NODULES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP GREGERMAN, RI (reprint author), AUDIE L MURPHY MEM VET AFFAIRS HOSP,SAN ANTONIO,TX 78284, 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 JUL 29 PY 1993 VL 329 IS 5 BP 360 EP 360 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LN621 UT WOS:A1993LN62100019 PM 8321268 ER PT J AU WINOGRAD, CH GERETY, MB AF WINOGRAD, CH GERETY, MB TI GERIATRIC-MEDICINE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID HIP FRACTURE; FALLS; RISK C1 VET AFFAIRS MED CTR,PALO ALTO,CA. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP WINOGRAD, CH (reprint author), STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305, USA. NR 16 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 14 PY 1993 VL 270 IS 2 BP 213 EP 216 DI 10.1001/jama.270.2.213 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA LL368 UT WOS:A1993LL36800022 PM 8315736 ER PT J AU GALE, GR SMITH, AB JONES, MM SINGH, PK AF GALE, GR SMITH, AB JONES, MM SINGH, PK TI MESO-2,3-DIMERCAPTOSUCCINIC ACID MONOALKYL ESTERS - EFFECTS ON MERCURY LEVELS IN MICE SO TOXICOLOGY LA English DT Article DE MERCURY; MESO-2,3-DIMERCAPTOSUCCINIC ACID (DMSA); DMSA MONOESTERS; 2,3-DIMERCAPTOPROPANE-1-SULFONATE (DMPS); MICE; KIDNEY ID MESO-DIMERCAPTOSUCCINIC ACID; INTRACELLULAR CADMIUM; MOBILIZATION; 2,3-DIMERCAPTOPROPANOL; EXCRETION; INVIVO; AGENTS; LEAD AB Seven monoesters of meso-2,3-dimercaptosuccinic acid (DMSA) were evaluated for relative activities in mobilizing and promoting excretion of mercury in mercury-laden mice. Compounds assessed were the ethyl (M-EDMS), n-propyl (Mn-PDMS), isopropyl (Mi-PDMS), n-butyl (Mn-BDMS), isobutyl (Mi-BDMS), n-amyl (Mn-ADMS), and isoamyl (Mi-ADMS) esters. 2,3-Dimercaptopropane-1-sulfonate (DMPS) and DMSA were used as positive controls. After the first oral dose of each compound at 0.5 mmol/kg, DMSA and DMPS reduced the corporal mercury burden 16% and 24%, respectively, compared to controls, while the monoesters effected reductions of 35% (M-EDMS) to 49% (Mi-ADMS). After the second treatment at the same dose, the respective reductions produced by DMSA and DMPS were 24% and 38%, and those conferred by the monoesters ranged from 52% (M-EDMS) to 61% (Mn-BDMS). Determination of the comparative dose-response relationships of DMSA and Mi-ADMS on corporal and renal mercury concentrations revealed the monoester to be more active than DMSA on both parameters at each dose used. The cumulative amount of mercury excreted in urine by control mice over a 3-day period was 7.08 mug; this was increased 22%, 85%, and 94% by daily i.p. injections of DMSA, DMPS, and Mi-ADMS, respectively, at a daily dose of 0. 1 mmol/kg. The respective cumulative 3-day totals recovered in feces from control mice and from mice treated with DMSA, DMPS, and Mi-ADMS were 9.76, 8.2 1, 10.44, and 11.73 mug. Parallel daily measurements of retained whole body radioactivity from Hg-203 in mice were in good agreement with the values calculated from the excretion data. C1 MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29401. VANDERBILT UNIV,DEPT CHEM,NASHVILLE,TN 37235. VANDERBILT UNIV,CTR MOLEC TOXICOL,NASHVILLE,TN 37235. RP GALE, GR (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,RES SERV,109 BEE ST,CHARLESTON,SC 29401, USA. FU NIEHS NIH HHS [ES-0267, ES-02638] NR 16 TC 39 Z9 40 U1 1 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0300-483X J9 TOXICOLOGY JI Toxicology PD JUL 11 PY 1993 VL 81 IS 1 BP 49 EP 56 DI 10.1016/0300-483X(93)90155-L PG 8 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA LV764 UT WOS:A1993LV76400004 PM 8396277 ER PT J AU DATTA, AK TAKAYAMA, K AF DATTA, AK TAKAYAMA, K TI ISOLATION AND PURIFICATION OF TREHALOSE 6-MONO-CORYNOMYCOLATES AND 6,6'-DI-CORYNOMYCOLATES FROM CORYNEBACTERIUM-MATRUCHOTII - STRUCTURAL CHARACTERIZATION BY H-1-NMR SO CARBOHYDRATE RESEARCH LA English DT Note ID BACTERIONEMA-MATRUCHOTII C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,COLL PSYCHOL,DEPT BACTERIOL,MADISON,WI 53706. FU NCRR NIH HHS [RR02031, RR02301]; NIGMS NIH HHS [GM-36054] NR 19 TC 10 Z9 10 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD JUL 5 PY 1993 VL 245 IS 1 BP 151 EP 158 DI 10.1016/0008-6215(93)80068-P PG 8 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA LL889 UT WOS:A1993LL88900014 PM 8358747 ER PT J AU GARRICK, T GRIJALVA, CV TRAUNER, M AF GARRICK, T GRIJALVA, CV TRAUNER, M TI LATERAL HYPOTHALAMIC-LESIONS CAUSE GASTRIC INJURY BY STIMULATING GASTRIC CONTRACTILITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GASTRIC MOTILITY; PEPTIC ULCERS; GASTRIC MUCOSAL DAMAGE ID EFFERENT CONNECTIONS; SOLITARY TRACT; BRAIN-STEM; RATS; PROJECTIONS; NUCLEUS; AREA; APHAGIA; SECRETION; PATHOLOGY AB Changes in gastric contractility following lateral hypothalamic (LH) lesions with and without bilateral cervical vagotomy were measured in urethan-anesthetized rats. LH lesions were induced with direct current passed through stereotaxically placed electrodes. Gastric contractility was recorded continuously for 4 h with acutely implanted strain gauge force transducers and analyzed by computer. LH lesions consistently stimulated gastric contractility and caused more gastric mucosal injury than control conditions. Vagotomy blocked both gastric mucosal injury and high-amplitude gastric contractions. In rats with LH lesions and exogenously infused intragastric hydrochloric acid, atropine methyl nitrate inhibited high-amplitude gastric contractions and gastric erosions. These findings indicate that LH lesions stimulate vagally mediated high-amplitude gastric contractions, which, in the presence of hydrochloric acid, cause gastric mucosal erosions. C1 W LOS ANGELES VET AFFAIRS MED CTR,CTR ULCER RES & EDUC,DEPT RES,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90024. RP GARRICK, T (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,CTR ULCER RES & EDUC,DEPT PSYCHIAT,PSYCHIAT SERV W116A,LOS ANGELES,CA 90073, USA. NR 39 TC 7 Z9 9 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUL PY 1993 VL 265 IS 1 BP G138 EP G142 PN 1 PG 5 WC Physiology SC Physiology GA LP431 UT WOS:A1993LP43100082 PM 8338162 ER PT J AU FILLEY, CM CULLUM, CM AF FILLEY, CM CULLUM, CM TI EARLY DETECTION OF FRONTOTEMPORAL DEGENERATION BY CLINICAL-EVALUATION SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Article ID PICKS DISEASE AB Although Alzheimer's Disease (AD) is the most common degenerative dementia, other neuropathological processes are well known to cause dementia syndromes. Fronto-temporal degeneration (FTD) is one such entity, and often produces a clinical presentation distinct from that of AD. Some FTD cases are shown at autopsy to be classic Pick's Disease, but others defy precise classification at this point because they lack characteristic Pick bodies. We describe a case of putative FTD in a 54-year-old man with personality change and complete Kluver-Bucy syndrome. Neuropsychological evaluation disclosed evidence of extensive frontal system dysfunction, with lesser problems in memory, language, and visuospatial skills. Magnetic resonance imaging studies after 17 months of the illness were largely nonspecific, but a follow-up scan 16 months later revealed bifrontal and bitemporal atrophy with ventricular enlargement. Neuromorphometric analysis suggested an increase in cortical atrophy and ventricular dilation over time. This case emphasizes the value of careful clinical evaluation in unusual non-AD degenerative demential and suggests that neuroimaging studies may be less sensitive in the early diagnosis of such cases. C1 DENVER VET AFFAIRS MED CTR,DENVER,CO. UNIV COLORADO,SCH MED,DEPT PSYCHIAT,DENVER,CO 80262. RP FILLEY, CM (reprint author), UNIV COLORADO,SCH MED,DEPT NEUROL,B-183,4200 E 9TH AVE,DENVER,CO 80262, USA. NR 20 TC 6 Z9 6 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6177 J9 ARCH CLIN NEUROPSYCH JI Arch. Clin. Neuropsychol. PD JUL-AUG PY 1993 VL 8 IS 4 BP 359 EP 367 DI 10.1016/0887-6177(93)90025-V PG 9 WC Psychology, Clinical; Psychology SC Psychology GA LM108 UT WOS:A1993LM10800005 PM 14589665 ER PT J AU YEHUDA, R BOISONEAU, D MASON, JW GILLER, EL AF YEHUDA, R BOISONEAU, D MASON, JW GILLER, EL TI GLUCOCORTICOID RECEPTOR NUMBER AND CORTISOL EXCRETION IN MOOD, ANXIETY, AND PSYCHOTIC DISORDERS SO BIOLOGICAL PSYCHIATRY LA English DT Article DE GLUCOCORTICOID RECEPTORS; LYMPHOCYTES; CORTISOL; DEPRESSION; BIPOLAR MANIA; PANIC DISORDER; POSTTRAUMATIC STRESS DISORDER; SCHIZOPHRENIA ID DEXAMETHASONE SUPPRESSION TEST; POSTTRAUMATIC-STRESS-DISORDER; ADRENAL-STEROID RECEPTORS; PANIC DISORDER; DEPRESSION; BINDING; TISSUES; SYSTEM AB In the present study, we measured cytosolic lymphocyte glucocorticoid receptor and 24-hour urinary cortisol excretion in patients with major depressive disorder, bipolar mania, posttraumatic stress disorder, panic disorder, and schizophrenia. Patients with major depression had the smallest, and posttraumatic stress disordered patients the largest, mean number of glucocorticoid receptors per cell compared to patients in the other groups. Bipolar manic and panic patients did not differ from each other in regard to the number of lymphocyte glucocorticoid receptors. Bipolar manic and panic patients did have significantly more glucocorticoid receptors/cell than schizophrenic patients. The mean 24-hour urinary cortisol excretion was significantly higher in patients with major depression and bipolar mania than in those in the other diagnostic groups. Lymphocyte glucocorticoid receptor number and cortisol excretion tended to be inversely related, when the entire sample was considered as a whole, but this effect did not reach statistical significance. It is concluded that lymphocyte glucocorticoid receptors may be modulated by multiple influences, not just ambient cortisol levels. These preliminary data suggest that the assessment of lymphocyte glucocorticoid receptor number in tandem with cortisol levels may provide a more meaningful estimate of hypothalamic-pituitary-adrenal axis activity than is achieved using cortisol alone. C1 W HAVEN VET ADM,PSYCHIAT SERV,W HAVEN,CT. UNIV CONNECTICUT,CTR HLTH,DEPT PSYCHIAT,FARMINGTON,CT 06032. YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06510. RP YEHUDA, R (reprint author), MT SINAI SCH MED,BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,PSYCHIATRY 116-A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIMH NIH HHS [MH 49555-01, MH 49536-01, MH41125-01A2] NR 36 TC 170 Z9 173 U1 1 U2 5 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 JUL 1 PY 1993 VL 34 IS 1-2 BP 18 EP 25 DI 10.1016/0006-3223(93)90252-9 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LQ802 UT WOS:A1993LQ80200005 PM 8373936 ER PT J AU VONANDRIAN, UH CHAMBERS, JD BERG, EL MICHIE, SA BROWN, DA KAROLAK, D RAMEZANI, L BERGER, EM ARFORS, KE BUTCHER, EC AF VONANDRIAN, UH CHAMBERS, JD BERG, EL MICHIE, SA BROWN, DA KAROLAK, D RAMEZANI, L BERGER, EM ARFORS, KE BUTCHER, EC TI L-SELECTIN MEDIATES NEUTROPHIL ROLLING IN INFLAMED VENULES THROUGH SIALYL LEWIS(X)-DEPENDENT AND LEWIS(X)-INDEPENDENT RECOGNITION PATHWAYS SO BLOOD LA English DT Article ID NODE HOMING RECEPTOR; VASCULAR ENDOTHELIAL-CELLS; CHEMOTACTIC FACTORS; ADHESION MOLECULE; CD18-INDEPENDENT ADHESION; MESENTERIC VENULES; LEUKOCYTE ADHESION; MEL-14 ANTIGEN; LYMPH-NODES; LECAM-1 C1 LA JOLLA INST EXPTL MED,LA JOLLA,CA. LIPOSOME CO,PRINCETON,NJ. US DEPT VET AFFAIRS,CTR MOLEC BIOL MED,PALO ALTO,CA. RP VONANDRIAN, UH (reprint author), STANFORD UNIV,MED CTR L235,DEPT PATHOL,IMMUNOL & VASC BIOL LAB,STANFORD,CA 94305, USA. RI von Andrian, Ulrich/A-5775-2008; Berg, Ellen/D-9076-2014 OI Berg, Ellen/0000-0001-5149-6665 FU NIAID NIH HHS [AI19957]; NIGMS NIH HHS [GM41965, GM37734] NR 56 TC 132 Z9 132 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 JUL 1 PY 1993 VL 82 IS 1 BP 182 EP 191 PG 10 WC Hematology SC Hematology GA LL366 UT WOS:A1993LL36600025 PM 7686786 ER PT J AU SUN, Y OBERLEY, LW OBERLEY, TD ELWELL, JH SIERRARIVERA, E AF SUN, Y OBERLEY, LW OBERLEY, TD ELWELL, JH SIERRARIVERA, E TI LOWERED ANTIOXIDANT ENZYMES IN SPONTANEOUSLY TRANSFORMED EMBRYONIC MOUSE-LIVER CELLS IN CULTURE SO CARCINOGENESIS LA English DT Article ID CHINESE-HAMSTER CELLS; SPONTANEOUS NEOPLASTIC EVOLUTION; MULTISTEP PROGRESSION; CATALASE; LINES AB Normal embryonal mouse liver cells in culture were shown to undergo spontaneous transformation during prolonged subculture. The spontaneously transformed cells lost their anchorage dependence, as measured by a soft agar assay, and gave rise to tumors in nude mice. Accompanying this transformation, the antioxidant enzymes, copper- and zinc-containing superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), catalase (CAT) and glutathione reductase, decreased significantly in activity; the decline in enzymatic activity of CuZnSOD, MnSOD and CAT was due to a decline in the levels of immunoreactive protein. These spontaneously transformed high passage in vitro liver cells appeared similar in morphology, antioxidant enzyme activity and tumorigenicity to their counterparts transformed by N-methyl-N-nitro-N-nitrosoguanidine and Simian virus 40. These data provide experimental evidence that changes in antioxidant enzymes are associated with spontaneous in vitro cellular transformation of mouse embryonal liver cells. C1 UNIV IOWA,MED LABS 14,RADIAT RES LAB,IOWA CITY,IA 52242. WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,MADISON,WI 53705. FU NCI NIH HHS [R01-CA41267, T32-CA-09125] NR 33 TC 47 Z9 47 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JUL PY 1993 VL 14 IS 7 BP 1457 EP 1463 DI 10.1093/carcin/14.7.1457 PG 7 WC Oncology SC Oncology GA LM978 UT WOS:A1993LM97800033 PM 8330364 ER PT J AU KAWAMURA, J TERAYAMA, Y TAKASHIMA, S OBARA, K PAVOL, MA MEYER, JS MORTEL, KF WEATHERS, S AF KAWAMURA, J TERAYAMA, Y TAKASHIMA, S OBARA, K PAVOL, MA MEYER, JS MORTEL, KF WEATHERS, S TI LEUKOARAIOSIS AND CEREBRAL PERFUSION IN NORMAL AGING SO EXPERIMENTAL AGING RESEARCH LA English DT Article ID WHITE MATTER LUCENCIES; ENCEPHALOPATHY BINSWANGERS DISEASE; CEREBROVASCULAR RISK-FACTORS; MAGNETIC-RESONANCE; COMPUTED-TOMOGRAPHY; VASCULAR DEMENTIA; BRAIN LUCENCIES; BLOOD-FLOW; LEUKOENCEPHALOPATHY; ATROPHY AB To clarify the incidence, age relationships and pathogenesis of white matter lesions of unknown origin (leuko-araiosis) detected by neuroimaging among normal elderly volunteers, we measured the severity of leuko-araiosis using computerized tomographic (CT) densitometry among 42 healthy self-supporting men and women of different ages, all with normal neurological and cognitive test performance. Results were correlated with local cerebral perfusion using xenon-contrasted CT. The 42 volunteers, who are followed in this laboratory for studies of normal aging, were divided into two groups in order to determine aging effects by an extremes design. One group consisted of 19 adults below age 60 (M = 53.3, SD 6.0). The index group comprised 23 individuals all over the age of 60 (M = 71.6, SD = 8.7). Leuko-araiosis around the anterior horns of the lateral ventricles (frontal leuko-araiosis) was more severe (p < .01) among the older group, however, occipital leuko-araiosis did not significantly differ between older and younger groups. Cerebral perfusion in frontal, temporal, and parietal cortex was decreased among older compared with younger volunteers (ps < .001, .01, and .05, respectively). Multiple regression analyses disclosed significant and direct relationships between severity of frontal leuko-araiosis and (a) frontal cortical atrophy and (b) reductions of cerebral perfusion within frontal white matter and caudate nucleus. We conclude that cortical atrophy with hypoperfusion and ischemia of frontal white matter play a part in the pathogenesis of frontal leuko-araiosis associated with normal aging and this may be a predictor for later cognitive declines. C1 DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,2002 HOLCOMBE BLVD,ROOM 225,BLDG 110,HOUSTON,TX 77030. BAYLOR COLL MED,HOUSTON,TX 77030. NR 31 TC 29 Z9 30 U1 0 U2 0 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0361-073X J9 EXP AGING RES JI Exp. Aging Res. PD JUL-SEP PY 1993 VL 19 IS 3 BP 225 EP 240 DI 10.1080/03610739308253935 PG 16 WC Geriatrics & Gerontology; Psychology SC Geriatrics & Gerontology; Psychology GA LX513 UT WOS:A1993LX51300004 PM 8223824 ER PT J AU KATZ, MS DAX, EM GREGERMAN, RI AF KATZ, MS DAX, EM GREGERMAN, RI TI BETA-ADRENERGIC REGULATION OF RAT-LIVER GLYCOGENOLYSIS DURING AGING SO EXPERIMENTAL GERONTOLOGY LA English DT Article DE ADENYLATE CYCLASE; BETA-ADRENERGIC RECEPTOR; G-PROTEIN; HEPATOCYTE; CATECHOLAMINES ID ADENYLATE-CYCLASE ACTIVITY; AGE-RELATED-CHANGES; C-MYC TRANSCRIPT; CYCLIC-AMP; HEPATIC GLYCOGENOLYSIS; BETA-2-ADRENERGIC RECEPTORS; GLUCOSE-PRODUCTION; HORMONE ACTION; CELLS; PHOSPHORYLASE AB Studies from a number of laboratories demonstrate a biphasic change in beta adrenergic regulation of hepatic glycogenolysis over the life span of the male rat. The beta adrenergic response is prominent in immature animals, declines rapidly during subsequent development to a minimum by the time of young adulthood, and then reemerges during postmaturational development. Age changes in beta adrenergic-responsive adenylate cyclase activity follow a ''U''-shaped curve similar to that described by changes in liver glycogenolytic responsiveness during aging. Developmental and postmaturational changes in beta adrenergic-sensitive adenylate cyclase activation are related to parallel alterations in the density of beta adrenergic receptors and also to functional changes in nonreceptor components of the enzyme. The prevailing view that catecholamines stimulate hepatic glycogenolysis by an alpha adrenergic receptor-mediated, cyclic AMP-independent mechanism is based almost entirely on evidence from young adult male rats. We propose that current concepts of alpha adrenergic-responsive liver glycogenolysis underestimate a physiological role for beta adrenergic responsiveness over the majority of the life span. C1 FAIRFIELD HOSP,NATL HIV REF LAB,FAIRFIELD,VIC 3078,AUSTRALIA. JOHNS HOPKINS UNIV,FRANCIS SCOTT KEY MED CTR,SCH MED,DEPT MED,BALTIMORE,MD 21224. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP KATZ, MS (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 49 TC 26 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD JUL-OCT PY 1993 VL 28 IS 4-5 BP 329 EP 340 DI 10.1016/0531-5565(93)90060-Q PG 12 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LQ417 UT WOS:A1993LQ41700005 PM 8224032 ER PT J AU LORENZSONN, V LLOYD, M OLSEN, WA AF LORENZSONN, V LLOYD, M OLSEN, WA TI IMMUNOCYTOCHEMICAL HETEROGENEITY OF LACTASE-PHLORHIZIN HYDROLASE IN ADULT LACTASE DEFICIENCY SO GASTROENTEROLOGY LA English DT Article ID IMMUNOELECTRON MICROSCOPY; SUCRASE-ISOMALTASE; SMALL-INTESTINE; EXPRESSION; HYPOLACTASIA; LOCALIZATION; ENTEROCYTES; RECEPTOR; ENZYMES; RATS C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR, GASTROENTEROL RES LAB, 2500 OVERLOOK TERRACE, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT MED, MADISON, WI 53706 USA. FU NIDDK NIH HHS [K08-DK01789, DK-13927] NR 20 TC 10 Z9 10 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 JUL PY 1993 VL 105 IS 1 BP 51 EP 59 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LJ984 UT WOS:A1993LJ98400007 PM 8514062 ER PT J AU GRAHAM, DY GO, MF AF GRAHAM, DY GO, MF TI HELICOBACTER-PYLORI - CURRENT STATUS SO GASTROENTEROLOGY LA English DT Article ID PEPTIC-ULCERATION C1 VET ADM MED CTR 111D,DIV MOLEC VIROL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. RP GRAHAM, DY (reprint author), VET ADM MED CTR 111D,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NIDDK NIH HHS [DK 39919] NR 24 TC 196 Z9 202 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JUL PY 1993 VL 105 IS 1 BP 279 EP 282 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LJ984 UT WOS:A1993LJ98400036 PM 8514046 ER PT J AU HUDNALL, SD BERENSON, JR AF HUDNALL, SD BERENSON, JR TI CLONAL HEAVY-CHAIN ISOTYPE SWITCHING WITHIN THE PROLIFERATION CENTERS OF A SMALL LYMPHOCYTIC LYMPHOMA - IMPLICATIONS REGARDING THE ORIGIN OF PROLIFERATION CENTERS SO HUMAN PATHOLOGY LA English DT Article DE LYMPHOMA; PROLIFERATION CENTERS; IMMUNOGLOBULIN GENE REARRANGEMENT; CHRONIC LYMPHOCYTIC LEUKEMIA; ISOTYPE SWITCHING ID DIFFUSE HISTIOCYTIC LYMPHOMA; IMMUNOGLOBULIN GENE REARRANGEMENTS; EPSTEIN-BARR VIRUS; B-CELL CLONES; RICHTERS SYNDROME; MULTIPLE-MYELOMA; MALIGNANT-LYMPHOMA; PERIPHERAL-BLOOD; LIGHT-CHAINS; LEUKEMIA C1 UNIV CALIF LOS ANGELES, SCH MED, JONSSON CANC CTR, DEPT PATHOL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR,SCH MED, WADSWORTH CANC CTR,DEPT MED, LOS ANGELES, CA USA. NR 55 TC 4 Z9 4 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 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JUL PY 1993 VL 24 IS 7 BP 796 EP 801 DI 10.1016/0046-8177(93)90018-C PG 6 WC Pathology SC Pathology GA LL763 UT WOS:A1993LL76300018 PM 8319958 ER PT J AU GONZALEZ, A OBERLEY, TD SCHULTZ, JL OSTROM, J LI, JJ AF GONZALEZ, A OBERLEY, TD SCHULTZ, JL OSTROM, J LI, JJ TI IN-VITRO CHARACTERIZATION OF ESTROGEN-INDUCED SYRIAN-HAMSTER RENAL TUMORS - COMPARISON WITH AN IMMORTALIZED CELL-LINE DERIVED FROM DIETHYLSTILBESTROL-TREATED ADULT HAMSTER-KIDNEY SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL LA English DT Article DE CELL CULTURE; HAMSTER; RENAL TUMOR ID PROXIMAL TUBULAR CELLS; MULTICELLULAR SPHEROIDS; COVALENT BINDING; GOLDEN-HAMSTER; DEFINED MEDIA; RECEPTOR; GROWTH; DIFFERENTIATION; PROLIFERATION; CARCINOMA AB Primary diethylstilbestrol-induced kidney tumors from Syrian hamsters were grown in vitro and maintained in culture for 6 mo. Combined immunohistochemical studies using antibodies to intermediate filaments and ultrastructural studies of tumor cells in culture exhibited characteristics similar to tumor cells in vivo. Furthermore, the cells manifested transformed properties in culture; they grew both as multilayered colonies attached to the tissue culture substrate and as floating multicellular colonies (spheroids). When cultured cells were injected into diethylstilbestrol-treated recipient hamsters, tumors developed at the injection sites. In contrast, renal tubules or whole kidney cortex from control hamsters cultured in the same medium underwent only short-term growth, with senescence developing after approximately 1 mo. However, cell cultures of kidney cortex from animals treated in vivo for 5 mo. with diethylstilbestrol formed a cell line. This diethylstilbestrol-induced cell line has been maintained in culture for 1.5 yr and has the following characteristics: a) it is anchorage-dependent, b) it is negative in in vivo tumorigenicity tests, and c) cultured cells are histochemically and ultrastructurally similar to cultured tumor cells. This culture system should prove to be of use in studying hormonal carcinogenesis in vitro. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SECT,OVERLOOK TERRACE,MADISON,WI 53705. UNIV UTAH,SCH MED,DEPT PATHOL,SALT LAKE CITY,UT 84148. WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SECT,MADISON,WI 53705. WASHINGTON STATE UNIV,COLL PHARM,DEPT PHARMACEUT SCI,HORMONAL CARCINOGENESIS LAB,PULLMAN,WA 99164. VET AFFAIRS MED CTR,LAB SERV,SALT LAKE CITY,UT 84148. FU NCI NIH HHS [CA-22008] NR 34 TC 7 Z9 7 U1 0 U2 0 PU SOC IN VITRO BIOLOGY PI UPPER MARLBORO PA 9315 LARGO DR W #255, UPPER MARLBORO, MD 20774-4755 SN 1071-2690 J9 IN VITRO CELL DEV-AN JI In Vitro Cell. Dev. Biol.-Anim. PD JUL PY 1993 VL 29A IS 7 BP 562 EP 573 PG 12 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA LR944 UT WOS:A1993LR94400009 PM 7689078 ER PT J AU RINALDI, MG AF RINALDI, MG TI IN-VITRO SUSCEPTIBILITY OF DERMATOPHYTES TO ANTIFUNGAL DRUGS SO INTERNATIONAL JOURNAL OF DERMATOLOGY LA English DT Note C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT VET AFFAIRS MYCOL REFERENCE LAB,SAN ANTONIO,TX. RP RINALDI, MG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0011-9059 J9 INT J DERMATOL JI Int. J. Dermatol. PD JUL PY 1993 VL 32 IS 7 BP 502 EP 503 DI 10.1111/j.1365-4362.1993.tb02833.x PG 2 WC Dermatology SC Dermatology GA LK425 UT WOS:A1993LK42500005 PM 8340184 ER PT J AU SHARKEYMATHIS, PK VELEZ, J FETCHICK, R GRAYBILL, JR AF SHARKEYMATHIS, PK VELEZ, J FETCHICK, R GRAYBILL, JR TI HISTOPLASMOSIS IN THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME (AIDS) - TREATMENT WITH ITRACONAZOLE AND FLUCONAZOLE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HISTOPLASMOSIS; AZOLES; ITRACONAZOLE; FLUCONAZOLE; AMPHOTERICIN-B ID IMMUNE-DEFICIENCY-SYNDROME; PROGRESSIVE DISSEMINATED HISTOPLASMOSIS; OPPORTUNISTIC INFECTIONS; ADRENAL INSUFFICIENCY; KETOCONAZOLE THERAPY; SYSTEMIC MYCOSES; AMPHOTERICIN-B; PARACOCCIDIOIDOMYCOSIS; COMPLICATION; DIAGNOSIS AB The manifestations of histoplasmosis in 20 patients with the acquired immunodeficiency syndrome are presented. In this series, patients were treated with either itraconazole or fluconazole. Twelve patients received treatment with itraconazole at 400 mg/day, including two patients who had not responded to treatment with fluconazole at 100 mg/day. Of the responses, seven were classified as remissions (mean treatment duration of 24 months), two as improvements, and three as failures. Ten patients received fluconazole. Of the responses, three were classified as remissions (mean treatment duration of 12 months), one as improvement, and six as failures. Of the 10 patients treated with fluconazole, five received doses of 100 mg/day, and five were given doses of 400 or 800 mg/day. The differences in outcome among the five patients receiving the lower dose of fluconazole (one remission, one improvement, and three failures) and the five patients given the higher doses of fluconazole (two remissions and three failures) were negligible. One other patient showed signs of histoplasmosis while receiving fluconazole at 50 mg/day for treatment of thrush. Three failures (two treated with itraconazole and one with fluconazole) followed lapses in azole therapy because of associated conditions. Azole therapy was well tolerated. The treatment responses in this pilot series appear promising in comparison with those reported in the literature with amphotericin B or ketoconazole. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. RP SHARKEYMATHIS, PK (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NCRR NIH HHS [M01-RR-01346] NR 65 TC 40 Z9 40 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUL PY 1993 VL 6 IS 7 BP 809 EP 819 PG 11 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LH852 UT WOS:A1993LH85200007 PM 8389850 ER PT J AU BRYAN, CL LEWIS, RE OWENS, SL EMANUEL, B JENKINSON, SG AF BRYAN, CL LEWIS, RE OWENS, SL EMANUEL, B JENKINSON, SG TI ALLOPURINOL INHIBITION OF NEUTROPHILIC ALVEOLAR RESPONSE DURING HYPEROXIA SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE OXYGEN TOXICITY; LUNG INFLAMMATION; RATS; BRONCHOALVEOLAR LAVAGE FLUID; FREE RADICALS ID RESPIRATORY-DISTRESS SYNDROME; PHORBOL-MYRISTATE ACETATE; LUNG INJURY; POLYMORPHONUCLEAR LEUKOCYTES; OXYGEN-TOXICITY; FREE-RADICALS; GRANULOCYTES; INFLAMMATION; ISCHEMIA; SHEEP AB Allopurinol is a potent xanthine oxidase inhibitor that has been administered to animals to protect tissues from oxidant injury. We hypothesized that allopurinol may protect against oxidant injury by inhibiting the inflammatory response. Male Sprague-Dawley rats were injected daily with vehicle or allopurinol and compared with noninjected controls. Animals were exposed to room air or 90% oxygen for 14 days. At the end of the exposure period, all animals were lavaged and bronchoalveolar lavage fluid (BALF) was examined for cell counts, lactate dehydrogenase (LDH), and protein. BALF neutrophils were significantly increased in oxygen-exposed noninjected controls (33 +/- 7 X 10(3)/mm3) and also in the vehicle-inoculated oxygen-exposed animals (43 +/- 6 X 10(3)/mm3). Allopurinol treatment resulted in a decrease in the neutrophilic alveolar response in oxygen-exposed animals (5.3 +/- 4 X 10(3)/mm3, P < 0.001). These data reveal that oxygen exposure produces a neutrophilic alveolar response that is attenuated by allopurinol treatment. BALF protein and LDH were significantly increased in all inoculated and noninoculated oxygen-exposed animals compared with air-exposed animals. Therefore, allopurinol decreases the neutrophilic alveolar response produced by a hyperoxic exposure in the rat but does not decrease lung injury as assessed by alveolar LDH and protein release. C1 WILFORD HALL USAF MED CTR,DEPT MED,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RP BRYAN, CL (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY VET ADM HOSP,DEPT MED,PULM DIS SECT 111E,SAN ANTONIO,TX 78284, USA. FU NHLBI NIH HHS [HL-30556] NR 24 TC 9 Z9 10 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JUL PY 1993 VL 75 IS 1 BP 357 EP 363 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA LN649 UT WOS:A1993LN64900049 PM 8376286 ER PT J AU HAAKE, DA CHAMPION, CI MARTINICH, C SHANG, ES BLANCO, DR MILLER, JN LOVETT, MA AF HAAKE, DA CHAMPION, CI MARTINICH, C SHANG, ES BLANCO, DR MILLER, JN LOVETT, MA TI MOLECULAR-CLONING AND SEQUENCE-ANALYSIS OF THE GENE ENCODING OMPL1, A TRANSMEMBRANE OUTER-MEMBRANE PROTEIN OF PATHOGENIC LEPTOSPIRA SPP SO JOURNAL OF BACTERIOLOGY LA English DT Article ID TREPONEMA-PALLIDUM; ESCHERICHIA-COLI; NEISSERIA-MENINGITIDIS; HEMOPHILUS-INFLUENZAE; BACTERIAL PORIN; ANTIBODY; INVASION; CELLS; ULTRASTRUCTURE; EXPRESSION AB Pathogenic Leptospira spp. are spirochetes that have a low transmembrane outer membrane protein content relative to that of enteric gram-negative bacteria. In a previous study we identified a 31-kDa surface Protein that was present in strains of Leptospira alstoni in amounts which correlated with the outer membrane particle density observed by freeze fracture electron microscopy (D. A. Haake, E. M. Walker, D. R. Blanco, C. A. Bolin, J. N. Miller, and M. A. Lovett, Infect. Immun. 59:1131-1140, 1991). The N-terminal amino acid sequence was used to design a pair of oligonucleotides which were utilized to screen a lambda ZAP II library containing EcoRI fragments of L. alstoni DNA. A 2.5-kb DNA fragment which contained the entire structural ompL1 gene was identified. The structural gene deduced from the sequence of this DNA fragment would encode a 320-amino-acid polypeptide with a 24-amino-acid leader peptide and a leader peptidase I cleavage site. Processing of OmpL1 results in a mature protein with a predicted molecular mass of 31,113 Da. Secondary-structure prediction identified repeated stretches of amphipathic beta-sheets typical of outer membrane protein membrane-spanning sequences. A topological model of OmpL1 containing 10 transmembrane segments is suggested. A recombinant OmpL1 fusion protein was expressed in Escherichia coli in order to immunize rabbits with the purified protein. Upon Triton X-114 extraction of L. alstoni and phase separation, anti-OmpL1 antiserum recognized a single band on immunoblots of the hydrophobic detergent fraction which was not present in the hydrophilic aqueous fraction. Immunoelectron microscopy with anti-Ompl1 antiserum demonstrates binding to the surface of intact L. alstoni. DNA hybridization studies indicate that the ompL1 gene is present in a single copy in all pathogenic Leptospira species that have been tested and is absent in nonpathogenic Leptospira species. OmpL1 may be the first spirochetal transmembrane outer membrane protein for which the structural gene has been cloned and sequenced. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MICROBIOL & IMMUNOL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, DIV INFECT DIS, LOS ANGELES, CA 90024 USA. RP HAAKE, DA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, DIV INFECT DIS, W111F, LOS ANGELES, CA 90073 USA. FU NIAID NIH HHS [5-T32-AI07323, AI-21352, AI-29733] NR 48 TC 87 Z9 113 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JUL PY 1993 VL 175 IS 13 BP 4225 EP 4234 PG 10 WC Microbiology SC Microbiology GA LL235 UT WOS:A1993LL23500036 PM 8320237 ER PT J AU KLEIN, BS HOGAN, LH JONES, JM AF KLEIN, BS HOGAN, LH JONES, JM TI IMMUNOLOGICAL RECOGNITION OF A 25-AMINO-ACID REPEAT ARRAYED IN TANDEM ON A MAJOR ANTIGEN OF BLASTOMYCES-DERMATITIDIS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE BLASTOMYCOSIS; TANDEM REPEAT; SERODIAGNOSIS; DIMORPHIC FUNGUS; CDNA ID MAMMALIAN-CELLS; PROTEIN; IDENTIFICATION; SEQUENCE; INVASIN; PURIFICATION; GLYCOPROTEIN; GENE AB A 120-kD glycoprotein antigen abundantly expressed on Blastomyces dermatitidis yeasts is a target of cellular and humoral immune responses in human infection. To investigate the antigen and immune response more carefully at the molecular level, we screened an expression library from B. dermatitidis to identify clones that encode this antigen, designated WI-1. A 942-bp cDNA was isolated by immunologic screening with polyclonal, rabbit anti-WI-1 antiserum. Northern hybridization analysis showed that the cDNA hybridized to yeast message congruent-to 3.9 kb. DNA and deduced protein sequence analysis of the clone demonstrated a 25-amino acid repeat arrayed in tandem, present in 4.5 copies near the 5' end, and rich in predicted antigenic epitopes. Further analysis showed strong homology in these tandem repeats with invasin, an adhesin of Yersiniae. Cloned cDNA was used to express a 30-kD fusion protein strongly recognized in western blots by rabbit anti-WI-1 antiserum, and by sera from all 35 blastomycosis patients studied. The fusion protein product of subcloned cDNA encoding only the tandem repeat also was strongly recognized in western blots by sera from the 35 blastomycosis patients, but not by sera from 10 histoplasmosis and 5 coccidioidomycosis patients. An antigen-inhibition radioimmunoassay showed that the tandem repeat alone completely eliminated rabbit and human anti-WI-1 antibody binding to radiolabeled native WI-1. From these results, we conclude that the 25-amino acid repeat of WI-1 displays an immunodominant B cell epitope, and that the carboxyl-terminus of the molecule exhibits an architecture that may promote adhesion of Blastomyces yeasts to host cells or extracellular matrix proteins and ultimately provide a clearer picture of the molecular pathogenesis of blastomycosis. C1 UNIV WISCONSIN,SCH MED,DEPT PEDIAT,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT MED MICROBIOL & IMMUNOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. RP KLEIN, BS (reprint author), UNIV WISCONSIN,HOSP & CLIN,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIAID NIH HHS [AI-00905, AI-31479] NR 29 TC 51 Z9 51 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 JUL PY 1993 VL 92 IS 1 BP 330 EP 337 DI 10.1172/JCI116571 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LL773 UT WOS:A1993LL77300044 PM 8326001 ER PT J AU BONADONNA, RC DELPRATO, S SACCOMANI, MP BONORA, E GULLI, G FERRANNINI, E BIER, D COBELLI, C DEFRONZO, RA AF BONADONNA, RC DELPRATO, S SACCOMANI, MP BONORA, E GULLI, G FERRANNINI, E BIER, D COBELLI, C DEFRONZO, RA TI TRANSMEMBRANE GLUCOSE-TRANSPORT IN SKELETAL-MUSCLE OF PATIENTS WITH NON-INSULIN-DEPENDENT DIABETES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE LIMB BALANCE; INSULIN RESISTANCE; HYPERGLYCEMIA ID GLYCOGEN-SYNTHASE ACTIVITY; RAT ADIPOSE-CELLS; POSTRECEPTOR DEFECT; RESPONSIVE TISSUES; PLASMA-MEMBRANE; SOLEUS MUSCLE; HUMAN FOREARM; PIMA-INDIANS; MELLITUS; RESISTANCE AB Insulin resistance for glucose metabolism in skeletal muscle is a key feature in non-insulin-dependent diabetes mellitus (NIDDM). Which cellular effectors of glucose metabolism are involved is still unknown. We investigated whether transmembrane glucose transport in vivo is impaired in skeletal muscle in nonobese NIDDM patients. We performed euglycemic insulin clamp studies in combination with the forearm balance technique (brachial artery and deep forearm vein catheterization) in six nonobese NIDDM patients and five age- and weight-matched controls. Unlabeled D-mannitol (a nontransportable molecule) and radioactive 3-0-methyl-D-glucose (the reference molecular probe to assess glucose transport activity) were simultaneously injected into the brachial artery, and the washout curves were measured in the deep venous effluent blood. In vivo transmembrane transport of 3-0-methyl-D-glucose in forearm muscle was determined by computerized analysis of the washout curves. At similar steady-state plasma concentrations of insulin (approximately 500 pmol/liter) and glucose (approximately 5.15 mmol/liter), transmembrane inward transport of 3-0-methyl-D-glucose in skeletal muscle was markedly reduced in the NIDDM patients (6.5 x 10(-2) +/- 0.56 x 10(-2) . min-1) compared with controls (12.5 x 10(-2) +/- 1.5 x 10(-2) - min-1, P < 0.005). Mean glucose uptake was also reduced in the diabetics both at the whole body level (9.25 +/- 1.84 vs. 28.3 +/- 2.44 mumol/min per kg, P < 0.02) and in the forearm tissues (5.84 +/- 1.51 vs. 37.5 +/- 7.95 mumol/min per kg, P < 0.02). When the latter rates were extrapolated to the whole body level, skeletal muscle accounted for - 80% of the defect in insulin action seen in NIDDM patients. We conclude that transmembrane glucose transport, when assessed in vivo in skeletal muscle, is insensitive to insulin in nonobese NIDDM patients, and plays a major role in determining whole body insulin resistance. C1 UNIV PADUA,DEPT ELECTR & INFORMAT,I-35100 PADUA,ITALY. WASHINGTON UNIV,SCH MED,DIV METAB,ST LOUIS,MO 63110. UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. UNIV TEXAS,AUDIE L MURPHY VET ADM HOSP,SAN ANTONIO,TX 78285. RP BONADONNA, RC (reprint author), UNIV PISA,CNR,INST CLIN PHYSIOL,METAB UNIT,VIA SAVI 8,I-56100 PISA,ITALY. RI Del Prato, Stefano/K-3405-2016 OI Del Prato, Stefano/0000-0002-5388-0270; BONORA, Enzo/0000-0003-1074-5164 FU NCRR NIH HHS [RR-00954]; NIDDK NIH HHS [DK-20579, DK-24092] NR 72 TC 126 Z9 128 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 JUL PY 1993 VL 92 IS 1 BP 486 EP 494 DI 10.1172/JCI116592 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LL773 UT WOS:A1993LL77300063 PM 8326013 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R WINE, DB AF SILVA, JA LEONG, GB WEINSTOCK, R WINE, DB TI DELUSIONAL MISIDENTIFICATION AND DANGEROUSNESS - A NEUROBIOLOGICAL HYPOTHESIS SO JOURNAL OF FORENSIC SCIENCES LA English DT Note DE FORENSIC PSYCHIATRY; DANGEROUSNESS; MENTAL DISORDER; SCHIZOPHRENIA; DELUSIONAL MISIDENTIFICATION SYNDROMES; FACE RECOGNITION ID CAPGRAS SYNDROME; FACIAL RECOGNITION; FREGOLI SYNDROME; KNOWLEDGE; TOMOGRAPHY; VIOLENCE; DEMENTIA; ATROPHY; SYSTEM AB Delusional misidentification syndromes have intrigued this century's psychiatric researchers. More recently, the dangerousness posed by individuals suffering from these syndromes has been a subject of scientific inquiry. A series of five individuals suffering from delusional misidentification syndromes was studied from a phenomenologic and neuropsy-chologic perspective. Using this information. a hypothesis involving the psychobiological contributions to the dangerousness of delusional misidentification can be generated. This may further our understanding of the dangerousness posed by psychotic individuals. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 52 TC 10 Z9 10 U1 0 U2 0 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD JUL PY 1993 VL 38 IS 4 BP 904 EP 913 PG 10 WC Medicine, Legal SC Legal Medicine GA LM756 UT WOS:A1993LM75600022 PM 8102637 ER PT J AU MULROW, CD LUCEY, CR FARNETT, LE AF MULROW, CD LUCEY, CR FARNETT, LE TI DISCRIMINATING CAUSES OF DYSPNEA THROUGH CLINICAL EXAMINATION SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Review RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 0 TC 46 Z9 49 U1 2 U2 4 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD JUL PY 1993 VL 8 IS 7 BP 383 EP 392 DI 10.1007/BF02600079 PG 10 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA LN093 UT WOS:A1993LN09300008 PM 8410400 ER PT J AU ORTIZBRAVO, E SCHUMACHER, HR AF ORTIZBRAVO, E SCHUMACHER, HR TI COMPONENTS GENERATED LOCALLY AS WELL AS SERUM ALTER THE PHLOGISTIC EFFECT OF MONOSODIUM URATE CRYSTALS IN-VIVO SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE GOUT; SELF-LIMITED INFLAMMATION; IN-VIVO ID CALCIUM PYROPHOSPHATE DIHYDRATE; INDUCED INFLAMMATION; HUMAN-NEUTROPHILS; PROTEIN ADSORPTION; KNEE JOINTS; BINDING; GOUT; MONOHYDRATE; STIMULATION; MEDIATOR AB Proteins binding monosodium urate (MSU) crystals alter their phlogistic potential in vitro and in vivo. These proteins and other materials capable of interacting with crystals could enter the joint space from the circulation and/or could be produced locally. Using the rat subcutaneous air pouch synovium-like model, we observed different effects of collected pouch fluid supernatants from acute (6 h) and from subsiding (72 h) inflammation, and from autologous rat serum on MSU crystal induced inflammation in new air pouches. Plain crystals at 6 h produced a mean leukocyte count (WBC) of 18,156/mm3 with 12% of cells showing phagocytosis of MSU; reaction to plain crystals at 72 h had subsided to only 75 WBC/mm3 and 1% phagocytosis; new crystals preincubated in supernatant from acutely inflamed 6 h air pouches produced higher numbers of WBC in new pouches at 6 h (34,044/mm3); while crystals preincubated in 72 h supernatant gave only 9,825/mm3 and 7% phagocytosis; crystals preincubated in rat serum produced similar pouch WBC to plain crystals at 6 h, but resulted in only 2% phagocytosis. Our study provides evidence that components generated locally during subsiding inflammation as well as serum components could bind to MSU crystals and affect the generation of chemotactic factors and/or crystal phagocytosis contributing in the self-limited nature of acute gouty arthritis. C1 UNIV PENN,SCH MED,VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL 151K,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. NR 45 TC 7 Z9 7 U1 0 U2 2 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JUL PY 1993 VL 20 IS 7 BP 1162 EP 1166 PG 5 WC Rheumatology SC Rheumatology GA LM769 UT WOS:A1993LM76900014 PM 8371210 ER PT J AU RIPPLE, M MULCAHY, RT WILDING, G AF RIPPLE, M MULCAHY, RT WILDING, G TI CHARACTERISTICS OF THE GLUTATHIONE GLUTATHIONE-S-TRANSFERASE DETOXIFICATION SYSTEM IN MELPHALAN RESISTANT HUMAN PROSTATE-CANCER CELLS SO JOURNAL OF UROLOGY LA English DT Article DE PROSTATE NEOPLASMS; GLUTATHIONE; GLUTATHIONE TRANSFERASES; MELPHALAN ID CYTO-TOXICITY; RAT-LIVER; BUTHIONINE SULFOXIMINE; CARCINOMA; LINE; ASSAY; ESTABLISHMENT; INHIBITION; DEPLETION; SURVIVAL AB Glutathione (GSH) and glutathione-S-transferases (GST) have been implicated in resistance of tumor cells to certain alkylating agents, including melphalan. Glutathione levels and GST activities were determined in melphalan-resistant sublines of the human prostate carcinoma cell lines DU 145, PC-3 and LNCaP produced by serial treatment with melphalan at progressively increasing concentrations. The resistant sublines M4.5DU145, M5DU145, M6DU145, M6PC-3 and M6LNCaP were 27-, 7-, 3-, 6- and 2-fold more resistant to melphalan than the parental lines. The melphalan-resistant DU 145 and PC-3 lines showed cross-resistance to cisplatin and tetraplatin, but retained sensitivity to vinblastine, colchicine and etoposide. Interestingly, both sublines were also resistant to methotrexate and adriamycin. The melphalan-resistant LNCaP line showed slight resistance to cisplatin and adriamycin, but remained sensitive to tetraplatin and methotrexate. This line also retained sensitivity to vinblastine while developing resistance to colchicine. Intracellular GSH levels were increased 2.8 fold for M5DU145, 1.7 fold for M6PC-3 and 2.1 fold for M6LNCaP compared to the parental lines, whereas GST activity using chlorodinitro-benzene as a substrate was comparable for all lines. When cumene hydroperoxide was used as a substrate, an increase in GST activity was noted only in the M6PC-3 line as compared with the parent line. Western blot analysis showed no change in GST isozyme profile between parent and resistant DU 145 lines; however a mu class isoenzyme was detected in the resistant, but not in the parent PC-3 line, using a Y(b1) antibody. M5DU145 cells maintained in the absence of melphalan for seven months maintained their resistance to melphalan. Depletion of GSH, with buthionine sulfoximine, to control levels reversed melphalan resistance to control levels. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP RIPPLE, M (reprint author), UNIV WISCONSIN,CTR COMPREHENS CANC,DEPT HUMAN ONCOL,K4-666 CSC,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [CA 50590] NR 37 TC 28 Z9 28 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 JUL PY 1993 VL 150 IS 1 BP 209 EP 214 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA LH013 UT WOS:A1993LH01300072 PM 8510259 ER PT J AU MARTI, HP LOVETT, DH AF MARTI, HP LOVETT, DH TI MESANGIAL MATRIX METALLOPROTEINASES AND THEIR ROLE IN GLOMERULONEPHRITIS SO KIDNEY INTERNATIONAL LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO VET ADM MED CTR,DEPT MED,SAN FRANCISCO,CA 94143. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JUL PY 1993 VL 44 IS 1 BP 258 EP 258 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA LG816 UT WOS:A1993LG81600131 ER PT J AU LEVITTE, SS AF LEVITTE, SS TI COEXISTENT HYPOMANIA AND SEVERE HYPOTHYROIDISM - IN REPLY SO PSYCHOSOMATICS LA English DT Letter RP LEVITTE, SS (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97207, USA. NR 4 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 JUL-AUG PY 1993 VL 34 IS 4 BP 374 EP 375 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA LJ932 UT WOS:A1993LJ93200019 ER PT J AU GUO, ZZ WEINSTEIN, MJ PHILLIPS, MD KROLL, MH AF GUO, ZZ WEINSTEIN, MJ PHILLIPS, MD KROLL, MH TI MR 6,400 AURIN TRICARBOXYLIC-ACID DIRECTLY ACTIVATES PLATELETS SO THROMBOSIS RESEARCH LA English DT Article DE THROMBOSIS; PROTEIN KINASES; PHOSPHOLIPASE; CYCLIC NUCLEOTIDES; AURIN TRICARBOXYLIC ACID ID MURINE MONOCLONAL-ANTIBODY; VONWILLEBRAND-FACTOR; AURINTRICARBOXYLIC ACID; FIBRINOGEN; BINDING; AGGREGATION; RECEPTOR; HEPARIN; GPIB; IIIA AB ATA is a novel anticoagulant polymeric anionic aromatic compound that inhibits von Willebrand factor binding to platelet glycoprotein Ib and thereby prevents ristocetin- and shear stress-induced platelet aggregation. To investigate its mechanism of action, ATA fractions of homogeneous M(r) have been prepared by size exclusion chromatography. ATA fractions of M(r) greater-than-or-equal-to 2,500 are most effective at inhibiting vWF-mediated platelet aggregation, and ATA of M(r) = 2,500 also inhibits thrombin-induced platelet activation. Paradoxical results were observed in studies of ATA with M(r) = 6,400. This fraction of ATA stimulates aggregation of washed platelets or platelet-rich-plasma. The dose/response of aggregation shows a bell-shaped curve with maximal aggregation at approximately 2 mug/ml. Platelet aggregation is associated with phosphoinositide turnover and protein kinase C- and calcium-dependent protein phosphorylation. Platelet signalling responses to ATA are inhibited by platelet pretreatment with PGI2 or dibutyryl-cyclic AMP, but are unaffected by inhibiting platelet cyclooxygenase with aspirin. These results suggest that M(r) 6,400 ATA directly activates platelet phospholipase C to initiate platelet aggregation. This effect, unique to M(r) 6,400 ATA, could potentially mitigate ATA's beneficial anti-thrombotic effect on vWF-mediated platelet responses, and should be considered when analyzing results of experiments that utilize unfractionated ATA. C1 BAYLOR COLL MED,VA MED CTR,HEMATOL SECT,MS 902 6565,HOUSTON,TX 77030. RICE UNIV,HOUSTON,TX 77251. BOSTON UNIV,SCH MED,BOSTON,MA 02118. FU NHLBI NIH HHS [HL02311, HL46981, HL22355] NR 24 TC 17 Z9 17 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0049-3848 J9 THROMB RES JI Thromb. Res. PD JUL 1 PY 1993 VL 71 IS 1 BP 77 EP 88 DI 10.1016/0049-3848(93)90207-5 PG 12 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA LJ163 UT WOS:A1993LJ16300005 PM 8367837 ER PT J AU GANZINI, L CASEY, DE HOFFMAN, WF MCCALL, AL AF GANZINI, L CASEY, DE HOFFMAN, WF MCCALL, AL TI THE PREVALENCE OF METOCLOPRAMIDE-INDUCED TARDIVE-DYSKINESIA AND ACUTE EXTRAPYRAMIDAL MOVEMENT-DISORDERS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article AB Background: Metoclopramide hydrochloride, a neuroleptic dopamine receptor antagonist used to treat gastric ailments, is reported to cause extrapyramidal movement disorders. The goals of this study were (1) to determine the prevalence and severity of tardive dyskinesia and acute extrapyramidal movement syndromes including akathisia, acute dystonia, and drug-induced parkinsonism in metoclopramide-treated patients and (2) to compare the prevalence and severity of tardive dyskinesia in metoclopramide-treated diabetics and nondiabetics. Methods: From a list of metoclopramide-treated patients received from the Portland (Ore) Veterans Affairs Medical Center pharmacy, 53 patients met inclusion criteria and 51 (96%) agreed to participate. Controls consisted of a convenience sample drawn from the Portland Veterans Affairs Medical Center Outpatient Clinic who were matched to subjects on age (+/-10 years), gender, and presence or absence of diabetes. Of 61 potential controls contacted, 51 (84%) agreed to participate. Metoclopramide-treated subjects and controls were seen by a rater who was ''blind'' to all diagnoses and treatments. The rater performed a standardized examination used to elicit signs and symptoms of tardive dyskinesia and acute extrapyramidal movement syndromes. Results: The relative risk for tardive dyskinesia was 1.67 (95% confidence interval, 0.93 to 2.97), and the relative risk for drug-induced parkinsonism was 4.0 (95% confidence interval, 1.5 to 10.5). Metoclopramide-treated patients had significantly greater severity of tardive dyskinesia, drug-induced parkinsonism, and subjective akathisia than controls. Use of metoclopramide was associated with impairment in ambulation and increased use of benzodiazepines. Metoclopramide-treated diabetics had significantly greater severity of tardive dyskinesia than metoclopramide-treated nondiabetics. Conclusions: Metoclopramide use is associated with a significantly increased prevalence and severity of several extrapyramidal movement disorders. C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. RP GANZINI, L (reprint author), PORTLAND VET AFFAIRS MED CTR,PSYCHIAT SERV,116A-P,POB 1034,PORTLAND,OR 97207, USA. FU NINDS NIH HHS [NS22213]; PHS HHS [43586, 36657] NR 30 TC 127 Z9 127 U1 1 U2 2 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 JUN 28 PY 1993 VL 153 IS 12 BP 1469 EP 1475 DI 10.1001/archinte.153.12.1469 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LJ892 UT WOS:A1993LJ89200007 PM 8512437 ER PT J AU HAMMOND, TG MAJEWSKI, RR ONORATO, JJ BRAZY, PC MORRE, DJ AF HAMMOND, TG MAJEWSKI, RR ONORATO, JJ BRAZY, PC MORRE, DJ TI ISOLATION AND CHARACTERIZATION OF RENAL CORTICAL MEMBRANES USING AN AQUEOUS 2-PHASE PARTITION TECHNIQUE SO BIOCHEMICAL JOURNAL LA English DT Article ID BRUSH-BORDER MEMBRANE; TRANSPORT; PROTEIN; ENDOSOMES; VESICLES; ASSAY AB The aqueous two-phase partition technique is a simple, rapid and inexpensive method for the fractionation of membrane preparations. Aqueous two-phase partitioning separates according to surface properties such as charge and hydrophobicity, making it complementary to established centrifugation techniques, which separate on the basis of density. Although aqueous two-phase partitioning has been successfully applied to animal tissues, there are limited data on the functional properties of the isolated membranes. We have applied the aqueous two-phase partition technique to rat renal brush-border membrane vesicles and sheets. Our aim was to remove organelle contamination while maintaining the functional properties of the membranes. Evidence from marker enzyme analysis and electron microscopy supports the conclusion that renal brush-border membranes are fractionated separate from the mitochondria and endoplasmic reticulum. This separation procedure did not alter the Na+-dependent transport of brush-border membrane vesicles. Na+-D-glucose symporter and Na+-H+ antiporter activity in the fractionated preparation increased to the same extent as did the enrichment of enzyme markers for brush-border membranes. C1 PURDUE UNIV,DEPT MED CHEM & PHARMACOGNOSY,W LAFAYETTE,IN 47907. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP HAMMOND, TG (reprint author), UNIV WISCONSIN,DEPT MED,NEPHROL SECT,CTR CLIN SCI H4-510,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 28 TC 3 Z9 3 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JUN 15 PY 1993 VL 292 BP 743 EP 748 PN 3 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LJ401 UT WOS:A1993LJ40100020 PM 7686365 ER PT J AU HUNG, L RICHARDSON, A AF HUNG, L RICHARDSON, A TI THE EFFECT OF AGING ON THE GENETIC EXPRESSION OF RENIN BY MOUSE KIDNEY SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE AGING; MOUSE KIDNEY; RENIN MESSENGER RNA AB The effect of aging on the genetic expression of renin was studied in kidney tissue by measuring renin mRNA levels. RNA was isolated from the kidneys of 5- to 37-month-old male C57BL/6J mice. The relative levels of the renin mRNA were measured by dot blot hybridization using a cDNA probe to renin. The size of renin mRNA as determined by northern blot analysis was found to be 1.6 Kb. The size of renin mRNA did not change with increasing age. However, the levels of renin mRNA in kidney RNA decreased 70% after 12 months of age. C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG 01548] NR 0 TC 1 Z9 1 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD JUN PY 1993 VL 5 IS 3 BP 193 EP 198 PG 6 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LH825 UT WOS:A1993LH82500005 PM 8399464 ER PT J AU SCHENKER, S HU, ZQ JOHNSON, RF YANG, YQ FROSTO, T ELLIOTT, BD HENDERSON, GI MOCK, DM AF SCHENKER, S HU, ZQ JOHNSON, RF YANG, YQ FROSTO, T ELLIOTT, BD HENDERSON, GI MOCK, DM TI HUMAN PLACENTAL BIOTIN TRANSPORT - NORMAL CHARACTERISTICS AND EFFECT OF ETHANOL SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE BIOTIN; PLACENTA; ALCOHOL ID THIAMINE TRANSPORT; MEMBRANE-VESICLES; RAT; DEFICIENCY; INVITRO; DIFFERENTIATION; ANTIPYRINE; EXPOSURE; GLUCOSE; MICE AB Biotin, a vitamin essential for many metabolic reactions, is supplied to the fetus exclusively from the mother. Deficiency of biotin in pregnancy leads to impaired fetal growth and development. Alcohol taken in pregnancy likewise may cause fetal growth abnormalities. Normal biotin transport via the placenta and the effects of ethanol on this transport apparently have not been studied. Our aims were to characterize these phenomena for the normal human-term placenta. Using maternal-facing placental membrane vesicles, biotin uptake was sodium- and temperature-dependent, saturable, and inhibited by structural analogs of biotin (desthiobiotin, biocytin, and biotin methyl ester), as well as by 4 and 10 hr exposure to 3 g/liter ethanol. Using the isolated perfused single cotyiedon method to measure placental transport of biotin at a perfusion concentration of 1 nm, the overall rate of biotin transport was found to be only 30% that of antipyrine, a freely diffusible marker. Clearance of biotin was approximately 2 ml/hr.g placenta, which was equal to the clearance of passively transferred L-glucose; biotin clearance was similar in both maternal to fetal and fetal to maternal directions. Overall transfer of biotin from maternal to fetal compartments was not inhibited by 500-fold greater concentrations of the three analogs, did not proceed against a biotin concentration gradient, and was not inhibited by 90-240 min exposure to an initial concentration of 4 g/liter ethanol. Concentration of biotin in the fetal compartment at the end of the study was not higher than on the maternal side (after maternal to fetal infusion), but placental concentration was 2- to 3-fold greater. No significant metabolism of biotin was detected. Exposing human placental cultured trophoblast on day 3 to 24 hr of ethanol (2 g/liter) had no effect on the net uptake of biotin by these cells. These studies provide evidence that maternal-facing placental membranes take up biotin by a mediated, carrier-dependent process that is inhibited by ethanol; however, based on the perfusion studies, we conclude that the overall (maternal-fetal) rate-limiting transfer of biotin by the human placenta is most consistent with a passive process, which is not inhibited by short-term exposure to ethanol. C1 UNIV TEXAS,HLTH SCI CTR,DEPT OBSTET & GYNECOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV IOWA,COLL MED,DEPT PEDIAT,DIV GASTROENTEROL & HEPATOL,IOWA CITY,IA 52242. RP SCHENKER, S (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07541, KO2 AA00121]; NIDDK NIH HHS [DK36823] NR 44 TC 23 Z9 24 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD JUN PY 1993 VL 17 IS 3 BP 566 EP 575 DI 10.1111/j.1530-0277.1993.tb00801.x PG 10 WC Substance Abuse SC Substance Abuse GA LH409 UT WOS:A1993LH40900008 PM 8333586 ER PT J AU BROWN, FR VOIGT, R SINGH, AK SINGH, I AF BROWN, FR VOIGT, R SINGH, AK SINGH, I TI PEROXISOMAL DISORDERS - NEURODEVELOPMENTAL AND BIOCHEMICAL ASPECTS SO AMERICAN JOURNAL OF DISEASES OF CHILDREN LA English DT Article ID RAT-LIVER PEROXISOMES; RHIZOMELIC CHONDRODYSPLASIA PUNCTATA; INFANTILE REFSUMS DISEASE; RENAL ZELLWEGER SYNDROME; ACID STORAGE DISEASE; CHAIN FATTY-ACIDS; X-LINKED ADRENOLEUKODYSTROPHY; CULTURED SKIN FIBROBLASTS; NEONATAL ADRENOLEUKODYSTROPHY; PHYTANIC ACID AB The peroxisomal disorders represent a group of inherited metabolic disorders that derive from defects of peroxisomal biogenesis and/or from dysfunction of single or multiple peroxisomal enzymes. Because peroxisomes are involved in the metabolism of lipids critical to the functioning of the nervous system, many of the peroxisomal disorders manifest with significant degrees of progressive psychomotor dysfunction. These disorders should be considered in the differential diagnosis of the infant with hypotonia and psychomotor delay (especially if accompanied by facial dysmorphisms, hepatomegaly, cataracts and/or retinitis, calcific stippling, short limbs, or combinations of these features), in the school-aged child with progressive neurologic dysfunction, and in adults with slowly progressive motor dysfunction. Current knowledge of peroxisomal biochemical and enzymatic processes permits precise identification of particular disorders within the peroxisomal disorder grouping. An effort should be made to identify the specific peroxisomal disorder to provide a precise explanation for neurodevelopmental deficits, to potentially prevent recurrence through genetic counseling, and to provide appropriate therapies when available. C1 MED UNIV S CAROLINA,DEPT PATHOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH JOHNSON VET ADM MED CTR,CHARLESTON,SC. RP BROWN, FR (reprint author), TEXAS CHILDRENS HOSP,CTR CLIN CARE,MEYER CTR DEV PEDIAT,1102 BATES ST,SUITE 530,HOUSTON,TX 77030, USA. FU NINDS NIH HHS [NS-22576] NR 83 TC 57 Z9 57 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0002-922X J9 AM J DIS CHILD JI Am. J. Dis. Child. PD JUN PY 1993 VL 147 IS 6 BP 617 EP 626 PG 10 WC Pediatrics SC Pediatrics GA LF301 UT WOS:A1993LF30100014 PM 7685145 ER PT J AU BEALL, AC JONES, JW GUINN, GA SVENSSON, LG NAHAS, C AF BEALL, AC JONES, JW GUINN, GA SVENSSON, LG NAHAS, C TI CARDIOPULMONARY BYPASS IN PATIENTS WITH PREVIOUSLY COMPLETED STROKE SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT 29TH Annual Meeting of the Society-of-Thoracic-Surgeons CY JAN 25-27, 1993 CL SAN ANTONIO, TX SP SOC THORAC SURGEONS ID ASCENDING AORTA; SURGERY AB It has been assumed that patients with neurological residua after a completed stroke are at increased risk of neurological complications associated with cardiac operations requiring cardiopulmonary bypass. To evaluate these assumptions, we reviewed retrospectively 1,163 consecutive patients undergoing cardiac operations with cardiopulmonary bypass. Among these 1,163 patients were 43 patients having a previously completed stroke with neurological residua, but without clinically significant extracranial carotid artery disease. Forty-one underwent coronary artery bypass grafting; of these, 1 required concomitant aortic valve replacement, 1 had mitral valve replacement, and 1 had aortic valve replacement. There was one death in this group of 43 patients, due to massive pulmonary embolism. Only 1 of these 43 patients experienced new neurological symptoms after operation, which would appear to indicate that patients with a previous, completed stroke may not be at increased risk of neurological complications from cardiac operations requiring cardiopulmonary bypass. C1 BAYLOR COLL MED,CORA & WEBB MADING DEPT SURG,HOUSTON,TX 77030. HOUSTON VET AFFAIRS MED CTR,HOUSTON,TX. NR 11 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD JUN PY 1993 VL 55 IS 6 BP 1382 EP 1385 PG 4 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA LH441 UT WOS:A1993LH44100007 ER PT J AU WALSH, TJ STANDIFORD, HC REBOLI, AC JOHN, JF MULLIGAN, ME RIBNER, BS MONTGOMERIE, JZ GOETZ, MB MAYHALL, CG RIMLAND, D STEVENS, DA HANSEN, SL GERARD, GC RAGUAL, RJ AF WALSH, TJ STANDIFORD, HC REBOLI, AC JOHN, JF MULLIGAN, ME RIBNER, BS MONTGOMERIE, JZ GOETZ, MB MAYHALL, CG RIMLAND, D STEVENS, DA HANSEN, SL GERARD, GC RAGUAL, RJ TI RANDOMIZED DOUBLE-BLINDED TRIAL OF RIFAMPIN WITH EITHER NOVOBIOCIN OR TRIMETHOPRIM-SULFAMETHOXAZOLE AGAINST METHICILLIN-RESISTANT STAPHYLOCOCCUS-AUREUS COLONIZATION - PREVENTION OF ANTIMICROBIAL RESISTANCE AND EFFECT OF HOST FACTORS ON OUTCOME SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID NASAL CARRIAGE; HOSPITAL OUTBREAK; UNITED-STATES; INFECTIONS; MUPIROCIN; ERADICATION; EFFICACY; THERAPY; HEMODIALYSIS; PROPHYLAXIS AB Methicillin-resistant Staphylococcus aureus (MRSA) is a major pathogen in hospitals. Current antimicrobial regimens for eradicating colonizing strains are not well defined and are often complicated by the emergence of resistance. The combination of novobiocin plus rifampin in vitro and in vivo was found to prevent the emergence of resistant populations of initially susceptible strains of MRSA, particularly resistance to rifampin. We therefore studied, in a randomized, double-blind, multicenter comparative trial, the combination of novobiocin plus rifampin versus trimethoprim-sulfamethoxazole (T/S) plus rifampin in order to determine the efficacy of each regimen in eradicating MRSA colonization and to further characterize the host factors involved in the response to this antimicrobial therapy. Among the 126 individuals enrolled in the study, 94 (80 patients; 14 hospital personnel) were evaluable. Among the 94 evaluable subjects, no significant demographic or medical differences existed between the two treatment groups. Successful clearance of the colonizing MRSA strains was achieved in 30 of 45 (67%) subjects receiving novobiocin plus rifampin, whereas successful clearance was achieved in 26 of 49 (53%) subjects treated with T/S plus rifampin (P = 0.18). The emergence of resistance to rifampin developed more frequently in 14% (7 of 49) of subjects treated with T/S plus rifampin than in 2% (1 of 45) of subjects treated with novobiocin plus rifampin (P = 0.04). Restriction endonuclease studies of large plasmid DNA demonstrated that the same strain was present at pretherapy and posttherapy in most refractory cases (24 of 29 [83%] subjects). Among the 56 successfully treated subjects, clearance of MRSA was age dependent: 29 of 36 (80%) subjects in the 18- to 49-year-old age group, 19 of 35 (54%) subjects in the 50- to 69-year-old age group, and 8 of 23 (35%) in the 70- to 94-year-old age group (P < 0.01). Clearance was also site dependent; culture-positive samples from wounds were related to a successful outcome in only 22 (48%) of 46 subjects, whereas culture-positive samples from sites other than wounds (e.g., nares, rectum, and sputum) were associated with a success rate of 34 of 48 (71%) subjects (P = 0.02). Foreign bodies in wounds did not prevent the eradication of MRSA by either regimen. T/S plus rifampin was less effective in clearing pressure wounds compared with other wounds, whereas novobiocin plus rifampin was equally effective in clearing both pressure and other wounds. There were no significant differences in toxicity between the two regimens. Thus, the combination of novobiocin plus rifampin, in comparison with T/S plus rifampin, was more effective in preventing the emergence of resistance to rifampin and demonstrated a trend toward greater activity in clearing the MRSA carrier state. The response to either combination depended on host factors, particularly age and the site of MRSA colonization. C1 BALTIMORE VET AFFAIRS MED CTR,INFECT DIS SECT,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. MED UNIV S CAROLINA,CHARLESTON,SC 29425. NCI,BETHESDA,MD 20892. VET AFFAIRS MED CTR,CHARLESTON,SC 29425. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. ASHEVILLE VET AFFAIRS MED CTR,ASHEVILLE,NC 28805. DUKE UNIV,MED CTR,DURHAM,NC 27710. RANCHO LOS AMIGOS MED CTR,DOWNEY,CA 90242. UNIV CALIF LOS ANGELES,SEPULVEDA VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. VIRGINIA COMMONWEALTH UNIV MED COLL VIRGINIA,RICHMOND,VA 23219. VET AFFAIRS MED CTR,DECATUR,GA 30033. EMORY UNIV,SCH MED,ATLANTA,GA 30322. SANTA CLARA VALLEY MED CTR,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,CALIF INST MED RES,SAN JOSE,CA 94305. UPJOHN CO,KALAMAZOO,MI 49001. OI Goetz, Matthew/0000-0003-4542-992X NR 56 TC 88 Z9 89 U1 1 U2 7 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 JUN PY 1993 VL 37 IS 6 BP 1334 EP 1342 PG 9 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA LF135 UT WOS:A1993LF13500022 PM 8328783 ER PT J AU FAUSTI, SA HENRY, JA SCHAFFER, HI OLSON, DJ FREY, RH BAGBY, GC AF FAUSTI, SA HENRY, JA SCHAFFER, HI OLSON, DJ FREY, RH BAGBY, GC TI HIGH-FREQUENCY MONITORING FOR EARLY DETECTION OF CISPLATIN OTOTOXICITY SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article ID HIGH-DOSE CISPLATIN; CIS-DICHLORODIAMMINEPLATINUM-II; CANCER-PATIENTS; HEARING-LOSS; PLATINUM; CHEMOTHERAPY; THERAPY; DIAMMINEDICHLOROPLATINUM; AUDIOMETRY; TOXICITY AB Cisplatin can cause irreversible hearing loss initially detectable as impairment of high-frequency hearing with progression to lower frequencies. Many patients receiving cisplatin are too ill to tolerate lengthy audiometric testing. Therefore, a rapid and sensitive high-frequency monitoring strategy to detect cisplatin-induced ototoxicity is needed. Serial conventional (0.25 to 8 kHz) and high-frequency (greater-than-or-equal-to 8 kHz) threshold monitoring was performed in patients receiving cisplatin, resulting in 84% of ears showing hearing loss, of which 71% were detected first in frequencies of 8 kHz or greater. By analysis according to an individualized, specific high-frequency range, early identification of hearing loss occurred in 94% of ears showing change. This five-frequency procedure is a sensitive detector of ototoxicity and is proposed as an alternative monitoring protocol for patients receiving cisplatin who cannot tolerate extended testing. C1 PORTLAND VET AFFAIRS MED CTR,AUDITORY RES LAB,PORTLAND,OR. PORTLAND VET AFFAIRS MED CTR,HEMATOL ONCOL SERV,PORTLAND,OR. OREGON HLTH SCI UNIV,MED ONCOL SERV,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT OTOLARYNGOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DIV HEMATOL,PORTLAND,OR 97201. RP FAUSTI, SA (reprint author), PORTLAND VET AFFAIRS MED CTR,DEPT VET AFFAIRS,POB 1034,PORTLAND,OR 97207, USA. NR 33 TC 48 Z9 52 U1 1 U2 3 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 JUN PY 1993 VL 119 IS 6 BP 661 EP 666 PG 6 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA LF783 UT WOS:A1993LF78300014 PM 8499098 ER PT J AU RESTREPO, D OKADA, Y TEETER, JH LOWRY, LD COWART, B BRAND, JG AF RESTREPO, D OKADA, Y TEETER, JH LOWRY, LD COWART, B BRAND, JG TI HUMAN OLFACTORY NEURONS RESPOND TO ODOR STIMULI WITH AN INCREASE IN CYTOPLASMIC CA2+ SO BIOPHYSICAL JOURNAL LA English DT Note ID RECEPTOR NEURONS; CALCIUM; CONDUCTANCE; MEMBRANE; CATFISH; CILIA; CELL AB The sense of smell allows terrestrial animals to collect information about the chemical nature of their environment through the detection of airborne molecules (7). In humans smell is believed to play an important role in protecting the organism from environmental hazards such as fire, gas leaks and spoiled food, in determining the flavor of foods, and perhaps in infant-parent bonding (8). In addition, the study of human olfaction is relevant to a number of medical problems that result in olfactory dysfunction, which can affect nutritional state, and to the study of the etiology of neurodegenerative diseases which manifest themselves in the olfactory epithelium (8, 26). Although much is known about behavioral aspects of human olfaction (8), little is understood about the underlying cellular mechanisms in humans. Here we report that viable human olfactory neurons (HON) can be isolated from olfactory tissue biopsies, and we find that HON respond to odorants with an increase in intracellular calcium concentration ([Ca(i)]). C1 UNIV PENN,SCH MED,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NAGASAKI UNIV,DEPT PHYSIOL,NAGASAKI 852,JAPAN. THOMAS JEFFERSON UNIV,DEPT OTOLARYNGOL,PHILADELPHIA,PA 19107. UNIV PENN,SCH DENT MED,DEPT BIOCHEM,PHILADELPHIA,PA 19104. RP RESTREPO, D (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. FU NIDCD NIH HHS [DC-00214, DC-00566, DC-01434] NR 27 TC 53 Z9 54 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JUN PY 1993 VL 64 IS 6 BP 1961 EP 1966 PG 6 WC Biophysics SC Biophysics GA LJ216 UT WOS:A1993LJ21600031 PM 8369416 ER PT J AU OGAWA, M AF OGAWA, M TI DIFFERENTIATION AND PROLIFERATION OF HEMATOPOIETIC STEM-CELLS SO BLOOD LA English DT Review ID COLONY-STIMULATING FACTOR; TRANSFORMING GROWTH FACTOR-BETA-1; RECOMBINANT GIBBON INTERLEUKIN-3; TUMOR NECROSIS FACTOR; PROGENITOR CELLS; GM-CSF; C-KIT; PAIRED PROGENITORS; FORMING-UNITS; SELF-RENEWAL C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. RP OGAWA, M (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. FU NIDDK NIH HHS [DK 32294] NR 126 TC 1077 Z9 1095 U1 4 U2 45 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 JUN 1 PY 1993 VL 81 IS 11 BP 2844 EP 2853 PG 10 WC Hematology SC Hematology GA LF065 UT WOS:A1993LF06500002 PM 8499622 ER PT J AU ANZUETO, A MUNOZ, J GLENN, ME WISE, D DUNCAN, C JENKINSON, S AF ANZUETO, A MUNOZ, J GLENN, ME WISE, D DUNCAN, C JENKINSON, S TI LEFT UPPER EXTREMITY EDEMA, RASH, AND VENOUS VARICOSITIES IN A 52-YEAR-OLD MAN SO CHEST LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT RADIOL,SAN ANTONIO,TX 78284. RP ANZUETO, A (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT 111E,SAN ANTONIO,TX 78284, USA. NR 6 TC 0 Z9 0 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 JUN PY 1993 VL 103 IS 6 BP 1849 EP 1850 DI 10.1378/chest.103.6.1849 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA LF719 UT WOS:A1993LF71900039 PM 8404111 ER PT J AU RECTOR, TS JOHNSON, G DUNKMAN, WB DANIELS, G FARRELL, L HENRICK, A SMITH, B COHN, JN AF RECTOR, TS JOHNSON, G DUNKMAN, WB DANIELS, G FARRELL, L HENRICK, A SMITH, B COHN, JN TI EVALUATION BY PATIENTS WITH HEART-FAILURE OF THE EFFECTS OF ENALAPRIL COMPARED WITH HYDRALAZINE PLUS ISOSORBIDE DINITRATE ON QUALITY-OF-LIFE - V-HEFT-II SO CIRCULATION LA English DT Article DE CLINICAL TRIALS; QUALITY OF LIFE; HEART FAILURE; QUESTIONNAIRES AB Background. Two new questionnaires concerning the quality of life of patients with heart failure were used in a randomized, controlled trial to determine if the patients' perceptions of the effects of enalapril on their daily activities and sense of well-being were different from those of a group treated with hydralazine and isosorbide dinitrate. Methods and Results. The questionnaires were completed at baseline and at 3 months, 6 months, and subsequently every 6 months during follow-up, which averaged 2.5 years (range, 0.5-5.7 years). Data from the questionnaires were reliable as indicated by correlation coefficients between repeated baseline scores of 0.88 and 0.87. Both treatment groups showed a progressive deterioration in quality of life as measured by both questionnaires. The questionnaire scores of the two treatment groups were not significantly different at any follow-up visit. Furthermore, there were no differences between treatments among subgroups defined by baseline questionnaire scores, peak oxygen consumption, ejection fraction, previous vasodilator use, and plasma norepinephrine concentration. Conclusions. Although several factors may limit the generalization of these results, the lack of a difference with regard to patients' quality of life is an important consideration for the evaluation of the relative therapeutic efficacy of these vasodilators. C1 UNIV MINNESOTA,SCH MED,DIV CARDIOVASC,BOX 488 UMHC,420 DELAWARE ST SE,MINNEAPOLIS,MN 55455. VET AFFAIRS MED CTR,W HAVEN,CT. VET AFFAIRS MED CTR,PHILADELPHIA,PA. VET AFFAIRS MED CTR,MILWAUKEE,WI. VET AFFAIRS MED CTR,HINES,IL. VET AFFAIRS MED CTR,NASHVILLE,TN. NR 5 TC 73 Z9 72 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 JUN PY 1993 VL 87 IS 6 SU 6 BP 71 EP 77 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG179 UT WOS:A1993LG17900010 ER PT J AU DUNKMAN, WB JOHNSON, GR CARSON, PE BHAT, G FARRELL, L COHN, JN AF DUNKMAN, WB JOHNSON, GR CARSON, PE BHAT, G FARRELL, L COHN, JN TI INCIDENCE OF THROMBOEMBOLIC EVENTS IN CONGESTIVE-HEART-FAILURE SO CIRCULATION LA English DT Article DE THROMBOEMBOLISM; STROKE; ANTICOAGULATION; ANTIPLATELETS ID IDIOPATHIC DILATED CARDIOMYOPATHY; CHRONIC ATRIAL-FIBRILLATION; ANTITHROMBOTIC THERAPY; NATURAL-HISTORY; ANTICOAGULANT-THERAPY; MYOCARDIAL-DISEASE; SYSTEMIC EMBOLISM; CARDIAC DISEASE; STROKE; RISK AB Background. The incidence of thromboembolism and the benefit of anticoagulation in congestive heart failure are controversial. Mdhods and Results. The data base provided by the Veterans Affairs Vasodilator-Heart Failure Trials (V-HeFT I and II) was examined retrospectively to address these issues. In V-HeFT I, 642 men with heart failure were followed an average of 2.28 years, providing 1,464 patient-years of follow-up. In V-HeFT II, 804 men were followed an average of 2.56 years, with 2,061 patient-years of follow-up. Mean left ventricular ejection fraction was 30% in V-HeFT I and 29% in V-HeFT II. Functional capacity was at the interface of classes II and III with a peak exercise oxygen consumption of 14.7 mL . kg-1 . min-1 in V-HeFT I and 13.7 mL . kg-1 . min-1 in V-HeFT II. Warfarin and antiplatelet agents were administered at the discretion of individual investigators. The incidence of all thromboembolic events during 1,068 patient-years without warfarin in V-HeFT I was 2.7/100 patient-years and during 1,188 patient-years in V-HeFT II was 2.1/100 patient-years and was not reduced in patients treated with warfarin. Patients experiencing events had a lower peak exercise oxygen consumption (p < 0.03 in V-HeFT I and p < 0.001 in V-HeFT II) and a lower mean ejection fraction (p=0.10 in V-HeFT I and p=0.07 in V-HeFT II). Atrial fibrillation was not associated with an increased risk of thromboembolic events. Conclusions. The incidence of thromboembolism and stroke in class II or III congestive heart failure is not high and may not be significantly reduced with warfarin treatment. Routine use of anticoagulants in patients with heart failure may not be justified. C1 VET AFFAIRS MED CTR,CINCINNATI,OH. VET AFFAIRS MED CTR,WASHINGTON,DC. VET AFFAIRS MED CTR,CTR COORDINATING,COOPERAT STUDIES PROGRAM,W HAVEN,CT. VET AFFAIRS MED CTR,MINNEAPOLIS,MN. UNIV PENN,SCH MED,DIV CARDIOVASC,PHILADELPHIA,PA 19104. GEORGETOWN UNIV,SCH MED,DIV CARDIOVASC,WASHINGTON,DC 20057. UNIV CINCINNATI,COLL MED,DIV CARDIOVASC,CINCINNATI,OH 45221. UNIV MINNESOTA,SCH MED,DIV CARDIOVASC,MINNEAPOLIS,MN 55455. RP DUNKMAN, WB (reprint author), VET AFFAIRS MED CTR,CARDIOL SECT 111C,PHILADELPHIA,PA 19104, USA. NR 59 TC 152 Z9 156 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 JUN PY 1993 VL 87 IS 6 SU 6 BP 94 EP 101 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG179 UT WOS:A1993LG17900013 ER PT J AU CARSON, PE JOHNSON, GR DUNKMAN, WB FLETCHER, RD FARRELL, L COHN, JN AF CARSON, PE JOHNSON, GR DUNKMAN, WB FLETCHER, RD FARRELL, L COHN, JN TI THE INFLUENCE OF ATRIAL-FIBRILLATION ON PROGNOSIS IN MILD-TO-MODERATE HEART-FAILURE - THE V-HEFT STUDIES SO CIRCULATION LA English DT Article DE ENALAPRIL; PRAZOSIN; HYDRALAZINE ISOSORBIDE DINITRATE; VASODILATORS ID IDIOPATHIC DILATED CARDIOMYOPATHY; CONGESTIVE CARDIOMYOPATHY; MORTALITY; SURVIVAL; PREDICTION; EXERCISE AB Background. Atrial fibrillation occurs commonly in heart failure; however, its importance in terms of prognosis is controversial. Methods and Results. We assessed the relation of atrial fibrillation on first Holter monitor to morbidity and mortality in mild to moderate heart failure in 632 patients in the Veterans Affairs Vasodilator-Heart Failure Trial (V-HeFT) I and 795 patients in V-HeFT II. Ninety-nine patients in atrial fibrillation and 533 patients in sinus rhythm were followed for a mean of 2.5 years (range, 6 months to 5.7 years) in V-HeFT I; 107 patients in atrial fibrillation and 688 patients in sinus rhythm in V-HeFT II were followed for a mean of 2.5 years (range, 6 months to 5.0 years). V-HeFT I compared treatment with prazosin, hydralazine-isosorbide dinitrate, and placebo, whereas V-HeFT II compared hydralazine-isosorbide dinitrate with enalapril. Follow-up evaluations included serial Holter monitors, serial metabolic exercise testing, hospitalization data, and clinical examinations. In V-HeFT I, cumulative mortality at 2 years was 0.34 for patients with atrial fibrillation and 0.30 for patients in sinus rhythm (p=0.25). Overall cumulative mortality was 0.54 for atrial fibrillation patients and 0.64 for sinus rhythm patients (p=0.86). In V-HeFT II, cumulative mortality at 2 years was 0.20 for patients with atrial fibrillation and 0.21 for patients with sinus rhythm (p=0.68), and overall cumulative mortality was 0.46 for atrial fibrillation patients and 0.52 for those in sinus rhythm (p<0.46). Sudden death was not increased with atrial fibrillation in V-HeFT I patients (p=0.64) or in V-HeFT II (p=0.68). By multivariate analysis, the relative mortality risk for atrial fibrillation was 0.95 in V-HeFT I and 0.76 in V-HeFT II. Metabolic exercise testing, showed no significant difference in mean change in peak oxygen consumption between patients with atrial fibrillation and those with sinus rhythm in V-HeFT I and a slight decrease late in V-HeFT II. Hospitalization rate for heart failure was not increased in either study. The embolic event rate was not increased for atrial fibrillation patients: 3% versus 4.9% of patients in sinus rhythm (p=0.41) in V-HeFT I and 4.0% versus 6.0% in V-HeFT II patients (p=0.44). A secondary analysis compared mortality of patients in atrial fibrillation with that of patients in sinus rhythm on all Holters: Mortality was not increased overall (p=0.72 in V-HeFT I and p=0.35 in V-HeFT II). Conclusions. Atrial fibrillation does not increase major morbidity or mortality in mild to moderate heart failure. C1 VET AFFAIRS MED CTR, CTR COOPERAT STUDIES COORDINATING, West Haven, CT USA. VET AFFAIRS MED CTR, MINNEAPOLIS, MN USA. UNIV PENN, VET AFFAIRS MED CTR, PHILADELPHIA, PA 19104 USA. UNIV PENN, DIV CARDIOVASC, PHILADELPHIA, PA 19104 USA. RP CARSON, PE (reprint author), VET AFFAIRS MED CTR, DEPT CARDIOL, 50 IRVING ST NW, WASHINGTON, DC 20422 USA. NR 31 TC 224 Z9 227 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0009-7322 EI 1524-4539 J9 CIRCULATION JI Circulation PD JUN PY 1993 VL 87 IS 6 SU 6 BP 102 EP 110 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LG179 UT WOS:A1993LG17900014 ER PT J AU DANG, H LAZARIDIS, K TALAL, N FISCHBACH, M SANZ, I AF DANG, H LAZARIDIS, K TALAL, N FISCHBACH, M SANZ, I TI CLONING OF A HUMAN-IGM AUTOANTIBODY BEARING A CROSS-REACTIVE IDIOTYPE IN A LAMBDA-EXPRESSION VECTOR - A NEW APPROACH TO STUDYING AUTOANTIBODIES SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTI-SM AUTOANTIBODY; INTERSPECIES IDIOTYPE; ESCHERICHIA-COLI; REPERTOIRE; DNA; ANTIBODIES; MICE; GENERATION; DIVERSITY C1 UNIV TEXAS,HLTH SCI CTR,RHEUMATOL SECT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DANG, H (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [AI 29003]; NIDCR NIH HHS [DE09311] NR 34 TC 3 Z9 3 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 JUN PY 1993 VL 67 IS 3 BP 249 EP 256 DI 10.1006/clin.1993.1072 PN 1 PG 8 WC Immunology; Pathology SC Immunology; Pathology GA LF995 UT WOS:A1993LF99500010 PM 8500272 ER PT J AU JOHNSON, CC AF JOHNSON, CC TI SUSCEPTIBILITY OF ANAEROBIC-BACTERIA TO BETA-LACTAM ANTIBIOTICS IN THE UNITED-STATES SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 1ST NORTH AMERICAN CONGRESS ON ANAEROBIC BACTERIA AND ANAEROBIC INFECTIONS CY JUL 24-26, 1992 CL MARINA DEL REY, CA SP ABBOTT LABS ID BACTEROIDES-FRAGILIS GROUP; ANTIMICROBIAL AGENTS; INVITRO ACTIVITY; TICARCILLIN-CLAVULANATE; CEFOPERAZONE SULBACTAM; RESISTANCE; IMIPENEM; PIPERACILLIN; INHIBITORS; CEFOXITIN AB Beta-lactam antibiotics are critical agents in the treatment of anaerobic infections. Susceptibility to these agents, however, varies widely, depending on the specific drug and organism; has not been constant over time; and differs in various geographic locations within the United States for many species. For the organisms in the Bacteroides fragilis group, the beta-lactam antibiotics with the most consistent activity are imipenem and combinations of a beta-lactam drug plus a beta-lactamase inhibitor, such as ticarcillin/clavulanate and ampicillin/sulbactam. Antibiotics with less activity include cefoxitin, piperacillin, cefotetan, and ceftizoxime. In other species of anaerobic gram-negative bacilli, beta-lactamase production is seen with increasing frequency. In vitro susceptibility of these strains is now similar to that of the B. fragilis group, with imipenem, ticarcillin/clavulanate, ampicillin/sulbactam, and cefoxitin being the most active drugs. The anaerobic gram-positive cocci and bacilli remain, for the most part, highly susceptible to penicillins and imipenem. C1 DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP JOHNSON, CC (reprint author), MED COLL PENN,3300 HENRY AVE,PHILADELPHIA,PA 19129, USA. NR 37 TC 16 Z9 16 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 JUN PY 1993 VL 16 SU 4 BP S371 EP S376 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LE919 UT WOS:A1993LE91900045 PM 8324150 ER PT J AU PUGH, JA JACOBSON, JM VANHEUVEN, WAJ WATTERS, JA TULEY, MR LAIRSON, DR LORIMOR, RJ KAPADIA, AS VELEZ, R AF PUGH, JA JACOBSON, JM VANHEUVEN, WAJ WATTERS, JA TULEY, MR LAIRSON, DR LORIMOR, RJ KAPADIA, AS VELEZ, R TI SCREENING FOR DIABETIC-RETINOPATHY - THE WIDE-ANGLE RETINAL CAMERA SO DIABETES CARE LA English DT Article ID MYDRIATIC FUNDUS PHOTOGRAPHY AB OBJECTIVE- To define the test characteristics of four methods of screening for diabetic retinopathy. RESEARCH DESIGN AND METHODS - Four screening methods (an exam by an ophthalmologist through dilated pupils using direct and indirect ophthalmoscopy, an exam by a physician's assistant through dilated pupils using direct ophthalmoscopy, a single 45-degrees retinal photograph without pharmacological dilation, and a set of three dilated 45-degrees retinal photographs) were compared with a reference standard of stereoscopic 30-degrees retinal photographs of seven standard fields read by a central reading center. Sensitivity, specificity, and positive and negative likelihood ratios were calculated after dichotomizing the retinopathy levels into none and mild nonproliferative versus moderate to severe nonproliferative and proliferative. Two sites were used. All patients with diabetes in a VA hospital outpatient clinic between June 1988 and May 1989 were asked to participate. Patients with diabetes identified from a laboratory list of elevated serum glucose values were recruited from a DOD medical center. RESULTS- The subjects (352) had complete exams excluding the exam by the physician's assistant that was added later. The sensitivities, specificities, and positive and negative likelihood ratios are as follows: ophthalmologist 0.33, 0.99, 72, 0.67; photographs without pharmacological dilation 0.61, 0.85, 4.1, 0.46; dilated photographs 0.81, 0.97, 24, 0.19; and physician's assistant 0.14, 0.99, 12, 0.87. CONCLUSIONS- Fundus photographs taken by the 45-degrees camera through pharmacologically dilated pupils and read by trained readers perform as well as ophthalmologists for detecting diabetic retinopathy. Physician extenders can effectively perform the photography with minimal training but would require more training to perform adequate eye exams. In this older population, many patients did not obtain adequate nonpharmacological dilation for use of the 45-degrees camera. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT OPHTHALMOL,SAN ANTONIO,TX 78284. USAF,WILFORD HALL MED CTR,LACKLAND AFB,TX 78236. 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 28 TC 91 Z9 93 U1 1 U2 5 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JUN PY 1993 VL 16 IS 6 BP 889 EP 895 DI 10.2337/diacare.16.6.889 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LD942 UT WOS:A1993LD94200004 PM 8100761 ER PT J AU ELLIOTT, ME GOODFRIEND, TL AF ELLIOTT, ME GOODFRIEND, TL TI MECHANISM OF FATTY-ACID INHIBITION OF ALDOSTERONE SYNTHESIS BY BOVINE ADRENAL GLOMERULOSA CELLS SO ENDOCRINOLOGY LA English DT Article ID GLUCOCORTICOID RECEPTORS; BINDING; SECRETION; RAT AB Previous work from this laboratory has suggested that the adrenal glomerulosa is under tonic inhibition by fatty acids. The purpose of the present work was to define the mechanism by which fatty acids inhibit aldosterone synthesis. Experiments with isolated bovine adrenocortical cells showed the following. 1) Fatty acids inhibited angiotensin-II-stimulated and (Bu)2cAMP-stimulated aldosterone synthesis with similar potencies. 2) Inhibition of aldosterone synthesis was highly dependent on fatty acid chain length and degree of unsaturation as well as on configuration of double bonds. Oleic acid was the most potent inhibitor among fatty acids prominent in plasma. 3) Cortisol synthesis was less sensitive to oleic acid inhibition than was aldosterone synthesis. 4) Pregnenolone synthesis by angiotensin-II-stimulated adrenal glomerulosa cells was relatively insensitive to oleic acid. 5) For both glomerulosa and fasciculata cells, cortisol synthesis from 21-deoxycortisol, which requires the participation of P450(21), was relatively insensitive to fatty acids. Cortisol synthesis from corticosterone by fasciculata cells, which requires the participation of P450(17alpha), was also insensitive to oleic acid. These are microsomal enzymes. 6) In glomerulosa cells, aldosterone synthesis from added corticosterone, which requires the 18-oxidase function of P450(11beta), a mitochondrial enzyme, was potently inhibited by fatty acids; cortisol synthesis from 11-deoxycortisol by glomerulosa cells, which requires P450(11beta), was less sensitive to inhibition, and cortisol synthesis from 11-deoxycortisol by fasciculata cells was even less sensitive. 7) Aldosterone synthesis from exogenous 18-hydroxycorticosterone was potently inhibited by oleic acid. Thus, fatty acids are potent inhibitors of the 18-oxidase function of the mitochondrial enzyme P450(11beta), whereas nonmitochondrial steroidogenic enzymes and the 11-hydroxylase function of P450(11beta) are relatively insensitive to fatty acids. The special sensitivity of aldosterone synthesis to fatty acid inhibition appears to result from the unusual susceptibility of the 18-oxidase function of the mitochondrial steroidogenic enzyme P450(11beta). This mechanism would allow differential regulation of aldosterone vs. cortisol production by unesterified fatty acids. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,MADISON,WI 53706. RP ELLIOTT, ME (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,HYPERTENS RES LAB,ROOM C4114,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 16 TC 14 Z9 14 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JUN PY 1993 VL 132 IS 6 BP 2453 EP 2460 DI 10.1210/en.132.6.2453 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LE170 UT WOS:A1993LE17000024 PM 8504749 ER PT J AU CUFF, CF CEBRA, CK RUBIN, DH CEBRA, JJ AF CUFF, CF CEBRA, CK RUBIN, DH CEBRA, JJ TI DEVELOPMENTAL RELATIONSHIP BETWEEN CYTOTOXIC ALPHA/BETA T-CELL RECEPTOR-POSITIVE INTRAEPITHELIAL LYMPHOCYTES AND PEYER PATCH LYMPHOCYTES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE REOVIRUS; INTRAEPITHELIAL LYMPHOCYTES; PEYER PATCH LYMPHOCYTES; CYTOTOXIC T-CELLS ID MURINE INTESTINAL EPITHELIUM; NATURAL-KILLER CELLS; MONOCLONAL-ANTIBODY; LAMINA PROPRIA; GAMMA-DELTA; REOVIRUS; DIFFERENTIATION; POPULATIONS; FREQUENCIES; PRECURSORS AB Following intraduodenal priming of mice with reovirus, precursor cytotoxic T lymphocytes (pCTL) rapidly appear in intraepithelial lymphocytes (IEL) and Peyer's patches. These cells express CTL activity after secondary in vitro stimulation with reovirus-infected cells. Adoptive transfer of Peyer's patch lymphocytes from normal BALB/c mice into reovirus-infected CB. 17 severe combined immunodeficiency mice results in the infection-dependent appearance of large numbers of both CD8+Thy-l+ and CD8-Thy-l+, IEL that express the alpha/beta T cell receptor (TcR). Phenotypic and functional characterization of IEL derived from conventionally reared, reovirus-infected mice also points to extensive similarities in the pCTL derived from Peyer's patches and IEL. As in the Peyer's patches, pCTL are persistent in the IEL compartment for up to 4 weeks after infection. A large percentage of IEL that are recovered from reovirus-primed mice after in vitro culture are CD8+Thy-1+ cells that express alpha/beta TcR. Furthermore, depletion experiments demonstrate that the CD8+Thy-1+ population mediates the virus-specific CTL activity. Using limiting dilution analyses, it was estimated that 7 days after intraduodenal infection the average frequency of virus-specific pCTL was 197/10(6) CD8+Thy-l+ IEL and 190/10(6) CD8+Thy-l+ Peyer's patch lymphocytes. Taken together, these observations provide evidence that specific cellular immunity to reovirus in IEL is mediated, at least in part, by conventional cytotoxic T lymphocytes and that these cells are functionally and phenotypically similar to the pCTL derived from the Peyer's patches. C1 UNIV PENN,DEPT BIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNIV PENN,DEPT MICROBIOL,PHILADELPHIA,PA 19104. FU NCI NIH HHS [T-32-CA-09140]; NIAID NIH HHS [AI-23970, AI-17997] NR 36 TC 62 Z9 62 U1 0 U2 1 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JUN PY 1993 VL 23 IS 6 BP 1333 EP 1339 DI 10.1002/eji.1830230622 PG 7 WC Immunology SC Immunology GA LG517 UT WOS:A1993LG51700021 PM 8388798 ER PT J AU GRAHAM, DY LEW, GM LECHAGO, J AF GRAHAM, DY LEW, GM LECHAGO, J TI ANTRAL G-CELL AND D-CELL NUMBERS IN HELICOBACTER-PYLORI INFECTION - EFFECT OF HELICOBACTER-PYLORI ERADICATION SO GASTROENTEROLOGY LA English DT Article ID DUODENAL-ULCER PATIENTS; GASTRIC-ACID SECRETION; PEPTIC-ULCER; CAMPYLOBACTER-PYLORI; RESECTED STOMACHS; PLASMA GASTRIN; PARIETAL-CELLS; DISEASE; SERUM; HYPERGASTRINEMIA C1 VET AFFAIRS MED CTR,DEPT PATHOL,HOUSTON,TX. VET AFFAIRS MED CTR,DIV MOLEC VIROL,HOUSTON,TX. BAYLOR COLL MED,HOUSTON,TX 77030. RP GRAHAM, DY (reprint author), VET AFFAIRS MED CTR 111D,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NIDDK NIH HHS [DK 39919] NR 47 TC 77 Z9 79 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JUN PY 1993 VL 104 IS 6 BP 1655 EP 1660 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LE468 UT WOS:A1993LE46800010 PM 8500723 ER PT J AU LEO, MA ROSMAN, AS LIEBER, CS AF LEO, MA ROSMAN, AS LIEBER, CS TI DIFFERENTIAL DEPLETION OF CAROTENOIDS AND TOCOPHEROL IN LIVER-DISEASE SO HEPATOLOGY LA English DT Article ID HEPATIC VITAMIN-A; BETA-CAROTENE; RETINOIC ACID; RAT; ETHANOL; METABOLISM; TISSUE; DEHYDROGENASE; CONVERSION; MICROSOMES AB Carotenoids and tocopherols are major natural protective agents against free radical-mediated liver damage, but their levels in diseased liver are largely uncharted. Therefore we carried out measurements with high-pressure liquid chromatography of alpha- and beta-carotene, lycopene, cryptoxanthin, lutein and zeaxanthin, total retinoids and alpha- and gamma-tocopherol. Liver tissue was obtained from percutaneous needle biopsies, livers of transplant recipients or a donor bank. Compared with controls (transplant donors; n = 13), levels of all carotenoids and retinoids were extremely low at all stages of liver disease. Patients with alcoholic cirrhosis (n = 11) had 20- and 25-fold decreases of levels of lycopene (p < 0.001) and alpha- and beta-carotene (p < 0.005), respectively. Even in subjects with less severe alcoholic liver disease (steatosis, perivenular fibrosis, portal fibrosis; n = 14) and in patients with nonalcoholic liver disease (n = 13), levels were four to six times lower than those in normal subjects. By contrast, levels of alpha-tocopherol were decreased significantly only in patients with cirrhosis, who displayed a threefold reduction. In the serum of most patients, lycopene and tocopherol concentrations were not depressed, whereas one third of alpha- and beta-carotene levels were low, probably reflecting poor dietary intake. A significant correlation was observed between serum and liver alpha- and beta-carotene levels (p < 0.0001; r = 0.715). However, of the patients with extremely low liver alpha- and beta-carotene concentrations, more than half had blood levels in the normal range, suggesting that liver disease interferes with the uptake, excretion or, perhaps, metabolism of alpha- and beta-carotene. In the cirrhotic livers of eight candidates for liver transplantation, the ratios of alpha- and beta-carotene to total retinoids and of beta-carotene to retinoids were much higher than those in normal livers, suggesting some impairment in the conversion of alpha- and beta-carotene to retinoids. In most cases, even with high ratios, absolute levels of hepatic alpha- and beta-carotene and retinoids were severely depressed. We concluded that, even in the presence of normal serum levels alpha- and beta-carotene, tocopherol and lycopene, patients with cirrhosis have extremely low hepatic levels. C1 MT SINAI SCH MED,NEW YORK,NY 10468. BRONX VET AFFAIRS MED CTR,LIVER DIS & NUTR SECT,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,ALCOHOL RES & TREATMENT CTR 151-G,130 W KINGSBRIDGE RD,BRONX,NY 10468. FU NIAAA NIH HHS [AA03508]; NIDDK NIH HHS [DK32810] NR 38 TC 103 Z9 105 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD JUN PY 1993 VL 17 IS 6 BP 977 EP 986 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LJ985 UT WOS:A1993LJ98500005 PM 8514270 ER PT J AU HAMNER, MB AF HAMNER, MB TI PTSD AND COCAINE ABUSE SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Letter ID STRESS DISORDER RP HAMNER, MB (reprint author), RALPH HENRY JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC, USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD JUN PY 1993 VL 44 IS 6 BP 591 EP 592 PG 2 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA LC960 UT WOS:A1993LC96000021 PM 8514313 ER PT J AU LEI, MG QURESHI, N MORRISON, DC AF LEI, MG QURESHI, N MORRISON, DC TI LIPOPOLYSACCHARIDE (LPS) BINDING TO 73-KDA AND 38-KDA SURFACE-PROTEINS ON LYMPHORETICULAR CELLS - PREFERENTIAL INHIBITION OF LPS BINDING TO THE FORMER BY RHODOPSEUDOMONAS-SPHAEROIDES LIPID-A SO IMMUNOLOGY LETTERS LA English DT Article DE LPS-BINDING PROTEIN; KDO DETERMINANT; LIPID-A; RS-DPLA ID MURINE SPLENOCYTES; ENDOTOXIN; MACROPHAGES; RECEPTOR; IDENTIFICATION; REQUIREMENTS; ASSOCIATION; INDUCTION; MICE AB Using a photoactivable, radioiodinated lipopolysaccharide probe, [I-125]ASD-LPS (derivatized from purified E. coli 0111:B4 S-LPS), we earlier reported the presence of a 73-kDa (p73) predominant LPS-binding protein on mouse lymphocytes and macrophages with specificity for the lipid A region of LPS. Both Re-LPS from Salmonella minnesota and purified lipid A will inhibit the binding of LPS to the p73 LPS receptor. In the studies reported here, we have found that nontoxic diphosphoryl lipid A purified from Rhodopseudomonas sphaeroides has the capability to inhibit the binding of [I-125]ASD-LPS to the p73 protein. However, using the same LPS probe and photoaffinity cross-linking techniques, our data suggest that a less dominant 38-kDa (p38) LPS-specific binding protein identified on mouse splenocytes, J774.1 macrophage-like cell line, and 70Z/3 pre B-cell line by SDS-PAGE is not inhibited by purified lipid A, even at a concentration in 50-fold excess of that of [I-125]ASD-LPS. The binding of the LPS probe to the p38 protein could be inhibited in a dose-dependent manner by underivatized native S. minnesota Re-LPS (composed only of Kdo and lipid A). We speculate that this p38 LPS-binding protein may manifest a specificity for inner core oligosaccharide determinants on LPS. C1 UNIV KANSAS,MED CTR,CTR CANC,KANSAS CITY,KS 66160. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL LAB,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. RP LEI, MG (reprint author), UNIV KANSAS,MED CTR,DEPT MICROBIOL MOLEC GENET & IMMUNOL,KANSAS CITY,KS 66160, USA. FU NCI NIH HHS [P01-CA54474]; NIAID NIH HHS [R37-AI-23447]; NIGMS NIH HHS [GM-36054] NR 26 TC 20 Z9 20 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD JUN PY 1993 VL 36 IS 3 BP 245 EP 250 DI 10.1016/0165-2478(93)90096-K PG 6 WC Immunology SC Immunology GA LM836 UT WOS:A1993LM83600003 PM 7690343 ER PT J AU PFALLER, MA RINALDI, MG AF PFALLER, MA RINALDI, MG TI ANTIFUNGAL SUSCEPTIBILITY TESTING - CURRENT STATE OF TECHNOLOGY, LIMITATIONS, AND STANDARDIZATION SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID FUNGAL-INFECTIONS; AMPHOTERICIN-B; UNITED-STATES; INVITRO; AGENTS; FLUCONAZOLE; INVIVO; THERAPY; YEASTS; KETOCONAZOLE C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP PFALLER, MA (reprint author), OREGON HLTH SCI UNIV,DEPT PATHOL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. NR 55 TC 46 Z9 46 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0891-5520 J9 INFECT DIS CLIN N AM JI Infect. Dis. Clin. North Am. PD JUN PY 1993 VL 7 IS 2 BP 435 EP 444 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LK347 UT WOS:A1993LK34700016 PM 8345178 ER PT J AU ORWOLL, ES OVIATT, SK BIDDLE, JA AF ORWOLL, ES OVIATT, SK BIDDLE, JA TI PRECISION OF DUAL-ENERGY X-RAY ABSORPTIOMETRY - DEVELOPMENT OF QUALITY-CONTROL RULES AND THEIR APPLICATION IN LONGITUDINAL-STUDIES SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID BONE MASS; FRACTURE; DENSITY; WOMEN; AGE AB In research settings, longitudinal measurements of bone mineral density have become an integral part of the assessment of patients with metabolic skeletal disorders. To adequately utilize longitudinal measures, confidence in the long-term precision of the measurement technique must be very high. Dual-energy x-ray absorptiometry (DXA) has become commonly utilized in this context, and to better understand its long-term precision and to develop quality assurance protocols for its use, we examined the performance of eight DXA machines over a 3 year period. Anthropomorphic spine phantoms were measured frequently on each machine during the period of observation, and precision was estimated from the consistency of these determinations. Overall precision was excellent (mean longitudinal coefficient of variation, 0.4%). Nevertheless, by using a series of objective quality control criteria, small alterations in the performance of each machine were identified (mean number of changes, 4.6 in 3 years; mean magnitude, 0.0039 g/cm2, or 0.4%). The cumulative effects of those changes were sufficient to cause a significant (albeit minor) change in the regression slopes (phantom mineral density versus time) of most machines. The same quality control rules were also used to quantitate the magnitude of change and to adjust retrospectively machine performance during the period of observation, such that alterations were minimal and regression slopes were not significantly different from zero. Although the precision of DXA is excellent, alterations in machine function must be anticipated during longitudinal use. The development of quality control protocols provides the means to detect change objectively and to adjust for alterations in performance during the course of longitudinal evaluations. C1 PORTLAND VA MED CTR,BONE & MINERAL RES UNIT,PORTLAND,OR. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. OI Orwoll, Eric/0000-0002-8520-7355 NR 12 TC 85 Z9 85 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JUN PY 1993 VL 8 IS 6 BP 693 EP 699 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LE193 UT WOS:A1993LE19300006 PM 8328311 ER PT J AU DYER, DG DUNN, JA THORPE, SR BAILIE, KE LYONS, TJ MCCANCE, DR BAYNES, JW AF DYER, DG DUNN, JA THORPE, SR BAILIE, KE LYONS, TJ MCCANCE, DR BAYNES, JW TI ACCUMULATION OF MAILLARD REACTION-PRODUCTS IN SKIN COLLAGEN IN DIABETES AND AGING SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE AGING; COLLAGEN; DIABETES; GLYCATION; OXIDATION ID AGE-DEPENDENT ACCUMULATION; OXIDATIVE STRESS; CROSS-LINK; MELLITUS; N-EPSILON-(CARBOXYMETHYL)LYSINE; GLYCATION; PROTEIN; COMPLICATIONS; PENTOSIDINE; PRECURSORS AB To investigate the contribution of glycation and oxidation reactions to the modification of insoluble collagen in aging and diabetes, Maillard reaction products were measured in skin collagen from 39 type 1 diabetic patients and 52 nondiabetic control subjects. Compounds studied included fructoselysine (FL), the initial glycation product, and the glycoxidation products, N(epsilon)-(carboxymethyl)lysine (CML) and pentosidine, formed during later Maillard reactions. Collagen-linked fluorescence was also studied. In nondiabetic subjects, glycation of collagen (FL content) increased only 33% between 20 and 85 yr of age. In contrast, CML, pentosidine and fluorescence increased five-fold, correlating strongly with age. In diabetic patients, collagen FL was increased threefold compared with nondiabetic subjects, correlating strongly with glycated hemoglobin but not with age. Collagen CML, pentosidine and fluorescence were increased up to twofold in diabetic compared with control patients: this could be explained by the increase in glycation alone, without invoking increased oxidative stress. There were strong correlations among CML, pentosidine and fluorescence in both groups, providing evidence for age-dependent chemical modification of collagen via the Maillard reaction, and acceleration of this process in diabetes. These results support the description of diabetes as a disease characterized by accelerated chemical aging of long-lived tissue proteins. C1 MED UNIV S CAROLINA,DEPT CHEM & BIOCHEM,DIV ENDOCRINOL DIABET & METAB,171 ASHLEY AVE,CHARLESTON,SC 29425. UNIV S CAROLINA,DEPT CHEM & BIOCHEM,COLUMBIA,SC 29208. UNIV S CAROLINA,SCH MED,COLUMBIA,SC 29208. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. ALTNAGELVIN HOSP,DEPT MED,LONDONDERRY BT47 1JE,NORTH IRELAND. ROYAL VICTORIA HOSP,SIR GEORGE E CLARK METAB UNIT,BELFAST BT12 6BA,NORTH IRELAND. FU NIDDK NIH HHS [DK-19971] NR 25 TC 485 Z9 494 U1 4 U2 36 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 JUN PY 1993 VL 91 IS 6 BP 2463 EP 2469 DI 10.1172/JCI116481 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LH121 UT WOS:A1993LH12100018 PM 8514858 ER PT J AU MCCANCE, DR DYER, DG DUNN, JA BAILIE, KE THORPE, SR BAYNES, JW LYONS, TJ AF MCCANCE, DR DYER, DG DUNN, JA BAILIE, KE THORPE, SR BAYNES, JW LYONS, TJ TI MAILLARD REACTION-PRODUCTS AND THEIR RELATION TO COMPLICATIONS IN INSULIN-DEPENDENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE COLLAGEN; COMPLICATIONS OF DIABETES; GLYCATION; OXIDATION; NONENZYMATIC BROWNING ID NON-ENZYMATIC GLYCOSYLATION; HUMAN-SKIN COLLAGEN; LIMITED JOINT MOBILITY; GLYCEMIC CONTROL; LINKED FLUORESCENCE; GLYCATED PROTEINS; CROSS-LINKING; END-PRODUCTS; RETINOPATHY; AGE AB Glycation, oxidation, and browning of proteins have all been implicated in the development of diabetic complications. We measured the initial Amadori adduct, fructoselysine (FL); two Maillard products, N(epsilon)-(carboxymethyl) lysine (CML) and pentosidine; and fluorescence (excitation = 328 nm, emission = 378 nm) in skin collagen from 39 type 1 diabetic patients (aged 41.5 +/- 15.3 117-731 yr; duration of diabetes 17.9 +/- 11.5 10-461 yr, [mean +/- SD, range]). The measurements were related to the presence of background (n = 9) or proliferative (n = 16) retinopathy; early nephropathy (24-h albumin excretion rate [AER24] greater-than-or-equal-to 20 mug/min; n = 9); and limited joint mobility (LJM; n = 20). FL, CML, pentosidine, and fluorescence increased progressively across diabetic retinopathy (P < 0.05, P < 0.001, P < 0.05, P < 0.01, respectively). FL, CML, pentosidine, and fluorescence were also elevated in patients with early nephropathy (P < 0.05, P < 0.001, P < 0.01, P < 0.01, respectively). There was no association with LJM. Controlling for age, sex, and duration of diabetes using logistic regression, FL and CML were independently associated with retinopathy (FL odds ratio (OR) = 1.06, 95% confidence interval (CI) = 1.011. 12, P < 0.05; CML OR = 6.77, 95% CI = 1.33-34.56, P < 0.05) and with early nephropathy (FL OR = 1.05, 95% CI = 1.01-1.10, P < 0.05; CML OR = 13.44,95% CI = 2.0093. 30, P < 0.01). The associations between fluorescence and retinopathy and between pentosidine and nephropathy approached significance (P = 0.05). These data show that FL and Maillard products in skin correlate with functional abnormalities in other tissues and suggest that protein glycation and oxidation (glycoxidation) may be implicated in the development of diabetic retinopathy and early nephropathy. C1 MED UNIV S CAROLINA, DIV ENDOCRINOL DIABET & METAB, 171 ASHLEY AVE, CHARLESTON, SC 29425 USA. ROYAL VICTORIA HOSP, SIR GEORGE E CLARK METAB UNIT, BELFAST BT12 6BA, NORTH IRELAND. UNIV S CAROLINA, DEPT CHEM & BIOCHEM, COLUMBIA, SC 29208 USA. UNIV S CAROLINA, SCH MED, COLUMBIA, SC 29208 USA. ALTNAGELVIN HOSP, DEPT MED, LONDONDERRY BT47 1JB, NORTH IRELAND. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR, CHARLESTON, SC 29401 USA. FU NIDDK NIH HHS [DK-19971] NR 67 TC 338 Z9 343 U1 2 U2 18 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 EI 1558-8238 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1993 VL 91 IS 6 BP 2470 EP 2478 DI 10.1172/JCI116482 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LH121 UT WOS:A1993LH12100019 PM 8514859 ER PT J AU MELCHER, GP MCGOUGH, DA FOTHERGILL, AW NORRIS, C RINALDI, MG AF MELCHER, GP MCGOUGH, DA FOTHERGILL, AW NORRIS, C RINALDI, MG TI DISSEMINATED HYALOHYPHOMYCOSIS CAUSED BY A NOVEL HUMAN PATHOGEN, FUSARIUM-NAPIFORME SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; FUNGAL INFECTION; LEUKEMIA; PATIENT; SOLANI; HOST AB Fusarium species are saprophytic molds and important plant pathogens, although they are increasingly recognized as agents of human mycosis. Frequently, the infection is superficial. Deep tissue infection may occur as an opportunistic hyalohyphomycosis, and wide dissemination is common in immunocompromised hosts. We describe a novel case of disseminated hyalohyphomycosis caused by F. napiforme in a patient with acute myelogenous leukemia. The clinical manifestations of this infection were similar to those attributed to infection with other species. In vitro susceptibility testing demonstrated resistance to amphotericin B and flucytosine, and progressive infection was documented until recovery of granulocyte function. The distinguishing clinical mycologic characteristics of this opportunistic mold are the unique turnip- or lemon-shaped microconidia. F. napiforme is a new agent of hyalohyphomycosis, further emphasizing the importance of Fusarium species as opportunistic molds. C1 WILFORD HALL USAF MED CTR,DEPT PATHOL,LACKLAND AFB,TX 78236. UNIV TEXAS,HLTH SCI CTR,FUNGUS TESTING LAB,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RP MELCHER, GP (reprint author), WILFORD HALL USAF MED CTR,DEPT INFECT DIS,LACKLAND AFB,TX 78236, USA. NR 34 TC 24 Z9 24 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JUN PY 1993 VL 31 IS 6 BP 1461 EP 1467 PG 7 WC Microbiology SC Microbiology GA LC728 UT WOS:A1993LC72800012 PM 8314987 ER PT J AU SMITH, DL LUCAS, LM AF SMITH, DL LUCAS, LM TI THE HUMAN SKELETON - AN OVERLOOKED BUT EFFECTIVE VISUAL AID SO JOURNAL OF RHEUMATOLOGY LA English DT Letter C1 OREGON HLTH SCI UNIV,DIV GEN MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,GEN MED SECT,PORTLAND,OR 97207. RP SMITH, DL (reprint author), PORTLAND VET AFFAIRS MED CTR,GEN MED RHEUMAT DIS SECT,PORTLAND,OR 97207, USA. NR 2 TC 1 Z9 3 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JUN PY 1993 VL 20 IS 6 BP 1088 EP 1089 PG 2 WC Rheumatology SC Rheumatology GA LH112 UT WOS:A1993LH11200044 PM 7688813 ER PT J AU LEUCHTER, AF DALY, KA ROSENBERGTHOMPSON, S ABRAMS, M AF LEUCHTER, AF DALY, KA ROSENBERGTHOMPSON, S ABRAMS, M TI PREVALENCE AND SIGNIFICANCE OF ELECTROENCEPHALOGRAPHIC ABNORMALITIES IN PATIENTS WITH SUSPECTED ORGANIC MENTAL SYNDROMES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID DEPRESSED SUBJECTS; EEG; DEMENTIA; AGE AB Objective: To determine the prevalence of electroencephalogram (EEG) abnormalities at different levels of cognitive impairment and to assess the possible diagnostic usefulness of the test. Design: Combined prospective assessment of subjects receiving EEGs and retrospective chart review of symptoms and medications. Setting: Academic geriatric psychiatry service. Patients: 350 adults age 50 and above; 312 were patients being evaluated for possible organic mental syndrome and 38 were normal controls. Measurements: All subjects had EEGs and Mini-Mental State Examinations (MMSE) performed at the time of the EEG. EEGs were rated for the presence and type of abnormality, and subjects were stratified according to the severity of impairment. Charts were reviewed by a person blinded to EEG results to determine clinical diagnosis and medications received. Main Results: Abnormal EEGs were significantly more common among all patients (67%) in the study than among controls (11%), and the prevalence of abnormality increased with increasing impairment. Many demented patients with equivocal impairment (42%), and most with mild-to-moderate impairment (65%) had abnormal EEGs. An abnormal EEG was not indicative of dementia even when clear cognitive impairment was present, since patients with depression frequently also had abnormal EEG results. Conclusions: These findings suggest that the EEG is a moderately sensitive but non-specific indicator of brain dysfunction in the elderly. The significance of abnormalities among patients with equivocal impairment should be more fully assessed by longitudinal follow-up to determine if greater cognitive impairment develops. C1 UNIV CALIF LOS ANGELES, HOSP NEUROPSYCHIAT, QUANTITAT EEG LAB, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, ROBERT WOOD JOHNSON CLIN SCHOLARS PROGRAM, W LOS ANGELES VET ADM MED CTR, VET ADM, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, ROBERT WOOD JOHNSON CLIN SCHOLARS PROGRAM, W LOS ANGELES VET ADM MED CTR, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA USA. RP LEUCHTER, AF (reprint author), UNIV CALIF LOS ANGELES, INST NEUROPSYCHIAT, QUANTITAT EEG LAB, 760 WESTWOOD PLAZA, LOS ANGELES, CA 90024 USA. FU NIA NIH HHS [P30 AG10123]; NIMH NIH HHS [MH 00665, MH 40705] NR 24 TC 17 Z9 19 U1 1 U2 1 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JUN PY 1993 VL 41 IS 6 BP 605 EP 611 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA LF776 UT WOS:A1993LF77600002 PM 8505456 ER PT J AU KANTEN, DN MULROW, CD GERETY, MB LICHTENSTEIN, MJ AGUILAR, C CORNELL, JE AF KANTEN, DN MULROW, CD GERETY, MB LICHTENSTEIN, MJ AGUILAR, C CORNELL, JE TI FALLS - AN EXAMINATION OF 3 REPORTING METHODS IN NURSING-HOMES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article AB Objective: To examine the concordance of various fall reporting methods and to use the results to recommend a preferred method of ascertaining fall frequency for residents of nursing homes, both for research and in the collection of federally mandated nursing home data. Design: A cohort study followed for 858 patient months, with a mean individual follow-up of 6.6 months. Measurements: Falls were independently ascertained monthly by three methods: review of administrative incident reports, nursing home chart abstraction, and structured interview of subjects. Concordance of events was assessed using measures of simple agreement and Kendall's Tau-b. Simple correlation and multiple regression were used to evaluate the relation of age, sex, gender, depression, mental status, and functional status with degree of concordance between self-reported falls and chart-recorded falls. Setting: One academic and six community nursing homes in San Antonio, Texas. Participants: 131 long-stay nursing home residents, greater than 60 years of age, dependent in at least two activities of daily living, and mildly cognitively impaired. Results: Falls were ascertained in 74 of the 131 individuals; 53 subjects fell 124 times by incident report, 58 had 140 falls according to chart review, and 66 subjects self-reported 232 falls. Greatest agreement between reporting methods was shown for incident report and chart review, with a Kendall's Tau-b of 0.88; self-report and chart-review agreement was 0.56; and self-report and incident agreement was 0.53. Estimated total fall events were more often (P = 0.001) identified by chart review (92%) than incident report (82%). Although concordance was higher for non-fallers, no significant relationships were observed between concordance and age, sex, race, depression, mental status, and functional status. Also, there was no systematic relationship between length of follow-up and degree of concordance. Conclusions: Fall frequency varies by ascertainment method, with chart review reflecting a greater number of fall events than the traditionally counted incident reports. C1 UNIV TEXAS,HLTH SCI CTR,DIV GERIATR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. RP KANTEN, DN (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [U01AG09117-01] NR 18 TC 54 Z9 55 U1 5 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JUN PY 1993 VL 41 IS 6 BP 662 EP 666 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA LF776 UT WOS:A1993LF77600013 PM 8505465 ER PT J AU HAFFNER, SM BAUER, RL AF HAFFNER, SM BAUER, RL TI THE ASSOCIATION OF OBESITY AND GLUCOSE AND INSULIN CONCENTRATIONS WITH BONE-DENSITY IN PREMENOPAUSAL AND POSTMENOPAUSAL WOMEN SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID MEXICAN-AMERICANS; DIABETES-MELLITUS; RISK; BODY; MASS C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN EPIDEMIOL,SAN ANTONIO,TX 78284. FU NHLBI NIH HHS [R01 HL24799, R37 HL36820]; NIAMS NIH HHS [R01 AR39794] NR 24 TC 60 Z9 62 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD JUN PY 1993 VL 42 IS 6 BP 735 EP 738 DI 10.1016/0026-0495(93)90241-F PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LG442 UT WOS:A1993LG44200012 PM 8510518 ER PT J AU TYAN, ML AF TYAN, ML TI EFFECTS OF H-2 AND DIETARY VITAMIN-A ON THE FREQUENCY OF DORSOVENTRAL VAGINAL SEPTUM SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLEFT-PALATE; MICE; GENE AB The frequency of dorsoventral vaginal septum (DVS) in mice is determined in part by genes associated with the major histocompatibility complex H-2. Data presented here confirm that one locus (DVS-1) maps centromeric to Ealpha and that the second (DVS-2), previously shown to be associated with the S-to-D region, maps to the C4:B144 interval, most likely between Dcp-2 which contributes to glucocorticoid-induced cleft palate susceptibility and Acp which enhances cleft palate susceptibility through the action of vitamin A. Comparisons of data obtained in this laboratory in the periods 1981-1983 and 1985-1990 and observations from the production colony from which many of the strains were purchased revealed minor variations in frequencies of DVS within strains which may be due to differences in ascertainment and/or to environmental factors. The addition of vitamin A to the diet of pregnant mice at a dose that increases the frequency of cleft palate in susceptible strains had no effect on the incidence of DVS. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90073 USA. RP TYAN, ML (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, W 111M, LOS ANGELES, CA 90073 USA. NR 14 TC 1 Z9 1 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JUN PY 1993 VL 203 IS 2 BP 175 EP 178 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LD339 UT WOS:A1993LD33900007 PM 8502659 ER PT J AU STERN, RG KAHN, RS DAVIDSON, M AF STERN, RG KAHN, RS DAVIDSON, M TI PREDICTORS OF RESPONSE TO NEUROLEPTIC TREATMENT IN SCHIZOPHRENIA SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID PLASMA HOMOVANILLIC-ACID; LATERAL VENTRICULAR SIZE; SUBJECTIVE RESPONSE; SHORT-TERM; CATECHOLAMINE METABOLITES; ANTIPSYCHOTIC-DRUGS; CLINICAL-RESPONSE; COMPUTERIZED EEG; CT SCANS; HVA C1 BRONX VET AFFAIRS MED CTR,NEW YORK,NY. RP STERN, RG (reprint author), CUNY MT SINAI SCH MED,DEPT PSYCHIAT,BOX 1228,1 GUSTAVE LEVY PL,NEW YORK,NY 10029, USA. NR 58 TC 24 Z9 24 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0193-953X J9 PSYCHIAT CLIN N AM JI Psychiatr. Clin. North Amer. PD JUN PY 1993 VL 16 IS 2 BP 313 EP 338 PG 26 WC Psychiatry SC Psychiatry GA LG548 UT WOS:A1993LG54800007 PM 8101371 ER PT J AU MIDHA, KK MARDER, SR JAWORSKI, TJ MCKAY, G HUBBARD, JW HAWES, EM VANPUTTEN, T WIRSHING, WC ARAVAGIRI, M AF MIDHA, KK MARDER, SR JAWORSKI, TJ MCKAY, G HUBBARD, JW HAWES, EM VANPUTTEN, T WIRSHING, WC ARAVAGIRI, M TI CLINICAL PERSPECTIVES OF SOME NEUROLEPTICS THROUGH DEVELOPMENT AND APPLICATION OF THEIR ASSAYS SO THERAPEUTIC DRUG MONITORING LA English DT Article DE FLUPHENAZINE; FLUPHENAZINE DECANOATE; FLUPHENAZINE DIHYDROCHLORIDE; PLASMA LEVEL MONITORING; PHARMACOKINETICS; ASSAY; APPLICATIONS TO CLINICAL STUDIES ID FLUPHENAZINE PLASMA-LEVELS; LIQUID-CHROMATOGRAPHIC METHOD; SCHIZOPHRENIC-PATIENTS; MONOCLONAL-ANTIBODIES; BLOOD-LEVELS; N-OXIDE; DECANOATE; RADIOIMMUNOASSAY; PHARMACOKINETICS; CHLORPROMAZINE AB Attempts to investigate relationships between plasma levels of neuroleptics and therapeutic outcome in schizophrenic patients have been hampered due to such factors as the chemical nature of these drugs, their metabolism, and the very heterogeneous nature of the disease states. Two clinical studies are described that investigate the relationship between plasma levels of fluphenazine (FLU) and its metabolites and therapeutic outcome in schizophrenic patients. In the first of these studies the levels of FLU and fluphenazine sulfoxide (FLUSO) in schizophrenics receiving either 5 or 25 mg of fluphenazine decanoate (FLUD) intramuscularly every 2 weeks were monitored. Patients given 25 mg of FLUD required 3 months to reach plasma level steady state. The results suggest that such patients, when being switched from the oral to the depot formulation of FLU, should continue to receive oral supplementation during the 1st 3 months after conversion. The relationship between log-transformed plasma levels at 26 and 38 weeks with subsequent psychotic exacerbation was investigated with the use of logistic regression and survival analysis. Both demonstrated significant relationships between FLU plasma levels and a risk of psychotic exacerbation at 26 and 38 weeks. The possibility of any correlations between neurological side effects and plasma concentrations were also investigated, with statistically significant correlations between FLU levels and akinesia found at 2 and 26 weeks. In the second of these studies the levels of FLU, FLUSO, 7-hydroxyfluphenazine (7-OHFLU), and fluphenazine N4'-oxide (FLUNO) in schizophrenics receiving 5, 10, or 20 mg of oral fluphenazine dihydrochloride daily for 4 weeks were monitored. The relationships between log-transformed plasma levels, disabling side effects, and global improvement were examined by logistic regression for the 4-week period. The study showed a significant correlation between increases in both plasma levels and disabling side effects such that at a plasma level of 2.7 ng/ml, approximately 90% of acutely ill patients experienced disabling side effects. Conversely, the study also showed that at a plasma level of 0.67 ng/ml, 48% of patients experienced improvement without the development of disabling side effects. When relationships between metabolite levels, disabling side effects, and global improvement were examined by logistic regression, a stronger correlation between disabling side effects and FLUNO levels than between side effects and FLU levels was found. No correlations between disabling side effects and plasma levels of FLUSO or 7-OHFLU were observed. These studies illustrate the usefulness of measuring plasma levels of neuroleptic drugs. C1 UNIV SASKATCHEWAN,COLL MED,SASKATOON S7N 0W0,SASKATCHEWAN,CANADA. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. RP MIDHA, KK (reprint author), UNIV SASKATCHEWAN,COLL PHARM,SASKATOON S7N 0W0,SASKATCHEWAN,CANADA. NR 58 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0163-4356 J9 THER DRUG MONIT JI Ther. Drug Monit. PD JUN PY 1993 VL 15 IS 3 BP 179 EP 189 DI 10.1097/00007691-199306000-00001 PG 11 WC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology SC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology GA LF859 UT WOS:A1993LF85900001 PM 8101398 ER PT J AU GABRIEL, SM BIERER, LM HAROTUNIAN, V PUROHIT, DP PERL, DP DAVIS, KL AF GABRIEL, SM BIERER, LM HAROTUNIAN, V PUROHIT, DP PERL, DP DAVIS, KL TI WIDESPREAD DEFICITS IN SOMATOSTATIN BUT NOT NEUROPEPTIDE-Y CONCENTRATIONS IN ALZHEIMERS-DISEASE CEREBRAL-CORTEX SO NEUROSCIENCE LETTERS LA English DT Article DE ALZHEIMERS DISEASE; SOMATOSTATIN; NEUROPEPTIDE-Y; DEMENTIA; NEUROPEPTIDE; NEURODEGENERATION; NITRIC OXIDE SYNTHASE; NADPH-DIAPHORASE ID CHOLINE-ACETYLTRANSFERASE ACTIVITY; SENILE DEMENTIA; NADPH-DIAPHORASE; PARKINSONS-DISEASE; DOWNS-SYNDROME; IMMUNOREACTIVITY; NEURONS; COEXISTENCE; POLYPEPTIDE AB Somatostatin-like immunoreactivity (SLI) and neuropeptide Y-like immunoreactivity (NPYLI) were measured in the cerebral cortex of 49 patients with Alzheimer's disease (AD), and 9 elderly controls. Concentrations of SLI were lower in AD patients relative to controls in 9 of 10 cortical regions. In contrast, no significant differences in NPYLI concentrations between the two groups were observed in any of 10 regions. These studies suggest a dissociation between SLI deficits and NPYLI concentrations in the postmortem cerebral cortex of AD patients. The apparent sparing of NPYLI-containing neurons suggests that neuropeptide Y may be located within a separate group of neurons compared to somatostatin. C1 CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. RP GABRIEL, SM (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIA NIH HHS [NIA AG00408, NIA AG02219, NIA AG05138] NR 33 TC 33 Z9 36 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAY 28 PY 1993 VL 155 IS 1 BP 116 EP 120 DI 10.1016/0304-3940(93)90686-F PG 5 WC Neurosciences SC Neurosciences & Neurology GA LK125 UT WOS:A1993LK12500027 PM 8103205 ER PT J AU ABBOUD, SL AF ABBOUD, SL TI A BONE-MARROW STROMAL CELL-LINE IS A SOURCE AND TARGET FOR PLATELET-DERIVED GROWTH-FACTOR SO BLOOD LA English DT Article ID MICROVASCULAR ENDOTHELIAL-CELLS; FACTOR-LIKE PROTEIN; FACTOR-BETA; C-SIS; MESSENGER-RNA; FACTOR PDGF; A-CHAIN; B-CHAIN; PROGENITOR CELLS; EXPRESSION C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP ABBOUD, SL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 47 TC 23 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 0006-4971 J9 BLOOD JI Blood PD MAY 15 PY 1993 VL 81 IS 10 BP 2547 EP 2553 PG 7 WC Hematology SC Hematology GA LC496 UT WOS:A1993LC49600011 PM 7683921 ER PT J AU LOVE, RR CARBONE, PP VERMA, AK GILMORE, D CAREY, P TUTSCH, KD POMPLUN, M WILDING, G AF LOVE, RR CARBONE, PP VERMA, AK GILMORE, D CAREY, P TUTSCH, KD POMPLUN, M WILDING, G TI RANDOMIZED PHASE-I CHEMOPREVENTION DOSE-SEEKING STUDY OF ALPHA-DIFLUOROMETHYLORNITHINE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ORNITHINE DECARBOXYLASE; POLYAMINE BIOSYNTHESIS; INHIBITOR AB Background: Alpha-difluoromethylornithine (DFMO) is an irreversible inhibitor of ornithine decarboxylase (ODC), the key enzyme in mammalian polyamine biosynthesis. Levels of ODC are closely related to tumor promotion, and inhibition of ODC is associated with suppression of tumor development in laboratory animals. DFMO has shown a dose-response effect in tumor inhibition in mice. Purpose: A randomized phase I study of DFMO was conducted to determine the lowest daily oral dose that can achieve at least 50% inhibition of ODC activity induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in human skin, with minimal clinical toxicity (grade 1 or lower; Eastern Cooperative Oncology Group [ECOG]). Methods: Cancer patients entered in steps 1 and 2 of the study had been treated and had no clinical evidence of cancer. In step 1, 13 patients received 0.125, 0.25, 0.5, or 0.75 g/m2 DFMO four times a day. In step 2, 13 patients received 0.125 or 0.25 g/m2 four times a day or 0.5 or 1.0 g/m2 every day. The 26 patients treated in steps 1 and 2 (range, <1-6 months) had colon, prostate, or bladder cancer. In step 3, six cancer-free subjects at risk for colorectal cancer received 0.5 g/m2 every day for 5-12 months. To evaluate the effectiveness of DFMO in reducing TPA-induced ODC activity, we calculated the percent change from pretreatment ODC levels in skin biopsy specimens and the percentage of subjects with at least a 50% reduction in ODC levels. Results: In step 1 of the study, treatment-limiting audiotoxicity was observed at the three highest doses. Because the only dose with no major toxic effects in step 2 was 0.5 g/m2 every day, that dose was administered in step 3, with no major toxic effects. Seven subjects treated with 0.5 g/m2 every day had pretreatment ODC levels in the normal range; five averaged a reduction in ODC activity of at least 50%. DFMO had linear pharmacokinetics over the entire dose range. When 0.5 g/m2 was given every day, the peak plasma concentration was 47.1 +/- 5.1 muM at 3-4 hours (monthly mean +/- SE, 14.5 +/- 5.2 muM); half-life was 3.5 hours; and area under the curve for plasma concentration X time for a single dose of DFMO was 311 +/- 39 muM X hour. Conclusions: These data support phase II chemoprevention studies with DFMO given at a dose of 0.5 g/m2 every day. Implications: Studies investigating prevention of cancers with DFMO are under consideration. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP LOVE, RR (reprint author), UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI 53792, USA. FU NCI NIH HHS [N01-CN-85109] NR 13 TC 95 Z9 95 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 MAY 5 PY 1993 VL 85 IS 9 BP 732 EP 737 DI 10.1093/jnci/85.9.732 PG 6 WC Oncology SC Oncology GA LA672 UT WOS:A1993LA67200014 PM 8478959 ER PT J AU DIN, ZZ MUKERJEE, P KASTOWSKY, M TAKAYAMA, K AF DIN, ZZ MUKERJEE, P KASTOWSKY, M TAKAYAMA, K TI EFFECT OF PH ON SOLUBILITY AND IONIC STATE OF LIPOPOLYSACCHARIDE OBTAINED FROM THE DEEP ROUGH MUTANT OF ESCHERICHIA-COLI SO BIOCHEMISTRY LA English DT Article ID DIPHOSPHORYL-LIPID-A; PHOTOAFFINITY CROSS-LINKING; RHODOPSEUDOMONAS-SPHAEROIDES; BINDING-SITES; STRUCTURAL CHARACTERISTICS; 70Z/3 CELLS; FATTY-ACIDS; LYMPHOCYTES; MACROPHAGES; INDUCTION AB The dissociation of the highly aggregated form of lipopolysaccharide (LPS) from Gram-negative bacteria to the monomeric (or soluble) form is though to be the initial step in the activation of responding cells (macrophages, B-cells, neutrophils, monocytes, and endothelial cells) by LPS. This process is presently not adequately understood. Using the equilibrium dialysis apparatus and a highly purified and well-characterized radiolabeled deep rough chemotype LPS ([C-14]ReLPS) from Escherichia coli D31m4, we have examined the effect of pH on its solubility (CT) and ionic states in aqueous media. The solubility range of [C-14]ReLPS suspended in 50 mM Tris-HCl-100 mM KCl buffer (or 50 mM MES-100 mM KCl buffer at pH 6.5) was determined to be from (2.91 +/- 0.01) X 10-8 to (4.55 +/- 0.07) X 10(-8) M over a pH range of 6.50-8.20, respectively. These experimental data satisfactorily fitted the curve generated by the solubility equation C(T)=S0(1+K5/[H+])/([H+]/K4'+1), where S0 is the concentration of the tetraanionic ReLPS, K5 is the dissociation constant of the tetraanionic ReLPS in solution, and K4' is the dissociation constant of the trianionic ReLPS at the surface of the solid particles in suspension. The increase in solubility of ReLPS with increase in pH from 7.00 to 8.20 is primarily caused by the formation of the pentaanionic form from the tetraanions. The pK5 (primarily the second dissociation of the l-phosphate) of ReLPS was determined to be 8.58 from experimental data. Theoretical arguments were presented to show that this value is higher than that for simple model compounds (monosaccharide monophosphates where pK = 6.1 for the second dissociation) because of electrostatic effects caused by the other phosphate and carboxylate groups of two 2-keto-3-deoxyoctonate (Kdo) moieties of ReLPS. Using the same theoretical arguments, pK6 was calculated to be much higher, 10.8. In the absence of Kdo groups, as is the case of 1,4'-diphosphoryl lipid A, the same theoretical approach showed that the pK values of the second dissociations of the two phosphate groups are lower and are separated by smaller numbers, giving calculated pK values of 6.9 and 7.8. The presence of nearby Kdo units in ReLPS gives the molecule fewer negative charges on the phosphate groups compared to lipid A. This may contribute to better binding of ReLPS to the LPS receptors and may explain its higher biological activity when compared to lipid A. From these results, we can now provide the monomeric concentrations, pK values, ionic states, and charge distribution of a model, toxic LPS dissolved in aqueous media. Such information is necessary to understand the molecular basis for the biological activities of LPS. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. FREE UNIV BERLIN,INST KRISTALLOG,W-1000 BERLIN 33,GERMANY. FU NIGMS NIH HHS [GM-36054] NR 49 TC 41 Z9 42 U1 1 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 MAY 4 PY 1993 VL 32 IS 17 BP 4579 EP 4586 DI 10.1021/bi00068a014 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LA560 UT WOS:A1993LA56000014 PM 8485134 ER PT J AU MORGAN, MB CINTRON, G BALIS, JU AF MORGAN, MB CINTRON, G BALIS, JU TI INFECTIVE MYCOTIC AORTIC ROOT ANEURYSM FOLLOWING CORONARY-ARTERY BYPASS-GRAFTING SO AMERICAN JOURNAL OF MEDICINE LA English DT Note C1 US DEPT VET AFFAIRS,JAMES A HALEY VET HOSP,TAMPA,FL. RP MORGAN, MB (reprint author), UNIV S FLORIDA,COLL MED,TAMPA,FL 33612, USA. NR 6 TC 4 Z9 4 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD MAY PY 1993 VL 94 IS 5 BP 550 EP 552 DI 10.1016/0002-9343(93)90096-8 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA LC874 UT WOS:A1993LC87400020 PM 8498404 ER PT J AU HOWIESON, J KAYE, JA HOLM, L HOWIESON, D AF HOWIESON, J KAYE, JA HOLM, L HOWIESON, D TI INTERUNCAL DISTANCE - MARKER OF AGING AND ALZHEIMER-DISEASE SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE DEMENTIA; BRAIN, MEASUREMENTS; BRAIN, MAGNETIC RESONANCE; AGE AND AGING; DEGENERATIVE BRAIN DISEASE ID DEMENTIA AB PURPOSE: To evaluate the utility of a recently reported simple measure of brain atrophy on MR imaging, the interuncal distance (IUD). METHODS: Measurements of the IUD were made over a 12-month interval in 10 patients with probable early Alzheimer disease and in a comparison group of age-matched healthy control subjects. The measurements were made in both the transaxial and coronal planes. RESULTS: Significant group differences for the coronal measurement of IUD were found in both the absolute value of the measurement and the IUD corrected for head size. There was overlap in IUD between the disease and the control groups. These differences were not found for the transaxial IUD. Significant positive correlations of the IUD with Mini-Mental State Examination score and Clinical Dementia Rating Scale stage were observed. Over the age range tested, age was not significantly correlated with IUD in the sample. CONCLUSIONS: The interuncal distance IUD is not a useful screening measurement for Alzheimer disease. C1 OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP HOWIESON, J (reprint author), OREGON HLTH SCI UNIV,DEPT DIAGNOST RADIOL,L340,3181 SAM JACKSON PK RD,PORTLAND,OR 97201, USA. OI Kaye, Jeffrey/0000-0002-9971-3478 FU NIA NIH HHS [AG 08017] NR 11 TC 17 Z9 17 U1 0 U2 0 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 MAY-JUN PY 1993 VL 14 IS 3 BP 647 EP 650 PG 4 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA LC082 UT WOS:A1993LC08200023 PM 8517353 ER PT J AU ZHOU, WG LEVINE, BA OLSON, MS AF ZHOU, WG LEVINE, BA OLSON, MS TI PLATELET-ACTIVATING-FACTOR - A MEDIATOR OF PANCREATIC INFLAMMATION DURING CERULEIN HYPERSTIMULATION SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID CALCIUM MOBILIZATION; RECEPTOR OCCUPATION; ENZYME-SECRETION; RAT; BN-52021; ACINI; AGGREGATION; NEUTROPHILS; ANTAGONIST; INCREASES AB Hyperstimulation of the exocrine pancreas with cerulein causes acute pancreatitis, characterized by intensive interstitial edema, acinar vacuolization, leukocytic infiltration, and hyperamylasemia Whereas the pathogenesis of cerulein-induced pancreatitis is not well-defined, a local inflammatory response may contribute to the full expression of acute pancreatitis. Platelet-activating factor (PAF) seems to be an important mediator of the inflammatory response. The present evidence includes: 1) pancreatic PAF levels increased in rats in which cerulein-induced pancreatitis was initiated, concomitant with an increase in calcium concentrations in the pancreatic tissue, 2) treatment of rats exposed to cerulein with WEB2170, a PAF receptor antagonist, was shown to reduce inflammatory injury, as demonstrated by decreases in pancreatic weight, Evan's blue extravasation, and myeloperoxidase activity and an improvement in pancreatic histology. In an idealized in vitro experiment mimicking cerulein-induced acute pancreatitis, in which pancreatic acini were employed, cerulein induced amylase release, an increase in [Ca2+]i, and an increase in PAF synthesis. Whereas amylase release was induced by low concentrations of cerulein (10(-11) mol/L), relatively high concentrations of cerulein (10(-9) mol/L) were required for the observed increases in PAF synthesis and the [Ca2+]i, indicating that these two responses may not occur under physiological conditions. The present study suggests that the pancreatic accumulation of PAF coupled with Ca2+ overload are important biochemical components of the pathophysiology of cerulein-induced acute pancreatitis. In fact, PAF production may serve as a primary mediator of inflammation observed during pancreatic hyperstimulation. This is an important observation that will allow a more detailed characterization of the molecular basis of cerulein-induced acute pancreatitis. C1 UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM-19473] NR 38 TC 49 Z9 52 U1 0 U2 1 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 MAY PY 1993 VL 142 IS 5 BP 1504 EP 1512 PG 9 WC Pathology SC Pathology GA LC123 UT WOS:A1993LC12300020 PM 8494049 ER PT J AU HWANG, SJ HARRIS, HW OTUECHERE, G YALLA, S SULLIVAN, MR KASHGARIAN, M BENOS, DJ KLEYMAN, TR ZEIDEL, ML AF HWANG, SJ HARRIS, HW OTUECHERE, G YALLA, S SULLIVAN, MR KASHGARIAN, M BENOS, DJ KLEYMAN, TR ZEIDEL, ML TI TRANSPORT DEFECTS OF RABBIT INNER MEDULLARY COLLECTING DUCT CELLS IN OBSTRUCTIVE NEPHROPATHY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE URETERAL OBSTRUCTION; SODIUM CHANNEL; SODIUM-POTASSIUM ADENOSINE-TRIPHOSPHATASE; KIDNEY MEDULLA ID NA-K-ATPASE; EPITHELIAL SODIUM-CHANNEL; IMMUNOCYTOCHEMICAL LOCALIZATION; POSTOBSTRUCTIVE DIURESIS; URETERAL OBSTRUCTION; RAT; TUBULE; MINERALOCORTICOIDS; MICROPUNCTURE; NA,K-ATPASE AB Urinary obstruction markedly reduces collecting duct Na+ reabsorption. To define the cellular mechanisms of this derangement in Na+ reabsorption in inner medullary collecting duct (IMCD) of obstructed kidneys, suspensions of intact IMCD cells and inner medulla plasma membranes (IMPM) were prepared from 24 h obstructed and untreated control kidneys. Oxygen consumption (QO2) studies revealed marked reductions in both amiloride-sensitive and ouabain-sensitive QO2 but not ouabain-insensitive QO2 in intact IMCD cells from obstructed, compared with control animals, indicating a reduction in oxygen-dependent transport activities of both the Na+ channel and the Na+-K+-adenosinetriphosphatase (ATPase). Amiloride-sensitive conductive Na-22+ uptake in intact IMCD cells from obstructed kidneys was significantly decreased by 45% at 10 s, 30 s, and 1-5 min (10 s: 2.42 +/- 0.63 vs. 4.49 +/- 0.64 nmol Na+ flux/mg protein, n = 7, P < 0.05; 1 min: 4.65 +/- 0.7 vs. 8.27 +/- 0.98 nmol Na+ flux/mg protein, n = 7, P < 0.05), indicating decreased activity of amiloride-sensitive Na+ channels in these cells. However, immunoblots of IMPM with antibodies to Na+ channel proteins did not show significant differences in content of Na+ channel proteins between membranes from obstructed and control groups. Ouabain-sensitive Na+-K+-ATPase activity in IMPM of obstructed kidneys was also reduced (61.1 +/- 18.1 vs. 152.6 +/- 25.8 nmol ATP degradation . min-1.mg protein-1, n = 6, P < 0.02), and immunoblots with monoclonal antibodies against the alpha1- and beta-subunits of rabbit Na+-K+-ATPase showed a 51 +/- 7% reduction of both subunits in IMPM from obstructed kidneys (n = 4). In summary, ureteral obstruction reduces the activities of apical Na+ channel and basolateral Na+-K+ATPase of the IMCD, probably contributing to the salt wasting that characterizes obstructive nephropathy. However, the lack of change in the amount of Na+ channel protein in contrast to the decreased numbers of Na+-K+-ATPase subunits suggests distinct regulatory mechanisms for these two transporters in obstructed kidneys. C1 W ROXBURY DEPT VET AFFAIRS MED CTR,RES SERV,BOSTON,MA 02132. KAOHSIUNG MED COLL,DEPT INTERNAL MED,KAOHSIUNG,TAIWAN. YALE UNIV,SCH MED,DEPT PATHOL,NEW HAVEN,CT 06510. UNIV ALABAMA,DEPT PHYSIOL & BIOPHYS,BIRMINGHAM,AL 35294. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. RI Hwang, Shang-Jyh /C-7270-2009 FU NIDDK NIH HHS [DK-38774, DK-43955, DK-17433] NR 46 TC 15 Z9 15 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 MAY PY 1993 VL 264 IS 5 BP F808 EP F815 PN 2 PG 8 WC Physiology SC Physiology GA LD347 UT WOS:A1993LD34700091 PM 8388652 ER PT J AU MOLITORIS, BA MEYER, C DAHL, R GEERDES, A AF MOLITORIS, BA MEYER, C DAHL, R GEERDES, A TI MECHANISM OF ISCHEMIA-ENHANCED AMINOGLYCOSIDE BINDING AND UPTAKE BY PROXIMAL TUBULE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GENTAMICIN; PHOSPHOLIPIDS; PHOSPHATIDYLINOSITOL; IMMUNOCYTOCHEMICAL TECHNIQUES; IMMUNOGOLD LABELING; ENDOCYTOSIS ID BORDER MEMBRANE-VESICLES; BRUSH-BORDER; GENTAMICIN-NEPHROTOXICITY; EPITHELIAL POLARITY; TEMPORARY ISCHEMIA; CELLULAR RECOVERY; RENAL-FAILURE; RAT-KIDNEY; INHIBITION; DYSFUNCTION AB Preceding ischemia or concurrent hypotension is known to enhance aminoglycoside nephrotoxicity; however, the underlying mechanisms responsible have not been determined. To investigate the effect of preceding mild ischemia on cellular gentamicin handling, brush-border membrane vesicle binding and in vivo cellular gentamicin uptake were quantified using [H-3]gentamicin as a tracer. Fifteen minutes of ischemia resulted in a marked increase in apical membrane gentamicin binding (2.8 +/- 0.4 vs. 4.9 +/- 0.8 nmol/mg protein, P < 0.01). This increase was associated with an increased number of binding sites (3.7 +/- 0.3 vs. 9.1 +/- 2.3 nmol/mg protein, P < 0.0 1) and a reduced binding affinity (11.8 +/- 2.2 vs. 27.7 +/- 10.4 muM, P < 0.01). This increase in gentamicin binding was accompanied by alterations in apical membrane phospholipids including a doubling of phosphatidylinositol ( PI) levels (13.8 +/- 0.4 vs. 27.5 +/- 3.1 nmol/mg protein, P < 0.01). Furthermore, treatment of apical membrane vesicles with PI-specific phospholipase C markedly reduced the difference in gentamicin binding between paired control and ischemic membrane fractions. Increased gentamicin binding was associated with increased in vivo uptake of gentamicin by SI/S2 and S3 cells. Outer cortical uptake of gentamicin increased from 2.18 +/- 0.39 to 2.68 +/- 0.27 nmol/mg protein (P < 0.01) after 15 min of ischemia and 4 h of reperfusion. Juxtamedullary uptake also increased from 1.39 +/- 0.31 to 1.75 +/- 0.12 nmol/mg protein (P < 0.01). Immunocytochemical techniques, utilizing immunogold labeling, showed gentamicin was taken up via the receptor-mediated endocytic pathway by S1/S2 and S3 cells. After ischemic injury gentamicin was localized in abnormal intracellular accumulations in S3 but not S1 or S2 cells. Taken together, these data indicate ischemia results in a marked increase in apical gentamicin binding due to increases in apical PI content. This is associated with increased internalization by S1/S2 and S3 cells and abnormal intracellular compartmentalization of gentamicin within S3 cells. C1 UNIV COLORADO,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. RP MOLITORIS, BA (reprint author), DENVER VET AFFAIRS MED CTR,111C,1055 CLERMONT ST,DENVER,CO 80220, USA. FU NIDDK NIH HHS [DK-41126] NR 37 TC 23 Z9 23 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 MAY PY 1993 VL 264 IS 5 BP F907 EP F916 PN 2 PG 10 WC Physiology SC Physiology GA LD347 UT WOS:A1993LD34700105 PM 8498544 ER PT J AU WHITING, J AF WHITING, J TI NOMINAL DYSPHASIA REDUX SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP WHITING, J (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97207, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAY PY 1993 VL 160 IS 5 BP 1146 EP 1146 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KY249 UT WOS:A1993KY24900048 PM 8470597 ER PT J AU BLACKBURN, WD CHATHAM, WW AF BLACKBURN, WD CHATHAM, WW TI NEUTROPHIL HYPOCHLOROUS ACID (HOCL) PRODUCTION IN RESPONSE TO SURFACE-ASSOCIATED IGG (SAIGG) IS DEPENDENT UPON BOTH FC-GAMMA-R-II AND FC-GAMMA-R-III AND THE INFLUX OF EXTRACELLULAR CALCIUM SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,BIRMINGHAM,AL. UNIV ALABAMA,BIRMINGHAM,AL 35294. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAY PY 1993 VL 36 IS 5 SU S BP R25 EP R25 PG 1 WC Rheumatology SC Rheumatology GA LD569 UT WOS:A1993LD56900113 ER PT J AU CHATHAM, WW BLACKBURN, WD AF CHATHAM, WW BLACKBURN, WD TI LIGATION OF CR-1 ON NEUTROPHILS ATTENUATES SURFACE-ASSOCIATED IGG-INDUCED HOCL GENERATION SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. US DEPT VET AFFAIRS,RES SERV,BIRMINGHAM,AL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAY PY 1993 VL 36 IS 5 SU S BP R25 EP R25 PG 1 WC Rheumatology SC Rheumatology GA LD569 UT WOS:A1993LD56900114 ER PT J AU CHATHAM, WW BLACKBURN, WD AF CHATHAM, WW BLACKBURN, WD TI SOLID-PHASE IGA INDUCES NEUTROPHIL DEGRANULATION AND OXIDANT GENERATION THROUGH A PERTUSSIS TOXIN-INSENSITIVE PATHWAY SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,RES SERV,BIRMINGHAM,AL. UNIV ALABAMA,UNIVERSITY,AL 35486. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAY PY 1993 VL 36 IS 5 SU S BP R18 EP R18 PG 1 WC Rheumatology SC Rheumatology GA LD569 UT WOS:A1993LD56900069 ER PT J AU SILVA, JA LEONG, GB WINE, DB AF SILVA, JA LEONG, GB WINE, DB TI MISIDENTIFICATION DELUSIONS, FACIAL MISRECOGNITION, AND RIGHT BRAIN INJURY SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Note ID CAPGRAS SYNDROME; INTERMETAMORPHOSIS; PROSOPAGNOSIA AB Individuals suffering from misidentification syndromes may present with right hemispheric pathology and deficits in facial recognition. In addition, misidentification delusions have been associated with aggressive behaviour. The possible linkage between misidentification phenomena,facial recognition, and aggression is discussed, illustrated by the case of a patient suffering from an organic delusional disorder. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 23 TC 19 Z9 19 U1 0 U2 1 PU CANADIAN PSYCHIATRIC ASSOC PI OTTAWA PA SUITE 200, 237 ARGYLE AVE, OTTAWA ON K2P 1B8, CANADA SN 0706-7437 J9 CAN J PSYCHIAT JI Can. J. Psychiat.-Rev. Can. Psychiat. PD MAY PY 1993 VL 38 IS 4 BP 239 EP 241 PG 3 WC Psychiatry SC Psychiatry GA LF032 UT WOS:A1993LF03200001 PM 8518973 ER PT J AU BONORA, E BONADONNA, RC DELPRATO, S GULLI, G SOLINI, A MATSUDA, M DEFRONZO, RA AF BONORA, E BONADONNA, RC DELPRATO, S GULLI, G SOLINI, A MATSUDA, M DEFRONZO, RA TI INVIVO GLUCOSE-METABOLISM IN OBESE AND TYPE-II DIABETIC SUBJECTS WITH OR WITHOUT HYPERTENSION SO DIABETES LA English DT Article ID INSULIN RESISTANCE; ANTIHYPERTENSIVE DRUGS; LIPOPROTEIN METABOLISM; LIPID-METABOLISM; BODY-COMPOSITION; BLOOD-PRESSURE; DOUBLE-BLIND; MELLITUS; HYPERINSULINEMIA; MUSCLE AB This study examined whether the presence of hypertension, an insulin-resistant condition, exacerbates the defect in insulin action observed in obesity and type II diabetes mellitus. Glucose metabolism in the basal state and in response to insulin was quantitated by using the euglycemic insulin (20 mU . min-1 . m-2) clamp in combination with 3-[H-3]glucose infusion and indirect calorimetry in 20 obese nondiabetic subjects (10 hypertensive and 10 normotensive), 26 type II diabetic subjects (13 hypertensive and 13 normotensive), and 11 normal nondiabetic subjects. The two groups of obese subjects and the two groups of diabetic subjects were matched for sex, age, race, body mass index, and fat distribution. Both in the basal state and during insulin infusion, glucose disposal rates (total, oxidative, and nonoxidative) were similar in obese subjects with or without hypertension. Compared with control subjects, both groups of obese subjects were markedly insulin resistant. Similarly, type II diabetic individuals, whether normotensive or hypertensive, were equally insulin resistant. The severity of insulin resistance was nearly identical in obese and diabetic groups. In diabetic subjects, the inhibitory effect of insulin on hepatic glucose output, lipolysis, and lipid oxidation was blunted compared with normal subjects. In obese subjects the ability of insulin to inhibit lipolysis and lipid oxidation was impaired. However, hypertension did not alter the suppressive effects of insulin on hepatic glucose production, plasma free fatty acid levels, or lipid oxidation in either obese or type II diabetic subjects. These results indicate that hypertension does not confer a greater severity of insulin resistance than that already is present in obesity and type II diabetes mellitus. C1 UNIV TEXAS,HLTH SCI CTR,DEPT INTERNAL MED,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RI Del Prato, Stefano/K-3405-2016; Solini, Anna/K-4666-2016 OI Del Prato, Stefano/0000-0002-5388-0270; Solini, Anna/0000-0002-7855-8253; BONORA, Enzo/0000-0003-1074-5164; Matsuda, Masafumi/0000-0001-8543-1616 FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 53 TC 40 Z9 40 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 MAY PY 1993 VL 42 IS 5 BP 764 EP 772 DI 10.2337/diabetes.42.5.764 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KZ308 UT WOS:A1993KZ30800018 PM 8482434 ER PT J AU BERRY, J VANGORP, WG HERZBERG, DS HINKIN, C BOONE, K STEINMAN, L WILKINS, JN AF BERRY, J VANGORP, WG HERZBERG, DS HINKIN, C BOONE, K STEINMAN, L WILKINS, JN TI NEUROPSYCHOLOGICAL DEFICITS IN ABSTINENT COCAINE ABUSERS - PRELIMINARY FINDINGS AFTER 2 WEEKS OF ABSTINENCE SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE NEUROPSYCHOLOGY; COCAINE ABUSE; COGNITION ID ADDICTION AB Sixteen subjects hospitalized for treatment of cocaine dependence were administered a battery of neuropsychological tests within 72 h of last cocaine use and again approximately 2 weeks later. Twenty-one non-cocaine using control subjects, matched for age, gender, ethnicity and education, also received neuropsychological testing. Abstinence from mood altering substances during the 2-week study period was verified for both groups on three occasions using quantitative urine analysis. The results suggest that recent cocaine use is associated with impairment in memory, visuospatial abilities, and concentration during the acute phase of withdrawal, independent of withdrawal-related depression. Furthermore, many of these deficits appear to persist at least 2 weeks beyond cessation of cocaine use. C1 W LOS ANGELES VA MED CTR,DIV BRENTWOOD,ALCOHOL & DRUG TREATMENT PROGRAM,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073. NR 20 TC 108 Z9 109 U1 0 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD MAY PY 1993 VL 32 IS 3 BP 231 EP 237 DI 10.1016/0376-8716(93)90087-7 PG 7 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA LK717 UT WOS:A1993LK71700004 PM 8394237 ER PT J AU KRISTAL, BS CONRAD, CC RICHARDSON, A YU, BP AF KRISTAL, BS CONRAD, CC RICHARDSON, A YU, BP TI IS POLY(A) TAIL LENGTH ALTERED BY AGING OR DIETARY RESTRICTION SO GERONTOLOGY LA English DT Article DE POLYADENYLATION; DIETARY RESTRICTION; POLY(A) TAIL LENGTH ID AGE-RELATED-CHANGES; MESSENGER-RNA; RIBONUCLEIC-ACID; GENE-EXPRESSION; RATS; TRANSCRIPTION; SEQUENCES; LONGEVITY; LEVEL AB We examined age- and diet-related alterations in RNA poly(A) tail length using high-resolution gel electrophoresis followed by Northern hybridization. The results demonstrate conclusively that there is no age-related decrease in the size of the Poly(A) tail of RNA isolated from the male Fischer 344 rat. In contrast, our results suggest that there is actually a slight age-related increase in the length of the poly(A) tail isolated from the liver and hypothalamus of these rats. Dietary restriction did not affect either poly(A) tail length or its age-related increase. These data demonstrate conclusively that oligo(dT) probes can be used to standardize RNA hybridization experiments between animals of different ages and dietary groups. In addition, these data provide further evidence that the ratio between RNA polymerase I and RNA polymerase II activity does not change with age. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR CLIN & EDUC,SAN ANTONIO,TX. FU NIA NIH HHS [AG01048, NIA T32 AG00205, AG01188] NR 25 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0304-324X J9 GERONTOLOGY JI Gerontology PD MAY-JUN PY 1993 VL 39 IS 3 BP 152 EP 162 PG 11 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LU211 UT WOS:A1993LU21100005 PM 7691690 ER PT J AU CRAIG, WA AF CRAIG, WA TI POSTANTIBIOTIC EFFECTS IN EXPERIMENTAL-INFECTION MODELS - RELATIONSHIP TO INVITRO PHENOMENA AND TO TREATMENT OF INFECTIONS IN MAN SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article; Proceedings Paper CT SYMP ON BACTERIAL INFECTION MODELS IN ANTIMICROBIAL CHEMOTHERAPY CY OCT 26-28, 1992 CL HELSINORE, DENMARK SP BRIT SOC ANTIMICROBIAL CHEMOTHERAPY, COMMISS EUROPEAN COMMUNITIES, EUROPEAN SOC CLIN MICROBIAL & INFECTIOUS DIS, DANISH SOC CLIN MICROBIOL, STATENS SERUMINISTUT, DANISH RESEARCH COUNCIL ID EXPERIMENTAL PSEUDOMONAS ENDOCARDITIS; STREPTOCOCCUS-PNEUMONIAE; EXPERIMENTAL MENINGITIS; AMIKACIN INVITRO; THIGH-INFECTION; INVIVO; EFFICACY; THERAPY; AMINOGLYCOSIDE; GENTAMICIN C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 36 TC 91 Z9 92 U1 0 U2 3 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD MAY PY 1993 VL 31 SU D BP 149 EP 158 PG 10 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA LF614 UT WOS:A1993LF61400014 PM 8335516 ER PT J AU GUDMUNDSSON, S EINARSSON, S ERLENDSDOTTIR, H MOFFAT, J BAYER, W CRAIG, WA AF GUDMUNDSSON, S EINARSSON, S ERLENDSDOTTIR, H MOFFAT, J BAYER, W CRAIG, WA TI THE POSTANTIBIOTIC EFFECT OF ANTIMICROBIAL COMBINATIONS IN A NEUTROPENIC MURINE THIGH INFECTION MODEL SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID PSEUDOMONAS-AERUGINOSA; ENTEROCOCCUS-FAECALIS; IMIPENEM; INVIVO; INVITRO; GENTAMICIN; RIFAMPIN C1 BORGARSPITALINN, DEPT MED, REYKJAVIK, ICELAND. UNIV WISCONSIN, DEPT MED, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MED SERV, MADISON, WI 53705 USA. BORGARSPITALINN, CLIN MICROBIOL LAB, REYKJAVIK, ICELAND. UNIV ICELAND, SCH MED, REYKJAVIK, ICELAND. NR 31 TC 23 Z9 23 U1 1 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD MAY PY 1993 VL 31 SU D BP 177 EP 191 PG 15 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA LF614 UT WOS:A1993LF61400017 PM 8335520 ER PT J AU ALLENDOERFER, R MAGEE, DM SMITH, JG BONEWALD, L GRAYBILL, JR AF ALLENDOERFER, R MAGEE, DM SMITH, JG BONEWALD, L GRAYBILL, JR TI INDUCTION OF TUMOR-NECROSIS-FACTOR-ALPHA IN MURINE CANDIDA-ALBICANS INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID LISTERIA-MONOCYTOGENES INFECTION; CACHECTIN; MICE; ENDOTOXIN; SHOCK; TNF AB Candidemia in humans is often associated with an endotoxic shock-like syndrome, comparable to gram-negative sepsis. Tumor necrosis factor-alpha (TNFalpha) has been implicated as a mediator in the endotoxic shock syndrome. The possible role of TNFalpha causing early deaths was explored in a murine model of acute infection with Candida albicans. In vitro data from three mouse strains (BALB/c, C3H/HeJ, and C3H/HeN) and in vivo data from BALB/c mice were obtained. Peritoneal macrophages from all three strains produced TNFalpha in vitro when stimulated with C albicans. After intravenous infection with 10(8) cfu of C. albicans, mice died within 12 h. TNF concentrations in sera from these mice were significantly greater than in controls. Pretreatment of BALB/c mice with anti-murine TNFalpha did not alter mortality of C. albicans-infected mice, but pretreatment with murine TNFalpha reduced mortality. Therefore, in contrast to what was anticipated, TNFalpha may serve a protective role in murine candidiasis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. RP ALLENDOERFER, R (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 21 TC 48 Z9 48 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAY PY 1993 VL 167 IS 5 BP 1168 EP 1172 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KZ499 UT WOS:A1993KZ49900026 PM 8486950 ER PT J AU BEERS, DR HENKEL, JS SCHAEFER, DC ROSE, JW STROOP, WG AF BEERS, DR HENKEL, JS SCHAEFER, DC ROSE, JW STROOP, WG TI NEUROPATHOLOGY OF HERPES-SIMPLEX VIRUS ENCEPHALITIS IN A RAT SEIZURE MODEL SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ENCEPHALITIS; HERPES SIMPLEX VIRUS; HISTOPATHOLOGY; HSV-1; NEUROANATOMY; RAT; SEIZURES ID CENTRAL-NERVOUS-SYSTEM; INFLUENCE VIRAL NEUROTROPISM; TYPE-1 STRAINS; INFECTIONS; SPREAD; BRAIN; MICE; REACTIVATION; ANTIBODY; HOST AB Herpes simplex virus type 1 (HSV-1) is the cause of a serious and often fatal encephalitis. Patients who survive herpes simplex encephalitis (HSE) experience behavioral abnormalities including profound cognitive dysfunctions. We have developed a rat model of acute HSE to investigate the cognitive impairments caused by HSV-1 central nervous system (CNS) infection. Following intranasal inoculation of Lewis rats with a neurovirulent strain of HSV-1, animals shed virus in both ocular and nasal secretions and developed clinical signs of infection, including partial complex motor seizures that eventually generalized. Homogenization assays demonstrated infectious virus in the trigeminal ganglia, olfactory bulbs, and the piriform and entorhinal cortices. Histopathological assessment revealed inflammatory and hemorrhagic lesions in the trigeminal ganglia, olfactory bulbs, amygdala, hippocampus, the piriform and entorhinal cortices, and the spinal trigeminal nuclei. Viral antigens and nucleic acids were also detected within these structures by immunofluorescence microscopy and in situ hybridization, respectively. Viral-induced astrocytic hypertrophy in the CNS was demonstrated by glial fibrillary acidic protein immunoreactivity. Together, these results indicate that HSV-1 has the ability to invade, replicate, and induce site-specific CNS damage in the Lewis rat. C1 DEPT VET AFFAIRS MED CTR,HOUSTON,TX. DEPT VET AFFAIRS MED CTR,SALT LAKE CITY,UT. UNIV UTAH,PROGRAM NEUROSCI,SALT LAKE CITY,UT 84112. UNIV UTAH,DEPT NEUROL,SALT LAKE CITY,UT 84112. BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT OPHTHALMOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. CONNAUGHT LABS INC,DEPT RES,SWIFTWATER,PA. RP BEERS, DR (reprint author), BAYLOR COLL MED,CULLEN EYE INST,6501 FANNIN NC-200,HOUSTON,TX 77030, USA. FU NEI NIH HHS [F32 EY07001]; NIDCD NIH HHS [1RO1 DC1706]; NIMH NIH HHS [1 F31 MH10094-01A1] NR 56 TC 29 Z9 29 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1993 VL 52 IS 3 BP 241 EP 252 PG 12 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LB785 UT WOS:A1993LB78500008 PM 8388040 ER PT J AU SCHAEFER, C MACHAC, J KEILP, J WAKEMAN, J DORFMAN, D BRICHTSWEIN, K CHAYES, Z STRITZKE, P INTRATOR, J AF SCHAEFER, C MACHAC, J KEILP, J WAKEMAN, J DORFMAN, D BRICHTSWEIN, K CHAYES, Z STRITZKE, P INTRATOR, J TI CEREBRAL ACTIVATION OF LEXICAL DECISION IN PSYCHOPATHS USING SINGLE-PHOTON EMISSION TOMOGRAPHY (SPECT) SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,BRONX,NY. MT SINAI MED CTR,NEW YORK,NY 10029. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1993 VL 34 IS 5 SU S BP P77 EP P78 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LB138 UT WOS:A1993LB13800306 ER PT J AU EISENBERG, JM GLICK, HA BUZBY, GP KINOSIAN, B WILLIFORD, WO AF EISENBERG, JM GLICK, HA BUZBY, GP KINOSIAN, B WILLIFORD, WO TI DOES PERIOPERATIVE TOTAL PARENTERAL-NUTRITION REDUCE MEDICAL-CARE COSTS SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID GASTROINTESTINAL SURGERY; SUPPORT AB An economic analysis accompanied a multicenter Department of Veterans Affairs randomized, controlled trial of perioperative total parenteral nutrition (TPN). The cost of providing TPN for an average of 16.15 days before and after surgery was $2405, more than half of which ($1025) included costs of purchasing, preparing, and delivering the TPN solution itself; lipid solutions accounted for another $181, additional nursing care for $843, and miscellaneous costs for $356. Prolonged hospital stay added another $764 per patient to the $2405 cost of providing TPN, bringing the total to $3169. The incremental costs attributed to perioperative TPN were highest ($3921) for the patients least likely to benefit, that is, those who were less malnourished and at low risk of nutrition-related complications. Incremental costs were lowest ($3071) for high-risk patients. On the basis of the hospital-based method of administering TPN that was used in the clinical trial, perioperative TPN did not result in decreased costs for any subgroup of patients. C1 UNIV PENN, LEONARD DAVIS INST HLTH ECON, PHILADELPHIA, PA 19104 USA. UNIV PENN, DEPT MED, DEPT SURG, GEN INTERNAL MED SECT, PHILADELPHIA, PA 19104 USA. PHILADELPHIA DEPT VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. DEPT VET AFFAIRS MED RES SERV, DEPT COOPERAT STUDIES PROGRAM, PERRY POINT, MD USA. GEORGETOWN UNIV, MED CTR, DEPT MED, 3800 RESERVOIR RD, WASHINGTON, DC 20007 USA. NR 20 TC 25 Z9 27 U1 0 U2 1 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD MAY-JUN PY 1993 VL 17 IS 3 BP 201 EP 209 DI 10.1177/0148607193017003201 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA LA456 UT WOS:A1993LA45600002 PM 8505824 ER PT J AU SCHUMACHER, HR HUDSON, AP BARDIN, T AF SCHUMACHER, HR HUDSON, AP BARDIN, T TI SHOULD WE TREAT POSTVENEREAL REITERS-SYNDROME BY ANTIBIOTICS - REPLY SO JOURNAL OF RHEUMATOLOGY LA English DT Letter C1 HOP LARIBOISIERE,RHUMATOL CLIN,F-75475 PARIS 10,FRANCE. RP SCHUMACHER, HR (reprint author), UNIV PENN,SCH MED,VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA 19104, USA. NR 15 TC 2 Z9 2 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD MAY PY 1993 VL 20 IS 5 BP 907 EP 908 PG 2 WC Rheumatology SC Rheumatology GA LC727 UT WOS:A1993LC72700032 ER PT J AU MCLELLAN, AT GRISSOM, GR BRILL, P DURELL, J METZGER, DS OBRIEN, CP AF MCLELLAN, AT GRISSOM, GR BRILL, P DURELL, J METZGER, DS OBRIEN, CP TI PRIVATE SUBSTANCE-ABUSE TREATMENTS - ARE SOME PROGRAMS MORE EFFECTIVE THAN OTHERS SO JOURNAL OF SUBSTANCE ABUSE TREATMENT LA English DT Article DE SUBSTANCE ABUSE; TREATMENT; OUTCOME; EFFICACY ID ALCOHOLISM AB There have been few studies of treatments for substance dependence among private programs. The present study compared the patient populations, treatment services provided and six-month outcomes of employed, insured patients referred by an employee assistance program to four private treatment programs (two inpatient and two outpatient). Subjects were alcohol and/or cocaine dependent males referred from a single employer. Ninety-four percent were successfully contacted at six-month follow-up, with confirmatory urinalysis and breathalyzer samples taken. Three results were obtained. First, there were significant and pervasive improvements shown in the total sample at follow-up. Fifty-nine percent were completely abstinent, 82% were working and only 8% required re-treatment. Second, there were significant differences among the programs in levels of improvement and six-month outcomes. Finally, the differences in efficacy were related to the differences in the nature and amount of treatment services provided. C1 INTEGRA INC,RADNOR,PA. RP MCLELLAN, AT (reprint author), VET AFFAIRS MED CTR,DEPT PSYCHIAT,CTR STUDIES ADDICT,BLD 7,UNIV AVE,PHILADELPHIA,PA 19104, USA. RI Metzger, David/D-9499-2012 NR 22 TC 80 Z9 80 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0740-5472 J9 J SUBST ABUSE TREAT JI J. Subst. Abus. Treat. PD MAY-JUN PY 1993 VL 10 IS 3 BP 243 EP 254 DI 10.1016/0740-5472(93)90071-9 PG 12 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA LE199 UT WOS:A1993LE19900001 PM 8391086 ER PT J AU ROYALL, DR MAHURIN, RK GRAY, KF AF ROYALL, DR MAHURIN, RK GRAY, KF TI EXECUTIVE COGNITIVE IMPAIRMENT - REPLY SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Letter C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAY PY 1993 VL 41 IS 5 BP 577 EP 578 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA LA893 UT WOS:A1993LA89300022 ER PT J AU HUTCHISON, FN AF HUTCHISON, FN TI PROTEINURIA, HYPERLIPIDEMIA, AND THE KIDNEY SO MINERAL AND ELECTROLYTE METABOLISM LA English DT Review DE ALBUMIN SYNTHESIS; ANALBUMINEMIA; CHOLESTEROL; CHRONIC RENAL FAILURE; DIETARY PROTEIN; LIPOPROTEIN; NEPHROTIC SYNDROME; ONCOTIC PRESSURE; PROTEINURIA; TRIGLYCERIDE ID CHRONIC AMINONUCLEOSIDE NEPHROSIS; HIGH-DENSITY LIPOPROTEINS; APOLIPOPROTEIN-A-I; PERFUSED-RAT-LIVER; ANALBUMINEMIC RATS; ALBUMIN SYNTHESIS; FOCAL GLOMERULOSCLEROSIS; GLOMERULAR LIPIDOSIS; RENAL-DISEASE; METABOLISM AB Hyperlipidemia in the nephrotic syndrome is the result of abnormalities in both synthesis and catabolism of lipids and lipoproteins. The etiology of nephrotic hyperlipidemia has not been established, but both abnormal glomerular permeability to plasma proteins and reduced serum oncotic pressure may contribute. Although standard hypolipemic drugs are effective in nephrotic patients, therapies such as dietary protein restriction and angiotensin-converting enzyme inhibitors which reduce proteinuria and increase serum oncotic pressure ameliorate hyperlipidemia as well. Hyperlipidemia may also induce proteinuric renal disease in normal animals and worsen renal injury in a variety of animal models of kidney disease. Conversely, treatment of hyperlipidemia prevents renal injury and lessens proteinuria. Potential mechanisms by which hyperlipidemia may cause renal injury include inflammatory and immunologically mediated injury and alteration of glomerular paracrine function. C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. RP HUTCHISON, FN (reprint author), RALPH H JOHNSON VET AFFAIRS MED CTR,DIALYSIS UNIT,109 BEE ST,CHARLESTON,SC 29401, USA. NR 105 TC 17 Z9 17 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-0392 J9 MINER ELECTROL METAB JI Miner. Electrolyte Metab. PD MAY-JUN PY 1993 VL 19 IS 3 BP 127 EP 136 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MB319 UT WOS:A1993MB31900003 PM 8232099 ER PT J AU HEYDARI, AR WU, B TAKAHASHI, R STRONG, R RICHARDSON, A AF HEYDARI, AR WU, B TAKAHASHI, R STRONG, R RICHARDSON, A TI EXPRESSION OF HEAT-SHOCK PROTEIN 70 IS ALTERED BY AGE AND DIET AT THE LEVEL OF TRANSCRIPTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SEQUENCE-SPECIFIC BINDING; HUMAN-DIPLOID FIBROBLASTS; MESSENGER-RNA; GENE-EXPRESSION; DNA-BINDING; CELLS; PROMOTER; HSP70; RESTRICTION; ACTIVATION AB Because heat shock proteins have been shown to play a critical role in protecting cells from hyperthermia and other types of physiological stresses, it was of interest to determine what effect age and caloric restriction have on the ability of cells to regulate the expression of heat shock protein 70 (hsp70), the most prominent and most evolutionarily conserved of the heat shock proteins. Caloric restriction is the only experimental manipulation known to retard aging and increase survival of mammals. The ability of hepatocytes isolated from young/adult (4- to 7-month-old) and old (22- to 28-month-old) male Fischer F344 rats fed ad libitum or a caloric restriction diet (60% of the content of the ad libitum diet) to express hsp70 was determined after a mild heat shock (42.5-degrees-C for 30 min). We found that the induction of hsp70 synthesis and mRNA levels by heat shock was 40 to 50% lower in hepatocytes isolated from old rats than in hepatocytes isolated from young rats. Using in situ hybridization, we found that essentially all hepatocytes from the young/adult and old rats expressed hsp70 in response to heat shock, therefore, the age-related decrease in the induction of hsp70 expression was not due to an age-related accumulation of cells that do not respond to heat shock. Measurements of bsp70 mRNA stability and hsp70 transcription demonstrated that the age-related decline in hsp70 expression arose from a decline in hsp70 transcription. Interestingly, the age-related decline in the induction of hsp70 expression was reversed by caloric restriction; e.g., the induction of hsp70 synthesis, mRNA levels, and nuclear transcription were significantly higher in hepatocytes isolated from old rats fed the caloric restricted diet than in hepatocytes isolated from old rats fed ad libitum. The levels of the heat shock transcription factor in nuclear extracts isolated from heat-shocked hepatocytes were measured in a gel shift assay. Binding of the heat shock transcription factor to the heat shock element decreased with age and was significantly higher in hepatocyte extracts isolated from old rats fed the caloric restriction diet than in those from old rats fed ad libitum. Thus, our study demonstrates that the ability of hepatocytes to respond to hyperthermia and express hsp70 decreases significantly with age and that this decrease occurs at the transcriptional level. In addition, caloric restriction, which retards aging, reversed the age-related decline in the induction of hsp70 transcription in hepatocytes. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG01548, AG09557] NR 55 TC 227 Z9 235 U1 1 U2 8 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 MAY PY 1993 VL 13 IS 5 BP 2909 EP 2918 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KY632 UT WOS:A1993KY63200026 PM 7682654 ER PT J AU HANDELSMAN, L SONG, IS LOSONCZY, M PARK, S JACOBSON, J WIENER, J ARONSON, M AF HANDELSMAN, L SONG, IS LOSONCZY, M PARK, S JACOBSON, J WIENER, J ARONSON, M TI MAGNETIC-RESONANCE ABNORMALITIES IN HIV-INFECTION - A STUDY IN THE DRUG-USER RISK GROUP SO PSYCHIATRY RESEARCH LA English DT Article DE MAGNETIC RESONANCE IMAGING; HUMAN IMMUNODEFICIENCY VIRUS; COGNITIVE IMPAIRMENT; ACQUIRED IMMUNE DEFICIENCY SYNDROME ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS DEMENTIA COMPLEX; BASE-LINE ASSESSMENT; HOMOSEXUAL MEN; CT; NEUROPATHOLOGY AB Cognitive impairment is a frequent complication of advanced human immunodeficiency virus-1 (HIV-1) infection. However, structural imaging of the brain has not revealed abnormalities that precede the onset of clinical abnormalities. Cranial magnetic resonance (MR) studies were performed in 28 male subjects with intravenous drug use histories; nine were HIV-1 seronegative, 11 were HIV-1 seropositive but asymptomatic, and eight were seropositive and met symptomatic criteria for acquired immune deficiency syndrome (AIDS). Cortical atrophy, but not the degree of ventricular enlargement or signal abnormalities, was increased in the seropositive group compared with the seronegative group and also differed between asymptomatic seropositive and seronegative patients. An increased level of cortical atrophy may reflect the early impact of HIV-1 infection on the brain. C1 BRONX VET AFFAIRS MED CTR,RADIOL SERV,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,NEUROL SERV,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,INFECT DIS SERV,BRONX,NY 10468. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP HANDELSMAN, L (reprint author), BRONX VET AFFAIRS MED CTR,PSYCHIAT SERV,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 31 TC 6 Z9 6 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 MAY PY 1993 VL 47 IS 2 BP 175 EP 186 DI 10.1016/0165-1781(93)90047-K PG 12 WC Psychiatry SC Psychiatry GA LG163 UT WOS:A1993LG16300007 PM 8341770 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R AF SILVA, JA LEONG, GB WEINSTOCK, R TI DELUSIONS OF TRANSFORMATION OF THE SELF SO PSYCHOPATHOLOGY LA English DT Article ID CAPGRAS SYNDROME; LYCANTHROPY; SYSTEM AB A series of 20 patients suffering from delusions of physical and psychological transformation of the self is studied. Nosological, psychosocial, and biological aspects are discussed. Two cases are presented in detail. C1 W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA. UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 40 TC 13 Z9 13 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD MAY-AUG PY 1993 VL 26 IS 3-4 BP 181 EP 188 PG 8 WC Psychiatry SC Psychiatry GA LW106 UT WOS:A1993LW10600011 PM 8234633 ER PT J AU SCHENKER, S HALFF, GA AF SCHENKER, S HALFF, GA TI NUTRITIONAL THERAPY IN ALCOHOLIC LIVER-DISEASE SO SEMINARS IN LIVER DISEASE LA English DT Review ID PROTEIN-CALORIE MALNUTRITION; RANDOMIZED CONTROLLED TRIAL; AMINO-ACID SUPPLEMENTATION; PARENTERAL-NUTRITION; SHORT-TERM; CIRRHOTIC-PATIENTS; CLINICAL-TRIAL; PYRIDOXAL 5'-PHOSPHATE; ABDOMINAL OPERATIONS; HEPATIC CIRRHOSIS C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED GASTROENTEROL & NUTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG LIVER TRANSPLANTAT,SAN ANTONIO,TX 78284. RP SCHENKER, S (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07514] NR 114 TC 17 Z9 19 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 MAY PY 1993 VL 13 IS 2 BP 196 EP 209 DI 10.1055/s-2007-1007349 PG 14 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LL293 UT WOS:A1993LL29300008 PM 8337604 ER PT J AU MCLELLAN, AT ARNDT, IO METZGER, DS WOODY, GE OBRIEN, CP AF MCLELLAN, AT ARNDT, IO METZGER, DS WOODY, GE OBRIEN, CP TI THE EFFECTS OF PSYCHOSOCIAL SERVICES IN SUBSTANCE-ABUSE TREATMENT SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID METHADONE-MAINTENANCE; DRUG-ABUSE; SEVERITY; PSYCHOTHERAPY; SUCCESS AB Objective.-To examine whether the addition of counseling, medical care, and psychosocial services improves the efficacy of methadone hydrochloride therapy in the rehabilitation of opiate-dependent patients. Design.-Random assignment to one of three treatment groups for a 6-month clinical trial: (1) minimum methadone services (MMS)-methadone alone (a minimum of 60 mg/d) with no other services; (2) standard methadone services (SMS) -same dose of methadone plus counseling; or (3) enhanced methadone services (EMS)-same dose of methadone plus counseling and on-site medical/psychiatric, employment, and family therapy. Setting.-The methadone maintenance program of the Philadelphia (Pa) Veterans Affairs Medical Center. Subjects.-Ninety-two male intravenous opiate users in methadone maintenance treatment. Results.-While methadone treatment alone (MMS) was associated with reductions in opiate use, 69% of these subjects had to be ''protectively transferred'' from the trial because of unremitting use of opiates or cocaine, or medical/psychiatric emergencies. This was significantly different from the 41% of SMS subjects and 19% of EMS subjects who met the criteria. End-of-treatment data (at 24 weeks) showed minimal improvements among the 10 MMS patients who completed the trial. The SMS group showed significantly more and larger improvements than did the MMS group; and the EMS group showed significantly better outcomes than did the SMS group. Minimum methadone services subjects who had been ''protectively transferred'' to standard care showed significant reductions in opiate and cocaine use within 4 weeks. Conclusions.-Methadone alone (even in substantial doses) may only be effective for a minority of eligible patients. The addition of basic counseling was associated with major increases in efficacy; and the addition of on-site professional services was even more effective. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. RP MCLELLAN, AT (reprint author), PHILADELPHIA VET AFFAIRS MED CTR,PENN VA CTR STUDIES ADDICT,DEPT PSYCHIAT,UNIV AVE,BLDG 7,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [DA05634] NR 19 TC 569 Z9 574 U1 3 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 APR 21 PY 1993 VL 269 IS 15 BP 1953 EP 1959 DI 10.1001/jama.269.15.1953 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA KX215 UT WOS:A1993KX21500024 PM 8385230 ER PT J AU WHEAT, J HAFNER, R WULFSOHN, M SPENCER, P SQUIRES, K POWDERLY, W WONG, B RINALDI, M SAAG, M HAMILL, R MURPHY, R CONNOLLYSTRINGFIELD, P BRIGGS, N OWENS, S AF WHEAT, J HAFNER, R WULFSOHN, M SPENCER, P SQUIRES, K POWDERLY, W WONG, B RINALDI, M SAAG, M HAMILL, R MURPHY, R CONNOLLYSTRINGFIELD, P BRIGGS, N OWENS, S TI PREVENTION OF RELAPSE OF HISTOPLASMOSIS WITH ITRACONAZOLE IN PATIENTS WITH THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; HISTOPLASMOSIS; ASTERISK-ITRACONAZOLE; AMPHOTERICIN-B; HUMAN IMMUNODEFICIENCY VIRUS INFECTIONS ID CAPSULATUM ANTIGEN; AMPHOTERICIN-B; AIDS; DIAGNOSIS; FLUCONAZOLE; THERAPY AB Objective: To assess the efficacy and safety of itraconazole in preventing relapse of histoplasmosis after induction therapy with amphotericin B in patients with the acquired immunodeficiency syndrome (AIDS) and disseminated histoplasmosis. Design: A prospective, multicenter, open-label clinical trial, with follow-up for at least 52 weeks. Setting: Tertiary care hospitals participating in a clinical investigation sponsored by the National Institutes of Allergy and Infectious Diseases (AIDS Clinical Trial Group and Mycoses Study Group). Patients: Forty-two patients with AIDS who had successfully completed induction therapy for disseminated histoplasmosis amphotericin B, at least 15 mg/kg body weight given over 4 to 12 weeks. Interventions: Itraconazole, 200 mg given orally twice daily. Main Outcome Measures: Response to therapy, specifically prevention of histoplasmosis relapse, was the main outcome measure. Secondary end points were survival and the effect of therapy on Histoplasma capsulatum variety capsulatum antigen levels in urine and serum. Plasma itraconazole concentrations were measured to document drug absorption and compliance with therapy. Results: The median follow-up was 109 weeks, and median survival was 98 weeks. Two relapses occurred (5%; 95% CI, 0.5% to 16%), one in a patient withdrawn from the study 18 weeks earlier and one in a patient who did not comply with the study therapy. Patients with elevated antigen levels at study entry showed clearance of antigen from urine and serum; urine specimens became negative in 43% of patients (CI, 26% to 59%), and serum specimens became negative in 75% of patients (CI, 56% to 94%). Only one patient discontinued treatment because of itraconazole toxicity (hypokalemia). Conclusions: Itraconazole, 200 mg twice daily, is safe and effective in preventing relapse of disseminated histoplasmosis in patients with AIDS. Antigen clearance from blood and urine correlates with clinical efficacy. C1 UNIV CINCINNATI,COLL MED,DEPT INTERNAL MED,CINCINNATI,OH 45221. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RICHARD L ROUDEBUSH VET AFFAIRS HOSP,INDIANAPOLIS,IN. DEPT VET AFFAIRS MED CTR,BIRMINGHAM,AL 35233. DEPT VET AFFAIRS MED CTR,DIV INFECT DIS 111G,HOUSTON,TX 77030. FRONTIER SCI & TECH RES FDN,AMHERST,NY 14226. WASHINGTON UNIV,CLIN TRIALS UNIT,ST LOUIS,MO 63130. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. INDIANA UNIV,SCH MED,IDRC,INDIANAPOLIS,IN 46202. CORNELL UNIV,ITHACA,NY 14853. RICHARD L ROUDEBUSH VET ADM MED CTR,INDIANAPOLIS,IN 46202. NIH,DIV AIDS,BETHESDA,MD 20892. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. OI Murphy, Robert/0000-0003-3936-2052 FU NIAID NIH HHS [1-AI-15082] NR 19 TC 150 Z9 153 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 15 PY 1993 VL 118 IS 8 BP 610 EP 616 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA KW470 UT WOS:A1993KW47000006 PM 8383934 ER PT J AU PAHLAVANI, MA RICHARDSON, A AF PAHLAVANI, MA RICHARDSON, A TI AGE-RELATED-CHANGES IN HEAT-SHOCK GENE-EXPRESSION IN RAT LYMPHOCYTES (NIA AG-00165 AND AG-01548) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT CELL & STR BIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1993 VL 150 IS 8 BP A22 EP A22 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95600117 ER PT J AU VIRELLA, G LOPESVIRELLA, MF AF VIRELLA, G LOPESVIRELLA, MF TI AUTOIMMUNITY AND ATHEROSCLEROSIS SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT MICROBIOL & IMMUNOL,CHARLESTON,SC 29425. RALPH H JOHNSON VET ADM MED CTR,CHARLESTON,SC 29425. NR 0 TC 0 Z9 0 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 APR 15 PY 1993 VL 150 IS 8 BP A238 EP A238 PN 2 PG 1 WC Immunology SC Immunology GA KX956 UT WOS:A1993KX95601370 ER PT J AU KRANER, JC LASKER, JM CORCORAN, GB RAY, SD RAUCY, JL AF KRANER, JC LASKER, JM CORCORAN, GB RAY, SD RAUCY, JL TI INDUCTION OF P4502E1 BY ACETONE IN ISOLATED RABBIT HEPATOCYTES SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID N-NITROSODIMETHYLAMINE DEMETHYLASE; ETHANOL-INDUCIBLE CYTOCHROME-P-450; LIVER-MICROSOMES; TREATED RABBITS; DIABETIC RAT; EXPRESSION; P450IIE1; STABILIZATION; MAINTENANCE; ACTIVATION AB The molecular mechanism(s) underlying induction of the hepatic microsomal cytochrome P4502E1 (2E1) by xenobiotics (e.g. ethanol and acetone) is controversial. Proposed mechanisms include increased rates of enzyme synthesis due to elevated 2E1 mRNA levels, enhanced translation of pre-existing mRNA, or stabilization of 2E1 protein. To further assess which, if any, of these events predominates during the initial stages of 2E1 protein induction, we investigated the effects of acetone treatment on 2E1 content in cultured rabbit hepatocytes, an in vitro system that allows for precise control of the cellular mileau. Hepatocytes harvested from female rabbits and plated on plastic dishes with serum-supplemented medium were 90-100% viable for at least 48 hr in culture. Analysis of immunoreactive 2E1 content and aniline hydroxylase activity in microsomes isolated from hepatocytes cultured for up to 24 hr revealed that 2E1 expression was equal to that of microsomes from unplated cells and by 48 hr of culture, 2E1 levels decreased by only 35%. Moreover, microsomes isolated from cells exposed to 17 mM acetone for 24 hr exhibited a 53 and 62% increase in aniline hydroxylase activity and 2E1 content, respectively, compared to untreated cells. To explain these increases, the rate of 2E1 protein synthesis was determined in untreated cells or in cells treated with 17 mM acetone by first exposing hepatocytes to medium supplemented with S-35-labeled methionine and cysteine ([S-35]Met/Cys) and subsequently assessing radiolabel incorporation into 2E1 protein. While no difference was found between untreated and acetone-treated cells in the incorporation of [S-35]Met/Cys into trichloroacetic acid-precipitable microsomal proteins, immunoaffinity purification of 2E1 revealed that incorporation of S-35-labeled amino acids specifically into 2E1 was elevated by acetone to 200% of control values. Treatment of hepatocytes with the transcriptional inhibitor, alpha-amanitin, markedly inhibited this acetone-mediated increase in [S-35]Met/Cys incorporation into 2E1. Analysis of hepatocyte RNA revealed that acetone increased 2E1 mRNA to 130 and 160% of control levels at 6 and 24 hr, respectively, and that these increases were prevented by pretreatment with alpha-amanitin. Our results indicate that acetone increases 2E1 protein levels in cultured rabbit hepatocytes by stimulating its rate of de novo synthesis. Since this increase in 2E1 synthesis stems, at least in part, from the acetone-mediated enhancement of hepatocyte 2E1 mRNA content and is inhibitable by alpha-amanitin, transcriptional activation of the rabbit CYP2E1 gene is apparently involved in the induction of 2E1 protein by acetone. C1 UNIV NEW MEXICO,COLL PHARM,TOXICOL PROGRAM,ALBUQUERQUE,NM 87131. BRONX VET ADM MED CTR,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY 10468. MT SINAI SCH MED,NEW YORK,NY 10468. FU NIAAA NIH HHS [AA-07842, AA-08139]; NIGMS NIH HHS [GM-41564] NR 42 TC 35 Z9 35 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 APR 6 PY 1993 VL 45 IS 7 BP 1483 EP 1492 DI 10.1016/0006-2952(93)90049-3 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KX573 UT WOS:A1993KX57300015 PM 8471070 ER PT J AU SANGUEZA, OP HYDER, DM BAKKE, AC WHITE, CR AF SANGUEZA, OP HYDER, DM BAKKE, AC WHITE, CR TI DNA DETERMINATION IN DYSPLASTIC NEVI - A COMPARATIVE-STUDY BETWEEN FLOW-CYTOMETRY AND IMAGE-ANALYSIS SO AMERICAN JOURNAL OF DERMATOPATHOLOGY LA English DT Article DE DYSPLASTIC NEVUS; DNA DETERMINATION; FLOW CYTOMETRY; IMAGE ANALYSIS ID MALIGNANT-MELANOMA; LESIONS AB Dysplastic nevi (DN), described in 1978, have been associated with increased risk of melanoma, but the role of DN as precursors of melanoma is still controversial. Recent studies have shown that DN are very common in the general population, bringing into question this purported association. Numerous investigations have attempted to correlate the presence of DN in individuals with specific phenotypic and genotypic features, including the presence of abnormal DNA content. Because the occurrence of such abnormal DNA stemlines in neoplasms may be associated with malignant behavior, we studied 38 biopsies from 19 patients that histologically fulfilled criteria for DN in order to ascertain characteristics of DNA content. Nuclear suspensions made from paraffin-embedded tissue were evaluated by both flow cytometry and image analysis techniques. All cases demonstrated diploid populations by both DNA measurement methods. Our results contradict previous reports of aneuploid populations in these melanocytic lesions. C1 OREGON HLTH SCI UNIV,DEPT DERMATOL,3181 S W SAM JACKSON PK RD,PORTLAND,OR 97201. SW WASHINGTON MED CTR,DEPT PATHOL,VANCOUVER,WA. PORTLAND VET AFFAIRS MED CTR,DERMATOL SERV,PORTLAND,OR. OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. NR 16 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0193-1091 J9 AM J DERMATOPATH JI Am. J. Dermatopathol. PD APR PY 1993 VL 15 IS 2 BP 99 EP 105 DI 10.1097/00000372-199304000-00001 PG 7 WC Dermatology SC Dermatology GA KV592 UT WOS:A1993KV59200001 PM 8494124 ER PT J AU HIBNER, CS MOSELEY, MJ SHANK, TL AF HIBNER, CS MOSELEY, MJ SHANK, TL TI WHAT IS TRANSESOPHAGEAL ECHOCARDIOGRAPHY SO AMERICAN JOURNAL OF NURSING LA English DT Article RP HIBNER, CS (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-936X J9 AM J NURS JI Am. J. Nurs. PD APR PY 1993 VL 93 IS 4 BP 74 EP & PG 0 WC Nursing SC Nursing GA KV594 UT WOS:A1993KV59400037 ER PT J AU SALORANTA, C KOIVISTO, V WIDEN, E FALHOLT, K DEFRONZO, RA HARKONEN, M GROOP, L AF SALORANTA, C KOIVISTO, V WIDEN, E FALHOLT, K DEFRONZO, RA HARKONEN, M GROOP, L TI CONTRIBUTION OF MUSCLE AND LIVER TO GLUCOSE-FATTY ACID CYCLE IN HUMANS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE FREE FATTY ACIDS; HEPATIC GLUCOSE PRODUCTION; GLYCOGEN SYNTHASE; PYRUVATE DEHYDROGENASE; CARNITINE PALMITOYLTRANSFERASE ID DEPENDENT DIABETES-MELLITUS; PERFUSED SKELETAL-MUSCLE; PYRUVATE-DEHYDROGENASE; INSULIN RESISTANCE; GLYCOGEN-SYNTHASE; METABOLISM; INFUSION; CARBOHYDRATE; AVAILABILITY; STARVATION AB To examine the influence of elevated free fatty acid (FFA) levels on hepatic glucose production (HGP) and oxidative and nonoxidative pathways of glucose metabolism, 12 healthy subjects participated in two euglycemic insulin-clamp studies performed with and without infusion of Intralipid plus heparin. To elucidate the role of skeletal muscle in this putative interaction, we performed muscle biopsies for the measurement of activities of glycogen synthase (GS), pyruvate dehydrogenase (PDH), and carnitine palmitoyltransferase (CPT). Infusion of Intralipid plus heparin caused an increase in plasma FFA concentrations and rate of lipid oxidation (measured by indirect calorimetry) that was not inhibited by insulin. Suppression of HGP by insulin was impaired by elevated plasma FFA levels. Furthermore, the increase in plasma FFA was associated with a 20% reduction in total glucose metabolism (P < 0.01), which was completely accounted for by a reduction in the rate of glucose oxidation. Although the fractional activity of GS was increased by insulin, elevation of plasma FFA had no influence on this key enzyme of glycogen synthesis. In addition, the activities of PDH and CPT were uninfluenced by the elevation of FFA, suggesting that oxidative processes in skeletal muscle were not a major target for the operative glucose-fatty acid cycle under the current conditions. Taken together, the data indicate that the interaction between FFA and glucose metabolism also involves impaired suppression of HGP by insulin. C1 HELSINKI UNIV HOSP,DEPT MED 4,UNIONINKATU 38,SF-00170 HELSINKI,FINLAND. HELSINKI UNIV HOSP,DEPT MED 2,SF-00170 HELSINKI,FINLAND. NOVO RES INST,COPENHAGEN,DENMARK. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM-24092] NR 37 TC 92 Z9 92 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 APR PY 1993 VL 264 IS 4 BP E599 EP E605 PN 1 PG 7 WC Physiology SC Physiology GA KZ603 UT WOS:A1993KZ60300056 PM 8476039 ER PT J AU MATALON, S BAUER, ML BENOS, DJ KLEYMAN, TR LIN, CM CRAGOE, EJ OBRODOVICH, H AF MATALON, S BAUER, ML BENOS, DJ KLEYMAN, TR LIN, CM CRAGOE, EJ OBRODOVICH, H TI FETAL LUNG EPITELIAL CELLS CONTAIN 2 POPULATIONS OF AMILORIDE-SENSITIVE NA+ CHANNELS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE 5-(N-ETHYL-N-ISOPROPYL)-2'-4'-AMILORIDE; BENZAMIL; BINDING SITES; IMMUNOFLUORESCENCE; POLYCLONAL ANTIBODIES; ANTIIDIOTYPIC ANTIBODIES; PLASMA MEMBRANE VESICLES, ALVEOLAR TYPE-II PNEUMOCYTES ID EPITHELIAL SODIUM-CHANNEL; WATER CLEARANCE; II PNEUMOCYTES; BINDING; PROTEIN; ANTIBODIES; AFFINITY AB Active Na+ transport by the alveolar epithelium plays a major role in reabsorption of the fetal lung fluid after birth. We characterized the biochemical and physiological characteristics of Na+ conductive pathways in distal fetal lung epithelial (FLE) cells isolated from 20-day-old rat fetuses. We demonstrated that a polyclonal antibody to Na+ channel protein (NaAb) binds to the plasma membranes of FLE cells. In Western blot studies, this NaAb and an anti-idiotypic monoclonal antibody to the amiloride-binding subunit of the Na+ channel protein recognized 150- and 90-kDa polypeptides in plasma membrane vesicles of FLE. Na-22+ flux measurements across plasma membrane vesicles of FLE revealed the existence of electrogenic Na+ transport, which was twice as high as the corresponding adult value. One hundred micromolars of amiloride, benzamil, and 5-(N-ethyl-N-isopropyl)-2'-4'-amiloride inhibited 30, 40, and 70% of the electrogenic Na+ transport across plasma membrane vesicles of FLE cells, respectively. The half-maximum inhibition of electrogenic Na+ transport by these substances occurred between 0.3 and 1 muM. [H-3]benzamil equilibrium binding studies in membrane vesicles of FLE cells revealed the existence of two binding sites that had dissociation constant values of 19 and 1,525 nM, respectively. These data indicate the presence of both high- and low-amiloride affinity Na+ conductive pathways (channels) in FLE cells. C1 UNIV ALABAMA,DEPT ANAESTHESIOL,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT PEDIAT,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT PHYSIOL & BIOPHYS,BIRMINGHAM,AL 35294. UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. UNIV TORONTO,HOSP SICK CHILDREN,DEPT PEDIAT RESP RES DIV,TORONTO M5G 1X8,ONTARIO,CANADA. FU NHLBI NIH HHS [HL-31197]; NIDDK NIH HHS [DK-37206] NR 31 TC 50 Z9 50 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 APR PY 1993 VL 264 IS 4 BP L357 EP L364 PN 1 PG 8 WC Physiology SC Physiology GA KZ603 UT WOS:A1993KZ60300101 PM 8386466 ER PT J AU ANDRADE, F ANZUETO, A GREENE, KE LEVINE, SM SILMAN, JB ROODMAN, GD MAXWELL, LC JENKINSON, SG BRYAN, CL AF ANDRADE, F ANZUETO, A GREENE, KE LEVINE, SM SILMAN, JB ROODMAN, GD MAXWELL, LC JENKINSON, SG BRYAN, CL TI DIAPHRAGM MUSCLE IMPAIRMENT IN MICE CHRONICALLY EXPOSED TO TUMOR-NECROSIS-FACTOR-ALPHA SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A235 EP A235 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900876 ER PT J AU ANZUETO, A BRYAN, CL LEVINE, SM PETERS, JI CRONIN, T CALHOON, JH JENKINSON, SG AF ANZUETO, A BRYAN, CL LEVINE, SM PETERS, JI CRONIN, T CALHOON, JH JENKINSON, SG TI PANEL REACTIVE ANTIBODIES AS A PREDICTOR OF GRAFT COMPLICATIONS IN SINGLE-LUNG TRANSPLANT RECIPIENTS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER 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 APR PY 1993 VL 147 IS 4 SU S BP A339 EP A339 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901270 ER PT J AU BRASSARD, JM ANZUETO, A LEVINE, SM ANDRADE, F MAXWELL, LC LAWRENCE, RA JENKINSON, SG AF BRASSARD, JM ANZUETO, A LEVINE, SM ANDRADE, F MAXWELL, LC LAWRENCE, RA JENKINSON, SG TI EFFECTS OF HYPEROXIA ON RAT DIAPHRAGM FUNCTION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A236 EP A236 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900878 ER PT J AU BRYAN, CL LEVINE, SM ANZUETO, A PETERS, JI COALSON, JJ TRINKLE, JK JENKINSON, SG AF BRYAN, CL LEVINE, SM ANZUETO, A PETERS, JI COALSON, JJ TRINKLE, JK JENKINSON, SG TI ISCHEMIC PRESERVATION TIME AS A PREDICTOR OF LUNG GRAFT COMPLICATIONS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 APR PY 1993 VL 147 IS 4 SU S BP A339 EP A339 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901271 ER PT J AU BUKOWSKI, DM LAWRENCE, RA DENEKE, SM JENKINSON, SG AF BUKOWSKI, DM LAWRENCE, RA DENEKE, SM JENKINSON, SG TI EFFECT OF GAMMA-GLUTAMYL-TRANSPEPTIDASE INHIBITION ON GLUTATHIONE UPTAKE AND METABOLISM IN RAT TYPE-II EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE 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 1 Z9 1 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A149 EP A149 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900540 ER PT J AU BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG AF BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG TI CHARACTERISTICS OF SODIUM-DEPENDENT CYSTINE UPTAKE IN RAT ALVEOLAR TYPE-II EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER 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 APR PY 1993 VL 147 IS 4 SU S BP A1005 EP A1005 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14903862 ER PT J AU CHIANG, YY ZACHMAN, RD THET, LA AF CHIANG, YY ZACHMAN, RD THET, LA TI CHANGES IN RETINOIC ACID RECEPTORS (RAR) IN TYPE-I AND TYPE-2 ALVEOLAR EPITHELIAL-CELLS DURING REPAIR OF HYPEROXIC LUNG INJURY SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A150 EP A150 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900546 ER PT J AU DHANANI, S HUANG, M DUBINETT, SM AF DHANANI, S HUANG, M DUBINETT, SM TI INTERFERON-ALPHA INHIBITS MURINE MACROPHAGE TRANSFORMING GROWTH-FACTOR-BETA PRODUCTION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA 90024 USA. W LOS ANGELES VAMC, DIV PULM & CRIT CARE MED, LOS ANGELES, CA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER THORACIC SOC PI NEW YORK PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A758 EP A758 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902907 ER PT J AU GREENE, KE SMITH, DB KING, RJ AF GREENE, KE SMITH, DB KING, RJ TI THE EFFECTS OF TUMOR-NECROSIS-FACTOR-ALPHA ON SURFACTANT PROTEIN-A SYNTHESIS AND SECRETION IN ADULT-RAT TYPE-II CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE 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,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A250 EP A250 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900924 ER PT J AU HOO, GWS ELLISON, MJ ZHANG, C WILLIAMS, AJ AF HOO, GWS ELLISON, MJ ZHANG, C WILLIAMS, AJ TI COMPARISON OF 4 MODES OF NASAL MECHANICAL VENTILATION IN PATIENTS WITH COPD SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 W LOS ANGELES VAMC, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER THORACIC SOC PI NEW YORK PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A322 EP A322 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901204 ER PT J AU HUANG, M DHANANI, S MINTZ, LE DUBINETT, SM AF HUANG, M DHANANI, S MINTZ, LE DUBINETT, SM TI DOWN-REGULATION OF INTERLEUKIN-2-INDUCED TRANSFORMING GROWTH-FACTOR-BETA BY INTERLEUKIN-7 SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, JONSSON COMPREHENS CANC CTR,SCH MED, DIV PULM & CRIT CARE MED,PULM IMMUNOL LAB, LOS ANGELES, CA USA. W LOS ANGELES VA MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER THORACIC SOC PI NEW YORK PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A757 EP A757 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902904 ER PT J AU LEEVERS, AM SIMON, PM MURTY, JL LANDRY, DM DEMPSEY, JA AF LEEVERS, AM SIMON, PM MURTY, JL LANDRY, DM DEMPSEY, JA TI EFFECTS OF INSPIRATORY FLOW-RATE DURING MECHANICAL VENTILATION ON NEUROMECHANICAL INHIBITION OF INSPIRATORY MUSCLE-ACTIVITY SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53705. MIDDLETON VET ADM HOSP,MADISON,WI 53705. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A163 EP A163 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900595 ER PT J AU LEVINE, SM PETERS, JI ANZUETO, A TILLIS, WP CALHOON, J TRINKLE, JK JENKINSON, SG BRYAN, CL AF LEVINE, SM PETERS, JI ANZUETO, A TILLIS, WP CALHOON, J TRINKLE, JK JENKINSON, SG BRYAN, CL TI ASPERGILLUS INFECTION IN SINGLE-LUNG TRANSPLANT RECIPIENTS SO AMERICAN REVIEW OF RESPIRATORY DISEASE 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 4 Z9 4 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A599 EP A599 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902284 ER PT J AU LEVINE, SM PETERS, JI BRYAN, CL ANZUETO, A TRINKLE, K JENKINSON, SG AF LEVINE, SM PETERS, JI BRYAN, CL ANZUETO, A TRINKLE, K JENKINSON, SG TI MEDICAL COMPLICATIONS IN LUNG-TRANSPLANT RECIPIENTS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER 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 APR PY 1993 VL 147 IS 4 SU S BP A602 EP A602 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902297 ER PT J AU PETERS, JI LEVINE, SM ANZUETO, A BRYAN, CL CALHOON, JH TRINKLE, JK JENKINSON, SG AF PETERS, JI LEVINE, SM ANZUETO, A BRYAN, CL CALHOON, JH TRINKLE, JK JENKINSON, SG TI INFECTIOUS COMPLICATIONS IN SINGLE-LUNG TRANSPLANT RECIPIENTS - A 5-YEAR EXPERIENCE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER 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 APR PY 1993 VL 147 IS 4 SU S BP A601 EP A601 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902292 ER PT J AU SILMAN, JB BRYAN, CL CALHOON, JH AF SILMAN, JB BRYAN, CL CALHOON, JH TI CRYOPRESERVATION WITH LAZAROID U74006F IN DOG LUNG AUTOTRANSPLANTATION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER 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 APR PY 1993 VL 147 IS 4 SU S BP A263 EP A263 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900975 ER PT J AU SILMAN, JB ANDRADE, F ANZUETO, A LEVINE, SM MAXWELL, LC JENKINSON, SG AF SILMAN, JB ANDRADE, F ANZUETO, A LEVINE, SM MAXWELL, LC JENKINSON, SG TI DIAPHRAGM MUSCLE FUNCTION AFTER LAZAROIDS (U74006F) EXPOSURE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A237 EP A237 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900883 ER PT J AU SIMON, PM LEEVERS, AM MURTY, JL LANDRY, DM AF SIMON, PM LEEVERS, AM MURTY, JL LANDRY, DM TI VOLUME AND FREQUENCY THRESHOLDS FOR INHIBITION OF INSPIRATORY MOTOR OUTPUT DURING MECHANICAL VENTILATION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53705. MIDDLETON VET ADM HOSP,MADISON,WI 53705. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A166 EP A166 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900608 ER PT J AU SUSANTO, I LAWRENCE, RA DENEKE, SM BUKOWSKI, DM JENKINSON, SG AF SUSANTO, I LAWRENCE, RA DENEKE, SM BUKOWSKI, DM JENKINSON, SG TI GLUTATHIONE REDOX CYCLE IS IMPORTANT IN PROTECTION AGAINST TYPE-II ALVEOLAR EPITHELIAL-CELL INJURY CAUSED BY H2O2 SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER 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 APR PY 1993 VL 147 IS 4 SU S BP A152 EP A152 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900552 ER PT J AU TILLIS, WP ANZUETO, A LEVINE, SM PETERS, JI CALHOON, JH TRINKLE, JK JENKINSON, SG BRYAN, CL AF TILLIS, WP ANZUETO, A LEVINE, SM PETERS, JI CALHOON, JH TRINKLE, JK JENKINSON, SG BRYAN, CL TI OUTCOME OF OBLITERATIVE BRONCHIOLITIS IN SINGLE-LUNG TRANSPLANT RECIPIENTS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER 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 APR PY 1993 VL 147 IS 4 SU S BP A198 EP A198 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900734 ER PT J AU ROOK, AH VOWELS, BR JAWORSKY, C SINGH, A LESSIN, SR AF ROOK, AH VOWELS, BR JAWORSKY, C SINGH, A LESSIN, SR TI THE IMMUNOPATHOGENESIS OF CUTANEOUS T-CELL LYMPHOMA - ABNORMAL CYTOKINE PRODUCTION BY SEZARY T-CELLS SO ARCHIVES OF DERMATOLOGY LA English DT Editorial Material ID INTERCELLULAR-ADHESION MOLECULE-1; TUMOR NECROSIS FACTOR; MYCOSIS-FUNGOIDES; EXTRACORPOREAL PHOTOCHEMOTHERAPY; GAMMA-INTERFERON; PROLIFERATION; EXPRESSION; SUBSETS; CLONES C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. RP ROOK, AH (reprint author), UNIV PENN,DEPT DERMATOL,CUTANEOUS LYMPHONA GRP,PHILADELPHIA,PA 19104, USA. FU NCI NIH HHS [R29-CA 55017] NR 30 TC 75 Z9 75 U1 0 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD APR PY 1993 VL 129 IS 4 BP 486 EP 489 DI 10.1001/archderm.129.4.486 PG 4 WC Dermatology SC Dermatology GA KW765 UT WOS:A1993KW76500014 PM 8466223 ER PT J AU NAITO, HK KWAK, YS HARTFIEL, JL PARK, JK TRAVERS, EM MYERS, GL ROSS, JW ECKFELDT, JH HARTMANN, AE AF NAITO, HK KWAK, YS HARTFIEL, JL PARK, JK TRAVERS, EM MYERS, GL ROSS, JW ECKFELDT, JH HARTMANN, AE TI MATRIX EFFECTS ON PROFICIENCY TESTING MATERIALS - IMPACT ON ACCURACY OF CHOLESTEROL MEASUREMENT IN LABORATORIES IN THE NATIONS LARGEST HOSPITAL SYSTEM SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID HYDROLYSIS AB The objective of this collaborative study with the Department of Veterans Affairs (VA), College of American Pathologists (CAP), and the Centers for Disease Control and Prevention (CDC) was to quantitate the matrix-induced biases of cholesterol measurements on the CAP Comprehensive Chemistry Surveys materials used in proficiency testing (PT). A total of 174 VA Medical Centers outpatient clinics and clinical laboratories participate in the VA-CDC National Cholesterol Standardization and Certification Program. This study was conducted in 112 VA laboratories that have been standardized for measuring cholesterol accurately (within +/- 3.0% of the CDC reference-method values) using fresh, unfrozen, unadulterated human serum samples. Fresh serum samples and 1990 CAP Surveys materials were sent by overnight mail, and the laboratories were asked to analyze them simultaneously in triplicate in a single analytic batch run. The results showed significant matrix-effect biases with the CAP Surveys materials with six of the eight major peer groups, despite the fact that accuracy of cholesterol measurements was maintained with fresh serum samples. The magnitude and direction (positive or negative) of the matrix-effect biases were instrument, reagent, and method specific using the following peer groups: du Pont Dimension (-8.9%); Beckman CX4, CX5, and CX7 (-5.5%); Kodak Ektachem 400, 500, and 700 (+4.4%); Instrumentation Laboratory Monarch (-3.1%); Baxter Paramax (-2.4%); Technicon SMAC and RA (+1.3%); Hitachi/BMD 704 through 747 (+0.4%); and Abbott Spectrum (-0.3%). The CAP PT materials used currently do not behave in a manner identical to fresh human serum when measuring cholesterol on many, but not all, analytic systems. The observed biases due to ''matrix effects' with PT materials will cause incorrect conclusions about the accuracy of many laboratory procedures performed on fresh patient specimens. This matrix-effect phenomenon will severely hamper interlaboratory accuracy transfer, standardization efforts, and monitoring performance of a laboratory's testing accuracy with the use of the current survey materials used in PT programs. Collaborative efforts are needed to (1) improve PT fluids to analytically behave more like fresh, human serum; (2) improve instrument design and reagent formulation; and (3) select methods and methodologic parameters that are more ''robust'' and less sensitive to the exact character of processed calibrators, quality control, and PT materials. C1 CASE WESTERN RESERVE UNIV,SCH MED,DEPT PATHOL,CLEVELAND,OH 44106. US DEPT VET AFFAIRS,CENT OFF,PATHOL & LAB MED SERV,WASHINGTON,DC. CTR DIS CONTROL,NATL CTR ENVIRONM HLTH,DIV ENVIRONM HLTH LAB SCI,ATLANTA,GA 30333. KENNESTONE HOSP,DEPT PATHOL,MARIETTA,GA. UNIV MINNESOTA HOSP & CLIN,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. PHYSICIANS LAB,SIOUX FALLS,SD. COLL AMER PATHOLOGISTS,COMM CHEM RESOURCE,NORTHFIELD,IL. RP NAITO, HK (reprint author), VET AFFAIRS MED CTR,NATL CTR LAB ACCURACY & STANDARDIZAT,PATHOL & LAB MED SERV,10701 EAST BLVD,CLEVELAND,OH 44106, USA. NR 29 TC 26 Z9 26 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 APR PY 1993 VL 117 IS 4 BP 345 EP 351 PG 7 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA KV587 UT WOS:A1993KV58700002 PM 8466396 ER PT J AU HOWANITZ, JH AF HOWANITZ, JH TI REVIEW OF THE INFLUENCE OF POLYPEPTIDE HORMONE FORMS ON IMMUNOASSAY RESULTS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID HUMAN GROWTH-HORMONE; BETA-SUBUNIT; CHORIO-GONADOTROPIN; HUMAN-PROLACTIN; SERUM; HCG; REEVALUATION; THYROTROPIN; SECRETION; AFFINITY AB Various forms of the polypeptide hormones that occur in blood, fluids, or tissues can differ according to physiologic and pathologic states. Forms include subunits of luteinizing hormone, follicle-stimulating hormone, human chorionic gonadotropin, and thyroid-stimulating hormone. Hormonal isoforms occur for these hormones as well as for prolactin and growth hormone. Variation in hormonal forms appears to contribute significantly to the wide variation in immunoassay results for these polypeptide hormones. Subunits and isoforms of the polypeptide hormones can overreact or underreact in monoclonal antibody assays. The underreaction or overreaction can occur with standards, controls, and patient specimens as well as with the assay label. C1 UNIV CALIF LOS ANGELES, DEPT PATHOL & LAB MED, LOS ANGELES, CA 90024 USA. RP HOWANITZ, JH (reprint author), W LOS ANGELES DEPT VET AFFAIRS MED CTR, LAB SERV, LOS ANGELES, CA USA. NR 22 TC 11 Z9 12 U1 0 U2 1 PU COLL AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA SN 0003-9985 EI 1543-2165 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD APR PY 1993 VL 117 IS 4 BP 369 EP 372 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA KV587 UT WOS:A1993KV58700005 PM 8466399 ER PT J AU WONG, ML EDELSTEIN, J WOLLMAN, J BOND, MG AF WONG, ML EDELSTEIN, J WOLLMAN, J BOND, MG TI ULTRASONIC PATHOLOGICAL COMPARISON OF THE HUMAN ARTERIAL-WALL - VERIFICATION OF INTIMA MEDIA THICKNESS SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE ULTRASONOGRAPHY; ARTERIAL WALL; TUNICA THICKNESS AB Recent intravascular ultrasound experience challenges the accuracy of ultrasonic measurement of arterial wall thickness. We reevaluated the correlation between histological and sonographic measurements of intima-media thickness using standard transcutaneous vascular technology. Carotid and femoral arterial segments were imaged before and after fixation using a 7-MHz linear-array vascular transducer. Log compression and beam orientation were varied. Mean intima, media, and adventitia thicknesses were measured and compared with corresponding histological tunica. Tissue processing caused 2.5% shrinkage. Intraobserver reading error was 0.7% for histology and 5.4% for sonography. Ultrasound overestimated the thickness of the intima and adventitia and underestimated the thickness of the media. For combined intima-media thickness, the differences between histology and imaging were insignificant, averaging 4% for the carotid artery and 9% for the femoral artery in the far-wall projection. In the near-wall projection, sonographic intima-media thickness was 20% less than that determined histologically. We conclude that ultrasonography is limited mainly by axial resolution in quantifying the dimensions of individual arterial tunica but is capable of accurately measuring far-wall intima-media thickness. C1 W LOS ANGELES DEPT VET AFFAIRS MED CTR,ANAT PATHOL SECT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DIV VASC ULTRASOUND RES,WINSTON SALEM,NC 27103. RP WONG, ML (reprint author), W LOS ANGELES DEPT VET AFFAIRS MED CTR,CARDIOL SECT WIIIE,LOS ANGELES,CA 90073, USA. NR 12 TC 208 Z9 231 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD APR PY 1993 VL 13 IS 4 BP 482 EP 486 PG 5 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KW817 UT WOS:A1993KW81700003 PM 8466883 ER PT J AU CUMMINGS, JL GORMAN, DG SHAPIRA, J AF CUMMINGS, JL GORMAN, DG SHAPIRA, J TI PHYSOSTIGMINE AMELIORATES THE DELUSIONS OF ALZHEIMERS-DISEASE SO BIOLOGICAL PSYCHIATRY LA English DT Article DE ALZHEIMERS DISEASE; DELUSIONS; PHYSOSTIGMINE; HALOPERIDOL; ACETYLCHOLINE; ACETYLCHOLINESTERASE; ACETYLCHOLINESTERASE INHIBITOR ID ORAL PHYSOSTIGMINE; DEMENTIA; DEPRESSION; PSYCHOSIS AB Alzheimer's disease (AD) patients frequently manifest delusions, and the cholinergic deficiency of AD may contribute to this aspect of the psychopathology of the disorder. In a double-blind, crossover study involving two patients, we compared the antidelusional efficacy of physostigmine, an acetylcholinesterase inhibitor, with haloperidol, a widely used neuroleptic agent. Physostigmine ameliorated the delusions and produced fewer side effects. These preliminary observations suggest that the cholinergic deficiency contributes to the occurrence of delusions in AD and cholinergic therapy may have a role in the treatment of the delusional symptoms. C1 W LOS ANGELES VET AFFAIRS MED CTR, NURSING SERV, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, CTR ALZHEIMERS DIS, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH NURSING, LOS ANGELES, CA USA. RP CUMMINGS, JL (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, PSYCHIAT SERV, NEUROBEHAV UNIT, BEHAV NEUROSCI SECT, BLDG 256B, LOS ANGELES, CA 90073 USA. FU NIA NIH HHS [AG 10123] NR 29 TC 98 Z9 98 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1993 VL 33 IS 7 BP 536 EP 541 DI 10.1016/0006-3223(93)90009-3 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LD103 UT WOS:A1993LD10300009 PM 8513039 ER PT J AU BAUER, RL HAFFNER, SM AF BAUER, RL HAFFNER, SM TI AXIAL SKELETAL BONE DENSITIES IN DIABETICS IN A POPULATION-BASED SURVEY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A123 EP A123 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100055 ER PT J AU BOLDT, DH ALCANTARA, O ONER, T OBEID, L HANNUN, YA AF BOLDT, DH ALCANTARA, O ONER, T OBEID, L HANNUN, YA TI REGULATION OF LUCIFERASE EXPRESSION BY FERRIC TRANSFERRIN IN STABLE HREH9 TRANSFECTANTS CONTAINING PKC-BETA-LUCIFERASE GENE CONSTRUCTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. DUKE UNIV,MED CTR,DURHAM,NC 27710. NR 1 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A308 EP A308 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101074 ER PT J AU DICPINIGAITIS, PV ALMENOFF, PL SPUNGEN, AM ABSGARTEN, A BAUMAN, WA AF DICPINIGAITIS, PV ALMENOFF, PL SPUNGEN, AM ABSGARTEN, A BAUMAN, WA TI EFFECT OF A GABA-AGONIST ON BRONCHIAL RESPONSIVENESS IN SUBJECTS WITH SPINAL-CORD INJURY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CUNY MT SINAI SCH MED,DIV PULM & CRIT CARE MED,NEW YORK,NY 10029. BRONX VET ADM MED CTR,SPINAL CORD DAMAGE RES CTR,BRONX,NY. NR 1 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A176 EP A176 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100361 ER PT J AU GRANDALIANO, G BISWAS, P CHOUDHURY, GG BARNES, JL ABBOUD, HE AF GRANDALIANO, G BISWAS, P CHOUDHURY, GG BARNES, JL ABBOUD, HE TI PGE1 ANALOG MISOPROSTOL INHIBITS THROMBIN-INDUCED DNA-SYNTHESIS AND PDGF B-CHAIN GENE-EXPRESSION IN CULTURED HUMAN MESANGIAL CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RI Grandaliano, Giuseppe/G-2963-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A141 EP A141 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100159 ER PT J AU HERBERT, V STOPLERKASDAN, T AF HERBERT, V STOPLERKASDAN, T TI CAN GENETIC NUTRITION BE USED TO PREDICT AND PREVENT HEART-ATTACKS - THE MOUNT-SINAI HEART-ATTACK PREDICTION AND PREVENTION PROFILE (THE PROFILE) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,NEW YORK,NY. NR 1 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A397 EP A397 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101593 ER PT J AU KERBER, CA LAWRENCE, VA DHANDA, R AF KERBER, CA LAWRENCE, VA DHANDA, R TI CAN THE AMERICAN SOCIETY OF ANESTHESIOLOGISTS PHYSICAL STATUS CLASSIFICATION PREDICT OPERATIVE RISK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A520 EP A520 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102322 ER EF