FN Thomson Reuters Web of Science™ VR 1.0 PT J AU TAKAHASHI, LK HAGLIN, C KALIN, NH AF TAKAHASHI, LK HAGLIN, C KALIN, NH TI PRENATAL STRESS POTENTIATES STRESS-INDUCED BEHAVIOR AND REDUCES THE PROPENSITY TO PLAY IN JUVENILE RATS SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE PRENATAL STRESS; JUVENILE RATS; SOCIAL PLAY; FREEZING; STRESS; PITUITARY-ADRENAL HORMONES; DEFENSIVE BEHAVIOR ID CORTICOSTERONE LEVELS; PLASMA TESTOSTERONE; FEMALE RATS; CORTICOTROPIN; MALES AB We examined the hypothesis that prenatal stress potentiates defensive responsiveness which may interfere with the expression of appetitive behavioral activities. Sibling pairs of prenatally stressed and control juvenile rats were placed in an unfamiliar environment. The latency and frequency of social play, a sought-after activity of juvenile rats, were measured on 4 successive days beginning at 25 days of age. However, on Day 27, electric foot shock was administered in order to assess directly whether exposure to threat facilitates the occurrence of defensive behavior in prenatally stressed rats. In addition, to determine whether previous exposure to threat produces long-term suppressive effects on play, rats were retested on Day 28 in the absence of shock. Throughout the testing period, the latency to play, as indicated by one rat pouncing on the opponent, was significantly higher in prenatally stressed than control rats. The frequency of play, however, did not differ reliably between groups. These data suggest that prenatally stressed rats take longer to adapt to the test situation before initiating play than control rats. In both groups, exposure to shock on Day 27 significantly increased the latency to play. More importantly, prenatally stressed rats exhibited significantly higher durations of defensive freezing than control animals. When retested on Day 28, however, the duration of freezing declined significantly and no longer differed between groups. Data appear to support the hypothesis that prenatally stressed juvenile rats are responsive to stress which may modulate the inclination to exhibit social behavior. C1 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 29 TC 83 Z9 84 U1 2 U2 10 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 FEB PY 1992 VL 51 IS 2 BP 319 EP 323 DI 10.1016/0031-9384(92)90147-T PG 5 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA HA082 UT WOS:A1992HA08200015 PM 1313590 ER PT J AU KAHN, RS DAVIDSON, M HIRSCHOWITZ, J STERN, RG DAVIS, BM GABRIEL, S MOORE, C DAVIS, KL AF KAHN, RS DAVIDSON, M HIRSCHOWITZ, J STERN, RG DAVIS, BM GABRIEL, S MOORE, C DAVIS, KL TI NOCTURNAL GROWTH-HORMONE SECRETION IN SCHIZOPHRENIC-PATIENTS AND HEALTHY-SUBJECTS SO PSYCHIATRY RESEARCH LA English DT Article DE PSYCHOENDOCRINOLOGY; HORMONES; DOPAMINE; SEROTONIN ID SLOW-WAVE SLEEP; GH RELEASE; SOMATOSTATIN; SEROTONIN; DOPAMINE; HUMANS AB Plasma growth hormone concentrations were measured at hourly intervals between 10 p.m. and 8 a.m. the next morning in 15 drug-free chronic schizophrenic male inpatients and 14 healthy males. Growth hormone secretion was significantly lower in the patients as compared with the controls. Growth hormone release peaked around 1 a.m. in the controls, but a growth hormone peak was absent in the patient group. Increased dopamine activity, increased serotonin activity, or both could explain the absence of a nocturnal growth hormone surge in the schizophrenic patients. C1 BRONX VET ADM MED CTR,SERV PSYCHIAT,BRONX,NY 10468. CUNY MT SINAI SCH MED,NEUROENDOCRINOL LAB,NEW YORK,NY 10029. RP KAHN, RS (reprint author), BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,CLIN RES UNIT,140 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIMH NIH HHS [R01 MH-37922-07] NR 27 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD FEB PY 1992 VL 41 IS 2 BP 155 EP 161 DI 10.1016/0165-1781(92)90107-E PG 7 WC Psychiatry SC Psychiatry GA HJ675 UT WOS:A1992HJ67500007 PM 1574542 ER PT J AU RAHMAN, MU HUDSON, AP SCHUMACHER, HR AF RAHMAN, MU HUDSON, AP SCHUMACHER, HR TI CHLAMYDIA AND REITERS-SYNDROME (REACTIVE ARTHRITIS) SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID UROGENITAL INVOLVEMENTS; TRACHOMATIS INFECTIONS; BORRELIA-BURGDORFERI; SEXUAL PARTNERS; DISEASE; EPIDEMIOLOGY; CELLS; MICE; HYBRIDIZATION; PATHOGENESIS C1 MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA. DEPT VET AFFAIRS MED CTR,RES SERV,PHILADELPHIA,PA. NR 88 TC 36 Z9 38 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-857X J9 RHEUM DIS CLIN N AM JI Rheum. Dis. Clin. North Am. PD FEB PY 1992 VL 18 IS 1 BP 67 EP 79 PG 13 WC Rheumatology SC Rheumatology GA LA276 UT WOS:A1992LA27600007 PM 1561410 ER PT J AU RAHMAN, MU SCHUMACHER, HR HUDSON, AP AF RAHMAN, MU SCHUMACHER, HR HUDSON, AP TI RECURRENT ARTHRITIS IN REITERS-SYNDROME - A FUNCTION OF INAPPARENT CHLAMYDIAL INFECTION OF THE SYNOVIUM SO SEMINARS IN ARTHRITIS AND RHEUMATISM LA English DT Article DE INAPPARENT INFECTION; CHLAMYDIA; SYNOVIUM; REITERS SYNDROME ID REACTIVE ARTHRITIS; UROGENITAL INVOLVEMENTS; SEXUAL PARTNERS; TRACHOMATIS; DISEASE; EPIDEMIOLOGY; PATHOGENESIS; PERSISTENT; DISORDERS; FEATURES C1 UNIV PENN,SCH MED,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR 151K,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. DEPT VET AFFAIRS MED CTR,RES SERV,PHILADELPHIA,PA 19104. FU NCRR NIH HHS [RR00040] NR 70 TC 24 Z9 24 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0049-0172 J9 SEMIN ARTHRITIS RHEU JI Semin. Arthritis Rheum. PD FEB PY 1992 VL 21 IS 4 BP 259 EP 266 DI 10.1016/0049-0172(92)90057-K PG 8 WC Rheumatology SC Rheumatology GA HE979 UT WOS:A1992HE97900008 PM 1570519 ER PT J AU SAAG, MS POWDERLY, WG CLOUD, GA ROBINSON, P GRIECO, MH SHARKEY, PK THOMPSON, SE SUGAR, AM TUAZON, CU FISHER, JF HYSLOP, N JACOBSON, JM HAFNER, R DISMUKES, WE AF SAAG, MS POWDERLY, WG CLOUD, GA ROBINSON, P GRIECO, MH SHARKEY, PK THOMPSON, SE SUGAR, AM TUAZON, CU FISHER, JF HYSLOP, N JACOBSON, JM HAFNER, R DISMUKES, WE TI COMPARISON OF AMPHOTERICIN-B WITH FLUCONAZOLE IN THE TREATMENT OF ACUTE AIDS-ASSOCIATED CRYPTOCOCCAL MENINGITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; FLUCYTOSINE; NEOFORMANS; EXPERIENCE AB Background. Intravenous amphotericin B, with or without flucytosine, is usually standard therapy for cryptococcal meningitis in patients with the acquired immunodeficiency syndrome (AIDS): Fluconazole, an oral triazole agent, represents a promising new approach to the treatment of cryptococcal disease. Methods. In a randomized multicenter trial, we compared intravenous amphotericin B with oral fluconazole as primary therapy for AIDS-associated acute cryptococcal meningitis. Eligible patents, in all of whom the diagnosis had been confirmed by culture, were randomly assigned in a 2:1 ratio to receive either fluconazole (200 mg per day) or amphotericin B. Treatment was considered successful if the patient had had two consecutive negative cerebrospinal fluid cultures by the end of the 10-week treatment period. Results. Of the 194 eligible patients, 131 received fluconazole and 63 received amphotericin B (mean daily dose, 0.4 mg per kilogram of body weight in patients with successful treatment and 0.5 mg per kilogram in patients with treatment failure; P = 0.34). Treatment was successful in 25 of the 63 amphotericin B recipients (40 percent; 95 percent confidence interval, 26 percent to 53 percent) and in 44 of the 131 fluconazole recipients (34 percent; 95 percent confidence interval, 25 percent to 42 percent) (P = 0.40). There was no significant difference between the groups in overall mortality due to cryptococcosis (amphotericin vs. fluconazole, 9 of 63 [14 percent] vs. 24 of 131 [18 percent]; P = 0.48); however, mortality during the first two weeks of therapy was higher in the fluconazole group (15 percent vs. 8 percent; P = 0.25). The median length of time to the first negative cerebrospinal fluid culture was 42 days (95 percent confidence interval, 28 to 71) in the amphotericin B group and 64 days (95 percent confidence interval, 53 to 67) in the fluconazole group (P = 0.25). Multivariate analyses identified abnormal mental status (lethargy, somnolence, or obtundation) as the most important predictive factor of a high risk of death during therapy (P < 0.0001). Conclusions. Fluconazole is an effective alternative to amphotericin B as primary treatment of cryptococcal meningitis in patients with AIDS. Single-drug therapy with either drug is most effective in patients who are at low risk for treatment failure. The optimal therapy for patients at high risk remains to be determined. C1 UNIV ALABAMA, SCH MED, DEPT MED, DIV INFECT DIS, BIRMINGHAM, AL 35233 USA. UNIV ALABAMA, SCH MED, CTR COMPREHENS CANC, DIV BIOSTAT, BIRMINGHAM, AL 35233 USA. WASHINGTON UNIV, SCH MED, DIV INFECT DIS, ST LOUIS, MO 63110 USA. ST LOUIS VET AFFAIRS MED CTR, ST LOUIS, MO USA. COLUMBIA UNIV, ST LUKES ROOSEVELT HOSP, SCH MED, NEW YORK, NY 10027 USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. AUDIE L MURPHY VET AFFAIRS HOSP, SAN ANTONIO, TX USA. EMORY UNIV, GRADY MEM HOSP, ATLANTA, GA 30322 USA. BOSTON CITY HOSP, DEPT MED, BOSTON, MA 02118 USA. BOSTON UNIV, UNIV HOSP, DEPT MED, BOSTON, MA 02215 USA. GEORGE WASHINGTON UNIV, DEPT MED, WASHINGTON, DC 20052 USA. MED COLL GEORGIA, DEPT MED, AUGUSTA, GA 30912 USA. TULANE UNIV, DEPT MED, NEW ORLEANS, LA 70118 USA. MT SINAI MED CTR, DEPT MED, DIV INFECT DIS, NEW YORK, NY 10029 USA. BRONX VET AFFAIRS MED CTR, BRONX, NY USA. NIAID, DIV AIDS, BETHESDA, MD 20892 USA. NIAID, DIV MICROBIOL & INFECT DIS, BETHESDA, MD 20892 USA. PFIZER INC, CENT RES, GROTON, CT 06340 USA. RP SAAG, MS (reprint author), UNIV ALABAMA, BIRMINGHAM VET AFFAIRS MED CTR, 700 19TH ST S, RM 2B-108, BIRMINGHAM, AL 35233 USA. FU NCRR NIH HHS [RR-00032]; NIAID NIH HHS [N01-AI-15082, NIH-NIAID-DMID-91-04] NR 25 TC 477 Z9 493 U1 1 U2 4 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 JAN 9 PY 1992 VL 326 IS 2 BP 83 EP 89 DI 10.1056/NEJM199201093260202 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA GY045 UT WOS:A1992GY04500002 PM 1727236 ER PT J AU SAIKI, H CHAN, ET WONG, E YAMAMURO, W OOKHTENS, M KAPLOWITZ, N AF SAIKI, H CHAN, ET WONG, E YAMAMURO, W OOKHTENS, M KAPLOWITZ, N TI ZONAL DISTRIBUTION OF CYSTEINE UPTAKE IN THE PERFUSED-RAT-LIVER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GLUTATHIONE; HETEROGENEITY; HEPATOCYTES; TRANSPORT AB When in situ perfused rat livers were administered tracer or physiologic concentrations of [S-35]cysteine, a zone III (perivenous) predominance of uptake was observed in either antegrade or retrograde single-pass perfusion, as determined by quantitative densitometry of autoradiographs of liver section. This pattern remained unchanged from 30 s to 5 min observed. At higher supraphysiologic doses a more uniform acinar distribution of cysteine uptake was observed. Uptake rates of cysteine in antegrade perfusion indicated an apparent saturable component at low but physiologic cysteine concentrations. That uptake rather than metabolic trapping accounts for this perivenular pattern was supported by finding identical zonal distribution under conditions in which GSH and protein synthesis were markedly inhibited. Furthermore, increasing or decreasing hepatic cysteine pool sizes did not affect the extraction or zonation. These results suggest that a low K(m) transport system for cysteine is localized in zone III of the hepatic acinus. C1 UNIV SO CALIF,SCH MED,DEPT MED,DIV GASTROINTESTINAL & LIVER DIS,LOS ANGELES,CA 90033. US DEPT VET AFFAIRS,OUTPATIENT CLIN,LOS ANGELES,CA 90013. FU NIDDK NIH HHS [DK30312] NR 16 TC 18 Z9 18 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 JAN 5 PY 1992 VL 267 IS 1 BP 192 EP 196 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GY439 UT WOS:A1992GY43900035 PM 1730587 ER PT J AU TAYLOR, SL NORDLEE, JA BUSH, RK AF TAYLOR, SL NORDLEE, JA BUSH, RK TI FOOD ALLERGIES SO ACS SYMPOSIUM SERIES LA English DT Review ID BREAST-FED INFANTS; NATURAL-HISTORY; HYPERSENSITIVITY REACTIONS; ATOPIC-DERMATITIS; ADVERSE REACTIONS; COWS MILK; IMMEDIATE HYPERSENSITIVITY; SENSITIVE INDIVIDUALS; ASTHMATIC-PATIENTS; CHILDREN C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT MED, MADISON, WI 53792 USA. RP UNIV NEBRASKA, DEPT FOOD SCI & TECHNOL, LINCOLN, NE 68583 USA. NR 82 TC 6 Z9 6 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0097-6156 J9 ACS SYM SER JI ACS Symp. Ser. PY 1992 VL 484 BP 316 EP 329 PG 14 WC Chemistry, Multidisciplinary SC Chemistry GA HN997 UT WOS:A1992HN99700028 ER PT S AU HEYDARI, AR RICHARDSON, A AF HEYDARI, AR RICHARDSON, A BE Franceschi, C Crepaldi, G Cristofalo, VJ Vijg, J TI DOES GENE-EXPRESSION PLAY ANY ROLE IN THE MECHANISM OF THE ANTIAGING EFFECT OF DIETARY RESTRICTION SO AGING AND CELLULAR DEFENSE MECHANISMS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON AGING AND CELLULAR DEFENSE MECHANISMS CY SEP 22-26, 1991 CL MODENA, ITALY SP NEW YORK ACAD SCI, NIA, SIGMA TAU, EURAGE RP HEYDARI, AR (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284, USA. NR 0 TC 17 Z9 17 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-729-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1992 VL 663 BP 384 EP 395 DI 10.1111/j.1749-6632.1992.tb38682.x PG 12 WC Geriatrics & Gerontology; Immunology; Physiology SC Geriatrics & Gerontology; Immunology; Physiology GA BX33J UT WOS:A1992BX33J00041 PM 1482068 ER PT J AU SZERLIP, HM HEEGER, P FELDMAN, GM AF SZERLIP, HM HEEGER, P FELDMAN, GM TI COMPARISON BETWEEN ACETATE AND BICARBONATE DIALYSIS FOR THE TREATMENT OF LITHIUM INTOXICATION SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Article DE LITHIUM INTOXICATION; HEMODIALYSIS; ACETATE; BICARBONATE ID DATA-COLLECTION-SYSTEM AB Lithium is used to treat manic-depressive disorders, but toxic side effects commonly occur. The preferred treatment of severe lithium intoxication is hemodialysis. No data, however, exist comparing the effectiveness of acetate to bicarbonate dialysis for the removal of lithium. We present a case of lithium intoxication treated with both. During acetate dialysis, lithium removal occurred exclusively from the extracellular fluid space, while during bicarbonate dialysis. lithium removal occurred equally from both the extracellular and intracellular fluid spaces. We hypothesize that acetate but not bicarbonate activates the sodium-hydrogen antiporter on cell membranes, and that lithium, substituting for sodium, is driven into cells. This may explain the rebound in lithium levels commonly noted after conventional dialysis. We recommend bicarbonate hemodialysis as the therapy of choice for severe lithium intoxication. C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. NR 16 TC 11 Z9 11 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PD JAN-APR PY 1992 VL 12 IS 1-2 BP 116 EP 120 DI 10.1159/000168430 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA JJ236 UT WOS:A1992JJ23600021 PM 1415356 ER PT J AU FREYALDENHOVEN, AM GUTIERREZ, GE LIFSCHITZ, MD KATZ, MS AF FREYALDENHOVEN, AM GUTIERREZ, GE LIFSCHITZ, MD KATZ, MS TI PROTEIN-KINASE-C DIFFERENTIALLY MODULATES PTH-SENSITIVE AND PGE2-SENSITIVE ADENYLATE-CYCLASE IN OSTEOBLAST-LIKE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PHORBOL ESTER; G PROTEINS; PERTUSSIS TOXIN ID S49 LYMPHOMA-CELLS; NUCLEOTIDE REGULATORY PROTEIN; BETA-ADRENERGIC-RECEPTOR; EPIDERMAL GROWTH-FACTOR; PARATHYROID-HORMONE; PHORBOL-ESTER; SARCOMA CELLS; SIGNALING PATHWAYS; PERTUSSIS TOXIN; CYCLIC-AMP AB The effects of phorbol 12-myristate 13-acetate (PMA), a known activator of protein kinase C, on receptor-mediated stimulation of adenylate cyclase were evaluated in a rat osteosarcoma cell line (UMR-106) with the osteoblast phenotype. Pretreatment of UMR-106 cells with PMA increased parathyroid hormone (PTH)-stimulated adenylate cyclase activity and inhibited prostaglandin E2 (PGE2)-responsive enzyme activity. In addition, PMA enhanced enzyme activation by forskolin, which is thought to exert a direct stimulatory action on the catalytic subunit of adenylate cyclase. The regulatory effects of PMA were concentration dependent and of rapid onset (less-than-or-equal-to 1 min). Treatment with PMA also resulted in translocation of protein kinase C activity from the cytosol to the particulate cell fraction. Pertussis toxin, which attenuates inhibition of adenylate cyclase mediated by the inhibitory guanine nucleotide-binding regulatory protein (G(i)), augmented PTH-sensitive adenylate cyclase activity and reduced the incremental increase in PTH response produced by PMA. The results suggest that activation of protein kinase C increases PTH-stimulated adenylate cyclase activity by actions on G(i) and/or the catalytic subunit and decreases PGE2 responsiveness by a mechanism involving the PGE2 receptor. 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,CTR GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX 78284. NR 41 TC 20 Z9 20 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1992 VL 262 IS 1 BP E87 EP E95 PN 1 PG 9 WC Physiology SC Physiology GA HA742 UT WOS:A1992HA74200046 PM 1733255 ER PT J AU FREEMAN, GL WIDMAN, LE CAMPBELL, JM COLSTON, JT AF FREEMAN, GL WIDMAN, LE CAMPBELL, JM COLSTON, JT TI AN EVALUATION OF PULSUS ALTERNANS IN CLOSED-CHEST DOGS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CONTRACTILITY; ISOVOLUMIC RELAXATION; STARLINGS LAW ID CONSCIOUS DOGS; HEART; PERFORMANCE; VENTRICLE AB Pulsus alternans is a condition in which the arterial pressure generated by the heart oscillates between two levels on a beat-to-beat basis. We evaluated the onset of pulsus alternans in chronically instrumented dogs subjected to tachycardia and inferior vena caval occlusion. During pulsus alternans, the left ventricular (LV) end-diastolic volume (EDV) was larger before the strong beats (28.7 +/- 5.3 vs. 25.9 +/- 4.5 ml, P < 0.001 by paired t test), suggesting that the Frank-Starling mechanism participates in the alternating difference in end-systolic pressure. In addition, however, the ratio of pressure to volume at end systole was greater in the strong beats (2.01 +/- 0.36 vs. 1.46 +/- 0.45, P < 0.005 by paired t test), a difference that cannot be explained by the Frank-Starling mechanism alone. This indicates that there is also a difference in end-systolic inotropic states between strong and weak beats. These changes occurred without significant alterations in beat-to-beat levels of coronary flow. The time constant of isovolumic pressure fall (T) was faster for the strong beats (37.5 +/- 4.2 vs. 61.1 +/- 12.7 ms, P < 0.002 by paired t test). The onset of oscillation in T preceded the onset of changes in LVEDV and LV systolic pressure in every case by an average of seven beats (range 3-11), suggesting that abnormalities of intracellular calcium handling led to the occurrence of pulsus alternans. The data could be simulated using a three-compartment model of intracellular calcium in which calcium uptake from the contractile elements and rerelease to them occurs separately, with each following a monoexponential time course. Our results suggest that abnormalities of LV relaxation precede pulsus alternans, establishing the conditions for both oscillations in end-diastolic volume (Frank-Starling effect) and in beat-to-beat contractile state. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP FREEMAN, GL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. NR 28 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 JAN PY 1992 VL 262 IS 1 BP H278 EP H284 PN 2 PG 7 WC Physiology SC Physiology GA HA743 UT WOS:A1992HA74300038 PM 1733317 ER PT J AU FREEMAN, GL COLSTON, JT AF FREEMAN, GL COLSTON, JT TI MYOCARDIAL DEPRESSION PRODUCED BY SUSTAINED TACHYCARDIA IN RABBITS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HEART FAILURE; CONTRACTILITY; POSTREST CONTRACTION ID CONGESTIVE HEART-FAILURE; CHRONIC SUPRAVENTRICULAR TACHYCARDIA; CLOSED-CHEST DOGS; SARCOPLASMIC-RETICULUM; EXPERIMENTAL-MODEL; MUSCLE AB Much recent attention has been focused on the tachycardia-induced heart failure model. We hypothesized that sustained tachycardia would lead to myocardial depression in rabbits, as it does in dogs and swine. We evaluated the passive and active length-tension relations and postrest contraction behavior in right ventricular papillary muscles from 22 New Zealand White rabbits, 11 controls, and 11 subjected to ventricular pacing at a rate of 400 beats/min for 29.4 +/- 10.6 days. Studies were performed in oxygenated buffer at 22-degrees-C. Active tension was significantly reduced at muscle lengths of 0.95.L(max) and above; at L(max) it was 4.7 +/- 0.2 g/mm2 for the control group and 3.3 +/- 0.2 g/mm2 for the paced group (P < 0.005). Both groups showed increased force development when the concentration of calcium in the buffer was increased. There were no differences between the groups in the passive length-tension relations. Of note, postrest contraction data showed that the second postrest beat was smaller for the paced animals for rest intervals up to 2 min, suggesting that beat-to-beat transarcolemmal calcium handling may differ from normal in this model. We conclude that sustained tachycardia will lead to myocardial depression in rabbits; the extension of this model to a small animal species may offer new ways to explore its causative mechanisms. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP FREEMAN, GL (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 23 TC 14 Z9 14 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1992 VL 262 IS 1 BP H63 EP H67 PN 2 PG 5 WC Physiology SC Physiology GA HA743 UT WOS:A1992HA74300009 PM 1733323 ER PT J AU GARZATREVINO, ES OVERALL, JE HOLLISTER, LE AF GARZATREVINO, ES OVERALL, JE HOLLISTER, LE TI VERAPAMIL VERSUS LITHIUM IN ACUTE MANIA SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID SCALE AB Twenty acutely manic patients were studied in a double-blind randomized trial comparing verapamil with lithium. The Petterson Mania Scale, the Brief Psychiatric Rating Scale (BPRS), and the Clinical Global Impression (CGI) were administered before treatment and weekly during 4 weeks of treatment to evaluate response to verapamil and lithium. Both treatment groups improved significantly, and there were no significant overall differences between treatments. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. RP GARZATREVINO, ES (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 10 TC 68 Z9 68 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JAN PY 1992 VL 149 IS 1 BP 121 EP 122 PG 2 WC Psychiatry SC Psychiatry GA GX040 UT WOS:A1992GX04000019 PM 1728160 ER PT J AU TASHKIN, DP KHALSA, ME GORELICK, D CHANG, P SIMMONS, MS COULSON, AH GONG, H AF TASHKIN, DP KHALSA, ME GORELICK, D CHANG, P SIMMONS, MS COULSON, AH GONG, H TI PULMONARY STATUS OF HABITUAL COCAINE SMOKERS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID DIFFUSING-CAPACITY; LUNG-FUNCTION; SMOKING; ABUSE; PNEUMOMEDIASTINUM; TOBACCO; COMPLICATIONS; DYSFUNCTION; DERIVATION; MARIJUANA AB We determined the prevalence of respiratory symptoms and lung dysfunction in a large sample of habitual smokers of freebase cocaine ("crack") alone and in combination with tobacco and/or marijuana. In addition, we compared these findings with those in an age- and race-matched sample of nonusers of crack who did or did not smoke tobacco and/or marijuana. A detailed respiratory and drug use questionnaire and a battery of lung function tests were administered to (1) a convenience sample of 202 habitual smokers of cocaine (cases) who denied intravenous drug abuse and (2) a reference sample of 99 nonusers of cocaine (control subjects). The cocaine smokers (85% black) included the following: 68 never-smokers of marijuana, ot whom 43 currently smoked tobacco and 25 did not, and 134 ever-smokers of marijuana (42 current and 92 former), of whom 92 currently smoked tobacco and 42 did not. The control subjects (96% black) included the following: 69 never-smokers of marijuana, of whom 26 currently smoked tobacco and 43 did not, and 30 ever-smokers of marijuana (18 current and 12 former), of whom 21 currently smoked tobacco and 9 did not. Cases smoked an average of 6.5 g cocaine per week for a mean of 53 months. The median time of the most recent use of crack prior to study was 19 days (range < 1 to 180 days). After controlling for the use of other smoked substances, frequent crack use was associated with: (1) a high prevalence of at least occasional occurrences of acute cardiorespiratory symptoms within 1 to 12 h after smoking cocaine (cough productive of black sputum [43.7%], hemoptysis [5.7%], chest pain [38.5%], usually worse with deep breathing, and cardiac palpitations [52.6%]) and (2) a mild but significant impairment in the diffusing capacity of the lung. We conclude that heavy, habitual cocaine smoking produces evidence of respiratory tract injury manifested by a high prevalence of acute respiratory symptoms temporally related to freebase use, and an abnormality in gas transfer (diffusion) in the lung, which is evident weeks to months after most recent use. The mechanism of the defect in gas transfer is unknown, but it could reflect damage to the alveolar capillary membrane or an abnormality involving the precapillary pulmonary vasculature. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOSTAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT EPIDEMIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA. RP TASHKIN, DP (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024, USA. FU NIDA NIH HHS [R01 DA-03018] NR 54 TC 67 Z9 69 U1 1 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 JAN PY 1992 VL 145 IS 1 BP 92 EP 100 PG 9 WC Respiratory System SC Respiratory System GA GZ104 UT WOS:A1992GZ10400018 PM 1731605 ER PT J AU ALBIN, MS RITTER, RR REINHART, R ERICKSON, D ROCKWOOD, A AF ALBIN, MS RITTER, RR REINHART, R ERICKSON, D ROCKWOOD, A TI VENOUS AIR-EMBOLISM DURING RADICAL RETROPUBIC PROSTATECTOMY SO ANESTHESIA AND ANALGESIA LA English DT Article ID COMPLICATION; MANAGEMENT; SURGERY C1 UNIV TEXAS,HLTH SCI CTR,AUDIE MURPHY MEM VET HOSP,DEPT SURG UROL,SAN ANTONIO,TX 78284. RP ALBIN, MS (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE MURPHY MEM VET HOSP,DEPT ANESTHESIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 17 TC 16 Z9 16 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 JAN PY 1992 VL 74 IS 1 BP 151 EP 153 PG 3 WC Anesthesiology SC Anesthesiology GA GX025 UT WOS:A1992GX02500026 PM 1734780 ER PT J AU ANDERSON, DC ASINGER, RW NEWBURG, SM FARMER, CC WANG, K BUNDLIE, SR KOLLER, RL JAGIELLA, WM KREHER, S JORGENSEN, CR SHARKEY, SW FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J WRIGHT, W CHESEBRO, JH WIEBERS, DO HOLLAND, AE MILLER, DM BARDSLEY, WT LITIN, SC MEISSNER, I ZERBE, DM MCANULTY, JH MARCHANT, C COULL, BM FELDMAN, G HAYWARD, A GANDARA, E MACMILLAN, K BLANK, N LEONARD, AD KANTER, MC ISENSEE, LM QUIROGA, ES PRESTI, CH TEGELER, CH LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS REDD, RM CADELL, DJ GOMEZ, CR JANOSIK, DL LABOVITZ, AJ KELLEY, RE CHAHINE, R CRISTO, L PALERMO, M PEREZ, O FEINBERG, WM VOLD, BK KERN, KB APPLETON, C MILLER, VT HOCKERSMITH, CJ COHEN, BA MARTIN, GJ PAWLOW, AJ HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME FUSTER, V DITTRICH, HC ROTHROCK, JF HAGENHOFF, C HELGASON, CM KONDOS, GT HOFF, J KAUFMANN, L RABJOHNS, RR MCRAE, RP GHALI, J ADAMS, HP THEILEN, EO BILLER, J BROWN, DD MARSH, EE SIRNA, SJ MITCHELL, VL ROTHBART, RM BAILEY, GH BURKHARDT, C BLACKSHEAR, JL WEAVER, L LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA MCBRIDE, R ATHEARN, MW PEARCE, LA NASCO, E HART, RG SHERMAN, CP SHERMAN, DG TALBERT, RL DACY, TL HEBERLING, PA AF ANDERSON, DC ASINGER, RW NEWBURG, SM FARMER, CC WANG, K BUNDLIE, SR KOLLER, RL JAGIELLA, WM KREHER, S JORGENSEN, CR SHARKEY, SW FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J WRIGHT, W CHESEBRO, JH WIEBERS, DO HOLLAND, AE MILLER, DM BARDSLEY, WT LITIN, SC MEISSNER, I ZERBE, DM MCANULTY, JH MARCHANT, C COULL, BM FELDMAN, G HAYWARD, A GANDARA, E MACMILLAN, K BLANK, N LEONARD, AD KANTER, MC ISENSEE, LM QUIROGA, ES PRESTI, CH TEGELER, CH LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS REDD, RM CADELL, DJ GOMEZ, CR JANOSIK, DL LABOVITZ, AJ KELLEY, RE CHAHINE, R CRISTO, L PALERMO, M PEREZ, O FEINBERG, WM VOLD, BK KERN, KB APPLETON, C MILLER, VT HOCKERSMITH, CJ COHEN, BA MARTIN, GJ PAWLOW, AJ HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME FUSTER, V DITTRICH, HC ROTHROCK, JF HAGENHOFF, C HELGASON, CM KONDOS, GT HOFF, J KAUFMANN, L RABJOHNS, RR MCRAE, RP GHALI, J ADAMS, HP THEILEN, EO BILLER, J BROWN, DD MARSH, EE SIRNA, SJ MITCHELL, VL ROTHBART, RM BAILEY, GH BURKHARDT, C BLACKSHEAR, JL WEAVER, L LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA MCBRIDE, R ATHEARN, MW PEARCE, LA NASCO, E HART, RG SHERMAN, CP SHERMAN, DG TALBERT, RL DACY, TL HEBERLING, PA TI PREDICTORS OF THROMBOEMBOLISM IN ATRIAL-FIBRILLATION .1. CLINICAL-FEATURES OF PATIENTS AT RISK SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE ATRIAL FIBRILLATION; CEREBROVASCULAR DISORDERS; HEART FAILURE, CONGESTIVE; HYPERTENSION; THROMBOEMBOLISM ID SYSTEMIC EMBOLIZATION; STROKE; FRAMINGHAM; COMPLICATIONS; TRIAL AB Objective: To identify those patients with nonrheumatic atrial fibrillation who are at high risk and those at low risk for arterial thromboembolism. Design: Cohort study of patients assigned to placebo in a randomized clinical trial. Setting: Five hundred sixty-eight inpatients and outpatients with nonrheumatic atrial fibrillation assigned to placebo therapy at 15 U.S. medical centers from 1987 to 1989 in the Stroke Prevention in Atrial Fibrillation study. Patients were followed for a mean of 1.3 years. Measurements: Clinical variables were assessed at study entry and correlated with subsequent ischemic stroke and systemic embolism by multivariate analysis. Main Results: Recent (within 3 months) congestive heart failure, a history of hypertension, and previous arterial thromboembolism were each significantly and independently associated with a substantial risk for thromboembolism (> 7% per year; P less-than-or-equal-to 0.05). The presence of these three independent clinical predictors (recent congestive heart failure, history of hypertension, previous thromboembolism) defined patients with rates of thromboembolism of 2.5% per year (no risk factors), 7.2% per year (one risk factor), and 17.6% per year (two or three risk factors). Nondiabetic patients without these risk factors, comprising 38% of the cohort, had a low risk for thromboembolism (1.4% per year; 95% Cl, 0.05% to 3.7%). Patients without clinical risk factors who were under 60 years of age had no thromboembolic events. Conclusion: Patients with atrial fibrillation at high risk (> 7% per year) and low risk (< 3% per year) for thromboembolism can be identified by readily available clinical variables. C1 STAT & EPIDEMIOL RES CORP,SPAF STAT COORDINAT CTR,1107 NE 45TH ST,SUITE 520,SEATTLE,WA 98105. HENNEPIN CTY MED CTR,MINNEAPOLIS,MN 55415. ABBOTT NW HOSP,MINNEAPOLIS,MN. UNIV MISSOURI,COLUMBIA,MO 65201. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. KAISER PERMANENTE,PORTLAND,OR. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. ST JOHNS MERCY MED CTR,ST LOUIS,MO 63141. ST LOUIS UNIV,MED CTR,ST LOUIS,MO 63103. UNIV MIAMI,SCH MED,MIAMI,FL 33152. UNIV ARIZONA,COLL MED,TUCSON,AZ 85721. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. MT SINAI MED CTR,NEW YORK,NY 10029. UNIV CALIF SAN DIEGO,MED CTR,LA JOLLA,CA 92093. UNIV ILLINOIS,COLL MED,CHICAGO,IL 60680. UNIV ILLINOIS,COLL MED,PEORIA,IL 61656. UNIV IOWA,COLL MED,IOWA CITY,IA 52242. UNIV COLORADO,COLL MED,BOULDER,CO 80309. MAYO CLIN,JACKSONVILLE,FL. UNIV WASHINGTON,SEATTLE,WA 98195. UNIV TEXAS,HLTH SCI CTR,CTR CLIN COORDINAT,SAN ANTONIO,TX 78284. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 24 TC 301 Z9 306 U1 0 U2 3 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 JAN 1 PY 1992 VL 116 IS 1 BP 1 EP 5 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA GX157 UT WOS:A1992GX15700001 ER PT J AU ANDERSON, DC ASINGER, RW NEWBURG, SM FARMER, CC WANG, K BUNDLIE, SR KOLLER, RL JAGIELLA, WM KREHER, S JORGENSEN, CR SHARKEY, SW FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J WRIGHT, W CHESEBRO, JH WIEBERS, DO HOLLAND, AE MILLER, DM BARDSLEY, WT LITIN, SC MEISSNER, I ZERBE, DM MCANULTY, JH MARCHANT, C COULL, BM FELDMAN, G HAYWARD, A GANDARA, E MACMILLAN, K BLANK, N LEONARD, AD KANTER, MC ISENSEE, LM QUIROGA, ES PRESTI, CH TEGELER, CH LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS REDD, RM CADELL, DJ GOMEZ, CR JANOSIK, DL LABOVITZ, AJ KELLEY, RE CHAHINE, R CRISTO, L PALERMO, M PEREZ, O FEINBERG, WM VOLD, BK KERN, KB APPLETON, C MILLER, VT HOCKERSMITH, CJ COHEN, BA MARTIN, GJ PAWLOW, AJ HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME FUSTER, V DITTRICH, HC ROTHROCK, JF HAGENHOFF, C HELGASON, CM KONDOS, GT HOFF, J KAUFMANN, L RABJOHNS, RR MCRAE, RP GHALI, J ADAMS, HP THEILEN, EO BILLER, J BROWN, DD MARSH, EE SIRNA, SJ MITCHELL, VL ROTHBART, RM BAILEY, GH BURKHARDT, C BLACKSHEAR, JL WEAVER, L LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA MCBRIDE, R PEARCE, LA NASCO, E HART, RG SHERMAN, CP SHERMAN, DG TALBERT, RL DACY, TL HEBERLING, PA AF ANDERSON, DC ASINGER, RW NEWBURG, SM FARMER, CC WANG, K BUNDLIE, SR KOLLER, RL JAGIELLA, WM KREHER, S JORGENSEN, CR SHARKEY, SW FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J WRIGHT, W CHESEBRO, JH WIEBERS, DO HOLLAND, AE MILLER, DM BARDSLEY, WT LITIN, SC MEISSNER, I ZERBE, DM MCANULTY, JH MARCHANT, C COULL, BM FELDMAN, G HAYWARD, A GANDARA, E MACMILLAN, K BLANK, N LEONARD, AD KANTER, MC ISENSEE, LM QUIROGA, ES PRESTI, CH TEGELER, CH LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS REDD, RM CADELL, DJ GOMEZ, CR JANOSIK, DL LABOVITZ, AJ KELLEY, RE CHAHINE, R CRISTO, L PALERMO, M PEREZ, O FEINBERG, WM VOLD, BK KERN, KB APPLETON, C MILLER, VT HOCKERSMITH, CJ COHEN, BA MARTIN, GJ PAWLOW, AJ HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME FUSTER, V DITTRICH, HC ROTHROCK, JF HAGENHOFF, C HELGASON, CM KONDOS, GT HOFF, J KAUFMANN, L RABJOHNS, RR MCRAE, RP GHALI, J ADAMS, HP THEILEN, EO BILLER, J BROWN, DD MARSH, EE SIRNA, SJ MITCHELL, VL ROTHBART, RM BAILEY, GH BURKHARDT, C BLACKSHEAR, JL WEAVER, L LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA MCBRIDE, R PEARCE, LA NASCO, E HART, RG SHERMAN, CP SHERMAN, DG TALBERT, RL DACY, TL HEBERLING, PA TI PREDICTORS OF THROMBOEMBOLISM IN ATRIAL-FIBRILLATION .2. ECHOCARDIOGRAPHIC FEATURES OF PATIENTS AT RISK SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE THROMBOEMBOLISM; ATRIAL FIBRILLATION; CEREBROVASCULAR DISORDERS; HYPERTENSION; HEART FAILURE, CONGESTIVE ID LEFT-VENTRICULAR MASS; SYSTEMIC EMBOLIZATION; STROKE; COMPLICATIONS AB Objective: To identify echocardiographic predictors of arterial thromboembolism in patients with nonrheumatic atrial fibrillation and to determine whether these add to clinical variables for risk stratification. Design: Cohort study of patients assigned to placebo in a randomized clinical trial. Setting: Five hundred sixty-eight inpatients and outpatients with nonrheumatic atrial fibrillation assigned to placebo therapy at 15 U.S. medical centers from 1987 to 1989 in the Stroke Prevention in Atrial Fibrillation study. Patients were followed for a mean of 1.3 years. Measurements: M-mode and two-dimensional (2-D) echocardiograms performed at study entry and interpreted by local cardiologists. The predictive value of 14 echocardiographic variables for later ischemic stroke or systemic embolism was assessed by multivariate analysis. Main Results: Left ventricular dysfunction from 2-D echocardiograms (P = 0.003) and the size of the left atrium from M-mode echocardiograms (P = 0.02) were the strongest independent predictors of later thromboembolism. Multivariate analysis of these two independent echocardiographic predictors with the three independent clinical predictors of thromboembolism (history of hypertension, recent congestive heart failure, previous thromboembolism) identified 26% of the cohort with a low risk for thromboembolism (1.0% per year; 95% Cl, 0.2% to 4.0%). Compared with risk stratification using clinical variables alone, echocardiographic results altered thromboembolic risk stratification in 18% of the entire cohort and in 38% of those without clinical risk factors. Conclusions: Both left ventricular and left atrial variables are significant predictors of thromboembolism in patients with nonvalvular atrial fibrillation. Our results challenge traditional views of the pathogenesis of ischemic stroke in patients with atrial fibrillation and suggest that standard echocardiography contributes to risk stratification, differentiating the one third of patients without clinical risk factors who are at increased risk for stroke from the remainder who may not need antithrombotic prophylaxis. C1 STAT & EPIDEMIOL RES CORP,SPAF STAT COORDINAT CTR,1107 NE 45TH ST,SUITE 520,SEATTLE,WA 98105. HENNEPIN CTY MED CTR,MINNEAPOLIS,MN 55415. ABBOTT NW HOSP,MINNEAPOLIS,MN. UNIV MISSOURI,COLUMBIA,MO 65201. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. KAISER PERMANENTE,PORTLAND,OR. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. ST JOHNS MERCY MED CTR,ST LOUIS,MO 63141. ST LOUIS UNIV,MED CTR,ST LOUIS,MO 63103. UNIV MIAMI,SCH MED,MIAMI,FL 33152. UNIV ARIZONA,COLL MED,TUCSON,AZ 85721. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. MT SINAI MED CTR,NEW YORK,NY 10029. UNIV CALIF SAN DIEGO,MED CTR,LA JOLLA,CA 92093. UNIV ILLINOIS,COLL MED,CHICAGO,IL 60680. UNIV ILLINOIS,COLL MED,PEORIA,IL 61656. UNIV IOWA,COLL MED,IOWA CITY,IA 52242. UNIV COLORADO,COLL MED,BOULDER,CO 80309. MAYO CLIN,JACKSONVILLE,FL. UNIV WASHINGTON,SEATTLE,WA 98195. UNIV TEXAS,HLTH SCI CTR,CTR CLIN COORDINAT,SAN ANTONIO,TX 78284. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 25 TC 333 Z9 338 U1 0 U2 3 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 JAN 1 PY 1992 VL 116 IS 1 BP 6 EP 12 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA GX157 UT WOS:A1992GX15700002 ER PT J AU ALLENDOERFER, R YATES, RR MARQUIS, AJ LOEBENBERG, D RINALDI, MG GRAYBILL, JR AF ALLENDOERFER, R YATES, RR MARQUIS, AJ LOEBENBERG, D RINALDI, MG GRAYBILL, JR TI COMPARISON OF SCH-39304 AND ITS ISOMERS, RR-42427 AND SS-42426, FOR TREATMENT OF MURINE CRYPTOCOCCAL AND COCCIDIOIDAL MENINGITIS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID INVIVO EFFICACY; AMPHOTERICIN-B; FLUCONAZOLE; SCH39304; TRIAZOLE AB SCH 39304 (304) and its isomers, SCH 42426 (426) and SCH 42427 (427), are new orally administered antifungal azole derivatives. In this study, we compared the efficacy of 304 with that of 426 and 427 in murine models of cryptococcal and coccidioidal meningitis. On day 18 postinfection with Cryptococcus neoformans, controls showed 80% mortality. The 50% protective doses calculated at this day were 0.56 mg of 304 per kg of body weight, 23.5 mg of 426 per kg, and 0.11 mg of 427 per kg. Controls with coccidioidal meningitis all succumbed, and treated mice at the same time point showed 50% protective doses of 10.8 mg/kg for 304, 200 mg/kg for 426, and 2.1 mg/kg for 427. We conclude that isomer 427 is five times as potent, whereas 426 is 1/50th as potent as 304 in these experimental mycoses. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. SCHERING PLOUGH RES CORP,BLOOMFIELD,NJ 07003. RP ALLENDOERFER, R (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. NR 17 TC 9 Z9 9 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 1992 VL 36 IS 1 BP 217 EP 219 PG 3 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA GY477 UT WOS:A1992GY47700044 PM 1590692 ER PT J AU ROSS, NS HANSEN, TPB AF ROSS, NS HANSEN, TPB TI RIBOFLAVIN DEFICIENCY IS ASSOCIATED WITH SELECTIVE PRESERVATION OF CRITICAL FLAVOENZYME-DEPENDENT METABOLIC PATHWAYS SO BIOFACTORS LA English DT Review ID RAT-LIVER MITOCHONDRIA; COENZYME-A DEHYDROGENASE; ACIDURIA TYPE-II; GLUTATHIONE-REDUCTASE; SHORT-CHAIN; IRON; PURIFICATION; ADULT; STIMULATION; PYRIDOXINE AB Riboflavin is a water soluble vitamin that serves as a precursor of flavin mononucleotide and flavin adenine dinucleotide. These two compounds are coenzymes in a variety of electron transfer reactions that occur in energy producing, biosynthetic, detoxifying and electron scavenging pathways. When an organism is confronted with inadequate dietary riboflavin, characteristic changes occur in the cellular distribution of the various flavin fractions as well as in the activities of flavin-dependent enzymes. These changes suggest a specific hierarchic response to riboflavin deficiency, e.g. the core electron transfer chain required for ATP synthesis is preserved while the enzymes required for the first step of fatty acid beta-oxidation are diminished. The mechanisms by which the specific changes in enzyme activity are mediated have not been completely identified, but appear to result from a combination of diminished access of normal or near normal levels of apoenzyme to coenzyme and diminished abundance of apoenzyme. The changes in apoenzyme content potentially result from alterations in either protein stability or gene expression. The response to riboflavin deficiency of several kev enzyme systems and the pathways affected will be discussed and a hierarchic order by which specific enzyme activities are preserved while others are decreased will be proposed. The current understanding of the molecular mechanisms by which these changes are mediated will be discussed. RP ROSS, NS (reprint author), W LOS ANGELES DEPT VET AFFAIRS MED CTR,ENDOCRINE SECT W111D,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. FU NICHD NIH HHS [HD25299] NR 49 TC 28 Z9 28 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0951-6433 J9 BIOFACTORS JI Biofactors PD JAN PY 1992 VL 3 IS 3 BP 185 EP 190 PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA HA918 UT WOS:A1992HA91800004 PM 1599612 ER PT J AU JARLAIS, DCD EDWARDS, G MOORE, MH ALMOND, B KLEBER, HD NEGRETE JONES, JC WOOLVERTON, WL MUSTO, DF KALANT, H ANTHONY, JC OBRIEN, CP KUHAR, MJ AF JARLAIS, DCD EDWARDS, G MOORE, MH ALMOND, B KLEBER, HD NEGRETE JONES, JC WOOLVERTON, WL MUSTO, DF KALANT, H ANTHONY, JC OBRIEN, CP KUHAR, MJ TI AIDS AND HIV-INFECTION IN COCAINE USERS SO CIBA FOUNDATION SYMPOSIA LA English DT Discussion ID INTRAVENOUS-DRUG-USERS; INJECTION C1 NATL ADDICT CTR,ADDICT RES UNIT,LONDON SE5 8AF,ENGLAND. HARVARD UNIV,JOHN F KENNEDY SCH GOVT,CAMBRIDGE,MA 02138. UNIV HULL,SOCIAL VALUES RES CTR,HULL HU6 7RX,N HUMBERSIDE,ENGLAND. OFF NATL DRUG CONTROL POLICY,EXECUT OFF PRESIDENT,WASHINGTON,DC 20500. MCGILL UNIV,MONTREAL GEN HOSP,DEPT PSYCHIAT,MONTREAL H3G 1A4,QUEBEC,CANADA. DRUG DEPENDENCE UNIT,MONTREAL H3G 1A4,QUEBEC,CANADA. UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,LANGLEY PORTER PSYCHIAT INST,SAN FRANCISCO,CA 94143. UNIV CHICAGO,DRUG ABUSE RES CTR,DEPT PHARMACOL & PHYSIOL SCI,CHICAGO,IL 60637. YALE UNIV,SCH MED,CHILD STUDY CTR PSYCHIAT & HIST MED,NEW HAVEN,CT 06510. UNIV TORONTO,DEPT PHARMACOL,ADDICT RES GRP,TORONTO M5S 1A8,ONTARIO,CANADA. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MENTAL HLTH,BALTIMORE,MD 21205. UNIV PENN,VET AFFAIRS MED CTR,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. RP JARLAIS, DCD (reprint author), BETH ISRAEL MED CTR,NARCOT & DRUG RES INC,11 BEACH ST,NEW YORK,NY 10013, USA. NR 15 TC 0 Z9 0 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1992 VL 166 BP 181 EP 194 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA HV055 UT WOS:A1992HV05500011 ER PT J AU OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR AF OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR TI PSYCHOTHERAPY FOR COCAINE DEPENDENCE SO CIBA FOUNDATION SYMPOSIA LA English DT Article AB Dependence on cocaine is a new disorder for contemporary US clinicians. Until the 1980s sufficient quantities of the drug were not available to produce a true dependence. Thus far the only models for pharmacological intervention involve an interaction between medication and psychotherapy; that is, medication may be able to facilitate a drug-free interval during which time the patient can be engaged in psychotherapy. Psychotherapy programmes for cocaine dependence have generally been modelled on group-oriented treatments of the type used by Alcoholics Anonymous. Controlled studies of therapy programmes for cocaine dependence are currently being conducted and one prospective random-assignment study comparing day hospital and in-patient rehabilitation shows generally good results. Behavioural treatments aimed at reducing or extinguishing conditioned responses in cocaine addicts have also shown efficacy in a controlled study. More general relapse prevention procedures including rehearsal and role-playing are also used in the treatment of cocaine dependence. Combinations of psychotherapy and pharmacotherapy have so far shown the most promise in the treatment of this disorder. RP OBRIEN, CP (reprint author), UNIV PENN,VET AFFAIRS MED CTR,DEPT PSYCHIAT,3900 CHESTNUT ST,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [R01 DA 000586, P50 DA 5186] NR 9 TC 6 Z9 6 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1992 VL 166 BP 207 EP 223 PG 17 WC Medicine, General & Internal SC General & Internal Medicine GA HV055 UT WOS:A1992HV05500013 PM 1638915 ER PT J AU PRABHU, SD FREEMAN, GL AF PRABHU, SD FREEMAN, GL TI KINETICS OF RESTITUTION OF LEFT-VENTRICULAR RELAXATION SO CIRCULATION RESEARCH LA English DT Article DE DIASTOLE; EXTRASYSTOLE; INTRACELLULAR CALCIUM; PRESSURE DECAY ID MECHANICAL RESTITUTION; PRESSURE; MYOCARDIUM; RYANODINE; DOGS AB Although the kinetics of cardiac systolic force restitution have been well described, the restitution kinetics of left ventricular relaxation have not been examined. To define relaxation restitution behavior, we studied seven dogs chronically instrumented with left ventricular high-fidelity micromanometers and piezoelectric dimension crystals. After a priming period at a basic cycle length of 375 msec, test extrastimuli were introduced after a range of extrasystolic intervals (ESIs). Relaxation behavior of control and extrasystolic beats was characterized by the time constant of isovolumic relaxation, tau. Relaxation restitution can be described by two concatenated monoexponential curves, an early phase described by a rapid time constant and a late phase described by a slower time constant (TC1, 36.21 +/- 7.90 msec; TC2, 75.94 +/- 10.65 msec; p < 0.05). The first phase of relaxation restitution parallels systolic force restitution over the same range and displays faster recovery (TC(s), 58.93 +/- 10.01 msec, p < 0.05). Postextrasystolic restitution of test pulses after beats at fixed ESIs depends on the initial ESI. Relaxation recovery of postextrasystolic beats proceeds faster with smaller initial ESIs (TC1 for ESI of 300 msec, 13.27 +/- 4.05 msec; TC1 for ESI of 450 msec, 72.85 +/- 21.72 msec; p < 0.0001). The monoexponential pattern of restitution was seen with model-independent descriptors of relaxation as well as with tau. 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 27 TC 14 Z9 14 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD JAN PY 1992 VL 70 IS 1 BP 29 EP 38 PG 10 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA HE089 UT WOS:A1992HE08900004 PM 1370136 ER PT J AU TUCKER, RM DENNING, DW HANSON, LH RINALDI, MG GRAYBILL, JR SHARKEY, PK PAPPAGIANIS, D STEVENS, DA AF TUCKER, RM DENNING, DW HANSON, LH RINALDI, MG GRAYBILL, JR SHARKEY, PK PAPPAGIANIS, D STEVENS, DA TI INTERACTION OF AZOLES WITH RIFAMPIN, PHENYTOIN, AND CARBAMAZEPINE - INVITRO AND CLINICAL OBSERVATIONS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID COCCIDIOIDES-IMMITIS; AMPHOTERICIN-B; ITRACONAZOLE INTERACTION; CYCLOSPORIN; THERAPY; KETOCONAZOLE; FLUCONAZOLE; ANTIFUNGAL; SERUM; SUSCEPTIBILITY AB Twelve patients receiving therapy with an azole agent (ketoconazole, itraconazole, and/or fluconazole) for systemic mycoses experienced drug interactions with rifampin, phenytoin, and/or carbamazepine resulting in substantial decreases in azole concentrations in serum. All four patients receiving azoles and concurrent phenytoin and/or carbamazepine failed to respond to treatment or suffered a relapse of their fungal infection. Four of five patients with cryptococcosis who received itraconazole and rifampin responded despite decreases in their serum itraconazole concentrations; synergy between itraconazole and rifampin was documented by in vitro analysis of inhibition and of killing of Cryptococcus neoformans isolates from all patients receiving this combination. In contrast, two patients with coccidioidomycosis failed to respond to itraconazole/rifampin. Moreover, two patients with cryptococcosis suffered a relapse or persistence of seborrheic dermatitis while receiving itraconazole/rifampin. The latter combination showed synergy in vitro in the inhibition of the mycelial phase of Coccidioides immitis and, to a lesser extent, of the pathogenic spherule phase of this fungus; synergy in the killing of C. immitis was not noted, nor was synergy seen against Malassezia furfur, the purported etiologic agent of seborrheic dermatitis. These findings illustrate several drug interactions that may affect clinical outcome and that must be considered in the management of antifungal therapy. C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,751 S BASCOM,SAN JOSE,CA 95128. CALIF INST MED RES,SAN JOSE,CA. STANFORD UNIV,MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,STANFORD,CA 94305. WENATCHEE VALLEY CLIN,DEPT INFECT DIS,DIV INTERNAL MED,WENATCHEE,WA. UNIV WASHINGTON,DEPT INTERNAL MED,SEATTLE,WA 98195. UNIV CALIF DAVIS,SCH MED,DEPT MED MICROBIOL,DAVIS,CA 95616. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,MYCOL TESTING LAB,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. OI Denning, David/0000-0001-5626-2251 NR 40 TC 141 Z9 142 U1 1 U2 1 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 JAN PY 1992 VL 14 IS 1 BP 165 EP 174 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HD517 UT WOS:A1992HD51700026 PM 1315160 ER PT B AU OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR AF OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR BE BOCK, GR WHELAN, J TI PSYCHOTHERAPY FOR COCAINE DEPENDENCE SO COCAINE : SCIENTIFIC AND SOCIAL DIMENSIONS SE CIBA FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT SYMP ON COCAINE : SCIENTIFIC AND SOCIAL DIMENSIONS CY JUL 20-22, 1991 CL CIBA FDN, LONDON, ENGLAND SP CIBA FDN HO CIBA FDN RP OBRIEN, CP (reprint author), UNIV PENN,VET AFFAIRS MED CTR,DEPT PSYCHIAT,3900 CHESTNUT ST,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [P50 DA 5186, R01 DA 000586] NR 0 TC 6 Z9 6 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI CHICHESTER PA CHICHESTER BN 0-471-93179-9 J9 CIBA F SYMP PY 1992 VL 166 BP 207 EP 223 PG 17 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry; Psychology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry; Psychology GA BV65D UT WOS:A1992BV65D00013 PM 1638915 ER PT J AU DEFRONZO, RA AF DEFRONZO, RA TI INSULIN RESISTANCE, HYPERINSULINEMIA, AND CORONARY-ARTERY DISEASE - A COMPLEX METABOLIC WEB SO CORONARY ARTERY DISEASE LA English DT Review DE INSULIN RESISTANCE; HYPERINSULINISM; CORONARY DISEASE; CHOLESTEROL; HYPERTENSION; DIABETES-MELLITUS; NON-INSULIN-DEPENDENT; OBESITY ID IMPAIRED GLUCOSE-TOLERANCE; DEPENDENT DIABETES-MELLITUS; CARDIOVASCULAR RISK-FACTORS; SODIUM-LITHIUM COUNTERTRANSPORT; HIGH-DENSITY LIPOPROTEIN; BLOOD-PRESSURE REGULATION; HEART-DISEASE; ESSENTIAL-HYPERTENSION; PIMA-INDIANS; FOLLOW-UP C1 UNIV TEXAS, HLTH SCI CTR, DIV NEPHROL, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX USA. RP DEFRONZO, RA (reprint author), UNIV TEXAS, HLTH SCI CTR, DIV DIABET, SAN ANTONIO, TX 78284 USA. NR 120 TC 22 Z9 22 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0954-6928 EI 1473-5830 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD JAN PY 1992 VL 3 IS 1 BP 11 EP 25 DI 10.1097/00019501-199201000-00003 PG 15 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HE751 UT WOS:A1992HE75100003 ER PT J AU SHAFFER, D WALKER, K WEISS, GR AF SHAFFER, D WALKER, K WEISS, GR TI MALIGNANT-MELANOMA IN A HISPANIC MALE WITH NEVUS OF OTA SO DERMATOLOGY LA English DT Article DE MALIGNANT MELANOMA; OCULODERMAL MELANOCYTOSIS; NEVUS OF OTA; BLADDER ID OCULODERMAL MELANOCYTOSIS; BLUE NEVUS AB Nevus of Ota is uncommon in the non-Oriental population. We report a case of malignant melanoma with metastasis to the genitourinary tract in a Hispanic male with nevus of Ota. Thirty-six prior cases of nevus of Ota with malignant melanoma reported in the English language are reviewed. Sixty-eight percent were women; 76% were Caucasians. Metastatic disease was reported in 16%. Three patients had liver metastases. Our case was the first involving the genito-urinary tract. All but one patient with metastatic disease died within 1 month of presentation. Despite the increased frequency of nevus of Ota in the Japanese, only 4 cases of malignant melanoma have been reported. Nevus of Ota would appear to be a risk factor for developing malignant melanoma in the Caucasian population. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. NR 44 TC 20 Z9 22 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1992 VL 185 IS 2 BP 146 EP 150 PG 5 WC Dermatology SC Dermatology GA JK178 UT WOS:A1992JK17800017 PM 1421629 ER PT J AU McIntire, WS AF McIntire, William S. TI Wither PQQ SO ESSAYS IN BIOCHEMISTRY, VOL 27 SE ESSAYS IN BIOCHEMISTRY LA English DT Review ID QUINONE BIOSYNTHESIS GENES; PYRROLOQUINOLINE QUINONE; METHYLAMINE DEHYDROGENASE; AMINE OXIDASES; ACTIVE-SITE; COFACTOR; ENZYMES; OXIDOREDUCTASES; 6-HYDROXYDOPA; QUINOPROTEINS C1 [McIntire, William S.] US Dept Vet Affairs, Div Mol Biol, Med Ctr, San Francisco, CA 94121 USA. [McIntire, William S.] Univ Calif San Francisco, Dept Biochem, San Francisco, CA 94143 USA. [McIntire, William S.] Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA. RP McIntire, WS (reprint author), US Dept Vet Affairs, Div Mol Biol, Med Ctr, San Francisco, CA 94121 USA. NR 33 TC 15 Z9 15 U1 0 U2 1 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON W1N 3AJ, ENGLAND SN 0071-1365 J9 ESSAYS BIOCHEM PY 1992 VL 27 BP 119 EP 134 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BHO25 UT WOS:000254740200009 PM 1330543 ER PT J AU SMALLEY, SL WOLKENSTEIN, BH LARUE, A WOODWARD, JA JARVIK, LF MATSUYAMA, SS AF SMALLEY, SL WOLKENSTEIN, BH LARUE, A WOODWARD, JA JARVIK, LF MATSUYAMA, SS TI COMMINGLING ANALYSIS OF MEMORY PERFORMANCE IN OFFSPRING OF ALZHEIMER PATIENTS SO GENETIC EPIDEMIOLOGY LA English DT Article DE ALZHEIMER; COMMINGLING ANALYSIS; HERITABILITY; MEMORY PERFORMANCE ID NEUROPATHOLOGICAL FINDINGS; 1ST-DEGREE RELATIVES; CLINICAL-DIAGNOSIS; GENETIC-LINKAGE; DISEASE; DEMENTIA; AGE; CHROMOSOME-21; SEGREGATION; MARKERS AB Dementia of the Alzheimer type (DAT) is a neurodegenerative disorder which afflicts approximately 3% of the population. Genetic influences are indicated from twin and family studies although genetic heterogeneity has been suggested from both pedigree analyses and linkage investigations. Autosomal dominant inheritance with age-dependent penetrance has been suggested in at least some families with DAT. In the present investigation, we examine memory and nonmemory task performance in 106 asymptomatic offspring (mean age 40.6 years) of 54 DAT probands. Intraclass sibling correlations revealed little evidence of sibling similarity for performance on three memory tasks which have been reported to be relatively sensitive to the memory losses accompanying DAT. Subsequent investigations of the distributions of the cognitive task scores in the offspring revealed evidence for a commingling of two distributions for the three memory tasks but not for the nonmemory measures. These findings are consistent with a hypothesis that these distributions reflect genotypic subgroups, carriers, and noncarriers, of a presumed DAT gene. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP SMALLEY, SL (reprint author), UNIV CALIF LOS ANGELES,SCH MED,NPI,DEPT PSYCHIAT,ROOM 48-241,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. FU NCRR NIH HHS [1 P41 RR03655]; NIMH NIH HHS [MH 36205] NR 41 TC 11 Z9 12 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1992 VL 9 IS 5 BP 333 EP 345 DI 10.1002/gepi.1370090505 PG 13 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA JW004 UT WOS:A1992JW00400004 PM 1427022 ER PT J AU GRAVENSTEIN, S MILLER, BA DRINKA, P AF GRAVENSTEIN, S MILLER, BA DRINKA, P TI PREVENTION AND CONTROL OF INFLUENZA-A OUTBREAKS IN LONG-TERM CARE FACILITIES SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID NURSING-HOME; ELDERLY PEOPLE; IMMUNIZATION; AMANTADINE; VACCINATION; REDUCTION; VIRUS; H3N2; PROPHYLAXIS; MORTALITY C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. WISCONSIN VET HOME,KING,WI. RP GRAVENSTEIN, S (reprint author), UNIV WISCONSIN,INST AGING & ADULT LIFE,DEPT MED,GERIATR SECT,425 HENRY MALL,MADISON,WI 53706, USA. RI Gravenstein, Stefan/G-1681-2011 FU NIA NIH HHS [AG09632, AG00548] NR 34 TC 26 Z9 26 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD JAN PY 1992 VL 13 IS 1 BP 49 EP 54 PG 6 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA GZ076 UT WOS:A1992GZ07600007 PM 1545112 ER PT J AU LAWRENCE, V MATTHAI, W HARTMAIER, S AF LAWRENCE, V MATTHAI, W HARTMAIER, S TI COMPARATIVE SAFETY OF HIGH-OSMOLALITY AND LOW-OSMOLALITY RADIOGRAPHIC CONTRAST AGENTS - REPORT OF A MULTIDISCIPLINARY WORKING GROUP SO INVESTIGATIVE RADIOLOGY LA English DT Article ID ACUTE RENAL DYSFUNCTION; HIGH-RISK PATIENTS; CARDIAC ANGIOGRAPHY; CORONARY ANGIOGRAPHY; ADVERSE REACTIONS; INTRAVENOUS UROGRAPHY; EXCRETORY UROGRAPHY; PROSPECTIVE TRIAL; MEDIA; COMPLICATIONS C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. COOPER HOSP UNIV MED CTR,ROBERT WOOD JOHNSON MED SCH,CAMDEN,NJ. UNIV N CAROLINA,SCH PUBL HLTH,DEPT EPIDEMIOL,CHAPEL HILL,NC 27514. RP LAWRENCE, V (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. NR 85 TC 54 Z9 55 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD JAN PY 1992 VL 27 IS 1 BP 2 EP 28 DI 10.1097/00004424-199201000-00002 PG 27 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GX894 UT WOS:A1992GX89400002 PM 1733876 ER PT J AU BENNETT, CL PASCAL, A CVITANIC, M GRAHAM, V KITCHENS, A DEHOVITZ, JA AF BENNETT, CL PASCAL, A CVITANIC, M GRAHAM, V KITCHENS, A DEHOVITZ, JA TI MEDICAL-CARE COSTS OF INTRAVENOUS-DRUG-USERS WITH AIDS IN BROOKLYN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE INPATIENT CHARGES; MEDICAID; MEDICAL COSTS; OUTPATIENT CHARGES ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; FORECASTS AB This article reports on a study of medical costs of intravenous drug users (IVDUs) with acquired immune deficiency syndrome (AIDS) in Brooklyn, NY, U.S.A. Sociodemographic and clinical data as well as information on medical resource use was gathered for 38 IVDUs with AIDS, all of whom belonged to minority racial/ethnic groups and were covered by Medicaid insurance. Data obtained through patient interviews and review of medical records indicated that the sample had mean annual medical charges of $33,002 per patient per year. Average inpatient charges were $24,171, with an average of 1.13 hospitalizations and 38.5 days of in-hospital care. Significantly more in-hospital care and higher inpatient changes on average were noted among patients who did not have a stable housing environment. Outpatient charges averaged $8,831, with 80% for pharmaceuticals. This estimate of medical charges and resource use, one of the first developed in a cohort of nonwhite individuals with i.v. drug use as a risk factor for human immunodeficiency virus infection, is about one third less than recent estimates reported from studies of cohorts of white homosexual men. C1 RAND CORP,SANTA MONICA,CA 90406. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM HOSP,SCH MED,DEPT MED,LOS ANGELES,CA 90024. VET ADM,WESTERN REG SPECIAL STUDIES GRP,LOS ANGELES,CA. SUNY HLTH SCI CTR,DEPT PREVENT MED,BROOKLYN,NY. KINGS CTY HOSP CTR,BROOKLYN,NY 11203. SUNY HLTH SCI CTR,DEPT COMMUNITY HLTH & MED,BROOKLYN,NY. RI Bennett, Charles/C-2050-2008 FU AHRQ HHS [1R01HS06494-01]; PHS HHS [6130] NR 22 TC 68 Z9 68 U1 0 U2 1 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 JAN PY 1992 VL 5 IS 1 BP 1 EP 6 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GW913 UT WOS:A1992GW91300001 PM 1738078 ER PT J AU ROODMAN, GD KURIHARA, N OHSAKI, Y KUKITA, A HOSKING, D DEMULDER, A SMITH, JF SINGER, FR AF ROODMAN, GD KURIHARA, N OHSAKI, Y KUKITA, A HOSKING, D DEMULDER, A SMITH, JF SINGER, FR TI INTERLEUKIN-6 - A POTENTIAL AUTOCRINE PARACRINE FACTOR IN PAGETS-DISEASE OF BONE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INTERLEUKIN-6; OSTEOCLASTS; PAGETS DISEASE; PRECURSORS ID OSTEOCLAST-LIKE CELLS; HUMAN MARROW CULTURES; MONOCLONAL-ANTIBODIES; PARATHYROID-HORMONE; MEASLES-VIRUS; GROWTH-FACTOR; INVITRO; TISSUE; ULTRASTRUCTURE; STIMULATE AB Pagetic osteoclasts are greatly increased in number and size and have increased numbers of nuclei per cell compared to normal osteoclasts. The mechanisms responsible for enhanced osteoclast formation in Paget's disease are unknown. We have used our recently described model system for pagetic osteoclast formation to evaluate culture media conditioned by these atypical multinucleated cells (MNC) to determine if pagetic osteoclasts produce an autocrine or paracrine factor that enhances osteoclast formation. Conditioned media from long-term bone marrow cultures from patients with Paget's disease stimulated osteoclast-like MNC formation in normal marrow cultures. At least part of this activity could be ascribed to interleukin 6 (IL-6). In contrast, conditioned media from normal marrow cultures contained lower levels of IL-6 and did not stimulate formation of osteoclast-like MNC. 7 of 8 bone marrow plasma samples taken from involved bones and 18 of 27 peripheral blood serum samples from Paget's patients had high levels of IL-6. Normal marrow plasma and peripheral blood serum had no or very low levels of IL-6. These results suggest that IL-6 produced by marrow and/or bone cells in patients with Paget's disease may be an autocrine/paracrine factor for pagetic osteoclasts. C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NOTTINGHAM HLTH AUTHOR,NOTTINGHAM NG5 1PB,ENGLAND. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90048. FU NCI NIH HHS [CA-40035]; NIAMS NIH HHS [AR-35188, AR-39539] NR 34 TC 275 Z9 280 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1992 VL 89 IS 1 BP 46 EP 52 DI 10.1172/JCI115584 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GY561 UT WOS:A1992GY56100006 PM 1729280 ER PT J AU ODDS, FC ARAI, T DISALVO, AF EVANS, EGV HAY, RJ RANDHAWA, HS RINALDI, MG WALSH, TJ AF ODDS, FC ARAI, T DISALVO, AF EVANS, EGV HAY, RJ RANDHAWA, HS RINALDI, MG WALSH, TJ TI NOMENCLATURE OF FUNGAL DISEASES - A REPORT AND RECOMMENDATIONS FROM A SUB-COMMITTEE OF THE INTERNATIONAL-SOCIETY-FOR-HUMAN-AND-ANIMAL-MYCOLOGY (ISHAM) SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article AB The ISHAM Mycoses Nomenclature Committee has considered the present status of fungal disease names. It suggests that the traditional approach to mycoses nomenclature in which the name of a causative taxon is suffixed with '-asis', '-iasis', '-osis' or '-mycosis' leads to names that are frequently unstable with respect to subsequent taxonomic and clinico-epidemiological changes. It is therefore recommended that individual mycoses should be named as often as possible in the form 'pathology A due to/caused by fungus X' or '[adjectival] fungus X pathology A' in preference to construction of names based solely on fungal taxa. A list of recommended mycosis names retained for their long tradition or intrinsic convenience is provided, together with a combined index and list of rejected names. C1 BIOTHERAPY RES ASSOC,BUNKYO KU,TOKYO,JAPAN. DEPT PATHOL & LAB MED 350,RENO,NV. VALLABH BHAI PATEL CHEST INST,DEPT MED MYCOL,DELHI,INDIA. UNIV LEEDS,DEPT MICROBIOL,REG MYCOL LAB,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. AUDIE L MURPHY MEM VET ADM MED CTR,AUDIE L MURPHY MEM VET ADM HOSP,LAB SERV 113,SAN ANTONIO,TX 78284. NIH,BETHESDA,MD 20892. GUYS HOSP,DEPT DERMATOL,LONDON SE1 9RT,ENGLAND. RP ODDS, FC (reprint author), JANSSEN RES FDN,DEPT BACTERIOL & MYCOL,B-2430 BEERSE,BELGIUM. NR 3 TC 40 Z9 42 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 1992 VL 30 IS 1 BP 1 EP 10 PG 10 WC Mycology SC Mycology GA HJ744 UT WOS:A1992HJ74400001 PM 1573518 ER PT J AU GALGIANI, JN RINALDI, MG POLAK, AM PFALLER, MA AF GALGIANI, JN RINALDI, MG POLAK, AM PFALLER, MA TI STANDARDIZATION OF ANTIFUNGAL SUSCEPTIBILITY TESTING SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT 11TH CONGRESS OF THE INTERNATIONAL SOC FOR HUMAN AND ANIMAL MYCOLOGY CY JUN 24-28, 1991 CL MONTREAL, CANADA SP INT SOC HUMAN & ANIM MYCOL ID INVITRO SUSCEPTIBILITY; CANDIDA-ALBICANS; AMPHOTERICIN-B; INOCULUM SIZE; 5-FLUOROCYTOSINE; YEASTS; KETOCONAZOLE; AGENTS; FLUCYTOSINE; FLUCONAZOLE C1 UNIV ARIZONA,TUCSON,AZ 85721. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. F HOFFMANN LA ROCHE & CO LTD,CH-4002 BASEL,SWITZERLAND. UNIV OREGON,EUGENE,OR 97403. RP GALGIANI, JN (reprint author), VET ADM MED CTR,MED SERV 111,TUCSON,AZ 85723, USA. NR 39 TC 22 Z9 23 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 1992 VL 30 SU 1 BP 213 EP 224 PG 12 WC Mycology SC Mycology GA KC681 UT WOS:A1992KC68100022 PM 1474447 ER PT J AU DOLAN, MJ LATTUADA, CP MELCHER, GP ZELLMER, R ALLENDOERFER, R RINALDI, MG AF DOLAN, MJ LATTUADA, CP MELCHER, GP ZELLMER, R ALLENDOERFER, R RINALDI, MG TI COCCIDIOIDES-IMMITIS PRESENTING AS A MYCELIAL PATHOGEN WITH EMPYEMA AND HYDROPNEUMOTHORAX SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID COCCIDIOIDES-IMMITIS; IDENTIFICATION; CULTURES AB A previously healthy Caucasian male developed hydropneumothorax and a pleural peel filled with pleomorphic, septate hyphae. The only organism grown from cultures of the lung and pleural fluid was Coccidioides immitis, confirmed by exoantigen testing. Spherule-endospore forms were produced, however, following injection of the arthroconidial tissue isolate into BALB/c mice. The patient had a positive immunodiffusion complement-fixation test and developed a positive coccidioidin skin test during therapy. He recovered following thoracotomy and wedge resection of the ruptured coccidioidal cavity, and therapy with amphotericin B followed by fluconazole. The sole presence of the mycelial form of the dimorphic fungus C. immitis in the pleural space may have been due to a low CO2 partial pressure at that site secondary to a bronchopleural fistula. The case shows a distinctive and uncommon presentation of coccidioidomycosis which demonstrates the specificity of both the immunodiffusion complement-fixation assay in diagnosing this disease and the exoantigen test in confirming culture results. C1 AUDIE L MURPHY MEM VET ADM MED CTR,MYCOL REFERENCE LAB,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MICROBIOL,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,DEPT PATHOL,LACKLAND AFB,TX 78236. RP DOLAN, MJ (reprint author), WILFORD HALL USAF MED CTR,DEPT INFECT DIS,LACKLAND AFB,TX 78236, USA. NR 20 TC 14 Z9 14 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 1992 VL 30 IS 3 BP 249 EP 255 PG 7 WC Mycology SC Mycology GA JG322 UT WOS:A1992JG32200008 PM 1517961 ER PT J AU ALLENDOERFER, R YATES, RR SUN, SH GRAYBILL, JR AF ALLENDOERFER, R YATES, RR SUN, SH GRAYBILL, JR TI COMPARISON OF AMPHOTERICIN-B LIPID COMPLEX WITH AMPHOTERICIN-B AND SCH-39304 IN THE TREATMENT OF MURINE COCCIDIOIDAL MENINGITIS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article AB To assess the efficacy of amphotericin B lipid complex (ABLC) in the treatment of coccidioidal meningitis, we compared a wide range of doses (0.35-15 mg kg-1, intravenously (IV)) of ABLC with amphotericin B deoxycholate (AmB) (0.3-7 mg kg-1, intraperitoneally (IP)) and (IV) and a new triazole, SCH 39304 (SCH), in an experimental murine model. Survival data showed high dose ABLC to be of equal efficacy to IV and high dose IP AmB and SCH. Quantitative studies confirmed this outcome. No acute toxicity with ABLC, at the doses employed, was found. We conclude that ABLC is effective in the treatment of murine coccidioidal meningitis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78242. 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 15 TC 23 Z9 23 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 1992 VL 30 IS 5 BP 377 EP 384 PG 8 WC Mycology SC Mycology GA JW048 UT WOS:A1992JW04800004 PM 1469539 ER PT J AU ROLAK, LA RUTECKI, P ASHIZAWA, T HARATI, Y AF ROLAK, LA RUTECKI, P ASHIZAWA, T HARATI, Y TI CLINICAL-FEATURES OF TODD POST-EPILEPTIC PARALYSIS SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Note ID FOCAL SEIZURES AB Two hundred and twenty nine patients with generalised tonic-clonic seizures were prospectively evaluated. Fourteen were identified who had transient focal neurological deficits thought to be Todd's post-epileptic paralysis (PEP). Eight of these 14 patients had underlying focal brain lesions associated with the postictal deficits. All patients with PEP were weak, but there was wide variation in the pattern (any combination of face, arm, leg), severity (plegia to mild), tone (spastic, flaccid, or normal), and reflexes (increased, decreased, or normal). Significant sensory loss occurred in only one patient. The only other signs of PEP were aphasia (in five patients all with underlying lesions) and gaze palsy (in four patients). Post-epileptic paralysis persisted from half an hour to 36 hours (mean of 15 hours). Post-epileptic paralysis may occur with the first seizure or after many years of seizures and does not appear after every seizure. The clinical features of PEP are thus heterogeneous. C1 HOUSTON VET AFFAIRS MED CTR,HOUSTON,TX. RP ROLAK, LA (reprint author), BAYLOR COLL MED,DEPT NEUROL,6501 FANNIN,NB302,HOUSTON,TX 77030, USA. NR 16 TC 60 Z9 62 U1 2 U2 2 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD JAN PY 1992 VL 55 IS 1 BP 63 EP 64 DI 10.1136/jnnp.55.1.63 PG 2 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA HA978 UT WOS:A1992HA97800018 PM 1548500 ER PT J AU LAVIZZOMOUREY, RJ ZINN, J TAYLOR, L AF LAVIZZOMOUREY, RJ ZINN, J TAYLOR, L TI ABILITY OF SURROGATES TO REPRESENT SATISFACTION OF NURSING-HOME RESIDENTS WITH QUALITY OF CARE SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID LONG-TERM CARE; PATIENT SATISFACTION; MEDICAL-CARE AB Objective: To measure the ability of surrogates to accurately represent nursing home residents' satisfaction with the nursing home care. Design: Comparison by correlation analysis of questionnaire answers by nursing-home residents and their designated surrogates. Setting: Four non-profit community nursing homes. Participants: One-hundred fifty-two resident-surrogate pairs were included, based on the following criteria: (1) the resident was able to respond to questions verbally and in English, had cognitive abilities sufficient to understand the questions, and had a responsible party who had a telephone number in the medical record; (2) both the resident and the surrogate agreed to be interviewed. Outcome Measures: A 26-item instrument (21 specific and 5 global items) was developed to measure surrogates' perceptions of residents' satisfaction with the quality of the physician services, nursing care, and the nursing home environment. The instrument was scored on a 4-point Likert scale in which higher scores indicated greater satisfaction and paralleled a similar instrument designed for nursing home residents. Correlation of residents' with surrogates' scores on the satisfaction instrument was examined. Results: The mean score for most items was greater than 3.0, indicating overall satisfaction with the care. Correlations between surrogates and residents on specific items ranged from 0.1 to 0.55. Correlations were highest for global items and items addressing satisfaction with the environment. Conclusion: We conclude that nursing home residents' surrogates cannot accurately express the residents' satisfaction with all areas of nursing home care and that their evaluations should not be taken in lieu of the residents' opinions. RP LAVIZZOMOUREY, RJ (reprint author), PHILADELPHIA VET AFFAIRS MED CTR,GEN INTERNAL MED SECT,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIA NIH HHS [K08AG00363-04] NR 25 TC 32 Z9 32 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 JAN PY 1992 VL 40 IS 1 BP 39 EP 47 PG 9 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA GY171 UT WOS:A1992GY17100008 PM 1727846 ER PT J AU WATSON, GR WRIGHT, V DEIAUNE, W AF WATSON, GR WRIGHT, V DEIAUNE, W TI THE EFFICACY OF COMPREHENSION TRAINING AND READING PRACTICE FOR PRINT READERS WITH MACULAR LOSS SO JOURNAL OF VISUAL IMPAIRMENT & BLINDNESS LA English DT Article ID LOW VISION; PSYCHOPHYSICS AB The objectives of the project reported here were to discover whether the rehabilitation of reading recognition allows comprehension of print for low vision individuals who were former readers and to develop and test training strategies for enhancing comprehension for those who do not achieve good comprehension. C1 PENN COLL OPTOMETRY,PHILADELPHIA,PA 19141. US DEPT VET AFFAIRS,CTR REHABIL RES & DEV,DECATUR,GA 30033. RP WATSON, GR (reprint author), PENN COLL OPTOMETRY,PHILADELPHIA,PA 19141, USA. NR 49 TC 22 Z9 23 U1 0 U2 0 PU AMER FOUNDATION BLIND PI NEW YORK PA J VISUAL IMPAIRMENT BLINDNESS 11 PENN PLAZA SUITE 300, NEW YORK, NY 10001 SN 0145-482X J9 J VISUAL IMPAIR BLIN JI J. Vis. Impair. Blind. PD JAN PY 1992 VL 86 IS 1 BP 37 EP 43 PG 7 WC Rehabilitation SC Rehabilitation GA HA111 UT WOS:A1992HA11100018 ER PT J AU SMITH, AJ DEIAUNE, W GERUSCHAT, DR AF SMITH, AJ DEIAUNE, W GERUSCHAT, DR TI LOW VISION MOBILITY PROBLEMS - PERCEPTIONS OF O-AND-M SPECIALISTS AND PERSONS WITH LOW VISION SO JOURNAL OF VISUAL IMPAIRMENT & BLINDNESS LA English DT Article AB Through national survey research. this study explored low vision mobility problems, including the effects of different lighting conditions and the relationship between the reported perceptions of mobility practitioners and persons with low vision. C1 US DEPT VET AFFAIRS,CTR REHABIL RES & DEV,DECATUR,GA 30033. MARYLAND SCH BLIND,RES,BALTIMORE,MD 21236. RP SMITH, AJ (reprint author), PENN COLL OPTOMETRY,1200 W GODFREY AVE,PHILADELPHIA,PA 19141, USA. NR 24 TC 17 Z9 17 U1 0 U2 1 PU AMER FOUNDATION BLIND PI NEW YORK PA J VISUAL IMPAIRMENT BLINDNESS 11 PENN PLAZA SUITE 300, NEW YORK, NY 10001 SN 0145-482X J9 J VISUAL IMPAIR BLIN JI J. Vis. Impair. Blind. PD JAN PY 1992 VL 86 IS 1 BP 58 EP 62 PG 5 WC Rehabilitation SC Rehabilitation GA HA111 UT WOS:A1992HA11100022 ER PT J AU RAY, WA TAYLOR, JA LICHTENSTEIN, MJ MEADOR, KG AF RAY, WA TAYLOR, JA LICHTENSTEIN, MJ MEADOR, KG TI THE NURSING-HOME BEHAVIOR PROBLEM SCALE SO JOURNALS OF GERONTOLOGY LA English DT Article ID ALZHEIMERS-DISEASE; RATING-SCALE; PSYCHOACTIVE MEDICATION; MENTAL IMPAIRMENT; DEMENTIA SCALE; SYMPTOMS; CARE; RELIABILITY; DISTURBANCE; INSTRUMENT AB Nursing home patients frequently have serious disturbances of behavior that can lead to use of chemical or physical restrains. To support research into better management of these problems, we developed the Nursing Home Behavior Problem Scale (NHBPS), a 29-item inventory of serious behavior problems designed to be completed by nurses and nursing assistants. NHBPS scores were obtained for two samples of nursing home residents: 431 in Tennessee and 122 in Texas. The interrater correlation was .754 in the Tennessee sample and .827 in the Texas sample. The NHBPS had a correlation of -.747 with the NOSIE scale and .911 with the CMAI. There was a pronounced association of increased NHBPS scores with mental impairment and use of sedative drugs or restrains. These data suggest the NHBPS is a useful research instrument for measuring serious behavior problems in nursing home residents. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,NASHVILLE,TN 37232. 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. RP RAY, WA (reprint author), VANDERBILT UNIV,MED CTR,SCH MED,DEPT PREVENT MED,NASHVILLE,TN 37232, USA. NR 52 TC 79 Z9 79 U1 0 U2 1 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 1992 VL 47 IS 1 BP M9 EP M16 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA GY680 UT WOS:A1992GY68000012 PM 1730851 ER PT J AU SESSIONS, C LAWRENCE, D CLINKINGBEARD, C SHENKER, Y AF SESSIONS, C LAWRENCE, D CLINKINGBEARD, C SHENKER, Y TI REGULATION OF ADRENAL ATRIAL NATRIURETIC HORMONE RECEPTOR SUBTYPES SO LIFE SCIENCES LA English DT Article ID SMOOTH-MUSCLE CELLS; ALDOSTERONE SECRETION; PHYSIOLOGICAL-ROLE; DECREASED DENSITY; ALPHA-HANP; PEPTIDE; RAT; INHIBITION; CGMP; STIMULATION AB Regulation of atrial natriuretic hormone (ANH) receptor binding and aldosterone suppression was studied in isolated adrenal glomerulosa cells from rats fed a high-salt (HS) or low-salt (LS) diet for 3 days. In plasma of HS rats, aldosterone levels were 5 times lower and immunoreactive ANH two times higher than in LS rats. Competitive binding studies showed the same affinity for human atrial natriuretic hormone (hANH) in both pools of cells, but receptor density was 50% higher on LS cells. A linear ANH analog that binds to non-guanylate-cyclase-coupled receptors did not show increased binding to LS cells. Cyclic GMP production in response to hANH was identical in both groups. The aldosterone-inhibitory effect of hANH on both groups of basal and angiotensin II-stimulated cells was also identical. Thus a short-term high-salt diet causes decreased density of ANH receptors in glomerulosa cells without changing biological activity of ANH. These results suggest that dietary salt content changes the number of ANH receptors and that non-guanylate-cyclase-coupled receptors contain at least two classes of receptors. C1 UNIV WISCONSIN,DEPT INTERNAL MED,ENDOCRINOL & METAB SECT,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NIDDK NIH HHS [R29-DK-39444] NR 36 TC 9 Z9 9 U1 0 U2 0 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 1992 VL 50 IS 15 BP 1087 EP 1095 DI 10.1016/0024-3205(92)90345-P PG 9 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA HG809 UT WOS:A1992HG80900003 PM 1313518 ER PT J AU PAVLIDIS, NA DROSOS, AA PAPADIMITRIOU, C TALAL, N MOUTSOPOULOS, HM AF PAVLIDIS, NA DROSOS, AA PAPADIMITRIOU, C TALAL, N MOUTSOPOULOS, HM TI LYMPHOMA IN SJOGRENS-SYNDROME SO MEDICAL AND PEDIATRIC ONCOLOGY LA English DT Article DE LYMPHOMA DEVELOPMENT; SPONTANEOUS REGRESSION; AUTOIMMUNE DISEASE ID MALIGNANT-LYMPHOMA AB Sjogren's syndrome is an autoimmune disease with a known predisposition for lymphoma development. Eight of 120 patients with primary Sjogren's syndrome followed at the University of loannina over the past 7 years developed non-Hodgkin's lymphoma diagnosed according to the Kiel classification. The lymphomas differed by location and grading. Six were called low grade (immunocytoma) and two intermediate grade non-Hodgkin's lymphomas. Five of the immunocytomas involved the minor salivary or lacrimal glands. Immunoperoxidase staining for light chains revealed monoclonal populations. Two patients showed spontaneous regression not previously reported in Sjogren's syndrome. Thus, in Sjogren's syndrome, low grade non-Hodgkin's lymphomas and especially immunocytomas are the most common lymphomas. These lymphomas tend to evolve very slowly and may regress spontaneously. Given these facts, a conservative approach to treatment is indicated in those patients with only localized disease. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. RP PAVLIDIS, NA (reprint author), UNIV IOANNINA,SCH MED,DEPT INTERNAL MED,GR-45110 IOANNINA,GREECE. NR 15 TC 39 Z9 41 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-1532 J9 MED PEDIATR ONCOL JI Med. Pediatr. Oncol. PY 1992 VL 20 IS 4 BP 279 EP 283 DI 10.1002/mpo.2950200403 PG 5 WC Oncology; Pediatrics SC Oncology; Pediatrics GA HZ956 UT WOS:A1992HZ95600002 PM 1608349 ER PT J AU SMITH, ME BAKER, CR BRANCH, LG WALLS, RC GRIMES, RM KARKLINS, JM KASHNER, M BURRAGE, R PARKS, A ROGERS, P SACZUK, A WAGSTERWEARE, M AF SMITH, ME BAKER, CR BRANCH, LG WALLS, RC GRIMES, RM KARKLINS, JM KASHNER, M BURRAGE, R PARKS, A ROGERS, P SACZUK, A WAGSTERWEARE, M TI CASE-MIX GROUPS FOR VA HOSPITAL-BASED HOME CARE SO MEDICAL CARE LA English DT Article DE HOSPITAL-BASED HOME CARE; LONG-TERM CARE REIMBURSEMENT; CASE MIX MODELS ID LONG-TERM CARE; RESOURCE UTILIZATION GROUPS; INSTITUTIONALIZATION; SERVICES; TRIAL AB The purpose of this study is to group hospital-based home care (HBHC) patients homogeneously by their characteristics with respect to cost of care to develop alternative case mix methods for management and reimbursement (allocation) purposes. Six Veterans Affairs (VA) HBHC programs in Fiscal Year (FY) 1986 that maximized patient, program, and regional variation were selected, all of which agreed to participate. All HBHC patients active in each program on October 1, 1987, in addition to all new admissions through September 30, 1988 (FY88), comprised the sample of 874 unique patients. Statistical methods include the use of classification and regression trees (CART software: Statistical Software; Lafayette, CA), analysis of variance, and multiple linear regression techniques. The resulting algorithm is a three-factor model that explains 20% of the cost variance (R2 = 20%, with a cross validation R2 of 12%). Similar classifications such as the RUG-II, which is utilized for VA nursing home and intermediate care, the VA outpatient resource allocation model, and the RUG-HHC, utilized in some states for reimbursing home health care in the private sector, explained less of the cost variance and, therefore, are less adequate for VA home care resource allocation. C1 VET HLTH ADM,MED CTR,SALT LAKE CITY,UT. VET HLTH ADM,MED CTR,MEMPHIS,TN. VET HLTH ADM,MED CTR,NEW ORLEANS,LA. US DEPT VET AFFAIRS,VET HLTH ADM,OFF GERIATR & EXTENDED CARE,WASHINGTON,DC. BOSTON UNIV,SCH MED,BOSTON,MA 02118. ABT ASSOCIATES INC,CAMBRIDGE,MA. UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,HOUSTON,TX 77225. VET HLTH ADM,MED CTR,BUFFALO,NY. VET HLTH ADM,MED CTR,BALTIMORE,MD. JOHN L MCCLELLAN MEM VET ADM MED CTR,US DEPT VET AFFAIRS,VET HLTH ADM,LITTLE ROCK,AR 72205. UNIV ARKANSAS MED SCI HOSP,COLL MED,LITTLE ROCK,AR 72205. NR 34 TC 13 Z9 13 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD JAN PY 1992 VL 30 IS 1 BP 1 EP 16 DI 10.1097/00005650-199201000-00001 PG 16 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GZ535 UT WOS:A1992GZ53500001 PM 1309585 ER PT J AU CARNES, M BROWNFIELD, M LENT, SJ NICHOLS, K SCHULER, L AF CARNES, M BROWNFIELD, M LENT, SJ NICHOLS, K SCHULER, L TI PULSATILE ACTH AND CORTISOL IN GOATS - EFFECTS OF INSULIN-INDUCED HYPOGLYCEMIA AND DEXAMETHASONE SO NEUROENDOCRINOLOGY LA English DT Article DE ACTH, PULSATILE; ULTRADIAN RHYTHM; HYPOGLYCEMIA, GOAT ID CORTICOTROPIN-RELEASING FACTOR; ANTERIOR-PITUITARY CELLS; ADRENOCORTICOTROPIN SECRETION; CORTICOSTEROID RESPONSES; INTERMEDIATE PITUITARY; ARGININE VASOPRESSIN; PLASMA CORTICOTROPIN; ACTION-POTENTIALS; OVINE ANTERIOR; CONSCIOUS DOGS AB Insulin-induced hypoglycemia is a metabolic stress that stimulates secretion of adrenocorticotropic hormone (ACTH) and cortisol in a number of animal species. Dexamethasone is a potent synthetic glucocorticoid that suppresses the secretion of ACTH and cortisol. Both ACTH and cortisol exhibit complex secretory patterns demonstrating ultradian and circadian rhythms. This work investigated the pattern of ACTH and cortisol response to hypoglycemia in goats and the effect of dexamethasone on this response. Five goats were pretreated with dexamethasone (0.1 mg/kg) and 5 with saline. Blood samples were taken every 2 min for 60 min before and 60 min after administration of insulin (2.5 IU/kg, i.v.). Immunoreactive ACTH and cortisol were measured in all samples and glucose in selected samples. Data sets were analyzed for significant pulses with the Cluster Analysis program. Complete data sets were compared as well as those for each 30-min interval. Plasma glucose was lower than preinsulin levels at 10 min, declined rapidly between 10 and 30 min, and remained low 30-60 min after insulin injection in both treatment groups. Controls showed a rapid rise in ACTH and cortisol beginning 30 +/- 10 min postinsulin. The increase in mean plasma hormone levels during hypoglycemia was predominantly due to an increase in amplitude of secretory pulses for ACTH and cortisol compared with the 30 min before insulin. Dexamethasone significantly lowered mean ACTH and cortisol levels and prevented alteration in plasma ACTH and cortisol secretion during hypoglycemia but did not totally ablate pulsatile activity of either hormone. The amplitude of ACTH and cortisol pulses was significantly decreased by dexamethasone treatment. The frequency of cortisol but not ACTH pulses was also significantly decreased. The highest cross-correlation between plasma ACTH and cortisol occurred at a lag of 0 min in control goats. Cross-correlation was lower and no consistent lag was seen in dexamethasone-treated goats. In control goats, during the fall in plasma glucose, before the rapid rise in plasma ACTH and cortisol, secretion appeared to be relatively quiescent compared to the prior 30 min. Specifically, a slight reduction occurred in frequency, amplitude, and area of ACTH pulses, in amplitude and area of cortisol pulses, and in cortisol levels. While this unexpected observation may have been an artifact of the sampling protocol, it bears further investigation. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT COMPARAT BIOSCI,MADISON,WI 53706. FU NIDDK NIH HHS [IR01-DK40759-01] NR 43 TC 11 Z9 11 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD JAN PY 1992 VL 55 IS 1 BP 97 EP 104 DI 10.1159/000126102 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA HB188 UT WOS:A1992HB18800014 PM 1319009 ER PT J AU TYAN, ML AF TYAN, ML TI EFFECTS OF H-2 AND VITAMIN-A ON EYE DEFECTS IN CONGENIC MICE SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID CRYSTALLIN; LOCUS; LENS AB Pregnant mice congenic with C57BL/10 (B10.A, B10.BR, B10.D2, B10.A(2R), B10.A(5R), B10.A(15R), B10.A(1R), B10.A(18R), and B10.OL) were fed Purina Mouse Chow or the same diet plus 200 IU of vitamin A daily. The pregnant dams were sacrificed on the 18th day of gestation and the fetuses were sexed and examined for defects in eye development. It was found that the frequency of microphthalmia and anophthalmia in the female progeny of mice fed Mouse Chow was 7.4-9.2% in B10.A and B10.BR, 4.0-5.5% in B10.A(18R), B10, B10.A(5R), B10.A(1R), B10.A(15R), and B10.A(2R), and 0.8% and 1.4% in B10.D2 and B10.OL mice, respectively. On average, the frequency of these defects in the female progeny was 6.2 times greater than that in males (P < 0.001). The right eye was 5.8 times more often affected than the left (P < 0.001). The addition of vitamin A to the diet increased the frequency of these eye abnormalities in all strains, suggesting that this effect is not mediated by loci associated with H-2, as is the case with vitamin A-enhanced cleft palate. The addition of vitamin A to the diet did not affect the ratios of affected males to females, affected right to left eye, or microphthalmia to anophthalmia. The results suggest that there are two loci on chromosome 17, one centromeric to E-beta and one telemeric to C4, that interact to determine to some degree the frequency of microphthalmia and anophthalmia. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RP TYAN, ML (reprint author), W LOS ANGELES VET ADM MED CTR 111M,LOS ANGELES,CA 90073, USA. NR 9 TC 11 Z9 11 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JAN PY 1992 VL 199 IS 1 BP 123 EP 127 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW106 UT WOS:A1992GW10600019 PM 1728030 ER PT J AU WIRSHING, WC MARDER, SR ECKMAN, T LIBERMAN, RP MINTZ, J AF WIRSHING, WC MARDER, SR ECKMAN, T LIBERMAN, RP MINTZ, J TI ACQUISITION AND RETENTION OF SKILLS TRAINING METHODS IN CHRONIC-SCHIZOPHRENIC OUTPATIENTS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 30TH ANNUAL MEETING OF THE AMERICAN COLLEGE OF NEUROPSYCHOPHARMACOLOGY CY DEC, 1991 CL SAN JUAN, PR SP AMER COLL NEUROPSYCHOPHARM ID DRUGS AB Forty-one DSM-III-R schizophrenic subjects on constant, low-dose maintenance neuroleptic drug therapy (5-10 mg of fluphenazine decanoate intramuscularly every 2 weeks) were randomly assigned to structured and modularized skills training or to supportive group psychotherapy. The skills training was designed by using cognitive and behavioral methods to compensate for the learning disabilities that plague many schizophrenic patients. Skill acquisition was assessed by using quantified performance on standardized role-play tests. Subjects who received skills training made significant gains In each of the areas taught, whereas those who participated in the control psychotherapy group did not. The knowledge and skills learned during training were retained without significant erosion over a 1-year followup period. These results suggest that the use of structured principles of learning and cognitive therapy can effectively train schizophrenics in skill areas pertinent to the self-management of their illness. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP WIRSHING, WC (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,B-151H,LOS ANGELES,CA 90073, USA. FU NIMH NIH HHS [MH-41573, MH-30911] NR 13 TC 19 Z9 20 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1992 VL 28 IS 3 BP 241 EP 245 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA JY721 UT WOS:A1992JY72100008 PM 1480726 ER PT J AU GANZINI, L CASEY, DE HOFFMAN, WF HEINTZ, RT AF GANZINI, L CASEY, DE HOFFMAN, WF HEINTZ, RT TI TARDIVE-DYSKINESIA AND DIABETES-MELLITUS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 30TH ANNUAL MEETING OF THE AMERICAN COLLEGE OF NEUROPSYCHOPHARMACOLOGY CY DEC, 1991 CL SAN JUAN, PR SP AMER COLL NEUROPSYCHOPHARM ID RISK-FACTORS; RATS; DOPAMINE; LESIONS; BRAIN; PREVALENCE; METOCLOPRAMIDE; METABOLISM; INSULIN; BINDING AB Two studies examine the prevalence of tardive dyskinesia (TD) in neuroleptic-treated diabetic patients. Study 1 compared 38 diabetic patients with 38 nondiabetic patients treated for psychotic disorders with low to moderate doses of neuroleptics (mean chlorpromazine equivalents = 300 mg/day) for an average of 18 years. Study 2 compared 24 diabetic and 27 nondiabetic patients treated for an average of 2.6 years with a mean 31 mg/day of metoclopramide for gastrointestinal disease. Patients were examined for TD using standardized scales by raters blind to all treatment and illness variables. In both studies, there were no differences between the diabetic and nondiabetic groups in age, sex, type of psychiatric illness, and dose and duration of neuroleptic treatment or severity of parkinsonism. In both studies, the diabetic patients had significantly greater prevalence and severity of TD. No measures of diabetes severity were associated with TD in either study. Possible pathophysiologic mechanisms for the increased prevalence of TD in neuroleptic-treated patients with diabetes will be discussed. C1 DAMMASCH STATE HOSP,WILSONVILLE,OR. OREGON HLTH SCI UNIV,DEPT PSYCHIAT,PORTLAND,OR 97201. RP GANZINI, L (reprint author), PORTLAND VET AFFAIRS MED CTR,PSYCHIAT SERV 116AP,POB 1034,3710 SW VET HOSP PK RD,PORTLAND,OR 97207, USA. FU NIMH NIH HHS [MH-36657, MH-43586] NR 37 TC 23 Z9 23 U1 1 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1992 VL 28 IS 3 BP 281 EP 286 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA JY721 UT WOS:A1992JY72100014 PM 1362276 ER PT J AU WALKER, EM SMITH, AB GALE, GR JONES, MM AF WALKER, EM SMITH, AB GALE, GR JONES, MM TI ENHANCED MOBILIZATION OF HEPATIC CADMIUM IN MICE UPON COADMINISTRATION OF AN N,N-DISUBSTITUTED DITHIOCARBAMATE AND AN ALKYL MONOESTER OF DIMERCAPTOSUCCINATE SO RESEARCH COMMUNICATIONS IN CHEMICAL PATHOLOGY AND PHARMACOLOGY LA English DT Article ID ORGAN DISTRIBUTION; EXCRETION; DIETHYLDITHIOCARBAMATE; DIETHYLENETRIAMINEPENTAACETATE; DIHYDROXYETHYLDITHIOCARBAMATE; ANTAGONISTS AB Oral (po) administration of mono-iso-amyl(2,3-dimercapto) succinate (Mi-ADMS), 0.5 mmol/kg for three consecutive days, to mice previously injected with cadmium (Cd) chloride reduced the whole body Cd burden 34%. Intraperitoneal (ip) administration of N-iso-amyl-N-glucaminedithiocarbamate (i-AmGDTC) by the same regimen reduced total body Cd 41%. Coadministration of the two compounds reduced the whole body Cd burden 60% (p < 0.05). The liver Cd concentration was reduced 56% and 50%, respectively, by Mi-ADMS given po and i-AmGDTC given ip, each at 0.5 mmol/kg for three consecutive days. Coadministration of the two chelators reduced the liver Cd concentration 90% (p < 0.05). The kidney Cd concentration was reduced 10% by Mi-ADMS alone, and 60% by i-AmGDTC alone, but there was only a 47% reduction when the two chelators were coadministered, probably as a result of redistribution of mobilized hepatic Cd to the kidneys. As 50-50% of the administered Cd is sequestered in the liver in this mouse model, it is concluded that coadministration of the two chemical classes of Cd complexing agents may offer a therapeutic advantage over administration of either agent alone. C1 JOHN L MCCLELLAN MEM VET ADM MED CTR,LITTLE ROCK,AR 72205. UNIV ARKANSAS MED SCI HOSP,DEPT PATHOL,LITTLE ROCK,AR 72205. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC. VANDERBILT UNIV,DEPT CHEM,NASHVILLE,TN 37235. VANDERBILT UNIV,CTR MOLEC TOXICOL,NASHVILLE,TN 37235. FU NIEHS NIH HHS [ES-02638] NR 12 TC 0 Z9 0 U1 0 U2 0 PU P J D PUBLICATIONS LTD PI WESTBURY PA PO BOX 966, WESTBURY, NY 11590 SN 0034-5164 J9 RES COMMUN CHEM PATH PD JAN PY 1992 VL 75 IS 1 BP 121 EP 124 PG 4 WC Pathology; Pharmacology & Pharmacy SC Pathology; Pharmacology & Pharmacy GA HB581 UT WOS:A1992HB58100012 PM 1626122 ER PT J AU AMIN, F DAVIDSON, M DAVIS, KL AF AMIN, F DAVIDSON, M DAVIS, KL TI HOMOVANILLIC-ACID MEASUREMENT IN CLINICAL RESEARCH - A REVIEW OF METHODOLOGY SO SCHIZOPHRENIA BULLETIN LA English DT Review ID HUMAN CEREBROSPINAL-FLUID; URINARY CATECHOLAMINE METABOLITE; NORADRENERGIC NEURONAL-ACTIVITY; CSF MONOAMINE METABOLITES; BRAIN DOPAMINE METABOLISM; AMINE METABOLITES; SCHIZOPHRENIC-PATIENTS; RAT-BRAIN; 3,4-DIHYDROXYPHENYLACETIC ACID; PLASMA DOPAMINE AB Despite its serious limitations, measuring the concentrations of homovanillic acid (HVA) in body fluids is perhaps the most direct method currently available to assess the changing activity of central dopamine (DA) neurons in living humans. The concentrations of HVA in body fluids are determined not only by the activity of central DA neurons but also by a number of unrelated factors such as the other sources of HVA and the elimination of HVA from the body. This article reviews many factors that help to determine the concentrations of HVA in body fluids and therefore must be considered in studies employing HVA as a possible index of central DA neuronal activity. The need for further methodological work is indicated to improve the use of body fluid HVA measurements in clinical research. C1 BRONX VET AFFAIRS MED CTR,MT SINAI SCH MED,NEW YORK,NY. RP AMIN, F (reprint author), VET ADM MED CTR,PSYCHIAT SERV,RM 3-B 50,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 196 TC 117 Z9 117 U1 1 U2 7 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 1992 VL 18 IS 1 BP 123 EP 148 PG 26 WC Psychiatry SC Psychiatry GA HH615 UT WOS:A1992HH61500018 PM 1553492 ER PT J AU WIRSHING, WC MARDER, SR JOHNSTONCRONK, K LEBELL, M MACKENZIE, J MINTZ, J ECKMAN, T LIBERMAN, RP AF WIRSHING, WC MARDER, SR JOHNSTONCRONK, K LEBELL, M MACKENZIE, J MINTZ, J ECKMAN, T LIBERMAN, RP TI MANAGEMENT OF RISK OF RELAPSE IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RI Mintz, Jim/N-7385-2014 OI Mintz, Jim/0000-0002-8299-5851 NR 0 TC 1 Z9 1 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 1992 VL 6 IS 2 BP 107 EP 108 DI 10.1016/0920-9964(92)90128-R PG 2 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800047 ER PT J AU STERN, RG KAHN, RS DAVIDSON, M HARVEY, PD AMIN, F APTER, SH DUMONT, K HIRSCHOWITZ, J DAVIS, KL AF STERN, RG KAHN, RS DAVIDSON, M HARVEY, PD AMIN, F APTER, SH DUMONT, K HIRSCHOWITZ, J DAVIS, KL TI SIGNIFICANT DECREASE IN PSYCHOPATHOLOGY WITHIN 3 DAYS OF HALOPERIDOL TREATMENT IN CHRONIC-SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,BRONX,NY 10468. MT SINAI MED SCH,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 1 Z9 1 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 1992 VL 6 IS 2 BP 109 EP 110 DI 10.1016/0920-9964(92)90134-Q PG 2 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800053 ER PT J AU AMES, D WIRSHING, WC LEE, MA CUMMINGS, JL VANPUTTEN, T MARDER, SR BARTZOKIS, G AF AMES, D WIRSHING, WC LEE, MA CUMMINGS, JL VANPUTTEN, T MARDER, SR BARTZOKIS, G TI SELEGILINE IN THE TREATMENT OF AKATHISIA, TARDIVE-DYSKINESIA, AND NEGATIVE SCHIZOPHRENIC SYMPTOMS SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RI Bartzokis, George/K-2409-2013 NR 0 TC 1 Z9 1 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 1992 VL 6 IS 2 BP 110 EP 111 DI 10.1016/0920-9964(92)90136-S PG 2 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800055 ER PT J AU KAHN, RS DAVIDSON, M KNOTT, P STERN, RG AMIN, F WEBSTER, L APTER, SA DAVIS, KL AF KAHN, RS DAVIDSON, M KNOTT, P STERN, RG AMIN, F WEBSTER, L APTER, SA DAVIS, KL TI EFFECT OF HALOPERIDOL ON CSF MONOAMINE METABOLITES IN SCHIZOPHRENIA - SYMPTOMATIC IMPROVEMENT IS RELATED TO ALTERED DOPAMINE-SEROTONIN INTERACTION SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 118 EP 118 DI 10.1016/0920-9964(92)90155-X PG 1 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800074 ER PT J AU KAHN, RS DAVIDSON, M HIRSCHOWITZ, J STERN, RG DAVIS, BM GABRIEL, S MOORE, C DAVIS, KL AF KAHN, RS DAVIDSON, M HIRSCHOWITZ, J STERN, RG DAVIS, BM GABRIEL, S MOORE, C DAVIS, KL TI NOCTURNAL GROWTH-HORMONE SECRETION IN SCHIZOPHRENIC-PATIENTS AND HEALTHY-SUBJECTS SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 125 EP 125 DI 10.1016/0920-9964(92)90169-6 PG 1 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800088 ER PT J AU KAHN, RS SIEVER, L KNOTT, P STERN, RG AMIN, F DUMONT, K APTER, SA DAVIDSON, M AF KAHN, RS SIEVER, L KNOTT, P STERN, RG AMIN, F DUMONT, K APTER, SA DAVIDSON, M TI M-CHLOROPHENYLPIPERAZINE AS A PROBE OF SEROTONIN FUNCTION IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 138 EP 138 DI 10.1016/0920-9964(92)90199-F PG 1 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800118 ER PT J AU LEVINE, RL JONES, JC BEE, N AF LEVINE, RL JONES, JC BEE, N TI STROKE AND PARKINSONS-DISEASE SO STROKE LA English DT Meeting Abstract C1 MIDDLETON VET ADM HOSP,MADISON,WI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1992 VL 23 IS 1 BP 136 EP 136 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HA876 UT WOS:A1992HA87600030 ER PT J AU WONG, TK HERSHMAN, JM AF WONG, TK HERSHMAN, JM TI CHANGES IN THYROID-FUNCTION IN NONTHYROID ILLNESS SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID FREE-THYROXINE; SERUM THYROTROPIN; TRIIODOTHYRONINE; HORMONE; ASSAY; ULTRAFILTRATION; SECRETION; DIALYSIS; BINDING; T4 AB Nonthyroid illness can cause changes in thyroid function that have been described as low triiodothyronine (T3) and low thyroxine (T4) states. Reduced peripheral conversion of T4 to T3 explains the low serum T3 concentration. The explanation for the low serum T4 level is multifactorial; whether free-thyroxine (FT4) level is normal or reduced remains controversial. Cytokines such as tumor necrosis factor alpha, which are produced by the immune system during severe illness, may inhibit thyroid function directly and be responsible for the changes in pituitary-thyroid function. RP WONG, TK (reprint author), UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,DEPT MED,DIV ENDOCRINOL,LOS ANGELES,CA 90073, USA. NR 28 TC 27 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD JAN-FEB PY 1992 VL 3 IS 1 BP 8 EP 12 DI 10.1016/1043-2760(92)90085-F PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GX703 UT WOS:A1992GX70300002 PM 18407071 ER PT J AU METZ, S HOLMES, D ROBERTSON, RP LEITNER, W DRAZNIN, B AF METZ, S HOLMES, D ROBERTSON, RP LEITNER, W DRAZNIN, B TI GENE-EXPRESSION OF TYPE-I PHOSPHOLIPASE-A2 IN PANCREATIC BETA-CELLS - REGULATION OF MESSENGER-RNA LEVELS BY STARVATION OR GLUCOSE EXCESS SO FEBS LETTERS LA English DT Article DE INSULIN; PANCREATIC ISLET; PHOSPHOLIPASE; GLUCOSE; BETA-CELL; FASTING ID MEMBRANE-ASSOCIATED PHOSPHOLIPASE-A2; INSULIN-SECRETION; RAT ISLETS; CDNA CLONING; HYPERGLYCEMIA; ACCUMULATION; SEQUENCE; CALCIUM AB Messenger RNA from intact rat pancreatic islets, or from transformed hamster beta (HIT) cells, hybridized with the cDNA probe for type I (but not type II) phospholipase A2. The levels of phospholipase A2 mRNA increased in islets from fasted rats; they decreased in islets cultured in a high glucose concentration (control values at 5.5 mM glucose = 150 +/- 6% of those at 22 mM) which impaired subsequent insulin secretion (reduction in second-phase release = 70 +/- 11%). These studies uniquely demonstrate that type I phospholipase A2 is expressed specifically in beta cells and that nutrient availability modulates transcript levels, an effect which could contribute to the detrimental influence of prolonged hyperglycemia on islet function. C1 VET ADM MED CTR,DENVER,CO 80220. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DIV ENDOCRINOL,MADISON,WI. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DIV ENDOCRINOL,MADISON,WI 53706. FU NIDDK NIH HHS [DK38325, DK37312] NR 26 TC 30 Z9 30 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD DEC 16 PY 1991 VL 295 IS 1-3 BP 110 EP 112 DI 10.1016/0014-5793(91)81397-Q PG 3 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA GZ363 UT WOS:A1991GZ36300029 PM 1662640 ER PT J AU RAGO, R MITCHEN, J CHENG, AL OBERLEY, T WILDING, G AF RAGO, R MITCHEN, J CHENG, AL OBERLEY, T WILDING, G TI DISRUPTION OF CELLULAR-ENERGY BALANCE BY SURAMIN IN INTACT HUMAN PROSTATIC-CARCINOMA CELLS, A LIKELY ANTIPROLIFERATIVE MECHANISM SO CANCER RESEARCH LA English DT Article ID TRANSFORMING GROWTH-FACTOR; FACTOR RECEPTOR-BINDING; LIVING CELLS; FACTOR-ALPHA; INHIBITION; ASSAY; DRUG; DIFFERENTIATION; PROLIFERATION; MITOCHONDRIA AB The antiparasitic drug, suramin, has antiproliferative effects in human carcinoma cells. It has been suggested that this occurs through blockade of growth factor-receptor interactions. Three types of evidence that suramin rapidly inhibits cellular respiration or disrupts cellular energy balance in intact cells of the human prostate carcinoma cell line, DU145, are presented. Beginning at approximately 10(-4) M, suramin rapidly causes dose-dependent inhibition of tetrazolium conversion by mitochondrial dehydrogenases in intact cells, demonstrating an inhibition of respiration. This effect is reversed by exchange with suramin-free media but not by pretreatment with serum, epidermal growth factor, insulin-like growth factor I, acidic and basic fibroblast growth factors, or calcium. Rhodamine 123 (10-mu-g/ml) uptake by mitochondria in intact DU145 cells is inhibited in the presence of 10(-3) M suramin. Treatment with 10(-4)-10(-3)M suramin causes the loss of rhodamine 123 from cells with mitochondria prestained with rhodamine 123, indicating that suramin is acting as an ionophore or respiratory poison. Also shown by electron microscopy are progressive toxic changes in mitochondria of DU145 cells within 1 h after treatment with 10(-4) M suramin. These data indicate that in intact DU145 cells 10(-4) M suramin rapidly disrupts cellular energy balance or respiration as seen by three studies of mitochondrial state. Disruption of energy balance or respiration represents a likely antiproliferative mechanism, as is thought to be a primary mechanism for the action of suramin in parasitic diseases. This proposed mechanism of action for suramin can explain the most prominent observed clinical toxicities of nephrotoxicity, adrenal toxicity, coagulopathy, and demyelinating neuropathy. C1 UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,K4-666 CSC,600 HIGHLAND AVE,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI 53705. OI Cheng, Ann-Lii/0000-0002-9152-6512 FU NCI NIH HHS [CA50590, T32 CA09614] NR 52 TC 42 Z9 43 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 15 PY 1991 VL 51 IS 24 BP 6629 EP 6635 PG 7 WC Oncology SC Oncology GA GU416 UT WOS:A1991GU41600022 PM 1742736 ER PT J AU LIEBER, CS AF LIEBER, CS TI PERSPECTIVES - DO ALCOHOL CALORIES COUNT SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE ETHANOL; ENERGY; DIETARY FAT; MICROSOMAL ETHANOL OXIDIZING SYSTEM; OXIDATIVE PHOSPHORYLATION ID CHRONIC ETHANOL-CONSUMPTION; UNITED-STATES ADULTS; MICROSOMAL-ENZYMES; OXIDIZING SYSTEM; ENERGY WASTAGE; BODY-WEIGHT; DIETARY-FAT; RAT-LIVER; ACETALDEHYDE; PHOSPHORYLATION AB Chronic consumption of substantial amounts of alcohol is not associated with the expected effect on body weight. Isocaloric substitution of carbohydrates by ethanol results in weight loss, and addition of ethanol to an otherwise normal diet does not produce the expected weight gain. This energy deficit cannot be explained by maldigestion or malabsorption but has been attributed to induction of the microsomal ethanol oxidizing system (a metabolic pathway that oxidizes ethanol without associated chemical energy production), increased sympathetic tone and associated thermogenesis, and/or enhanced ATP breakdown (with increased purine catabolism) secondary to the acetate produced from ethanol. All these hypotheses do not fully explain the lack of weight deficit when alcohol is consumed with a very-low-fat diet, which suggests that an alteration in the energy utilization derived from fat plays a major role, possibly through uncoupling of oxidation with phosphorylation in mitochondria damaged by chronic ethanol consumption. C1 BRONX VET AFFAIRS MED CTR,LIVER DIS & NUTR SECT,BRONX,NY. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151-G,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 64 TC 118 Z9 123 U1 0 U2 3 PU AMER SOC CLIN NUTRITION INC 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 DEC PY 1991 VL 54 IS 6 BP 976 EP 982 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA GT073 UT WOS:A1991GT07300004 PM 1957830 ER PT J AU LINDGRENFURMAGA, EM SCHUNA, AA AF LINDGRENFURMAGA, EM SCHUNA, AA TI SWITCHING FROM ENALAPRIL TO LISINOPRIL SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Letter C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PHARM SERV,MADISON,WI 53705. RP LINDGRENFURMAGA, EM (reprint author), UNIV ILLINOIS,COLL PHARM,DEPT PHARM PRACTICE,833 S WOOD ST,CHICAGO,IL 60680, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD DEC PY 1991 VL 48 IS 12 BP 2605 EP 2605 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GR456 UT WOS:A1991GR45600008 ER PT J AU BOELAERT, JR FENVES, AZ COBURN, JW AF BOELAERT, JR FENVES, AZ COBURN, JW TI DEFEROXAMINE THERAPY AND MUCORMYCOSIS IN DIALYSIS PATIENTS - REPORT OF AN INTERNATIONAL REGISTRY SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE DIALYSIS; DEFEROXAMINE; FEROXAMINE; MUCORMYCOSIS; RHIZOPUS; IRON OVERLOAD ID AMBULATORY PERITONEAL-DIALYSIS; HEMODIALYSIS-PATIENTS; RECEIVING DEFEROXAMINE; CHELATED ALUMINUM; IRON OVERLOAD; DESFERRIOXAMINE; PHYCOMYCOSIS; ZYGOMYCOSIS; RISK; ASSOCIATION C1 BAYLOR UNIV,MED CTR,NEPHROL SECT,WACO,TX 76798. UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,WADSWORTH DIV MED SERV,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,WADSWORTH DIV,RES SERV,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RP BOELAERT, JR (reprint author), ALGEMEEN ZIEKENHUIS ST JAN,RENAL & INFECT DIS UNIT,B-8000 BRUGES,BELGIUM. NR 53 TC 108 Z9 111 U1 1 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD DEC PY 1991 VL 18 IS 6 BP 660 EP 667 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA GT961 UT WOS:A1991GT96100006 PM 1962650 ER PT J AU SUNDERLAND, MC ROODMAN, GD AF SUNDERLAND, MC ROODMAN, GD TI INTERLEUKIN-3 - ITS BIOLOGY AND POTENTIAL USES IN PEDIATRIC HEMATOLOGY ONCOLOGY SO AMERICAN JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; RECOMBINANT HUMAN INTERLEUKIN-3; HUMAN GRANULOCYTE-MACROPHAGE; HEMATOPOIETIC GROWTH-FACTORS; MYELOBLASTIC-LEUKEMIA CELLS; HUMAN GM-CSF; PROGENITOR CELLS; BONE-MARROW; HUMAN IL-3; MYELODYSPLASTIC SYNDROMES AB The hematopoietic growth factor interleukin (IL)-3 is a potent regulator of blood cell proliferation. It promotes the survival, proliferation, and development of hematopoietic stem cells and committed progenitor cells of the granulocyte-macrophage, erythrocyte, eosinophil, basophil, megakaryocyte, mast cell, and lymphocyte lineages. In addition, IL-3 enhances mature myeloid cell functions such as phagocytosis and activation of basophils and eosinophils, as well as monocyte cytotoxicity. The first phase of clinical trials suggested that IL-3 may augment myelopoiesis in a number of clinical conditions. It may be efficacious for treatment of primary marrow disorders, including myelodysplastic syndromes and aplastic anemia. However, replacement therapy with IL-3 alone is probably not sufficient to obtain maximal stimulation of myelopoiesis. Preclinical and clinical studies published to date suggest that sequential use or combinations of growth factors will be needed to obtain optimal hematopoietic responses. C1 UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTON BLVD,SAN ANTONIO,TX 78284. NR 87 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-8562 J9 AM J PEDIAT HEMATOL PD WIN PY 1991 VL 13 IS 4 BP 414 EP 425 PG 12 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA GR302 UT WOS:A1991GR30200005 PM 1785668 ER PT J AU OISHI, SN PAGE, CP SCHWESINGER, WH AF OISHI, SN PAGE, CP SCHWESINGER, WH TI COMPLICATED PRESENTATIONS OF GROIN HERNIAS SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 43RD ANNUAL MEETING OF THE SOUTHWESTERN SURGICAL CONGRESS CY APR 21-24, 1991 CL LAS VEGAS, NV SP SW SURG CONGRESS ID REPAIR AB Elective repair of simple (uncomplicated) inguinal and femoral hernias avoids incarceration and bowel obstruction (complicated presentations). To identify factors that perturb this strategy, we analyzed the records of 1,859 consecutive nonpediatric patients with groin hernias. Incarceration or bowel obstruction prompted operation in 22 of 77 (29%) women and in 15 of 34 (44%) patients with femoral hernia. Patients presenting with bowel obstruction were significantly older than those with incarceration only and/or uncomplicated presentation, and 13 of 25 (52%) required resection of necrotic bowel. Mortality was limited to five patients of advanced age with groin hernia and bowel obstruction. Four of the five patients had undergone resection of necrotic bowel. Complicated presentations of groin hernias are associated with a higher proportion of women and patients with femoral hernias. Gangrenous bowel was encountered only in those patients with groin hernia and bowel obstruction. Early diagnosis and elective repair of uncomplicated hernias should remain our strategy in patients of all ages. C1 UNIV TEXAS,HLTH SCI CTR,DEPT SURG,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 8 TC 37 Z9 37 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD DEC PY 1991 VL 162 IS 6 BP 568 EP 571 DI 10.1016/0002-9610(91)90110-Y PG 4 WC Surgery SC Surgery GA GX232 UT WOS:A1991GX23200011 PM 1670226 ER PT J AU JENKINSON, SG DUNCAN, CA BRYAN, CL LAWRENCE, RA AF JENKINSON, SG DUNCAN, CA BRYAN, CL LAWRENCE, RA TI EFFECTS OF AGE ON RAT GLUTATHIONE METABOLISM SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Article DE GLUTATHIONE; GLUTATHIONE PEROXIDASE; AGING RATS; GAMMA-GLUTAMYL TRANSPEPTIDASE ID GAMMA-GLUTAMYL-TRANSPEPTIDASE; PEROXIDASE-ACTIVITY; SUPEROXIDE-DISMUTASE; SELENIUM DEFICIENCY; LIPID-PEROXIDATION; S-TRANSFERASES; LIVER; ERYTHROCYTE; SENSITIVITY; INHIBITION AB The authors hypothesized that rat plasma or tissue glutathione metabolism could change with age due to possible decreases in glutathione-related enzyme activities. To test this hypothesis, the authors measured plasma and tissue concentrations of glutathione and glutathione-related enzymes. Animals were 3 months, 12 months, or 24 months old at the time of experiments. Plasma glutathione was found to be significantly increased in both the 12-month-old and 24-month-old groups compared to the 3-month-old rats. Tissue enzyme measurements showed no significant differences between the groups in lung or liver glutathione peroxidase or glutathione S-transferase. gamma-Glutamyl transpeptidase activity was significantly decreased in kidney and lung with aging. Decreases in tissue gamma-glutamyl transpeptidase activity occur with age; this may contribute to increases in plasma glutathione concentrations. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP JENKINSON, SG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU PHS HHS [H-30556] NR 39 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9629 J9 AM J MED SCI JI Am. J. Med. Sci. PD DEC PY 1991 VL 302 IS 6 BP 347 EP 352 DI 10.1097/00000441-199112000-00004 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GU876 UT WOS:A1991GU87600004 PM 1685307 ER PT J AU DEFAVERI, J GRAYBILL, JR AF DEFAVERI, J GRAYBILL, JR TI IMMUNOHISTOPATHOLOGY OF MURINE PULMONARY HISTOPLASMOSIS DURING NORMAL AND HYPERSENSITIVE CONDITIONS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID PNEUMONITIS; MICE; CAPSULATUM; ANTIGENS; LYMPHOCYTES; DEFENSE; CELLS AB Pulmonary histoplasmosis was induced in nonimmunized and immunized Balb-C nu/+ mice. The lung tissue burden of H. capsulatum, histopathology, the size of the inflammatory area, and the numbers of total T lymphocytes and subtypes in situ were evaluated serially after challenge. Over 3 days previously immunized mice developed a large lymphocyte/macrophage inflammatory response. This rapidly decreased in the next 2 wk. In contrast, the nonimmunized control mice developed a predominantly polymorphonuclear infiltrate that evolved more slowly over the first week of infection. This initial response was nonspecific but, after the first week, shifted to lymphocytes and granuloma formation. The lymphocyte infiltration in both immunized and nonimmunized mice was predominantly CD4. Previously immunized mice had a rapid decrease in tissue counts of H. capsulatum after Day 3, but nonimmunized mice continued to have increased counts through Day 7 after infection. These studies reproduce in the mouse model a host response similar to acute reinfection histoplasmosis in the human. In this condition an intense cell-mediated inflammatory response is thought to be elicited by fungal antigens and to represent host reaction rather than fungal replication. Our experimental model added new information relevant to the understanding of the pathogenesis of this process. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV ESTADO SAO PAULO,BOTUCATU MED SCH,DEPT PATHOL,SAO PAULO,BRAZIL. RP GRAYBILL, JR (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 27 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 DEC PY 1991 VL 144 IS 6 BP 1366 EP 1372 PG 7 WC Respiratory System SC Respiratory System GA GU988 UT WOS:A1991GU98800026 PM 1741551 ER PT J AU SANTIAGO, S TOBIAS, J WILLIAMS, AJ AF SANTIAGO, S TOBIAS, J WILLIAMS, AJ TI A REAPPRAISAL OF THE CAUSES OF HEMOPTYSIS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID FIBEROPTIC BRONCHOSCOPY AB We reviewed the records of 264 patients who underwent fiberoptic bronchoscopy for unexplained hemoptysis to determine the various causes of hemoptysis. Bronchogenic carcinoma (29%), bronchitis (23%), and idiopathic hemoptysis (22%) accounted for the majority of causes of hemoptysis. In contrast to older studies, the incidence of hemoptysis secondary to tuberculosis and bronchiectasis has decreased. Although our patient population is predominantly male and elderly, our data may well be representative of more recent epidemiologic trends in causes of hemoptysis. C1 UNIV CALIF LOS ANGELES,SCH MED,PULM DIS SECT,LOS ANGELES,CA 90024. RP SANTIAGO, S (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,LOS ANGELES,CA 90073, USA. NR 10 TC 61 Z9 65 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD DEC PY 1991 VL 151 IS 12 BP 2449 EP 2451 DI 10.1001/archinte.151.12.2449 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA HF433 UT WOS:A1991HF43300015 PM 1747002 ER PT J AU RUCKDESCHEL, JC MOORES, D LEE, JY EINHORN, LH MANDELBAUM, I KOELLER, J WEISS, GR LOSADA, M KELLER, JH AF RUCKDESCHEL, JC MOORES, D LEE, JY EINHORN, LH MANDELBAUM, I KOELLER, J WEISS, GR LOSADA, M KELLER, JH TI INTRAPLEURAL THERAPY FOR MALIGNANT PLEURAL EFFUSIONS - A RANDOMIZED COMPARISON OF BLEOMYCIN AND TETRACYCLINE SO CHEST LA English DT Article ID INTRACAVITARY BLEOMYCIN; MANAGEMENT; PLEURODESIS AB Between December 1985 and August 1988, there were 115 patients at 13 centers who were entered on a randomized comparison of tetracycline and bleomycin for treatment of malignant pleural effusions. Fifteen patients were not treated, primarily due to rapid progression of systemic cancer. Fifteen patients entered on a high-dose regimen of bleomycin (120 units) were excluded from this analysis (following early closure of that arm), leaving 85 patients randomized to low-dose bleomycin (60 units; 44 patients) or tetracycline (1 g; 41 patients). Patients were required to have a cytologically positive pleural effusion, good performance status (0, 1, or 2), lung reexpansion following tube thoracostomy with drainage rates of 100 ml/24 or less, no prior intrapleural therapy, no prior systemic bleomycin therapy, no chest irradiation, and no recent (four weeks) change in systemic therapy. A total of 11 patients (five with bleomycin and six with tetracycline) were not evaluable due to technical problems with tube drainage (one), loss to follow-up (two), sudden death due to pulmonary embolus (one), and rapid progression of systemic disease (seven). There were no clinically significant differences in demographic factors, primary site, performance status, or presence of metastases other than pleural effusion. Overall survival did not differ between the two groups. Median time to recurrence or progression of the effusion was 32 days for tetracycline-treated patients and at least 46 days for bleomycin-treated patients (p = 0.037). The recurrence rate within 30 days of instillation was 36 percent (10/28) with bleomycin and 67 percent (18/27) with tetracycline (p = 0.023) (not all patients were restudied in the first 30 days). By 90 days the corresponding recurrence rates were 30 Percent (11/37) for bleomycin and 53 percent (19/36) for tetracycline (p = 0.047). Toxicity was similar between groups. C1 UNIV ALABAMA,DIV BIOSTAT,BIRMINGHAM,AL 35294. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. INDIANA UNIV,INDIANAPOLIS,IN 46204. BRISTOL MYERS US,PHARMACEUT GRP,EVANSVILLE,IN. RP RUCKDESCHEL, JC (reprint author), UNION UNIV,ALBANY,NY 12208, USA. NR 30 TC 109 Z9 112 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD DEC PY 1991 VL 100 IS 6 BP 1528 EP 1535 DI 10.1378/chest.100.6.1528 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GU051 UT WOS:A1991GU05100013 PM 1720370 ER PT J AU KOMADINA, KH SCHENK, DA LAVEAU, P DUNCAN, CA CHAMBERS, SL AF KOMADINA, KH SCHENK, DA LAVEAU, P DUNCAN, CA CHAMBERS, SL TI INTEROBSERVER VARIABILITY IN THE INTERPRETATION OF PULMONARY-ARTERY CATHETER PRESSURE TRACINGS SO CHEST LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; CRITICALLY ILL PATIENTS; WEDGE PRESSURE; HEMODYNAMIC STATUS; HEART; EXPERIENCE; FREQUENCY; BLOOD AB Study objective: We evaluated the ability of three independent reviewers (R1, R2, R3) using waveform analysis to accurately identify confirmed valid PCWP tracings, and their ability to consistently report the PCWP numerical value. Design: Sixty PA and PCWP tracings were prospectively obtained and blindly reviewed by three independent critical care physicians. Setting: The medical ICU of Wilford Hall USAF Medical Center. Patients or participants: Twenty mechanically ventilated patients with PA catheters inserted for hemodynamic assessment. Interventions: Sixty PA and PCWP tracings were reviewed blindly and independently for acceptability using waveform criteria by three critical care physicians. While recording all 60 tracings, blood was aspirated from the distal port of the PA catheter with the balloon "wedged" and blood gas analysis was done. Each reviewer analyzed the PCWP tracings for validity using waveform criteria, and reported a numerical PCWP reading for those tracings judged valid by waveform criteria. Reviewer sensitivity, specificity and accuracy in performing waveform analysis were assessed by comparing their predictions with those tracings that were confirmed valid by the aspiration of pulmonary capillary blood. Inter-reviewer agreement upon which validity of PCWP tracings was based and reviewer agreement on the numerical PCWP reading were also assessed. All tracings were blindly reviewed by each physician, first without and then with an AP tracing to define end-expiration. Measurements and results: Thirty-eight of 60 PCWP tracings were confirmed valid by the aspiration of pulmonary capillary blood. In the remaining 22 tracings, mixed venous blood was aspirated with the balloon wedged, and tracing validity was unconfirmed. Reviewer accuracy in identifying confirmed valid PCWP tracings, using waveform analysis, was 50 percent for R1, 65 percent for R2 and 57 percent for R3. No reviewer's accuracy was significantly different from a random guess which would yield an accuracy of 50 percent. Agreement by all three reviewers in identifying valid PCWP tracings using waveform analysis varied from 37 percent in the absence of an AP tracing to 66 percent when an AP tracing was available to identify end-expiration (p < 0.003). Agreement by all three reviewers on the PCWP numerical reading (within 4 mm Hg) was 79 percent without an AP tracing and 96 percent with an AP tracing (p = NS). The numerical reading reported by the ICU nurses and house staff correlated closely with the reviewers' readings. Agreement with the reported PCWP reading was improved only for R2 by the addition of an AP tracing. Conclusion: We conclude that the validation of PCWP tracings by waveform analysis is subject to interobserver variability, and reviewer accuracy in identifying confirmed valid tracings was no better than a random guess. Agreement on the numerical PCWP reading was high among the reviewers as was agreement by each individual reviewer with the reported PCWP. Finally, the presence of an AP tracing, to define end-expiration, adds little to the interpretation of the PCWP numerical reading by experienced physicians. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,PULM CRIT CARE SECT,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,CARDIOL SECT,LACKLAND AFB,TX 78236. WILFORD HALL USAF MED CTR,PULM CRIT CARE SECT,LACKLAND AFB,TX 78236. RP KOMADINA, KH (reprint author), PARK NICOLLET MED CTR,5000 W 39TH ST,MINNEAPOLIS,MN 55416, USA. NR 19 TC 37 Z9 42 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD DEC PY 1991 VL 100 IS 6 BP 1647 EP 1654 DI 10.1378/chest.100.6.1647 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GU051 UT WOS:A1991GU05100033 PM 1959409 ER PT J AU BRYAN, CL COHEN, DJ DEW, JA TRINKLE, JK JENKINSON, SG AF BRYAN, CL COHEN, DJ DEW, JA TRINKLE, JK JENKINSON, SG TI GLUTATHIONE DECREASES THE PULMONARY REIMPLANTATION RESPONSE IN CANINE LUNG AUTOTRANSPLANTS SO CHEST LA English DT Article ID OXIDATIVE STRESS; RAT LUNG; TRANSPLANTATION; HEART; PRESERVATION; REPERFUSION; DISULFIDE; ISCHEMIA; STORAGE; DAMAGE AB The pulmonary reimplantation response (PRR) is a form of membrane permeability pulmonary edema occurring in lung transplants. The severity of the PRR reflects the quality and duration of lung graft preservation. Free radicals formed during ischemia with reperfusion in the autotransplanted dog lung may play a role in producing PRR. We hypothesized that the addition of reduced glutathione (GSH) to the preservative solution could decrease PRR if hydroperoxides are being formed. Six dogs underwent left lung autotransplantation after the lung was flushed with Euro-Collins solution (EC). These dogs demonstrated radiographic and histopathologic evidence of bilateral pulmonary edema, greatest in the transplanted left lung. They also had increases in lung wet to dry weight (W/D) ratios in both lungs (left, 12.0 +/- 0.9; right, 10.1 +/- 0.8) as compared with a group of five unmanipulated control animals (left, 6.0 +/- 0.5; right, 7.0 +/- 0.4). Malondialdehyde (MDA) concentrations were significantly increased in the transplanted left lungs (14 +/- 4) from this group as compared with the controls (5 +/- 7). Five additional dogs underwent left lung autotransplantation with GSH added to the EC cryopreservation fluid. These animals did not develop histologic or radiographic evidence of pulmonary edema, and W/D ratios as well as MDA concentrations were not different from those in controls. To evaluate the effect of ischemia alone on changes in lung GSH concentrations, ten additional dogs underwent left pneumonectomy. Left lungs were cryopreserved in EC + GSH. In five of the animals, the right lung was removed and preserved in EC alone. In the other five animals, the right lung remained in vivo for 3 h and was then removed. Lung GSH concentrations were doubled after 3 h of ischemia when incubated in EC + GSH compared to in vivo controls and to EC-treated lungs. These data suggest that GSH added to the preservation fluid prevents PRR following transplantation and that lung GSH concentrations actually increase during preservation prior to reimplantation and reperfusion if the lung graft is exposed to GSH in the preservation fluid. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. USAF,WILFORD HALL MED CTR,LACKLAND AFB,TX 78236. UNIV TEXAS,HLTH SCI CTR,DEPT MED,LUNG METAB UNIT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. RP BRYAN, CL (reprint author), DIV PULM DIS,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 40 TC 18 Z9 19 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD DEC PY 1991 VL 100 IS 6 BP 1694 EP 1702 DI 10.1378/chest.100.6.1694 PG 9 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GU051 UT WOS:A1991GU05100040 PM 1959416 ER PT J AU BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G AF BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G TI A RANDOMIZED TRIAL OF AMBULATORY CARE IN THE 3RD YEAR CLERKSHIP 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 1991 VL 39 IS 4 BP A883 EP A883 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200468 ER PT J AU BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG AF BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG TI CYSTINE TRANSPORT IS NOT INDUCED IN ALVEOLAR TYPE-II CELLS STRESSED BY ARSENITE OR DIETHYLMALEATE (DEM) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,AUDIE L MURPHY VET ADM HOSP,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78285. 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 1991 VL 39 IS 4 BP A813 EP A813 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200095 ER PT J AU CROW, SE LICHTENSTEIN, MJ TULEY, MR MASCARENHAS, C AF CROW, SE LICHTENSTEIN, MJ TULEY, MR MASCARENHAS, C TI OBSERVER VARIABILITY AND ENVIRONMENTAL NOISE IN SCREENING FOR HEARING-LOSS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,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 1991 VL 39 IS 4 BP A884 EP A884 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200473 ER PT J AU GERETY, MB KADRI, AA CROW, S CHIODO, LK KANTEN, DN MULROW, CD AF GERETY, MB KADRI, AA CROW, S CHIODO, LK KANTEN, DN MULROW, CD TI SCREENING TOOLS FOR DEPRESSION IN NURSING-HOME RESIDENTS 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 1991 VL 39 IS 4 BP A884 EP A884 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200475 ER PT J AU GREENE, KE BRYAN, CL UTSET, OM ROODMAN, D JENKINSON, SG AF GREENE, KE BRYAN, CL UTSET, OM ROODMAN, D JENKINSON, SG TI LUNG INFLAMMATION AND FIBROSIS IN MICE CHRONICALLY EXPOSED TO TNF-ALPHA 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 1991 VL 39 IS 4 BP A846 EP A846 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200277 ER PT J AU LAWRENCE, VA HILSENBECK, SG PAGE, CP TULEY, MR AF LAWRENCE, VA HILSENBECK, SG PAGE, CP TULEY, MR TI PREDICTING OPERATIVE PULMONARY RISK 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 1991 VL 39 IS 4 BP A885 EP A885 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200483 ER PT J AU LEVINE, SM ANZUETO, A BRYAN, CL PETERS, JI ZAMORA, CA CALHOON, JH TRINKLE, JK JENKINSON, SG AF LEVINE, SM ANZUETO, A BRYAN, CL PETERS, JI ZAMORA, CA CALHOON, JH TRINKLE, JK JENKINSON, SG TI SINGLE LUNG TRANSPLANTATION IN PATIENTS WITH SYSTEMIC-DISEASE SO CLINICAL RESEARCH 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 SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A867 EP A867 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200390 ER PT J AU LICHTENSTEIN, MJ GRIFFIN, MR RAY, WA TULEY, MR AF LICHTENSTEIN, MJ GRIFFIN, MR RAY, WA TULEY, MR TI FACTORS ASSOCIATED WITH IN-HOSPITAL HIP-FRACTURES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX 78284. VANDERBILT UNIV,DEPT PREVENT MED,NASHVILLE,TN 37240. 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 1991 VL 39 IS 4 BP A886 EP A886 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200484 ER PT J AU MORALES, C ANDRADE, F ANZUETO, A LEVINE, S MAXWELL, L JENKINSON, S AF MORALES, C ANDRADE, F ANZUETO, A LEVINE, S MAXWELL, L JENKINSON, S TI DIETHYLMALATE IMPAIRS DIAPHRAGMATIC FUNCTION DURING INSPIRATORY RESISTIVE BREATHING SO CLINICAL RESEARCH 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. USAF,WILFORD HALL MED CTR,LACKLAND AFB,TX 78236. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A868 EP A868 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200393 ER PT J AU ROSSRUCKER, J BRYAN, C CALHOON, J JENKINSON, S AF ROSSRUCKER, J BRYAN, C CALHOON, J JENKINSON, S TI GLUTATHIONE DIMINISHES THE PULMONARY REIMPLANTATION RESPONSE IN CANINE LUNG AUTOTRANSPLANTATION AFTER 24 HOURS OF ISCHEMIC CRYOPRESERVATION 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 1991 VL 39 IS 4 BP A868 EP A868 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200394 ER PT J AU TILLIS, W BRYAN, C CHAMBERS, S DENEKE, S LAWRENCE, R JENKINSON, S AF TILLIS, W BRYAN, C CHAMBERS, S DENEKE, S LAWRENCE, R JENKINSON, S TI CATALASE ACTIVITY IN MESOTHELIAL CELLS, FIBROBLASTS, AND TYPE-II CELLS IS ASSOCIATED WITH VARIABLE RESISTANCE TO OXIDANT STRESS 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. USAF,WILFORD HALL MED CTR,LACKLAND AFB,TX 78236. 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 1991 VL 39 IS 4 BP A812 EP A812 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200092 ER PT J AU MOSS, JT KADMON, D AF MOSS, JT KADMON, D TI BCG AND THE TREATMENT OF SUPERFICIAL BLADDER-CANCER SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Review ID BACILLUS-CALMETTE-GUERIN; TRANSITIONAL CELL-CARCINOMA; LIVING MYCOBACTERIUM-BOVIS; TRANS-URETHRAL RESECTION; INTRAVESICAL MITOMYCIN-C; LYMPH-NODE METASTASES; DISEASE-FREE INTERVAL; TUMOR NECROSIS FACTOR; MALIGNANT-MELANOMA; RANDOMIZED TRIAL AB In this report, we review the evolution of bacillus Calmette-Guerin (BCG) immunotherapy as a legitimate form of treatment in superficial, nonmuscle-invasive bladder cancer. In the US, an estimated 45 000 new cases of bladder cancer are diagnosed each year and the annual death rate approaches 11 000. Approximately 70 percent of these cancers are superficial at the time of initial presentation. The treatment of superficial bladder cancer has three objectives: (1) eradication of existing disease, (2) prophylaxis against tumor recurrence, and (3) prevention of tumor progression (either muscular invasion, metastatic spread, or both). Cystectomy generally is reserved for muscle-invasive disease. Transurethral resection of the bladder tumor is the preferred initial therapy. Intravesical instillations of various chemotherapeutic agents following transurethral resection have been extensively investigated. Some of the common agents used include thiotepa, mitomycin, and doxorubicin. Despite such treatment efforts, however, over 40 percent of patients with superficial bladder cancer experience a recurrence of their tumor within three years. Approximately half of these recurrences either present as less-well-differentiated tumors or have already penetrated into the bladder musculature, metastasized, or both. Since Morales et al. first introduced intravesical BCG vaccine for prophylaxis as well as for treatment of superficial bladder tumors in 1976, support has grown rapidly for its use as an alternative to chemotherapy. When used with prophylactic intent following transurethral resection, recurrence rates are lower than those achieved with other agents. In addition, BCG is emerging as the consensus drug of choice for treating carcinoma in situ of the bladder. The mechanisms by which BCG exerts its antitumor activity remain largely unknown. BCG is thought to stimulate a localized, nonspecific inflammatory response that leads to subsequent shedding of tumor cells. A large body of clinical and experimental data suggest an association between the development of an immunologic response to BCG and successful antitumor activity. No universally accepted therapeutic regimen has been agreed upon. One regimen commonly used consists of an ampul of BCG mixed with 50 mL of NaCl 0.9%, instilled once a week for six weeks and retained for two hours prior to voiding. Maintenance therapy generally consists of intravesical doses given at three-month cycles for at least two years of recurrence-free follow-up. Because BCG is a biologic agent, the commercially available products may differ in weight, colony-forming units per vial, and antigenicity. How these product characteristics affect clinical responsiveness to different strains of BCG remains unanswered. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. BAYLOR COLL MED,SCOTT DEPT UROL,HOUSTON,TX 77030. RP MOSS, JT (reprint author), DEPT VET AFFAIRS MED CTR,PHARM SERV 119,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 183 TC 5 Z9 5 U1 0 U2 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD DEC PY 1991 VL 25 IS 12 BP 1355 EP 1367 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GV254 UT WOS:A1991GV25400017 PM 1815434 ER PT J AU CABALLERIA, J BARAONA, E DEULOFEU, R HERNANDEZMUNOZ, R RODES, J LIEBER, CS AF CABALLERIA, J BARAONA, E DEULOFEU, R HERNANDEZMUNOZ, R RODES, J LIEBER, CS TI EFFECTS OF H-2-RECEPTOR ANTAGONISTS ON GASTRIC ALCOHOL-DEHYDROGENASE ACTIVITY SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE H-2-RECEPTOR ANTAGONISTS; CIMETIDINE; RANITIDINE; NIZATIDINE, FAMOTIDIN; ETHANOL; STOMACH; ALCOHOL DEHYDROGENASE ID HUMAN GASTROINTESTINAL-TRACT; H2-RECEPTOR ANTAGONISTS; LIVER ALCOHOL; ETHANOL; CIMETIDINE; RAT; FAMOTIDINE; METABOLISM; HISTAMINE; LOCALIZATION AB Inhibition of gastric alcohol dehydrogenase (ADH) activity by cimetidine results in elevated blood levels of ethanol after moderate consumption. To search for alternative H2-blockers lacking such an effect, we compared cimetidine, ranitidine, nizatidine, and famotidine. They inhibited rat gastric ADH noncompetitively, with a K(i) for ethanol oxidation of 0.68 mM for cimetidine, 0.5 mM for ranitidine, 1 mM for nizatidine, and 4.5 mM for famotidine. These concentrations are higher than therapeutic plasma levels, but intracellular concentrations in the gastric mucosa (assessed with [H-3]cimetidine and [C-14]famotidine) were at least 10- and 2-fold greater than in the blood, respectively. These results suggests that, given at therapeutic doses in vivo, the degree of inhibition by cimetidine and ranitidine should be significant and comparable, that by nizatidine should be smaller, and that by famotidine should be negligible. These drugs also exerted either mixed or competitive inhibition of rat hepatic ADH, but the effects of cimetidine and famotidine were observed at concentrations unlikely to occur in vivo. Thus, in alcoholics and in social drinkers who require treatment with H2-receptor antagonists, famotidine might be preferable to the other H-2 blockers tested. C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151-G,130 W KINGSBRIDGE RD,NEW YORK,NY 10468. CUNY,MT SINAI SCH MED,NEW YORK,NY 10468. HOSP CLIN BARCELONA,LIVER UNIT,BARCELONA 36,SPAIN. HOSP CLIN BARCELONA,BIOCHEM LAB,BARCELONA 36,SPAIN. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151-G,130 W KINGSBRIDGE RD,NEW YORK,NY 10468, USA. FU NIAAA NIH HHS [AA 03508] NR 28 TC 58 Z9 58 U1 0 U2 3 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD DEC PY 1991 VL 36 IS 12 BP 1673 EP 1679 DI 10.1007/BF01296608 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GV255 UT WOS:A1991GV25500003 PM 1684149 ER PT J AU LEIGHTON, JA BAY, MK MALDONADO, AL SCHENKER, S SPEEG, KV AF LEIGHTON, JA BAY, MK MALDONADO, AL SCHENKER, S SPEEG, KV TI COLCHICINE CLEARANCE IS IMPAIRED IN ALCOHOLIC CIRRHOSIS SO HEPATOLOGY LA English DT Article ID PRIMARY BILIARY-CIRRHOSIS; TRIAL; PHARMACOKINETICS; VOLUNTEERS; LIVER AB Colchicine may have benefit in primary biliary cirrhosis and alcoholic liver disease. It is currently used in patients with impaired liver function, yet little is known about its elimination in such patients. Colchicine clearance in the rat is significantly impaired in various models of liver disease. To study this in human beings, colchicine pharmacokinetics were compared in normal subjects and patients with alcoholic cirrhosis. Colchicine clearance was impaired in the cirrhotic patients. Normal subjects had a mean clearance of 10.65 +/- 1.82 ml/min.kg, whereas cirrhotic patients had a mean clearance of 4.22 +/- 0.45 ml/min.kg (p < 0.01). The half-life was 57.4 +/- 14.2 min in control subjects vs. 114.4 +/- 19.7 min in cirrhotic patients (p = 0.054). Volume of distribution was not different in the two groups (0.718 +/- 0.1 L/kg in control subjects; 0.716 +/- 0.158 L/kg in cirrhotic patients, p > 0.99). No correlation was seen between colchicine clearance and bilirubin, albumin, prothrombin time or Child-Pugh classification, but this may be the result of the small number of patients studied. Based on the values measured, it is estimated that colchicine steady state would change from an average 1.12 ng/ml in normal individuals to 2.82 ng/ml in the cirrhotic patients if 0.6 mg were taken every 12 hr. It is unknown whether this change would be clinically significant. These data show that cirrhosis impairs colchicine clearance and demonstrates that the liver is a major route of colchicine elimination. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. FU NCRR NIH HHS [MO1-RR-01346] NR 15 TC 24 Z9 24 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD DEC PY 1991 VL 14 IS 6 BP 1013 EP 1015 DI 10.1016/0270-9139(91)90121-B PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GT559 UT WOS:A1991GT55900010 PM 1959847 ER PT J AU DEFRONZO, RA BARZILAI, N SIMONSON, DC AF DEFRONZO, RA BARZILAI, N SIMONSON, DC TI MECHANISM OF METFORMIN ACTION IN OBESE AND LEAN NONINSULIN-DEPENDENT DIABETIC SUBJECTS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HEPATIC GLUCOSE-PRODUCTION; INSULIN RESISTANCE; LACTIC-ACIDOSIS; METABOLISM; MELLITUS; THERAPY; HYPERGLYCEMIA; SECRETION; BINDING; MUSCLE AB The effect of metformin on glucose metabolism was examined in eight obese (percent ideal body weight, 151 +/- 9%) and six lean (percent ideal body weight, 104 +/- 4%) noninsulin-dependent diabetic (NIDD) subjects before and after 3 months of metformin treatment (2.5 g/day). Fasting plasma glucose (11.5-8.8 mmol/L), hemoglobin-A1c (9.8-7.7%), oral glucose tolerance test response (20.0-17.0 mmol/L; peak glucose), total cholesterol (5.67-4.71 mmol/L), and triglycerides (2.77-1.52 mmol/L) uniformly decreased (P < 0.05-0.001) after metformin treatment; fasting plasma lactate increased slightly from baseline (1.4 to 1.7 mmol/L; P = NS). Body weight decreased by 5 kg in obese NIDD subjects, but remained constant in lean NIDD. Basal hepatic glucose production declined in all diabetics from 83 to 61 mg/m2.min (P < 0.01), and the decrease correlated (r = 0.80; P < 0.01) closely with the fall in fasting glucose concentration. Fasting insulin (115 to 79 pmol/L) declined (P < 0.05) after metformin. During a 6.9 mmol/L hyperglycemic clamp, glucose uptake increased in every NIDD subject (113 +/- 15 to 141 +/- 12 mg/m2.min; P < 0.001) without a change in the plasma insulin response. During a euglycemic insulin clamp, total glucose uptake rose in obese NIDD subjects (121 +/- 10 to 146 +/- 9 mmol/m2.min; P < 0.05), but decreased slightly in lean NIDD (121 +/- 10 to 146 +/- 0.5; P = NS). Hepatic glucose production was suppressed by more than 80-90% in all insulin clamp studies before and after metformin treatment. In conclusion, metformin lowers the fasting plasma glucose and insulin concentrations, improves oral glucose tolerance, and decreases plasma lipid levels independent of changes in body weight. The improvement in fasting glucose results from a reduction in basal hepatic glucose production. Metformin per se does not enhance tissue sensitivity to insulin in NIDD subjects. The improvement in glucose metabolism under hyperglycemic, but not euglycemic, conditions suggests that metformin augments glucose-mediated glucose uptake. Metformin has no stimulatory effect on insulin secretion. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP DEFRONZO, RA (reprint author), UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV DIABET, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. NR 59 TC 267 Z9 268 U1 3 U2 7 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 1991 VL 73 IS 6 BP 1294 EP 1301 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GW879 UT WOS:A1991GW87900022 PM 1955512 ER PT J AU HARRISON, L TEPLOW, DB RINALDI, M STROBEL, G AF HARRISON, L TEPLOW, DB RINALDI, M STROBEL, G TI PSEUDOMYCINS, A FAMILY OF NOVEL PEPTIDES FROM PSEUDOMONAS-SYRINGAE POSSESSING BROAD-SPECTRUM ANTIFUNGAL ACTIVITY SO JOURNAL OF GENERAL MICROBIOLOGY LA English DT Article ID DUTCH ELM DISEASE; BIOLOGICAL-CONTROL; PV-SYRINGAE; SYRINGOMYCIN; FLUORESCENS; SYRINGOTOXIN; BACTERIA; ROT AB A family of peptide antimycotics, termed pseudomycins, has been isolated from liquid cultures of Pseudomonas syringae, a plant-associated bacterium. These compounds were purified using Amberlite XAD-2 and reverse-phase liquid chromatography. Pseudomycin A, the predominant peptide in a family of four, showed selective phytotoxicity, and had impressive activity against the human pathogen Candida albicans. Amino acid, mass spectroscopic, and comparative electrophoretic and chromatographic analyses revealed that the pseudomycins are different from previously described antimycotics from P. syringae, including syringomycin, syringotoxin and syringostatins. Pseudomycins A-C contain hydroxyaspartic acid, aspartic acid, serine, arginine, lysine and diaminobutyric acid. The molecular masses of pseudomycins A-C, as determined by plasma desorption mass spectrometry, are 1224, 1208 and 1252 Da, respectively. Pseudomycin D, on the other hand, has a molecular mass of 2401 Da and is more complex than pseudomycins A-C. C1 MONTANA STATE UNIV,DEPT PLANT PATHOL,BOZEMAN,MT 59717. CALTECH,BECKMAN INST,PASADENA,CA 91125. CALTECH,DIV BIOL,PASADENA,CA 91125. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 23 TC 47 Z9 50 U1 1 U2 4 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1287 J9 J GEN MICROBIOL JI J. Gen. Microbiol. PD DEC PY 1991 VL 137 BP 2857 EP 2865 PN 12 PG 9 WC Microbiology SC Microbiology GA GX946 UT WOS:A1991GX94600023 PM 1791440 ER PT J AU TEETER, JH KUMAZAWA, T BRAND, JG HONDA, E KALINOSKI, DL SMUTZER, G AF TEETER, JH KUMAZAWA, T BRAND, JG HONDA, E KALINOSKI, DL SMUTZER, G TI AMINO-ACID RECEPTOR CHANNELS IN TASTE CELLS SO JOURNAL OF GENERAL PHYSIOLOGY LA English DT Meeting Abstract C1 MONELL CHEM SENSES CTR,PHILADELPHIA,PA 19104. UNIV PENN,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1295 J9 J GEN PHYSIOL JI J. Gen. Physiol. PD DEC PY 1991 VL 98 IS 6 BP A9 EP A10 PG 2 WC Physiology SC Physiology GA GW479 UT WOS:A1991GW47900026 ER PT J AU RABINOWITZ, JL AF RABINOWITZ, JL TI [2-C-14] 5-FLUOROURACIL METABOLISM TO [(CO2)-C-14] SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE FLUOROURACIL; NOVIKOFF ASCITES; TUMOR TREATMENT; FIBROSARCOMA ID F-19 NMR; PHARMACOKINETICS; INVIVO AB The rate of (CO2)-C-14 production from 2-C-14-5-FU was measured in rats bearing the Novikoff ascites hepatoma. Tracer amounts were injected and (CO2)-C-14 collected over a 6-hour period. As the tumor cells proliferated the rate of 2-C-14-5-FU oxidation decreased markedly over the approximately 12 +/- 2 days between implantation of tumor cells and death. On the day of innoculation of tumor cells, oxidation proceeded nearly linearly until almost 50% of the injected 2-C-14-5-FU was converted to (CO2)-C-14 in about 4 hours. With time after tumor innoculation, the rate of (CO2)-C-14 collection declined; ten days after innoculation only about 27% was oxidized by 4 hours, and at the terminal stage it declined to about 18% over 4 hours. Calculated from the time curves, the time oxidation of 25% of the injected trace dose increased from 88 +/- 27 min to 195 +/- 42 min after ten days, to 300 +/- 59 min at the moribund state after 12 +/- 2 days. Similar decreases in oxidation rate of 5-FU were observed during growth of a solid implanted mammary carcinoma and for two other 2-C-14-labelled pyrimidines, uracil and thymine injected in trace quantities. By comparing cancer subjects with themselves at different time-intervals from the onset of the disease and treatment, it might be possible to guage treatment dosages in the progress of the disease. RP RABINOWITZ, JL (reprint author), UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 14 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD DEC PY 1991 VL 29 IS 12 BP 1277 EP 1282 DI 10.1002/jlcr.2580291203 PG 6 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA GV770 UT WOS:A1991GV77000002 ER PT J AU LEIDENHEIMER, NJ HARRIS, RA AF LEIDENHEIMER, NJ HARRIS, RA TI A TRANSIENT OSMOTIC PERMEABILIZATION METHOD FOR THE INTRODUCTION OF IMPERMEANT MOLECULES INTO FUNCTIONAL BRAIN MEMBRANE-VESICLES SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE BRAIN MEMBRANE VESICLES; MICROSACS; GABA-A RECEPTOR; PHOSPHORYLATION; PERMEABILIZATION ID CALCIUM-TRANSPORT; RECEPTOR FUNCTION; GABAA-RECEPTOR; GAINING ACCESS; RAT-BRAIN; PHOSPHORYLATION; SYNAPTOSOMES; DESENSITIZATION; CELLS AB Mouse brain membrane vesicles (microsacs) were transiently permeabilized by hypo-osmotic shock. This permeabilization method resulted in the encapsulation of both [C-14]sucrose and exogenous alkaline phosphatase. The efficiency of this method was estimated by [C-14]sucrose encapsulation experiments to be approximately 81%. External membrane binding experiments with the lectin [H-3]concanavalin A demonstrate that the microsacs were not inverted by permeabilization. Following permeabilization, the functional integrity of a ligand-gated ion channel, the GABA(A) receptor complex, was investigated. Muscimol-stimulated Cl-36- uptake experiments show that this receptor retains its functional properties including blockade by the receptor antagonist bicuculline and potentiation by the allosteric modulators flunitrazepam and pentobarbital. The osmotic permeabilization technique described here provides several advantages over other permeabilization methods. These advantages include a high trapping efficiency, the encapsulation of not only small solutes but large membrane impermeant compounds such as enzymes and the functional preservation of at least one transmembrane protein. Furthermore, this method does not require specialized equipment and does not result in large, permanent holes in the plasma membrane. C1 DENVER VET AFFAIRS MED CTR, DENVER, CO USA. RP UNIV COLORADO, HLTH SCI CTR, DEPT PHARMACOL, 4200 E 9TH AVE, DENVER, CO 80262 USA. FU NIAAA NIH HHS [AA03527, AA06399] NR 28 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 EI 1872-678X J9 J NEUROSCI METH JI J. Neurosci. Methods PD DEC PY 1991 VL 40 IS 2-3 BP 233 EP 241 DI 10.1016/0165-0270(91)90072-8 PG 9 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA GY148 UT WOS:A1991GY14800017 PM 1666165 ER PT J AU BARDIN, T SCHUMACHER, HR AF BARDIN, T SCHUMACHER, HR TI SHOULD WE TREAT POSTVENEREAL REITERS-SYNDROME BY ANTIBIOTICS SO JOURNAL OF RHEUMATOLOGY LA English DT Editorial Material ID CHLAMYDIA-TRACHOMATIS INFECTIONS; REACTIVE ARTHRITIS; DISEASE C1 UNIV PENN,SCH MED,RHEUMATOL SECT,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA 19104. HOP LARIBOISIERE,CTR VIGGO PETERSEN,RHUMATOL CLIN,F-75475 PARIS 10,FRANCE. NR 30 TC 16 Z9 16 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 DEC PY 1991 VL 18 IS 12 BP 1780 EP 1782 PG 3 WC Rheumatology SC Rheumatology GA HA099 UT WOS:A1991HA09900003 PM 1795310 ER PT J AU ROSENBEK, JC ROBBINS, J FISHBACK, B LEVINE, RL AF ROSENBEK, JC ROBBINS, J FISHBACK, B LEVINE, RL TI EFFECTS OF THERMAL APPLICATION ON DYSPHAGIA AFTER STROKE SO JOURNAL OF SPEECH AND HEARING RESEARCH LA English DT Article DE DYSPHAGIA; THERMAL APPLICATION; STROKE; REHABILITATION C1 UNIV WISCONSIN,SCH MED,DEPT NEUROL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP ROSENBEK, JC (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 21 TC 52 Z9 56 U1 0 U2 1 PU AMER SPEECH-LANG-HEARING ASSN 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 1991 VL 34 IS 6 BP 1257 EP 1268 PG 12 WC Language & Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA GU526 UT WOS:A1991GU52600004 PM 1787707 ER PT J AU SZERLIP, H PALEVSKY, P COX, M BLAZERYOST, B AF SZERLIP, H PALEVSKY, P COX, M BLAZERYOST, B TI RELATIONSHIP OF THE ALDOSTERONE-INDUCED PROTEIN, GP70, TO THE CONDUCTIVE NA+ CHANNEL SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE RENAL EPITHELIAL NA+ TRANSPORT; SODIUM CHANNEL; TOAD URINARY BLADDER (BUFO-MARINUS); GLYCOPROTEINS ID EPITHELIAL SODIUM-CHANNEL; MARINUS URINARY BLADDERS; TOAD BLADDER; HORMONAL-REGULATION; SUBUNIT; PUMP; PERMEABILITY; LOCALIZATION; SPECIFICITY; TRANSPORT AB Although one of the primary effects of aldosterone is to increase apical membrane Na+ conductance, as yet none of the proteins induced by the hormone in renal epithelia have been shown to be related to the conductive Na+ channel. Because the toad urinary bladder aldosterone-induced glycoprotein, GP70, has recently been localized to the apical surface of this Na+ transporting epithelium, whether GP70 is associated with the Na+ channel was examined. The specilicities of a monoclonal antibody used to characterize GP70 (mAb 20) and a polyclonal antibody raised against the purified bovine renal papillary Na+ channel (anti-CH) were compared: GP70 was specifically immunoprecipitated by both mAb 20 and anti-CH. Moreover, the sodium dodecyl sulfate-polyacrylamide gel electrophoresis profile of mAb 20 purified toad urinary bladder membrane preparations was similar to those reported for bovine and A6 cell Na+ channels. Under nonreducting conditions, a single, very large protein was evident; reduction yielded GP70, a 140-kd polypeptide, and a number of minor bands. Interestingly, only GP70 was induced by aldosterone. Thus, GP70 appears to be associated with the toad urinary bladder conductive Na+ channel; whether GP70 is an integral subunit of the channel or whether it functions as a regulatory moiety remains to be determined. Whatever the case, because GP70 is induced by aldosterone, it likely has a central role in Na+ channel modulation. C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. RP SZERLIP, H (reprint author), VET AFFAIRS MED CTR,MED SERV 3,DEPT MED,RENAL ELECTROLYTE SECT,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 31 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD DEC PY 1991 VL 2 IS 6 BP 1108 EP 1114 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA GV914 UT WOS:A1991GV91400008 PM 1663799 ER PT J AU TRODAHL, JN AF TRODAHL, JN TI DENTIST DISCRIMINATION SO MILITARY MEDICINE LA English DT Letter C1 US DEPT VET AFFAIRS,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 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 DEC PY 1991 VL 156 IS 12 BP A12 EP A12 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GV758 UT WOS:A1991GV75800005 ER PT J AU SIEVER, LJ KAHN, RS LAWLOR, BA TRESTMAN, RL LAWRENCE, TL COCCARO, EF AF SIEVER, LJ KAHN, RS LAWLOR, BA TRESTMAN, RL LAWRENCE, TL COCCARO, EF TI CRITICAL ISSUES IN DEFINING THE ROLE OF SEROTONIN IN PSYCHIATRIC-DISORDERS .2. SO PHARMACOLOGICAL REVIEWS LA English DT Article; Proceedings Paper CT CONF ON SEROTONIN AND NEUROPSYCHIATRIC DISORDERS : IMPLICATIONS FOR THE DISCOVERY OF NEW PSYCHOTHERAPEUTIC AGENTS CY OCT 03, 1990 CL HERSHEY, PA SP HOECHST ROUSSEL PHARM ID OBSESSIVE-COMPULSIVE DISORDER; CSF 5-HYDROXYINDOLEACETIC ACID; MAJOR AFFECTIVE-DISORDERS; CONTROLLED CLINICAL-TRIAL; IMIPRAMINE BINDING-SITES; NUCLEUS RAPHE DORSALIS; CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; NEURO-ENDOCRINE; PANIC DISORDER RP SIEVER, LJ (reprint author), MT SINAI MED SCH,BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,130 W KINGSBRIDGE,BRONX,NY 10469, USA. NR 184 TC 105 Z9 106 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-6997 J9 PHARMACOL REV JI Pharmacol. Rev. PD DEC PY 1991 VL 43 IS 4 BP 509 EP 525 PG 17 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GW852 UT WOS:A1991GW85200004 PM 1723206 ER PT J AU LEONG, GB ETH, S AF LEONG, GB ETH, S TI LEGAL AND ETHICAL ISSUES IN ELECTROCONVULSIVE-THERAPY SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID SUPREME-COURT HEARING; PSYCHIATRIC MALPRACTICE; BRAIN-DAMAGE; ECT; CALIFORNIA; RESTRAINT; FORM C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. RP LEONG, GB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV B116A12,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 41 TC 4 Z9 4 U1 1 U2 4 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 DEC PY 1991 VL 14 IS 4 BP 1007 EP 1020 PG 14 WC Psychiatry SC Psychiatry GA HL652 UT WOS:A1991HL65200014 PM 1771147 ER PT J AU DEMETER, JG DEJONG, SA LAWRENCE, AM PALOYAN, E AF DEMETER, JG DEJONG, SA LAWRENCE, AM PALOYAN, E TI ANAPLASTIC THYROID-CARCINOMA - RISK-FACTORS AND OUTCOME SO SURGERY LA English DT Article; Proceedings Paper CT 12TH ANNUAL MEETING OF THE AMERICAN ASSOC OF ENDOCRINE SURGEONS CY APR 14-16, 1991 CL SAN JOSE, CA SP AMER ASSOC ENDOCRINE SURGEONS ID CELL; ANEUPLOIDY; CANCER; GLAND AB Anaplastic thyroid carcinoma, in contrast to well-differentiated thyroid carcinoma, has a dismal prognosis, and little progress has been made in improving survival for this disease. We reviewed our experience during a 23-year period to identify risk factors and possible methods to improve outcome. Between 1966 and 1989, 340 patients with thyroid carcinoma underwent operation. Of these, 17 (5%) were undergoing operative treatment of anaplastic or undifferentiated thyroid carcinoma. The female/male ratio was 3.5:1, and mean age at presentation was 63 years. The most common presenting symptoms included neck mass, voice change, or dysphagia. Unusual presentations included symptomatic bradycardia from compression of the vagus nerve and superior vena cava syndrome. Four patients had a history of well-differentiated thyroid carcinoma. Nine patients had been diagnosed or treated in the past for "goiter" or a neck mass, and four patients had concurrent differentiated thyroid carcinoma associated with the anaplastic tumor. Thus 13 (76%) of 17 patients had a previous thyroid disorder, benign or differentiated malignant, and eight (47%) of 17 patients had previous or concurrent differentiated thyroid carcinoma. At the time of presentation, six patients had unilateral true vocal cord paralysis. At operation, 14 patients had local extension of the tumor and four required tracheostomy. Only five of 12 patients showed response to postoperative radiation therapy. Overall median survival was 12 months, and 13 (76%) of 17 patients died. The two patients alive longer than 12 months had only small foci of anaplastic carcinoma in association with well-differentiated carcinoma. Anaplastic thyroid carcinoma is a locally and systemically aggressive disease, with long-term survival seen only in those with well-localized anaplastic tumor. The major risk factor in this series is a history of previous benign or malignant thyroid disease. Because of this, a more aggressive approach to thyroid masses may be warranted. Long-standing goiters or benign nodules should be followed carefully and considered for resection if they grow or do not respond to medical therapy, and total thyroidectomy for malignant disease may obviate the subsequent development of anaplastic carcinoma. This method of early diagnosis and resection of abnormal thyroid tissue seems to be the only method currently available to improve the nearly uniform fatality of this disease. C1 US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,RES SERV,HINES,IL. LOYOLA UNIV,STRITCH SCH MED,DEPT SURG,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT BIOCHEM,MAYWOOD,IL 60153. NR 20 TC 104 Z9 106 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD DEC PY 1991 VL 110 IS 6 BP 956 EP 963 PG 8 WC Surgery SC Surgery GA GU130 UT WOS:A1991GU13000006 PM 1745983 ER PT J AU DEMETER, JG DEJONG, SA OSLAPAS, R ERNST, K HESSEL, P JAROSZ, H SMITH, M NAYYAR, R LAWRENCE, AM PALOYAN, E AF DEMETER, JG DEJONG, SA OSLAPAS, R ERNST, K HESSEL, P JAROSZ, H SMITH, M NAYYAR, R LAWRENCE, AM PALOYAN, E TI HIGH PHOSPHATE DIET-INDUCED PRIMARY HYPERPARATHYROIDISM - AN ANIMAL-MODEL SO SURGERY LA English DT Article; Proceedings Paper CT 12TH ANNUAL MEETING OF THE AMERICAN ASSOC OF ENDOCRINE SURGEONS CY APR 14-16, 1991 CL SAN JOSE, CA SP AMER ASSOC ENDOCRINE SURGEONS ID PARATHYROID-HORMONE; SECONDARY HYPERPARATHYROIDISM; RATS; METABOLISM; PHOSPHORUS; PREVENTION; CALCIUM; GENESIS; SERUM AB Primary hyperparathyroidism (PHPT) is increasing in incidence and detection, primarily because of the aging of our population and the widespread use of automated serum calcium determination. As a result, a substantial number of "early" cases or "biochemical" PHPT are being detected. The indications for parathyroidectomy in such early cases of PHPT are currently under debate, primarily because of economic issues. These factors underscore the importance of research into the basic mechanisms and natural history of PHPT. We investigated an animal model of diet-induced PHPT that retains two crucial aspects of PHPT: elevation of endogenously produced parathyroid hormone (PTH), accompanied by gross and microscopic changes in the native parathyroid glands. Female Long-Evans rats were divided into six groups of 15 each and fed a control diet (Ca/P of 1:2) or a high-phosphate diet (Ca/P of 1:7) for 1-, 2-, or 3-month intervals. Compared with the control animals, serum PTH levels were elevated at all three time intervals in the experimental group, whereas serum calcium levels were decreased at all time intervals. Serum creatine levels were also elevated at all time intervals, whereas serum phosphorus levels did not change. Parathyroid histopathologic studies demonstrated no change at 1 month, whereas nine of 15 experimental animals showed mild hyperplasia at 2 months and 13 of 14 showed mild to moderate hyperplasia with gland enlargement at 3 months compared with control animals. Histopathologic examination of the kidneys showed no change at 1 month but focal parenchymal inflammation with calcium deposition at 2 and 3 months in the experimental groups. In conclusion, the high-phosphate diet successfully induced the earliest changes of PHPT: elevated PTH levels and parathyroid hyperplasia. However, because renal function was mildly compromised early on, some element of early secondary (renal) hyperparathyroidism may have supervened quickly. Because this model is simple, it may be useful to investigate this complex syndrome further, as well as its natural history and the complications it produces in other organs such as the kidneys. C1 LOYOLA UNIV,STRITCH SCH MED,DEPT SURG,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT BIOCHEM,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,RES SERV,HINES,IL. NR 24 TC 10 Z9 12 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD DEC PY 1991 VL 110 IS 6 BP 1053 EP 1060 PG 8 WC Surgery SC Surgery GA GU130 UT WOS:A1991GU13000019 PM 1745975 ER PT J AU YOUNG, GP TAYLOR, AS AF YOUNG, GP TAYLOR, AS TI CONVERSION OF PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA IN A CHILD WITH A SLOW VERAPAMIL INFUSION - CASE-REPORT AND LITERATURE-REVIEW SO AMERICAN JOURNAL OF EMERGENCY MEDICINE LA English DT Article DE PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA; PEDIATRIC CARDIAC ARRHYTHMIAS; VERAPAMIL; ADENOSINE RP YOUNG, GP (reprint author), PORTLAND VET AFFAIRS MED CTR,EMERGENCY MED SERV,POB 1034 11C4,PORTLAND,OR 97207, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0735-6757 J9 AM J EMERG MED JI Am. J. Emerg. Med. PD NOV PY 1991 VL 9 IS 6 BP 603 EP 608 DI 10.1016/0735-6757(91)90123-2 PG 6 WC Emergency Medicine SC Emergency Medicine GA GM672 UT WOS:A1991GM67200019 PM 1834070 ER PT J AU SIMON, PM SKATRUD, JB BADR, MS GRIFFIN, DM IBER, C DEMPSEY, JA GARBER, E LANDRY, D AF SIMON, PM SKATRUD, JB BADR, MS GRIFFIN, DM IBER, C DEMPSEY, JA GARBER, E LANDRY, D TI ROLE OF AIRWAY MECHANORECEPTORS IN THE INHIBITION OF INSPIRATION DURING MECHANICAL VENTILATION IN HUMANS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID CHRONIC RESPIRATORY-FAILURE; BREATHING PATTERN; HYPERCAPNIC VENTILATION; MUSCLE-ACTIVITY; LUNG-VOLUME; ANESTHESIA; SLEEP; PRESSURE; AEROSOL; BREATHLESSNESS AB The purpose of this study was to demonstrate a neuromechanical inhibitory effect on respiratory muscle activity during mechanical ventilation and to determine whether upper and lower airway receptors provide this inhibitory feedback. Several protocols were completed during mechanical ventilation: (1) positive and negative pressure changes in the upper airway, (2) airway anesthesia to examine the consequences of receptor blockade on respiratory muscle activity, (3) increasing FRC with positive end-expiratory pressure to study the effect of hyperinflation or stretch on respiratory muscle activity, and (4) use of heart-lung transplant patients to determine the effects of vagal denervation on respiratory muscle activity. All subjects were mechanically hyperventilated with positive pressure until inspiratory muscle activity was undetectable and the end-tidal PCO2 decreased to less than 30 mm Hg. End-tidal PCO2 (PET(CO2)) was increased by either adding CO2 to the inspired gas or decreasing tidal volume (50 ml/min). The PET(CO2) where a change in inspiratory muscle activity occurred was taken as the recruitment threshold (PCO2RT). Neuromechanical feedback caused significant inspiratory muscle inhibition during mechanical ventilation, as evidenced by the difference between PCO2RT and PET(CO2) during spontaneous eupnea (45 +/- 4 versus 39 +/- 4 mm Hg) and a lower PCO2RT when tidal volume was reduced with a constant frequency and fraction of inspired CO2. Recruitment threshold was unchanged during positive and negative pressure ventilation, during upper and lower airway anesthesia, and in vagally denervated lung transplant patients. These findings demonstrate that neuromechanical feedback causes highly significant inhibition of inspiratory muscle activity during mechanical ventilation; upper and lower airway receptors do not appear to mediate this effect. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,MADISON,WI 53705. UNIV WISCONSIN,JOHN RANKIN LAB PULM MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT PREVENT MED,MADISON,WI 53706. HENNEPIN CTY MED CTR,DEPT MED,MINNEAPOLIS,MN 55415. FU NHLBI NIH HHS [P01 HL-42242] NR 37 TC 60 Z9 60 U1 0 U2 1 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 NOV PY 1991 VL 144 IS 5 BP 1033 EP 1041 PG 9 WC Respiratory System SC Respiratory System GA GP082 UT WOS:A1991GP08200006 PM 1952428 ER PT J AU WARD, W RICHARDSON, A AF WARD, W RICHARDSON, A TI EFFECT OF AGE ON LIVER PROTEIN-SYNTHESIS AND DEGRADATION SO HEPATOLOGY LA English DT Review ID SENESCENT HUMAN-FIBROBLASTS; TRANSFER-RNA-SYNTHETASES; LABILE ENZYME MOLECULES; AGING HUMAN-FIBROBLASTS; PERFUSED RAT-LIVER; MOUSE-LIVER; DIETARY RESTRICTION; PARENCHYMAL-CELLS; TRANSLATIONAL ACTIVITY; ALTERED DEGRADATION C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG01188, AG01548, AG06819] NR 130 TC 57 Z9 57 U1 1 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 NOV PY 1991 VL 14 IS 5 BP 935 EP 948 DI 10.1002/hep.1840140529 PG 14 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GN098 UT WOS:A1991GN09800028 PM 1937398 ER PT J AU GHASSEMI, M HEYDARI, AR RICHARDSON, A AF GHASSEMI, M HEYDARI, AR RICHARDSON, A TI INDUCTION OF HEAT-SHOCK PROTEINS IN LYMPHOCYTES INCREASES WITH MITOGEN STIMULATION SO IMMUNOLOGY LETTERS LA English DT Article DE HEAT SHOCK; LYMPHOCYTE; HEAT SHOCK PROTEIN; HYPERTHERMIA ID T STRESS RESPONSE; HUMAN HSP70 GENE; HYPERTHERMIC STRESS; EXPRESSION; FAMILY AB The effect of the growth state of a cell on the ability of hyperthermia to induce the synthesis of heat shock proteins (HSPs) was studied in resting and concanavalin A (ConA)-stimulated lymphocytes. Hyperthermia induced the synthesis of hsp 110, hsp 90, hsc 70, and hsp 70 in both resting and ConA-stimulated lymphocytes, and ConA-treatment induced the synthesis of the hsp 90 and hsc 70 at normal temperature. The induction of the synthesis of hsp 110 and hsp 70 by hyperthermia was 3- to 6-fold higher for lymphocytes cultured with ConA for 12 and 24 h than in non-stimulated lymphocytes. Thus, lymphocytes induced to undergo proliferation showed a greater response to hyperthermia than resting lymphocytes. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG 01548] NR 30 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD NOV PY 1991 VL 30 IS 3 BP 333 EP 337 DI 10.1016/0165-2478(91)90047-E PG 5 WC Immunology SC Immunology GA GP587 UT WOS:A1991GP58700010 PM 1800319 ER PT J AU KROLL, MH HARRIS, TS MOAKE, JL HANDIN, RI SCHAFER, AI AF KROLL, MH HARRIS, TS MOAKE, JL HANDIN, RI SCHAFER, AI TI VONWILLEBRAND-FACTOR BINDING TO PLATELET GPIB INITIATES SIGNALS FOR PLATELET ACTIVATION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE THROMBOSIS; ADHESION; PHOSPHOLIPASES; PROTEIN KINASE-C; CALCIUM ID MURINE MONOCLONAL-ANTIBODY; GLYCOPROTEIN-IIB/IIIA COMPLEX; VWF MULTIMERS; FACTOR-VIII; AGGREGATION; CELLS; FIBRINOGEN; INHIBITORS; METABOLISM; PROTEINS AB The hypothesis that von Willebrand factor (vWF) binding to platelet membrane glycoprotein Ib (GpIb) initiates intracellular pathways of platelet activation was studied. We measured the biochemical responses of intact human platelets treated with ristocetin plus vWF multimers purified from human cryo-precipitate. vWF plus ristocetin causes the breakdown of phosphatidylinositol 4,5-bisphosphate, the production of phosphatidic acid (PA), the activation of protein kinase C (PKC), increase of ionized cytoplasmic calcium ([Ca2+]i), and the synthesis of thromboxane A2. PA production, PKC activation, and the rise of [Ca2+]i stimulated by the ristocetin-induced binding of vWF multimers to platelets are inhibited by an anti-GpIb monoclonal antibody, but are unaffected by anti-GpIIb-IIIa monoclonal antibodies. Indomethacin also inhibits these responses without impairing platelet aggregation induced by vWF plus ristocetin. These results indicate that vWF binding to platelets initiates specific intraplatelet signaling pathways. The mechanism by which this occurs involves an arachidonic acid metabolite-dependent activation of phospholipase C after vWF binding to platelet membrane GpIb. This signal then causes PKC activation and increases of [Ca2+]i, which promote platelet secretion and potentiate aggregation. C1 BAYLOR COLL MED,HOUSTON VET AFFAIRS MED CTR,HOUSTON,TX 77030. RICE UNIV,HOUSTON,TX 77251. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL02311, HL35387, HL36045] NR 27 TC 228 Z9 231 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD NOV PY 1991 VL 88 IS 5 BP 1568 EP 1573 DI 10.1172/JCI115468 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GN727 UT WOS:A1991GN72700018 PM 1939645 ER PT J AU LYNN, WA RAETZ, CRH QURESHI, N GOLENBOCK, DT AF LYNN, WA RAETZ, CRH QURESHI, N GOLENBOCK, DT TI LIPOPOLYSACCHARIDE-INDUCED STIMULATION OF CD11B CD18 EXPRESSION ON NEUTROPHILS - EVIDENCE OF SPECIFIC RECEPTOR-BASED RESPONSE AND INHIBITION BY LIPID A-BASED ANTAGONISTS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; ESCHERICHIA-COLI; MURINE SPLENOCYTES; BINDING PROTEINS; HUMAN-MONOCYTES; LPS BINDING; ENDOTOXIN; INDUCTION; CACHECTIN; RELEASE AB Gram-negative bacterial septicemia is a common clinical syndrome resulting, in part, from the activation of phagocytic leukocytes by LPS. By using flow cytometry, we have characterized LPS-induced expression of the beta-2 integrin CD11b/CD18. After exposure to Salmonella minnesota R595 LPS, expression of neutrophil CD11b/CD18 is rapidly upregulated, beginning within 5 min and achieving a peak fluorescence (typically two- to threefold over base line) by 30 min. The increase in CD11b/CD18 expression was similar in kinetics and magnitude to that produced by FMLP, PMA, and human rTNF-alpha. Concentrations of LPS necessary to stimulate a response were as low as 1 ng/ml of R595 LPS; a maximal response was observed between 30 and 100 ng/ml. The upregulation of CD11b/CD18 due to LPS was not interrupted by protein synthesis inhibitors. A group of glucosamine disaccharide lipid A-like molecules: Rhodobacter sphaeroides lipid A, lipid IV(A), KDO2IV(A), and deacylated LPS were able to block the stimulatory effect of LPS. This inhibition was specific for the actions of LPS as stimulation of polymorphonuclear leukocytes (PMN) by FMLP, human rTNF-alpha, PMA, and rewarming were not altered by the disaccharide inhibitors. PMN which were exposed to the specific disaccharide LPS antagonists and then washed, were refractory to stimulation by LPS. The monosaccharide lipid A precursor lipid X also blocked stimulation of neutrophils by LPS, although with a 100-fold reduction in potency. Unlike the disaccharide inhibitors, PMN exposed to lipid X were still responsive to LPS stimulation after washing. The PMN response to LPS was less sensitive in the absence of serum, although upregulation of CD11b/CD18 could still be seen using higher concentrations of LPS. Monoclonal antibody directed against CD14 (clone 3C10), also specifically inhibited LPS induced PMN CD11b/CD18 expression both in the presence and absence of serum. These findings support the hypothesis that LPS stimulates neutrophils by interacting with specific cellular receptors. C1 BOSTON UNIV,BOSTON CITY HOSP,SCH MED,DEPT MED,MAXWELL FINLAND LAB INFECT DIS,ROOM 315,BOSTON,MA 02118. MERCK SHARP & DOHME LTD,DEPT BIOCHEM,RAHWAY,NJ 07065. 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. FU PHS HHS [K11-000840] NR 49 TC 144 Z9 145 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1991 VL 147 IS 9 BP 3072 EP 3079 PG 8 WC Immunology SC Immunology GA GL580 UT WOS:A1991GL58000037 PM 1717586 ER PT J AU BALDWIN, RD AF BALDWIN, RD TI PUTATIVE RADIONUCLIDE FEATURES OF LEFT-VENTRICULAR HYPERTROPHY SO MEDICAL HYPOTHESES LA English DT Article AB Distinctive changes in the left ventricular cavity seen with nuclear ventriculographic studies are described. These changes are postulated to be uniquely associated with left ventricular hypertrophy. RP BALDWIN, RD (reprint author), US DEPT VET AFFAIRS,NUCL MED SERV 115,MED & REG OFF CTR,TOGUS,ME 04330, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD NOV PY 1991 VL 36 IS 3 BP 221 EP 222 DI 10.1016/0306-9877(91)90136-M PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW727 UT WOS:A1991GW72700013 PM 1838575 ER PT J AU BRADLEY, TB AF BRADLEY, TB TI LITERARY RULES AND WRITING SO MILITARY MEDICINE LA English DT Letter RP BRADLEY, TB (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 1991 VL 156 IS 11 BP A6 EP A6 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GP395 UT WOS:A1991GP39500001 ER PT J AU VANKAMMEN, DP AF VANKAMMEN, DP TI THE BIOCHEMICAL BASIS OF RELAPSE AND DRUG RESPONSE IN SCHIZOPHRENIA - REVIEW AND HYPOTHESIS SO PSYCHOLOGICAL MEDICINE LA English DT Review ID PLASMA HOMOVANILLIC-ACID; DOPAMINE-BETA-HYDROXYLASE; THYROTROPIN-RELEASING-HORMONE; EARLY NEUROLEPTIC RESPONSE; PSYCHIATRIC-PATIENTS; CEREBROSPINAL-FLUID; GROWTH-HORMONE; MONOAMINE METABOLITES; ADENYLATE-CYCLASE; LONG-TERM AB This review of the literature suggests that antipsychotic drug response is determined by dopamine (DA) turnover and norepinephrine (NE) activity prior to treatment. The data suggest that NE modulates the DA system. Drug-free psychotic patients with relatively increased DA and NE activity, including release, are more likely to be treatment responsive, while patients who show evidence of enhanced DA and NE activity during treatment with antipsychotic drugs are likely to relapse soon after neuroleptic withdrawal. Basal release of DA and NE is decreased and associated with residual positive and negative symptoms. Improvement during neuroleptic treatment is associated with decreases in DA and NE phasic or stimulus induced release. The variable response to antipsychotic drugs is most likely to be a result of dysregulated DA and NE release, i.e. under state-dependent control, rather than evidence of a heterogeneous aetiology. Because catecholamines regulate gain, signal-to-noise ratio and gating in the brain, this model allows for environmental factors to interact with biochemical state and drug treatment. The author proposes that impaired homeostasis of NE and DA in schizophrenia causes instability in NE and DA neuronal firing and release, presumably related to mechanisms down-stream from the receptors, such as G proteins. This instability of catecholamine release may explain the observed variability in clinical states and drug response in schizophrenia. C1 UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,SCH MED,PITTSBURGH,PA 15213. RP VANKAMMEN, DP (reprint author), US DEP VET AFFAIRS,HIGHLAND DR VET ADM MED CTR,PITTSBURGH,PA 15206, USA. FU NIMH NIH HHS [R01-MH44841-01] NR 189 TC 18 Z9 19 U1 4 U2 5 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD NOV PY 1991 VL 21 IS 4 BP 881 EP 895 PG 15 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA GV147 UT WOS:A1991GV14700006 PM 1685791 ER PT J AU BRUMMELSMITH, K AF BRUMMELSMITH, K TI HOME HEALTH-CARE - HOW LONG WILL IT REMAIN LOW TECH SO SOUTHERN CALIFORNIA LAW REVIEW LA English DT Article ID PROGRAM C1 OREGON HLTH SCI UNIV,MED & FAMILY MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 26 TC 0 Z9 0 U1 0 U2 0 PU UNIV SOUTHERN CALIF PI LOS ANGELES PA LAW CENTER UNIV PARK, LOS ANGELES, CA 90089-0071 SN 0038-3910 J9 SOUTHERN CALIF LAW R JI South. Calif. Law Rev. PD NOV PY 1991 VL 65 IS 1 BP 491 EP 502 PG 12 WC Law SC Government & Law GA HF351 UT WOS:A1991HF35100021 PM 11645843 ER PT J AU TERAYAMA, Y MEYER, JS KAWAMURA, J AF TERAYAMA, Y MEYER, JS KAWAMURA, J TI COGNITIVE RECOVERY CORRELATES WITH LONG-TERM INCREASES OF CEREBRAL PERFUSION AFTER HEAD-INJURY SO SURGICAL NEUROLOGY LA English DT Article DE CHRONIC HEAD INJURY; COGNITIVE PROGNOSIS; CEREBRAL BLOOD FLOW ID MULTI-INFARCT DEMENTIA; GLASGOW OUTCOME SCALE; BLOOD-FLOW FLUCTUATE; AUTOREGULATION; INHALATION; PRESSURE AB Prospective measurements of cerebral blood flow (CBF) and Cognitive Capacity Screening Examinations (CCSE) were obtained following head injury among 42 patients for a mean total follow-up interval of 10 years. Clinical data obtained at the time of injury and detailed neurological examinations at each follow-up visit were correlated with serial CBF and CCSE scores. Comparisons of the group of patients who cognitively improved (n = 32) were made with the group that did not (n = 10). Of the total group, 76% showed cognitive improvements for as long as 10 years after injury, with CBF increases toward normal. Predictors for long-term cognitive improvements include: higher initial Glasgow Coma Scales, earlier recovery from coma, absence of signs of brain stem injury, and improvements of cerebral perfusion and autoregulation. Failure to improve correlated with low initial Glasgow Coma Scales, signs of brain stem injury, and persistent impairments of cerebral perfusion. C1 BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,2002 HOLCOMBE BLVD,HOUSTON,TX 77211. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77211. NR 35 TC 7 Z9 7 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0090-3019 J9 SURG NEUROL JI Surg. Neurol. PD NOV PY 1991 VL 36 IS 5 BP 335 EP 342 DI 10.1016/0090-3019(91)90021-Z PG 8 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA GK804 UT WOS:A1991GK80400001 PM 1745957 ER PT J AU ABRUTYN, E BERLIN, JA AF ABRUTYN, E BERLIN, JA TI INTRATHECAL THERAPY IN TETANUS - A METAANALYSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID MUHIMBILI-MEDICAL-CENTRE; DAR-ES-SALAAM; NEONATAL TETANUS; SERUM HORSE; IMMUNOGLOBULIN; SEROTHERAPY; EXPERIENCE; TRIAL AB Objective. - To assess the efficacy of intrathecal therapy with tetanus antibody (antitetanus equine serum or human tetanus immune globulin) in neonatal and adult tetanus using meta-analytical techniques. Data Sources. - Clinical trials identified by searching MEDLINE and by reviewing bibliographies of published articles. Study Selection. - Studies in English with concurrent controls treated without intrathecal therapy Data Extraction. - Data were extracted by one author and verified by the second; conflicts were resolved by discussion. Data Synthesis. - No major treatment effect was found in neonatal tetanus when all studies were considered. A benefit was suggested for antitetanus equine serum in adult disease, but this finding should be accepted with caution. Subgroup analyses were limited in power. Methodological difficulties in neonatal and adult trials were common and safety has not been established. Conclusions. - Intrathecal therapy for tetanus with either antitetanus equine serum or human tetanus immune globulin is not of proven benefit and should only be given in the context of well-designed, controlled trials. C1 UNIV PENN,SCH MED,GEN INTERNAL MED SECT,CLIN EPIDEMIOL UNIT,PHILADELPHIA,PA 19104. RP ABRUTYN, E (reprint author), MED COLL PENN,VET AFFAIRS MED CTR,INFECT DIS SECT,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19129, USA. NR 33 TC 33 Z9 33 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 23 PY 1991 VL 266 IS 16 BP 2262 EP 2267 DI 10.1001/jama.266.16.2262 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GK661 UT WOS:A1991GK66100036 PM 1833565 ER PT J AU GOLENBOCK, DT HAMPTON, RY QURESHI, N TAKAYAMA, K RAETZ, CRH AF GOLENBOCK, DT HAMPTON, RY QURESHI, N TAKAYAMA, K RAETZ, CRH TI LIPID-A-LIKE MOLECULES THAT ANTAGONIZE THE EFFECTS OF ENDOTOXINS ON HUMAN MONOCYTES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIPOPOLYSACCHARIDE-BINDING PROTEINS; MACROPHAGE TUMOR-CELLS; MURINE SPLENOCYTES; INDUCTION; PRECURSORS; CACHECTIN; INVITRO; SITES AB Lipopolysaccharide (LPS) endotoxin is implicated as the bacterial product responsible for the clinical syndrome of Gram-negative septicemia. Although the lipid A domain of LPS appears to be responsible for the toxicity of endotoxin, lipid A from the photosynthetic bacterium Rhodobacter sphaeroides (RSLA) and a disaccharide precursor of lipid A from enteric bacteria, termed lipid IV(A), have little activity on human cells. Using the human promonomyelocytic cell line THP-1 and human monocytic cells, we now show that both lipid IV(A) and RSLA are antagonists of LPS. Complete, apparently competitive, inhibition of LPS activity is possible at a 10-100-fold excess of antagonist, as judged by measuring the release of cytokines and prostaglandin E2. Both antagonists prevent monocyte stimulation by endotoxin extracted from a variety of Gram-negative bacteria. Cells pretreated with either inhibitor and subsequently washed still show attenuated responses to LPS. Stimulation of monocytes by whole Gram-negative bacteria is also antagonized in a dose-dependent manner. Lipid X has no inhibitory effect in the same dose range as lipid IV(A) and RSLA. These findings rule out LPS sequestration as the explanation for the observed antagonism. Neither inhibitor alters monocyte stimulation by phorbol 12-myristate 13-acetate, Staphylococcus aureus, or purified protein derivative, demonstrating specificity for LPS. Although RSLA appears to inhibit LPS when tested with macrophages from both humans and mice, lipid IV(A) had the unique ability to act as an LPS antagonist with human-derived cells but to exhibit LPS-like effects with murine-derived cells. Like LPS, lipid IV(A) Stimulated the release of both tumor necrosis factor-alpha and arachidonic acid from murine-derived RAW 264.7 macrophage tumor cells. The range of concentrations necessary for lipid IV(A) to induce LPS-like effects in murine cells was similar to that necessary to antagonize the actions of LPS in human monocytes. The agonist activities of lipid IV(A) were completely inhibitable by RSLA. This unique species-dependent pharmacology observed with lipid IV(A) may reflect differences between human and murine LPS receptors. RSLA and lipid IV(A) may be useful in defining the role of LPS in Gram-negative bacterial infections and may prove to be prototypical therapeutic agents for the treatment of Gram-negative septicemia. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BIOCHEM,MADISON,WI 53706. MERCK SHARP & DOHME LTD,DEPT BIOCHEM,W POINT,PA 19486. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. RP GOLENBOCK, DT (reprint author), UNIV WISCONSIN HOSP & CLIN,DEPT MED,MADISON,WI 53729, USA. FU NIAID NIH HHS [AI00840]; NIGMS NIH HHS [GM-36054] NR 33 TC 342 Z9 348 U1 2 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 15 PY 1991 VL 266 IS 29 BP 19490 EP 19498 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GK667 UT WOS:A1991GK66700057 PM 1918061 ER PT J AU YAN, X LASKER, JM ROSMAN, AS LIEBER, CS AF YAN, X LASKER, JM ROSMAN, AS LIEBER, CS TI ISOELECTRIC-FOCUSING WESTERN BLOTTING - A NOVEL AND PRACTICAL METHOD FOR QUANTITATION OF CARBOHYDRATE-DEFICIENT TRANSFERRIN IN ALCOHOLICS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Note DE CARBOHYDRATE-DEFICIENT TRANSFERRIN (CDT); ISOELECTRIC FOCUSING; WESTERN BLOTTING; ALCOHOLISM; MARKERS ID SERUM TRANSFERRIN; LIVER; ABUSE; CONSUMPTION; MARKERS; DISEASE; VARIANT; FORMS AB Carbohydrate-deficient transferrin (CDT) has been described as the single, most accurate marker of chronic alcohol consumption. Rapid, sensitive, and specific measurement of serum CDT levels can thus provide important clinical information concerning patient diagnosis and treatment. To date, however, methods used for assessing CDT concentrations [e.g., analytical isoelectric focusing combined with immunofixation and micro anion-exchange chromatography followed by radioimmunoassay (RIA)] have not been practical enough for widespread laboratory application. In the present study, we examined the use of a different technique, namely isoelectric focusing (IEF) combined with Western blotting (IEF/WB). Serum proteins (20-40-mu-g) were first focused according to isoelectric points (pI) on high-resolution agarose IEF gels (ampholyte pH range of 5-8) containing nonionic detergent. The focused proteins were transferred electrophoretically to nitrocellulose filters, and then stained immunochemically with antihuman transferrin IgG. IEF/WB completely resolved CDT (focusing at pI 5.7 and 5.9) from other serum transferring isoforms, as assessed with neuraminidase-generated CDT standards. Computerized densitometric scanning of the immunoblots allowed CDT levels to be quantitated directly rather than as a quotient. Serum CDT content determined by IEF/WB was highly correlated (r2 = 0.962; n = 17) with values determined previously by RIA. In a larger subject group, CDT levels (mg/liter) measured by IEF/WB were 139 +/- 54 in recently-drinking alcoholics (n = 58), 81 +/- 8 in abstaining alcoholics (n = 7), and 68 +/- 16 in healthy control subjects (n = 16). These IEF/WB values for serum CDT are highly similar to those reported using other quantitation methods. Importantly, CDT levels as measured by IEF/WB were not influenced by the severity of liver disease among the recently-drinking alcoholics nor did nondrinkers with liver disease exhibit elevated IEF/WB CDT values. Serum CDT/total transferrin ratios (the latter measured by ELISA) offered no advantage over serum CDT alone to distinguish active and heavy drinking. In conclusion, we have developed a sensitive, accurate, and most importantly, practical method for quantitation of serum CDT, a highly-reliable marker of chronic alcohol consumption. Routine implementation of this technique by clinical laboratories can rapidly provide the physician with a powerful diagnostic tool. C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,130 W KINGSBRIDGE RD,BRONX,NY 10468. MT SINAI MED SCH,NEW YORK,NY 10468. NR 28 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD OCT PY 1991 VL 15 IS 5 BP 814 EP 821 PG 8 WC Substance Abuse SC Substance Abuse GA GL409 UT WOS:A1991GL40900014 ER PT J AU WOLOSCHUK, DMM WERMELING, JR PRUEMER, JM AF WOLOSCHUK, DMM WERMELING, JR PRUEMER, JM TI STABILITY AND COMPATIBILITY OF FLUOROURACIL AND MANNITOL DURING SIMULATED Y-SITE ADMINISTRATION SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE ADDITIVES; ANTINEOPLASTIC AGENTS; CONCENTRATION; DEXTROSE; DIURETICS; FLUOROURACIL; INCOMPATIBILITIES; INJECTIONS; MANNITOL; SODIUM CHLORIDE; STABILITY; VEHICLES ID CISPLATIN; CHEMOTHERAPY; ADMIXTURES; RECURRENT; INFUSION; CANCER; HEAD; NECK AB The stability and compatibility of fluorouracil admixtures with mannitol during simulated Y-site administration was studied. Fluorouracil injection 50 mg/mL was diluted with 5% dextrose injection, 0.9% sodium chloride injection, and 5% dextrose and 0.45% sodium chloride injection to final concentrations of 1 and 2 mg/mL. Combinations of fluorouracil admixtures with 20% mannitol injection were made using equal volumes in glass test tubes; immediately after mixing and at one, two, and four hours, the samples were examined for visual incompatibilities. Duplicate combinations of fluorouracil admixtures with 20% mannitol injection were made using equal volumes in plastic syringes; immediately after mixing with internal standard in glass test tubes and at 2, 4, 8, and 24 hours, samples were removed for chemical analysis. A high-performance liquid chromatographic assay was used to determine fluorouracil concentrations. No evidence of precipitation, color change, or haze was observed. During the 24-hour study, fluorouracil concentrations remained within 6% of initial concentrations for all combinations with mannitol. Fluorouracil 1 and 2 mg/mL in 5% dextrose injection, 0.9% sodium chloride injection, and 5% dextrose and 0.45% sodium chloride injection was chemically stable and visually compatible when combined with 20% mannitol injection during simulated Y-site administration. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL RES LAB,MADISON,WI 53705. UNIV CINCINNATI HOSP,CINCINNATI,OH. RP WOLOSCHUK, DMM (reprint author), HLTH SCI CTR,DEPT PHARMACEUT SERV,ROOM MS-189,820 SHERBROOK ST,WINNIPEG R3A 1RD,MANITOBA,CANADA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD OCT PY 1991 VL 48 IS 10 BP 2158 EP 2160 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GH077 UT WOS:A1991GH07700021 PM 1781472 ER PT J AU DEGROOTKOSOLCHAROEN, J AF DEGROOTKOSOLCHAROEN, J TI PANDEMONIUM OVER GLOVES - USE AND ABUSE SO AMERICAN JOURNAL OF INFECTION CONTROL LA English DT Article RP DEGROOTKOSOLCHAROEN, J (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 0 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 0196-6553 J9 AM J INFECT CONTROL JI Am. J. Infect. Control PD OCT PY 1991 VL 19 IS 5 BP 225 EP 227 DI 10.1016/S0196-6553(05)80252-4 PG 3 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA GK193 UT WOS:A1991GK19300002 PM 1755546 ER PT J AU CHENG, SS PINSON, W LOPEZ, RR CRASS, RA JOHNSON, RS AF CHENG, SS PINSON, W LOPEZ, RR CRASS, RA JOHNSON, RS TI EFFECT OF DONOR-DISSEMINATED INTRAVASCULAR COAGULATION IN LIVER-TRANSPLANTATION SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 62ND ANNUAL SCIENTIFIC SESSION OF THE PACIFIC COAST SURGICAL ASSOC CY FEB 18, 1991 CL PEBBLE BEACH, CA SP PACIFIC COAST SURG ASSOC ID PRESERVATION; GENDER AB It is not known whether disseminated intravascular coagulation, present in a large percentage of organ donors, affects patient outcome after liver transplantation. We reviewed our first 55 liver transplantations and identified 10 donors with disseminated intravascular coagulation. We compared the perioperative courses of the 10 recipients of these transplanted livers with those of 10 matched controls whose donors did not have disseminated intravascular coagulation. Disseminated intravascular coagulation recipients did not require more blood products during or after surgery; their hepatic enzyme levels and prothrombin times after surgery were not statistically significantly higher than those of the controls. There was no difference in hospital stay, number of episodes of rejection, retransplantations, or deaths. The presence of disseminated intravascular coagulation in donors did not adversely affect graft function or patient outcome and should not be a sole criterion for rejecting a liver for transplantation. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT SURG,NASHVILLE,TN 37232. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. OREGON HLTH SCI UNIV,DEPT SURG,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT CLIN PATHOL,PORTLAND,OR 97201. NR 24 TC 3 Z9 3 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD OCT PY 1991 VL 126 IS 10 BP 1292 EP 1296 PG 5 WC Surgery SC Surgery GA GJ524 UT WOS:A1991GJ52400020 PM 1929832 ER PT J AU KALIN, NH SHELTON, SE TAKAHASHI, LK AF KALIN, NH SHELTON, SE TAKAHASHI, LK TI DEFENSIVE BEHAVIORS IN INFANT RHESUS-MONKEYS - ONTOGENY AND CONTEXT-DEPENDENT SELECTIVE EXPRESSION SO CHILD DEVELOPMENT LA English DT Article ID DORSOLATERAL PREFRONTAL CORTEX; INHIBITION; SEPARATION; VARIABLES; SHYNESS; LIFE; CUES; AGE C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP KALIN, NH (reprint author), UNIV WISCONSIN,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [1 RO1 MH-46729, R01 MH046729] NR 40 TC 70 Z9 70 U1 1 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0009-3920 J9 CHILD DEV JI Child Dev. PD OCT PY 1991 VL 62 IS 5 BP 1175 EP 1183 DI 10.1111/j.1467-8624.1991.tb01598.x PG 9 WC Psychology, Educational; Psychology, Developmental SC Psychology GA GR257 UT WOS:A1991GR25700022 PM 1756661 ER PT J AU CHARLAND, SL DICKERSON, RN RAJTER, JJ SETTLE, RG AF CHARLAND, SL DICKERSON, RN RAJTER, JJ SETTLE, RG TI THE EFFECT OF SEPSIS ON HEPATIC CYTOCHROME-P-450 ACTIVITY IN PARENTERALLY FED RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 PHILADELPHIA COLL PHARM & SCI,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RI Dickerson, Roland/C-5185-2008 NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD OCT PY 1991 VL 39 IS 3 BP A682 EP A682 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GF369 UT WOS:A1991GF36900125 ER PT J AU HAMMOND, TG ONORATO, JJ MORRE, DJ BRAZY, PC AF HAMMOND, TG ONORATO, JJ MORRE, DJ BRAZY, PC TI INCREASED SODIUM-DEPENDENT COTRANSPORT IN RENAL BRUSH-BORDER MEMBRANE-VESICLES (BBMVS) PURIFIED BY AQUEOUS 2 PHASE PARTITIONING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. PURDUE UNIV,W LAFAYETTE,IN 47907. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD OCT PY 1991 VL 39 IS 3 BP A771 EP A771 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GF369 UT WOS:A1991GF36900609 ER PT J AU GORELICK, FS AF GORELICK, FS TI PANCREAS - EDITORIAL OVERVIEW SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Editorial Material RP GORELICK, FS (reprint author), US DEP VET AFFAIRS,ADM OFF RES SERV,950 CAMPBELL AVE,W HAVEN,CT 06516, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD OCT PY 1991 VL 7 IS 5 BP 687 EP 690 DI 10.1097/00001574-199110000-00001 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GH010 UT WOS:A1991GH01000001 ER PT J AU ROSELLE, G MENDENHALL, C MORITZ, T WEESNER, R AF ROSELLE, G MENDENHALL, C MORITZ, T WEESNER, R TI IMMUNOLOGICAL PREDICTOR VARIABLES FOR SURVIVAL IN PATIENTS WITH MODERATE AND SEVERE ALCOHOLIC HEPATITIS (AH) SO HEPATOLOGY LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A235 EP A235 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100747 ER PT J AU SPEEG, KV MALDONADO, AL MUIRHEAD, D AF SPEEG, KV MALDONADO, AL MUIRHEAD, D TI THE INVIVO EFFECT OF CYCLOSPORINE (CSA) ON COLCHICINE SECRETION BY THE LIVER CANALICULAR MULTIDRUG TRANSPORTER SO HEPATOLOGY 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 W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A163 EP A163 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100463 ER PT J AU WEESNER, R MENDENHALL, C MORITZ, T ROSELLE, G AF WEESNER, R MENDENHALL, C MORITZ, T ROSELLE, G TI THE CLINICAL-SIGNIFICANCE OF LIVER-SPLEEN SCANS IN PATIENTS WITH MODERATE TO SEVERE ALCOHOLIC HEPATITIS SO HEPATOLOGY LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A236 EP A236 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100753 ER PT J AU KUSARI, J VERMA, US BUSE, JB HENRY, RR OLEFSKY, JM AF KUSARI, J VERMA, US BUSE, JB HENRY, RR OLEFSKY, JM TI ANALYSIS OF THE GENE-SEQUENCES OF THE INSULIN-RECEPTOR AND THE INSULIN-SENSITIVE GLUCOSE TRANSPORTER (GLUT-4) IN PATIENTS WITH COMMON-TYPE NON-INSULIN-DEPENDENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INSULIN RECEPTOR GENE; INSULIN RESISTANCE; INSULIN-SENSITIVE GLUCOSE TRANSPORTER (GLUT-4) GENE; NON-INSULIN-DEPENDENT DIABETES-MELLITUS; POLYMORPHISM; SEQUENCING ID POLYMERASE CHAIN-REACTION; HUMAN SKELETAL-MUSCLE; KINASE-ACTIVITY; ENZYMATIC AMPLIFICATION; MORBIDLY OBESE; PIMA-INDIANS; GENOMIC DNA; NIDDM; RESISTANCE; BINDING AB Insulin resistance is a common feature of non-insulin-dependent diabetes mellitus (NIDDM) and "diabetes susceptibility genes" may be involved in this abnormality. Two potential candidate genes are the insulin receptor (IR) and the insulin-sensitive glucose transporter (GLUT-4). To elucidate whether structural defects in the IR and/or GLUT-4 could be a primary cause of insulin resistance in NIDDM, we have sequenced the entire coding region of the GLUT-4 gene from DNA of six NIDDM patients. Since binding properties of the IRs from NIDDM subjects are normal, we also analyzed the sequence of exons 16-22 (encoding the entire cytoplasmic domain of the IR) of the IR gene from the same six patients. When compared with the normal IR sequence, no difference was found in the predicted amino acid sequence of the IR cytoplasmic domain derived from the NIDDM patients. Sequence analysis of the GLUT-4 gene revealed that one patient was heterozygous for a mutation in which isoleucine (ATC) was substituted for valine (GTC) at position 383. Consequently, the GLUT-4 sequence at position 383 was determined in 24 additional NIDDM patients and 30 nondiabetic controls and all showed only the normal sequence. From these studies, we conclude that the insulin resistance seen in the great majority of subjects with the common form of NIDDM is not due to genetic variation in the coding sequence of the IR-beta-subunit, nor to any single mutation in the GLUT-4 gene. Possibly, a subpopulation of NIDDM patients exists displaying variation in the GLUT-4 gene. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. RP KUSARI, J (reprint author), US DEPT VET AFFAIRS,VET ADM MED CTR,V-111G,3350 LA JOLLA VILLAGE DR,SAN DIEGO,CA 92161, USA. FU NIDDK NIH HHS [DK-33649] NR 44 TC 84 Z9 87 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT PY 1991 VL 88 IS 4 BP 1323 EP 1330 DI 10.1172/JCI115437 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GJ508 UT WOS:A1991GJ50800034 PM 1918382 ER PT J AU SCHILLER, JH LINDSTROM, M WITT, PL HANK, JA MAHVI, D WAGNER, RJ SONDEL, P BORDEN, EC AF SCHILLER, JH LINDSTROM, M WITT, PL HANK, JA MAHVI, D WAGNER, RJ SONDEL, P BORDEN, EC TI IMMUNOLOGICAL EFFECTS OF LEVAMISOLE INVITRO SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE LEVAMISOLE; DUKES C-COLORECTAL CARCINOMA; 5-FLUOROURACIL ID ADJUVANT THERAPY; HUMAN-MONOCYTES; 2',5'-OLIGOADENYLATE SYNTHETASE; INDOLEAMINE 2,3-DIOXYGENASE; THORACIC IRRADIATION; HUMAN-LYMPHOCYTES; RANDOMIZED TRIAL; HODGKINS-DISEASE; GENERATED INVIVO; COLON-CARCINOMA AB Levamisole, an antihelminthic drug with immunological properties, has recently been reported to have antitumor activity when administered with 5-fluorouracil in patients with Duke's C colorectal carcinoma. The mechanism of this antitumor effect is unknown, but has been postulated to be related to levamisole's immunomodulatory properties. To define further the immunomodulatory activities of levamisole, we studied the in vitro effects of levamisole on monocyte and lymphocyte cytotoxicity, activation, and proliferation; induction of cytokine-induced proteins; and expression of tumor-associated antigens. Experiments utilized peripheral blood mononuclear cells from normal donors incubated in the presence of increasing concentrations of levamisole (0.1 to 100-mu-g/ml). Levamisole had no consistent effect on induction of 2',5'-oligoadenylate synthetase activity or indoleamine-2,3-dioxygenase activity, or production of tumor necrosis factor. Levamisole had no effect on monocyte cytotoxicity or expression of HLA-DR, HLA-DQ, HLA-DP, and the Fc receptor. Similarly, levamisole had no significant effect on NK or LAK cytotoxicity or the immunological activation of T-lymphocytes, assessed by expression of CD3, CD4, CD8, CD16, CD25, and CD56. Proliferation of lymphocytes from normal donors, patients with benign polyps, and patients with malignancies, with or without IL-2 or irradiated LS174T cells, was not significantly increased overall. No significant enhancement in the expression of three tumor-associated antigens (880364, NRCO-4, and ING-1) and the intercellular adhesion molecule-1 (ICAM-1) antigen on four human cancer cell lines was observed following in vitro exposure to levamisole. We conclude that levamisole is not a potent modulator of the immune parameters we examined, and that the mechanism behind the unique clinical interaction between levamisole and 5-fluorouracil in colorectal carcinoma remains to be identified. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT BIOSTAT,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT SURG,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT HUMAN ONCOL,MADISON,WI 53705. UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53706. FU NCI NIH HHS [NCI-CM-87215-18] NR 43 TC 19 Z9 19 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD OCT PY 1991 VL 10 IS 5 BP 297 EP 306 DI 10.1097/00002371-199110000-00001 PG 10 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA GH358 UT WOS:A1991GH35800001 PM 1790137 ER PT J AU STRACK, S AF STRACK, S TI FACTOR-ANALYSIS OF MCMI-II AND PACL BASIC PERSONALITY-SCALES IN A COLLEGE SAMPLE SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article ID CLINICAL MULTIAXIAL INVENTORY; ADJECTIVE CHECK LIST; MILLON RP STRACK, S (reprint author), US DEPT VET AFFAIRS,OUTPATIENT CLIN,PSYCHOL SERV 116B,425 S HILL ST,LOS ANGELES,CA 90013, USA. NR 23 TC 12 Z9 12 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0022-3891 J9 J PERS ASSESS JI J. Pers. Assess. PD OCT PY 1991 VL 57 IS 2 BP 345 EP 355 DI 10.1207/s15327752jpa5702_12 PG 11 WC Psychology, Clinical; Psychology, Social SC Psychology GA GG107 UT WOS:A1991GG10700012 PM 16370885 ER PT J AU CLARK, HW AF CLARK, HW TI POLICY AND MEDICAL-LEGAL ISSUES IN THE PRESCRIBING OF CONTROLLED SUBSTANCES SO JOURNAL OF PSYCHOACTIVE DRUGS LA English DT Article DE PRESCRIBING; CHRONIC PAIN; MEDICAL-LEGAL; NATIONAL PRACTITIONER DATA BANK; ELECTRONIC DATA TRANSFER; STATE LAWS; FEDERAL LAWS; OPIOIDS; BENZODIAZEPINES AB The physician who prescribes controlled substances is faced with an array of laws, regulatory policies, and professional attitudes about their use. Prescriptions for these scheduled drugs are furthermore monitored by the pharmacists who dispense them. Certain drugs, such as the opioids and the benzodiazepines, are considered so potentially abusive that special programs have been recommended to track the behavior of physician prescribers. Multiple copy programs have been implemented in some states. More recent proposals recommend electronic data transfer (EDT) of pharmacy information to centralized processing points so that misprescribing physicians and doctor-shopping patients can be identified. Regulators concerned about physician behavior and confronted by demands of nonphysicians to prescribe controlled substances may find EDT a good solution. Physicians should be concerned about being censured for misprescribing, because such actions may lead to inclusion in the National Practitioner Data Bank. With all of the regulatory concerns about controlled substances, those physicians who would employ longterm opioid therapy for their chronic pain patients must follow certain basic guidelines to be able to defend themselves against allegations of deviant professional behavior. Such procedures as conducting a history and physical examination, maintaining a written treatment plan, consulting with knowledgeable colleagues, and assessing for addictive behavior can provide the practitioner with safeguards. C1 SAN FRANCISCO VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBST ABUSE SERV,SUBST ABUSE PROGRAM,SAN FRANCISCO,CA 94121. SAN FRANCISCO VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBST ABUSE SERV,HIV PROGRAM,SAN FRANCISCO,CA 94121. RP CLARK, HW (reprint author), UNIV CALIF SAN FRANCISCO,PSYCHIAT,SAN FRANCISCO,CA 94143, USA. FU NIDA NIH HHS [R18-DA06097] NR 13 TC 7 Z9 7 U1 0 U2 1 PU HAIGHT-ASHBURY PUBL PI SAN FRANCISCO PA 409 CLAYTON ST, SAN FRANCISCO, CA 94117 SN 0279-1072 J9 J PSYCHOACTIVE DRUGS JI J. Psychoact. Drugs PD OCT-DEC PY 1991 VL 23 IS 4 BP 321 EP 328 PG 8 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA HJ339 UT WOS:A1991HJ33900002 PM 1813603 ER PT J AU SHEVCHUK, O BARAONA, E MA, XL PIGNON, JP LIEBER, CS AF SHEVCHUK, O BARAONA, E MA, XL PIGNON, JP LIEBER, CS TI GENDER DIFFERENCES IN THE RESPONSE OF HEPATIC FATTY-ACIDS AND CYTOSOLIC FATTY ACID-BINDING CAPACITY TO ALCOHOL-CONSUMPTION IN RATS SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID CHOLESTEROL ACYLTRANSFERASE; LIVER; PROTEINS; PATHOGENESIS; METABOLISM; INCREASE; ASSAY AB To investigate possible gender differences in the response of hepatic fatty acids and cytosolic fatty acid-binding capacity to ethanol consumption, both female and male rats (41 days of age) were pair fed liquid diets (with a littermate of the same sex) for 28 days. The diets contained 36% of energy either as ethanol or as additional carbohydrate. After ethanol feeding, the hepatic concentration of fatty acids increased 155% in females (P < 0.01), whereas there was only a trend for an increase (22%) in males. This was associated with a much smaller increase of cytosolic fatty acid-binding capacity in females (58%) than in males (161%). Whereas the ethanol-induced increase in fatty acid-binding capacity provided an ample excess of binding sites for the fatty acids in the males, the increase in females was barely sufficient for the binding of the large increase of fatty acids produced by ethanol in the females. The cytosolic protein responsible for this binding, the liver fatty acid-binding protein of the cytosol (L-FABP(c)), also promotes esterification of the fatty acids. In keeping with the postulated role of this protein, the ethanol-induced increases in hepatic triacylglycerols, phospholipids, and cholesterol esters were smaller in females than in males. The gender difference in cholesterol esters was associated with parallel changes in acyl-CoA transferase activity. A possible implication of the relatively small and most likely inadequate increase in liver fatty acid-binding capacity and fatty acid esterification during alcohol consumption in the females is that under these circumstances the risk for development of a potentially deleterious accumulation of fatty acids in the liver is increased, thereby contributing to the enhanced vulnerability of females to alcohol-induced hepatotoxicity. C1 BRONX VET AFFAIRS MED CTR,ALCOHOL RES & TREATMENT CTR,130 W KINGSBRIDGE RD,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,LIVER DIS SECT,BRONX,NY 10468. MT SINAI MED SCH,NEW YORK,NY 10468. FU NIAAA NIH HHS [AA-03508, AA-07275] NR 41 TC 23 Z9 23 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 OCT PY 1991 VL 198 IS 1 BP 584 EP 590 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GF685 UT WOS:A1991GF68500012 PM 1891473 ER PT J AU COLWELL, JA AF COLWELL, JA TI CLINICAL-TRIALS OF ANTIPLATELET AGENTS IN DIABETES-MELLITUS - RATIONALE AND RESULTS SO SEMINARS IN THROMBOSIS AND HEMOSTASIS LA English DT Article; Proceedings Paper CT CHICAGO SATELLITE SYMP OF THE 10TH INTERNATIONAL CONGRESS OF FIBRINOLYSIS - THROMBOSIS AND FIBRINOLYSIS : CURRENT CLINICAL AND THERAPEUTIC ASPECTS CY AUG 02-03, 1990 CL CHICAGO, IL ID ATHEROSCLEROSIS; PATHOGENESIS; ASPIRIN; DIPYRIDAMOLE C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. RP COLWELL, JA (reprint author), US DEPT VET AFFAIRS,CHARLESTON VET ADM MED CTR 151,109 BEE ST,CHARLESTON,SC 29403, USA. NR 25 TC 7 Z9 7 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. PD OCT PY 1991 VL 17 IS 4 BP 439 EP 444 DI 10.1055/s-2007-1002651 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA GX822 UT WOS:A1991GX82200027 PM 1803515 ER PT J AU AAGAARD, J KNES, J MADSEN, PO AF AAGAARD, J KNES, J MADSEN, PO TI PROSTATIC TISSUE-LEVELS OF OFLOXACIN SO UROLOGY LA English DT Article AB The prostatic tissue levels of ofloxacin were determined in 20 patients undergoing transurethral resection of the prostate. Ofloxacin was administered in two separate dosages of 300 mg PO from twenty-two to two hours preoperatively. The ofloxacin plasma concentrations ranged from 3.73 to 1.85-mu-g/mL at the time of surgery, and the tissue concentrations ranged from 4.55 to 1.94-mu-g/mL. The ofloxacin tissue/plasma ratios ranged from 0.9 to 1.2. These findings indicate that ofloxacin may be useful in prophylaxis prior to transurethral prostatic surgery and also in the treatment of bacterial prostatitis. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI 53706. NR 4 TC 7 Z9 7 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD OCT PY 1991 VL 38 IS 4 BP 380 EP 382 DI 10.1016/0090-4295(91)80159-5 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA GJ133 UT WOS:A1991GJ13300023 PM 1755152 ER PT J AU DATTA, AK TAKAYAMA, K NASHED, MA ANDERSON, L AF DATTA, AK TAKAYAMA, K NASHED, MA ANDERSON, L TI AN IMPROVED SYNTHESIS OF TREHALOSE 6-MONO-CORYNOMYCOLATES AND 6,6'-DI-CORYNOMYCOLATES AND RELATED ESTERS SO CARBOHYDRATE RESEARCH LA English DT Article ID CORD-FACTOR ANALOGS; CORYNEBACTERIUM-DIPHTHERIAE; ESCHERICHIA-COLI; 6-O-CORYNOMYCOLOYL-ALPHA,ALPHA-TREHALOSE; PURIFICATION; MONOMYCOLATE; GLYCOLIPIDS; LETHAL; MUTANT AB A simplified synthesis of 6-mono- and 6,6'-di-corynomycolate esters of alpha,alpha-trehalose, and related compounds, was achieved by coupling the (hydroxyl-protected) acids to the partially trimethylsilylated sugar in the presence of dicyclohexylcarbodiimide and 4-dimethylaminopyridine. As acid reactants, (2-RS,3-RS)-3-hydroxy-2-tetradecyloctadecanoic acid (DL-corynomycolic acid) and its 2RS,3SR diastereomer were prepared from methyl palmitate by sequential Claisen condensation, reduction, chromatographic separation, and saponification. Reaction with tert-butylchlorodimethylsilane (imidazole) gave the disubstituted ether-esters. which were converted into the required 3-tert-butyldimethylsilyl ethers by partial hydrolysis. 6-Linked monocorynomycolate was obtained in excellent yield (78%) from the reaction of the RS,SR acid with the known heptakis-O-(trimethylsilyl)trehalose, and in good yield from equimolar portions of RS,RS acid and hexakis-O-(trimethylsilyl)trehalose. An excess (2.5-molar portions) of the RS,RS acid gave the 6,6'-diester (69%). The mono- and di-palmitate were similarly obtained from (Me3Si)6-trehalose. The mono (RS,RS)-(Me3Si)6-trehalose coupling product was partially resolved on a silica gel column into its RR and SS diastereomers, the former corresponding to the naturally occurring trehalose monocorynomycolate. All coupling products were deprotected to free trehalose esters by treatment first with K2CO3 in methanol, then tetrabutylammonium fluoride-trifluoroacetic acid in oxolane. 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 BIOCHEM,MADISON,WI 53706. FU NCRR NIH HHS [RR02031, RR02301]; NIGMS NIH HHS [GM-36054] NR 37 TC 39 Z9 39 U1 2 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD SEP 30 PY 1991 VL 218 BP 95 EP 109 DI 10.1016/0008-6215(91)84089-W PG 15 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA GM858 UT WOS:A1991GM85800009 PM 1802389 ER PT J AU GUNION, MW GRIJALVA, CV TACHE, Y NOVIN, D AF GUNION, MW GRIJALVA, CV TACHE, Y NOVIN, D TI DESTRUCTION OF DIFFERENT FIBER TRACTS UNDERLIES DEVELOPMENT OF LATERAL HYPOTHALAMIC LESION-INDUCED HYPERTHERMIA AND LOSS OF BOMBESIN-INDUCED HYPOTHERMIA SO BRAIN RESEARCH LA English DT Note DE BOMBESIN; CORE BODY TEMPERATURE; FIBER TRANSECTION; HYPERTHERMIA; HYPOTHERMIA; LATERAL HYPOTHALAMUS; LESION; THERMOREGULATION ID MEDIAL BASAL FOREBRAIN; PREOPTIC AREA; RAT; EFFERENTS AB The relative roles of lateral hypothalamic cell bodies and fibers of passage were assessed in the development of lesion-induced hyperthermia and bombesin-induced hypothermia. Electrolytic lesions or discrete fiber transections were combined with intracisternal bombesin injection to show that each of these two thermoregulatory effects involves fibers crossing the borders of the lateral hypothalamus; however, the two effects primarily involve fibers crossing different borders. Thus, the hyperthermia and the abolition of bombesin-induced hypothermia which follow lateral hypothalamic damage appear to result from disruption of separate thermoregulatory pathways. C1 SEPULVEDA VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,SEPULVEDA,CA 91343. UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,CTR ULCER RES & EDUC,LOS ANGELES,CA 90073. FU NIDDK NIH HHS [DK30110]; NIMH NIH HHS [MH00663]; NINDS NIH HHS [NS20660] NR 15 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD SEP 27 PY 1991 VL 560 IS 1-2 BP 326 EP 329 DI 10.1016/0006-8993(91)91252-V PG 4 WC Neurosciences SC Neurosciences & Neurology GA GM832 UT WOS:A1991GM83200046 PM 1760739 ER PT J AU KRANTZ, DD ZIDOVETZKI, R KAGAN, BL ZIPURSKY, SL AF KRANTZ, DD ZIDOVETZKI, R KAGAN, BL ZIPURSKY, SL TI AMPHIPATHIC BETA-STRUCTURE OF A LEUCINE-RICH REPEAT PEPTIDE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID-SEQUENCE; NUCLEAR MAGNETIC-RESONANCE; LIPID-PROTEIN INTERACTIONS; PLATELET GLYCOPROTEIN-IB; CYTOCHROME-C-OXIDASE; RIBONUCLEASE INHIBITOR; TRANSMEMBRANE PROTEIN; CIRCULAR-DICHROISM; ADENYLATE-CYCLASE; PROTEOGLYCAN-II AB Long tandem arrays of a characteristic leucine-rich repeat motif on the order of 24 amino acids in length have been found in the primary structure of an increasing number of proteins. The most striking feature of these repeats is an amphipathic sequence, with leucine as the predominant hydrophobic residue. Based on this amphipathic sequence and the function of the proteins in which they have been found, the repeats have been proposed to be involved in protein-protein and protein-lipid interactions. As a step toward elucidating the structure and biochemical properties of the leucine-rich repeat motif, we have studied a synthetic leucine-rich repeat peptide (LRP32) representing one of the repeats found in Drosophila chaoptin. We have shown that: (i) LRP32 is soluble in aqueous solution but will bind quantitatively to phospholipid vesicles; (ii) LRP32 has a partial beta-structure in aqueous solution and is predominantly a beta-structure in the presence of phospholipid; (iii) LRP32 integrates into lipid bilayers to form 60-angstrom intramembrane particles as seen using freeze-fracture electron microscopy (these putative oligomeric structures appear to contain a central aqueous core as indicated by their ability to generate conductances in planar lipid bilayers); and (iv) LRP32-lipid complexes generate H-2 NMR spectra characteristic of integral membrane proteins. This study is consistent with LRP32 forming an amphipathic beta-sheet. We propose that protein segments containing tandem arrays of leucine-rich repeats also may form amphipathic beta-sheets. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOL CHEM,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,INST MOLEC BIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,BRAIN RES INST,LOS ANGELES,CA 90024. W LOS ANGELES VET ADM HOSP,LOS ANGELES,CA 90024. UNIV CALIF RIVERSIDE,DEPT BIOL,RIVERSIDE,CA 92521. NR 72 TC 59 Z9 60 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 SEP 5 PY 1991 VL 266 IS 25 BP 16801 EP 16807 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GD635 UT WOS:A1991GD63500088 PM 1715870 ER PT J AU OBERLEY, TD SLATTERY, AF GONZALEZ, A LI, SA LI, JJ AF OBERLEY, TD SLATTERY, AF GONZALEZ, A LI, SA LI, JJ TI COMPARATIVE MORPHOLOGICAL AND IMMUNOHISTOCHEMICAL STUDIES OF ESTROGEN PLUS ALPHA-NAPHTHOFLAVONE INDUCED LIVER-TUMORS IN SYRIAN-HAMSTERS AND RATS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HEPATOCELLULAR-CARCINOMA; ORIGIN; CELL AB Syrian hamsters were treated with ethinylestradiol and maintained on a diet containing alpha-naphthoflavone (alpha-NF), a regimen that produces a high incidence of liver tumors. Morphologic analyses (light microscopy, immunoperoxidase studies, and electron microscopy) were performed on livers of these animals. After 4 months of hormone plus alpha-NF treatment, marked hepatocyte cell changes were already present, as demonstrated by loss of eosinophilic staining of hepatocyte cytoplasm. Large multinucleated hepatocytes exhibiting frequent mitoses were observed around central veins. After 5 months of treatment, there was proliferation of bile ducts, and small cells with eosinophilic cytoplasm resembling hepatocytes appeared surrounding these bile ducts. At 7 to 8 months, the first tumor nodules (foci) were seen. Tumor foci in the portal area consisted of small clusters of large cells resembling hepatocytes with irregular nuclei. At the same time, dysplastic glands were identified among proliferating bile ducts. By 8 to 10 months, large tumors were present. These were trabecular hepatocellular carcinomas with widely varying individual cell morphology. Compared with adjacent liver, dysplastic glands in the portal areas, microcarcinomas, and large tumors all showed intense immunostaining for cytokeratin. Rats treated with the same regimen also developed hepatic tumors, but the light and electron microscopy results and immunohistochemical profiles were very different. Altered hepatic foci composed of small hepatocytes were typically prominent; however, malignant tumors did not arise from the portal area. Neither altered foci nor tumors stained significantly for cytokeratin. These data suggest that the biochemical events giving rise to these liver tumors differ between the species studied, despite the animals being exposed to the same treatment regimens. C1 UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53706. VET AFFAIRS MED CTR,PATHOL SERV,SALT LAKE CITY,UT. UNIV UTAH,SCH MED,DEPT PATHOL,SALT LAKE CITY,UT 84112. WASHINGTON STATE UNIV,COLL PHARM,DEPT PHARMACEUT SCI,HORMONAL CARCINOGENESIS LAB,PULLMAN,WA 99164. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,PATHOL SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA41387] NR 9 TC 4 Z9 5 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD SEP PY 1991 VL 139 IS 3 BP 669 EP 679 PG 11 WC Pathology SC Pathology GA GE846 UT WOS:A1991GE84600022 PM 1887866 ER PT J AU ALBERT, MM GRAYBILL, JR RINALDI, MG AF ALBERT, MM GRAYBILL, JR RINALDI, MG TI TREATMENT OF MURINE CRYPTOCOCCAL MENINGITIS WITH AN SCH-39304-AMPHOTERICIN-B COMBINATION SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; SYSTEMIC FUNGAL-INFECTIONS; AMPHOTERICIN-B; CANDIDA-ALBICANS; THERAPY; ASPERGILLOSIS; KETOCONAZOLE; TRIAZOLES; AGENTS AB Cryptococcal meningitis was induced in BALB/c mice by intracerebral infection with Cryptococcus neoformans. Drug therapy was initiated 1 day later, with mice receiving amphotericin B (AMB), SCH 39304, combination therapy, or no drug therapy (controls). Most, but not all, combinations showed additive benefits, significantly prolonging survival and reducing organism counts in tissues compared with those in controls and groups which received the drugs independently. Optimum protection was obtained when a single dose of 10 mg of AMB per kg of body weight was combined with a fairly narrow SCH 39304 dose range. AMB antagonism did not occur with any regimen tested. AMB-azole combinations may be reasonable alternatives for patients who fail standard cryptococcosis therapeutic regimens. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. NR 32 TC 26 Z9 26 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 SEP PY 1991 VL 35 IS 9 BP 1721 EP 1725 PG 5 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA GE362 UT WOS:A1991GE36200005 PM 1952837 ER PT J AU DEMENDEZ, I YOUNG, KR BIGNON, J LAMBRE, CR AF DEMENDEZ, I YOUNG, KR BIGNON, J LAMBRE, CR TI BIOCHEMICAL CHARACTERISTICS OF ALVEOLAR MACROPHAGE-SPECIFIC PEROXIDASE-ACTIVITIES IN THE RAT SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID PERITONEAL-MACROPHAGES; ENDOGENOUS PEROXIDASE; HUMAN-MONOCYTES; ENDOPLASMIC-RETICULUM; DIFFERENTIATION; MYELOPEROXIDASE; INFLAMMATION; INVITRO C1 HOP HENRI MONDOR,INSERM,U139,F-94010 CRETEIL,FRANCE. UNIV ALABAMA,BIRMINGHAM,AL 35294. BIRMINGHAM VET AFFAIRS MED CTR,DIV PULM & CRIT CARE MED,BIRMINGHAM,AL 35294. NR 20 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD SEP PY 1991 VL 289 IS 2 BP 319 EP 323 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA GA870 UT WOS:A1991GA87000017 PM 1654854 ER PT J AU KERN, RS GREEN, MF SATZ, P WIRSHING, WC AF KERN, RS GREEN, MF SATZ, P WIRSHING, WC TI PATTERNS OF MANUAL DOMINANCE IN PATIENTS WITH NEUROLEPTIC-INDUCED MOVEMENT-DISORDERS SO BIOLOGICAL PSYCHIATRY LA English DT Article ID D2 DOPAMINE-RECEPTORS; POSITRON EMISSION TOMOGRAPHY; TARDIVE-DYSKINESIA; LEFT-HANDEDNESS; INDUCED PARKINSONISM; HUMAN-BRAIN; SCHIZOPHRENIA; ASYMMETRY; ASSOCIATION; SYMPTOMS AB To explore the association between patterns of manual dominance and extrapyramidal symptoms we examined 32 chronic schizophrenic inpatients at Camarillo State Hospital for signs of tardive dyskinesia (TD) and neuroleptic-induced parkinsonism (NIP) using clinical rating scales (Abnormal Involuntary Movement Scale and Columbia Unified Parkinsons Disease Rating Scale) and specialized electromechanical instruments. Manual dominance was assessed using an eight-item hand preference demonstration test. Patients were divided into dextral (consistent use of right hand) and nondextral (any use of the left hand) groups. Dextrals showed a higher prevalence of TD than nondextrals on clinical rating measures (p < 0.01). Orofacial ultrasound measures of TD revealed a similar association between TD and handedness. The two handedness groups did not differ on either the clinical or electromechanical measures of NIP. Interestingly, 28 of the 32 patients showed greater left than right facial movement. It is hypothesized that patients with more standard patterns of manual dominance may be at higher risk for TD than those with atypical patterns. C1 W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA. RP KERN, RS (reprint author), UNIV CALIF LOS ANGELES,CAMARILLO STATE HOSP,RES CTR,NEUROPSYCHIAT INST,BOX 6022,CAMARILLO,CA 93011, USA. NR 42 TC 9 Z9 9 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 SEP 1 PY 1991 VL 30 IS 5 BP 483 EP 492 DI 10.1016/0006-3223(91)90310-I PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA GE872 UT WOS:A1991GE87200008 PM 1681944 ER PT J AU FLETCHER, EC SHAH, A QIAN, W MILLER, CC AF FLETCHER, EC SHAH, A QIAN, W MILLER, CC TI NEAR MISS DEATH IN OBSTRUCTIVE SLEEP-APNEA - A CRITICAL CARE SYNDROME SO CRITICAL CARE MEDICINE LA English DT Article DE SLEEP APNEA, OBSTRUCTIVE; CRITICAL CARE; PICKWICKIAN SYNDROME; PULMONARY DISEASE; CHRONIC OBSTRUCTIVE; VENTILATION; MECHANICAL; RESPIRATORY FAILURE; INTUBATION; HYPERSOMNIA; MORTALITY; INTENSIVE CARE UNIT ID MORTALITY; AIRWAY AB Objective: The objective of this study was to alert critical care physicians to the syndrome of obstructive sleep apnea with respiratory failure ("near miss" death) and to elucidate characteristics that might allow earlier recognition and treatment of such patients. Design: We examined clinical and laboratory characteristics of eight patients with obstructive sleep apnea presenting to the ICU with respiratory failure. These characteristics were compared with those of eight stable apnea patients of similar severity but without a history of presentation with respiratory failure. Setting: Medical ICU and pulmonary outpatient clinic at the Houston Veterans Administration Medical Center, a teaching hospital affiliated with Baylor College of Medicine. Patients: Eight patients with obstructive sleep apnea who presented in, or developed, acute respiratory failure requiring tracheal intubation and mechanical ventilation were matched to eight stable obstructive sleep apnea outpatients from the chest clinic. Measurements and Main Results: The records of these 16 patients were reviewed and multiple characteristics that might predict these obstructive sleep apnea patients prone to respiratory failure and death (called the "near miss" death group; n = 8) were examined. The mean age of the near miss group was 57 yrs. All eight patients presented with respiratory acidosis (mean pH 7.22), hypercarbia (mean PaCO2 82 torr [10.9 kPa]), and hypoxemia (mean PaO2 45 torr [6.0 kPa]). Six of the eight patients had concomitant chronic obstructive pulmonary disease as determined by clinical characteristics and spirometry. Predisposing factors included facial trauma, lower respiratory tract infections or bronchospasm, and use of pain medication. All but one of the near miss subjects had awake hypercarbia (mean PaCO2 49 torr [6.5 kPa]) and hypoxemia (mean PaO2 58 torr [7.7 kPa]) during periods of clinical stability while only two controls had concomitant chronic obstructive pulmonary disease and none had hypercarbia. The prevalence of a history of wheezing and prior hospitalization for "respiratory problems" were greater in the near miss group. Once cured of apnea, no patient presented with recurrence of respiratory failure in follow-up ranging from 6 to 80 months, and cor pulmonale recurred in only one patient during subsequent onset of central apneas. Conclusion: Patients with obstructive sleep apnea who have concomitant chronic obstructive pulmonary disease or hypercarbia and hypoxemia are more prone to develop severe respiratory failure and probable death than those patients with apnea alone. The current study shows that recurrent respiratory failure and presumably mortality from this acute complication can be reversed with effective treatment of the obstructive apnea. RP FLETCHER, EC (reprint author), BAYLOR COLL MED,HOUSTON VET AFFAIRS MED CTR,DEPT MED,PULM DIS & CRIT CARE SECT,HOUSTON,TX 77030, USA. NR 10 TC 34 Z9 37 U1 0 U2 2 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 SEP PY 1991 VL 19 IS 9 BP 1158 EP 1164 DI 10.1097/00003246-199109000-00011 PG 7 WC Critical Care Medicine SC General & Internal Medicine GA GF175 UT WOS:A1991GF17500011 PM 1884615 ER PT J AU PETRIDES, AS LUZI, L REUBEN, A RIELY, C DEFRONZO, RA AF PETRIDES, AS LUZI, L REUBEN, A RIELY, C DEFRONZO, RA TI EFFECT OF INSULIN AND PLASMA AMINO-ACID CONCENTRATION ON LEUCINE METABOLISM IN CIRRHOSIS SO HEPATOLOGY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; DEPENDENT DIABETES-MELLITUS; WHOLE-BODY LEUCINE; PROTEIN-SYNTHESIS; ALPHA-KETOISOCAPROATE; GLUCOSE-METABOLISM; LIVER-DISEASE; HEPATIC ENCEPHALOPATHY; RESISTANCE; IMBALANCE AB Clinically stable patients with cirrhosis demonstrate insulin resistance with regard to glucose metabolism. However, much less is known about the two major factors, insulin and plasma amino acid concentration, that regulate protein metabolism in cirrhotic patients. To examine this question, we performed paired euglycemic insulin clamp studies in combination with C-14-leucine and indirect calorimetry. In the first study insulin alone was infused, and the plasma amino acid concentration was allowed to decline. During the second study a balanced amino acid solution was infused with insulin to increase the total plasma amino acid concentration approximately twofold. Insulin-mediated glucose disposal (4.68 vs. 6.45 mg/kg-min, p < 0.01) was significantly impaired by 30% in cirrhotic patients during both insulin clamp studies. In the postabsorptive state, cirrhotic patients manifested low plasma leucine (76 vs. 102-mu-mol/L) and alpha-ketoisocaproate (19 vs. 30-mu-mol/L) concentrations, but all parameters of leucine turnover were normal. When insulin alone was infused, the endogenous leucine flux (an index of protein degradation) declined similarly in cirrhotic patients (30.8-mu-mol/m2-min) and control (26.9) subjects, and this was accompanied by a similar decrease in plasma leucine concentration (31% vs. 33%). The decline in circulating leucine concentration was accompanied by a parallel decline in leucine oxidation (5.1 vs. 4.6-mu-mol/m2-min) and nonoxidative (28.9 vs. 26.0-mu-mol/m2-min) leucine disposal, which were of similar magnitude in cirrhotic patients and control subjects, respectively. In both cirrhotic patients and control subjects, combined hyperinsulinemia/hyperaminoacidemia elicited a similar stimulation of nonoxidative leucine disposal (an index of protein synthesis) and leucine oxidation while causing a greater suppression of endogenous leucine flux than observed with insulin alone. Thus the suppressive effect of insulin on protein degradation and the stimulatory effect of insulin/amino acid infusion on protein synthesis are not impaired in cirrhotic patients, demonstrating a clear-cut dissociation between the effects of insulin on protein and glucose metabolism. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Luzi, Livio/M-2696-2016 OI Luzi, Livio/0000-0003-3183-0552 FU NCRR NIH HHS [M01-RR-01346] NR 55 TC 44 Z9 44 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 SEP PY 1991 VL 14 IS 3 BP 432 EP 441 DI 10.1016/0270-9139(91)90180-4 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GD077 UT WOS:A1991GD07700005 PM 1874488 ER PT J AU SHUSTER, E AF SHUSTER, E TI NONGENETIC SURROGACY - NO CURE BUT PROBLEMS FOR INFERTILITY SO HUMAN REPRODUCTION LA English DT Article DE BABY SELLING; GENETIC MOTHER; GENETIC REDUCTIONISM; GESTATIONAL MOTHER; SURROGACY AGREEMENT AB Non-genetic surrogacy characterizes a situation where the gestational mother is not the genetic mother. It further widens a circle that started with the introduction of in-vitro fertilization (IVF) and creates problems in defining motherhood and identifying at birth the mother who will have the rights and responsibilities of rearing the child. RP SHUSTER, E (reprint author), DEPT VET AFFAIRS MED CTR,UNIV & WOODLAND AVE,PHILADELPHIA,PA, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0268-1161 J9 HUM REPROD JI Hum. Reprod. PD SEP PY 1991 VL 6 IS 8 BP 1176 EP 1180 PG 5 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA GQ346 UT WOS:A1991GQ34600029 PM 1806581 ER PT J AU TERAYAMA, Y MEYER, JS KAWAMURA, J WEATHERS, S AF TERAYAMA, Y MEYER, JS KAWAMURA, J WEATHERS, S TI ROLE OF THALAMUS AND WHITE MATTER IN COGNITIVE OUTCOME AFTER HEAD-INJURY SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE BRAIN TRAUMA; CEREBRAL BLOOD FLOW; COGNITIVE FUNCTION; PARTITION COEFFICIENTS ID CEREBRAL BLOOD-FLOW; ENHANCED COMPUTED-TOMOGRAPHY; POSITRON TOMOGRAPHY; CT; STROKE; METABOLISM; DEMENTIA; CORTEX AB Local CBF (LCBF) and local partition coefficients (L-lambda) were measured by xenon-enhanced computed tomography among 15 patients with remote cerebral trauma resulting from severe head injury. Results were compared with similar measures among age-matched normal volunteers (N = 20). The patients were divided into two groups according to different outcomes based on serial cognitive testing: Group I (N = 10) improved but Group D (N = 5) deteriorated throughout a mean interval of 10 years of follow-up. Initial LCBF measurements were performed at mean intervals of 6.8 years after injury. Cortical LCBF values were decreased in frontal (p < 0.01) and temporal (p < 0.05) regions among both groups, but only in Group D were flow values decreased in putamen and thalamus (p < 0.05). L-lambda values were reduced in frontotemporal cortex among both groups but in the thalamus only among Group D (p < 0.05). Mean white matter flow values were normal in Group I but were reduced in Group D (p < 0.05). Mean partition coefficients for white matter were reduced in both groups (p < 0.01) but were lower in Group D (p < 0.05). Reduced perfusion of frontotemporal gray matter is consonant with neuropathological reports following severe brain trauma of neuronal atrophy, gliosis, and infarction affecting these regions. Group comparisons between patients who cognitively improved versus those that deteriorated demonstrate an association between reductions of CBF in putamen, thalamus and subcortical white matter and impaired cognition after severe head injury. C1 DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT RADIOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. DEPT VET AFFAIRS MED CTR,RADIOL SERV,HOUSTON,TX. NR 31 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD SEP PY 1991 VL 11 IS 5 BP 852 EP 860 PG 9 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA GD344 UT WOS:A1991GD34400019 PM 1874818 ER PT J AU LEONG, GB SILVA, JA WEINSTOCK, R AF LEONG, GB SILVA, JA WEINSTOCK, R TI DANGEROUS MENTALLY DISORDERED CRIMINALS - UNRESOLVABLE SOCIETAL FEAR - RESPONSE SO JOURNAL OF FORENSIC SCIENCES LA English DT Letter RP LEONG, GB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 0 Z9 0 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 SEP PY 1991 VL 36 IS 5 BP 1281 EP 1281 PG 1 WC Medicine, Legal SC Legal Medicine GA GF647 UT WOS:A1991GF64700003 ER PT J AU FLYNN, FG CUMMINGS, JL GORNBEIN, J AF FLYNN, FG CUMMINGS, JL GORNBEIN, J TI DELUSIONS IN DEMENTIA SYNDROMES - INVESTIGATION OF BEHAVIORAL AND NEUROPSYCHOLOGICAL CORRELATES SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID MULTI-INFARCT DEMENTIA; ALZHEIMERS-DISEASE; SENILE DEMENTIA; PSYCHOSIS; SYMPTOMS; DISTURBANCE; DIAGNOSIS; EPILEPSY AB A prospective cross-sectional investigation examining the relationship of neuropsychological and behavioral changes to the occurrence of delusions in dementia syndromes was conducted. Nineteen patients had Alzheimer's disease (AD), and 14 had multi-infarct dementia (MID). Patients with and without delusions were compared with regard to demographic characteristics, neuropsychological and neurological features, and a variety of behavioral disturbances. Delusional patients were more aggressive and exhibited more severe activity disturbances than nondelusional patients. Delusional patients were more severely cognitively impaired, but the neuropsychological differences between the two groups were not outstanding. These observations suggest that specific neuropsychological deficits are not compelling predictors of delusions and that delusional patients are more behaviorally disturbed than those without delusions. It is hypothesized that delusions are independent noncognitive manifestations of the neurobiology of AD and MID. C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROBEHAV UNIT,BLDG 256B,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOMATH,BIOSTAT CONSULTING UNIT,LOS ANGELES,CA 90024. NR 36 TC 82 Z9 82 U1 1 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD FAL PY 1991 VL 3 IS 4 BP 364 EP 370 PG 7 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA GM866 UT WOS:A1991GM86600002 PM 1821254 ER PT J AU HADJOKAS, N GOODFRIEND, T AF HADJOKAS, N GOODFRIEND, T TI INHIBITION OF ALDOSTERONE PRODUCTION AND ANGIOTENSIN ACTION BY DRUGS AFFECTING POTASSIUM CHANNELS SO PHARMACOLOGY LA English DT Article DE ALDOSTERONE; ADRENAL GLOMERULOSA; ANGIOTENSIN-II; POTASSIUM CHANNELS; VASODILATORS; HYPERTENSION ID ADRENAL GLOMERULOSA CELLS; RABBIT AORTA; K+ CHANNELS; SECRETION; CALCIUM; RESPONSES; BLOCKERS; HYPERTENSION; CROMAKALIM; BRL-34915 AB We screened potassium channel agonists and antagonists in a search for pharmacologic probes of the channels that mediate potassium's effects on adrenal zona glomerulosa cells. Suspensions of bovine cells were tested, and aldosterone was measured by radioimmunoassay. The most potent inhibitors were pinacidil, capsaicin, glyburide, and quinine. These reagents were more potent against aldosterone production than against cortisol production. Aldosterone produced under basal conditions, as well as that stimulated by potassium, angiotensin II, or dibutyryl cyclic AMP, was antagonized. The vasodilatory and aldosterone-inhibiting potencies of potassium channel reagents were very different. Candidate antihypertensives with potassium channel activity should be tested for adrenal inhibition. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT PHARMACOL,MADISON,WI 53706. NR 38 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0031-7012 J9 PHARMACOLOGY JI Pharmacology PD SEP PY 1991 VL 43 IS 3 BP 141 EP 150 DI 10.1159/000138839 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GR373 UT WOS:A1991GR37300004 PM 1775517 ER PT J AU REDINGTON, J EBERT, SC CRAIG, WA AF REDINGTON, J EBERT, SC CRAIG, WA TI ROLE OF ANTIMICROBIAL PHARMACOKINETICS AND PHARMACODYNAMICS IN SURGICAL PROPHYLAXIS SO REVIEWS OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON PERIOPERATIVE ANTIBIOTIC PROPHYLAXIS CY MAR 04-07, 1990 CL SAN JUAN, PR SP GLAXO, SMITHKLINE BEECHAN, ELI LILLY, HOFFMANN LA ROCHE, ICI AMER ID OPEN-HEART SURGERY; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; BETA-LACTAM ANTIBIOTICS; TISSUE PENETRATION; PROTEIN-BINDING; SUBCUTANEOUS TISSUE; INVITRO MODEL; STAPHYLOCOCCUS-AUREUS; THIGH-INFECTION; PELVIC TISSUE AB The pharmacokinetic and pharmacodynamic properties of antimicrobial agents used for surgical prophylaxis are reviewed. Since levels in tissue homogenates depend on the amount of drug present intracellularly, they do not accurately describe the relation between concentrations in serum and those in interstitial fluid. Levels of free drug in serum are good predictors of the time course of concentrations of unbound drug in interstitial fluid. An increase in protein binding does not reduce the area under the curve (AUC) of free drug for beta-lactam agents eliminated predominantly by glomerular filtration. Pharmacodynamic studies of persistent growth suppression and bactericidal activity predict that the period for which the free-drug concentration exceeds the minimal inhibitory concentration (MIC) is an important parameter in the efficacy of beta-lactam antibiotics. In contrast, the AUC is the major parameter in the efficacy of aminoglycosides and quinolones. Although studies with animals support the above concepts, data for humans are limited. Until additional clinical trials dictate other conclusions, the goal of prophylaxis with beta-lactam agents should be to provide serum levels of free drug above the MIC for common contaminating bacteria for the entire surgical period. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,MADISON,WI 53706. NR 102 TC 22 Z9 23 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0162-0886 J9 REV INFECT DIS PD SEP-OCT PY 1991 VL 13 SU 10 BP S790 EP S799 PG 10 WC Immunology; Microbiology SC Immunology; Microbiology GA GM606 UT WOS:A1991GM60600003 PM 1754787 ER PT J AU HARMS, BA ROSENFELD, DJ CONHAIM, RL PAHL, AC SUBRAMANIAN, R STORM, FK AF HARMS, BA ROSENFELD, DJ CONHAIM, RL PAHL, AC SUBRAMANIAN, R STORM, FK TI PULMONARY AND SYSTEMIC FLUID FILTRATION AFTER CONTINUOUS VERSUS BOLUS INTERLEUKIN-2 INFUSION SO SURGERY LA English DT Article ID ACTIVATED KILLER CELLS; RECOMBINANT INTERLEUKIN-2; SHEEP; CANCER; HUMANS AB Interleukin-2 has been widely investigated as adjuvant therapy for advanced cancer and is administered by either bolus or continuous infusion. We compared the effects of bolus and continuous interleukin-2 infusion on pulmonary (Q(L)) and systemic microvascular fluid filtration in 11 adult sheep prepared with chronic lung and soft-tissue lymph fistulas. Interleukin-2 was administered as a bolus infusion (100,000 units/kg) every 8 hours for 3 days or as a continuous infusion at the same dose for 3 days. No significant changes in pulmonary hydrostatic pressures or pulmonary vascular resistance were noted after either bolus or continuous interleukin-2 infusion. However, significantly decreased (p less-than-or-equal-to 0.05) systemic vascular resistances were observed in both groups. Q(L) increased steadily throughout the infusion period in both groups, peaking at three times baseline on the third infusion day. The plasma/interstitial protein clearance (Q(L) X lymph/plasma protein ratio) rose similarly in both groups, indicating increased barrier permeability. Increased lymphocyte clearance into lung lymph occurred by day 3 but was not associated with lymphocytic sequestration in the lung interstitium. We conclude that pulmonary and systemic microvascular fluid and protein flux exhibit similar changes after bolus or continuous interleukin-2 infusion. These changes are associated with increased clearance of lymphocytes into lung lymph that are not sequestered in the pulmonary interstitium after infusions of shorter duration. C1 UNIV WISCONSIN, DEPT SURG, MADISON, WI 53706 USA. UNIV WISCONSIN, DEPT SURG ONCOL, MADISON, WI 53706 USA. UNIV WISCONSIN, DEPT PATHOL, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. NR 25 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0039-6060 J9 SURGERY JI Surgery PD SEP PY 1991 VL 110 IS 3 BP 500 EP 507 PG 8 WC Surgery SC Surgery GA GE315 UT WOS:A1991GE31500007 PM 1887373 ER PT J AU TAKAHASHI, LK KALIN, NH AF TAKAHASHI, LK KALIN, NH TI EARLY DEVELOPMENTAL AND TEMPORAL CHARACTERISTICS OF STRESS-INDUCED SECRETION OF PITUITARY-ADRENAL HORMONES IN PRENATALLY STRESSED RAT PUPS SO BRAIN RESEARCH LA English DT Article DE PRENATAL STRESS; HYPOTHALAMIC-PITUITARY-ADRENAL SYSTEM; ADRENOCORTICOTROPIN; CORTICOSTERONE; PREWEANLING RAT; STRESS; HORMONE ID CORTICOSTERONE LEVELS; PLASMA; BRAIN; TESTOSTERONE; HIPPOCAMPUS; RECEPTORS; PREGNANCY; FETUSES; ACTH AB Previous experiments revealed that 14-day-old prenatally stressed rats have significantly elevated concentrations of plasma adrenocortico-trophic hormone (ACTH) and corticosterone suggesting these animals have an overactive hypothalamic-pituitary-adrenal (HPA) system. In these studies, however, stress-induced hormone levels were determined only immediately after exposure to an acute stressor. Therefore, in the current study, we examined in postnatal days 7, 14 and 21 prenatally stressed rats the stress-induced time course of this pituitary-adrenal hormone elevation. Plasma ACTH and corticosterone were measured in the basal state and at 0.0, 0.5, 1.0, 2.0 and 4.0 h after a 10-min exposure period to foot shocks administered in the context of social isolation. Results indicated that at all 3 ages, plasma ACTH in prenatally stressed rats was significantly elevated. Corticosterone concentrations were also significantly higher in prenatally stressed than in control rats, especially in day 14 rats. Analysis of stress-induced hormone fluctuations over time indicated that by 14 days of age, both prenatally stressed and control rats had significant increases in plasma ACTH and corticosterone after exposure to stress. Furthermore, although prenatally stressed rats had significantly higher pituitary-adrenal hormone concentrations than control animals, the post-stress temporal patterns of decline in ACTH and corticosterone levels were similar between groups. Results suggest that throughout the preweaning period, prenatal stress produces an HPA system that functions in a manner similar to that of controls but at an increased level. C1 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 30 TC 117 Z9 119 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD AUG 30 PY 1991 VL 558 IS 1 BP 75 EP 78 DI 10.1016/0006-8993(91)90715-8 PG 4 WC Neurosciences SC Neurosciences & Neurology GA GE895 UT WOS:A1991GE89500009 PM 1657312 ER PT J AU HOLDCROFT, CJ ELLISON, RT AF HOLDCROFT, CJ ELLISON, RT TI TRIMETHOPRIM SULFAMETHOXAZOLE REACTION SIMULATING PNEUMOCYSTIS-CARINII PNEUMONIA SO AIDS LA English DT Letter RP HOLDCROFT, CJ (reprint author), DENVER VET AFFAIRS MED CTR,DEPT VET AFFAIRS,1055 CLERMONT ST,DENVER,CO 80220, USA. NR 5 TC 3 Z9 3 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD AUG PY 1991 VL 5 IS 8 BP 1029 EP 1029 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA GB651 UT WOS:A1991GB65100017 PM 1777163 ER PT J AU WOLBER, RA DUPUIS, BA WICK, MR AF WOLBER, RA DUPUIS, BA WICK, MR TI EXPRESSION OF C-ERBB-2 ONCOPROTEIN IN MAMMARY AND EXTRAMAMMARY PAGETS-DISEASE SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE C-ERBB-2; PAGETS DISEASE; BREAST; VULVA ID BREAST-CANCER; CARCINOMA INSITU; FLUID PROTEIN-15; PROTO-ONCOGENE; AMPLIFICATION; ADENOCARCINOMAS; PROTOONCOGENE; ASSOCIATION; RECEPTOR; TUMORS AB Formalin-fixed, paraffin-embedded tissue sections from 45 patients with mammary and extramammary Paget's disease were stained immunohistochemically with the use of a polyclonal antiserum directed against a 14-amino acid segment of the c-erbB-2 oncoprotein. Positive membrane staining, which correlates with gene amplification, was found in 15 of 19 cases (79%) of mammary Paget's disease, 4 of 13 cases (31%) of vulvar Paget's disease, none of 8 cases of scrotal Paget's disease, and none of 5 cases of perianal Paget's disease. Of the 19 patients with mammary Paget's disease, specimens of underlying breast tissue were available from 14; all contained a concurrent ductal adenocarcinoma. Concordance of c-erbB-2 antigen staining between the underlying breast carcinoma and the pagetoid component was observed in 12 cases. Of the 13 patients with vulvar Paget's disease, 2 had superficial stromal invasion, and 3 had underlying, deeply invasive adenocarcinomas. One superficially invasive case was positive for c-erbB-2 expression. One additional case of vulvar Paget's disease had an associated primary pagetoid endocervical adenocarcinoma that spread into the endometrium; both the endocervical and vulvar components stained positively for the c-erbB-2 antigen. The results of this study indicate that the c-erbB-2 oncoprotein may play a role in the pathogenesis of extramammary Paget's disease. These results also suggest that the c-erbB-2 oncoprotein may function in vivo to promote intraepithelial spread of adenocarcinoma cells. C1 UNIV BRITISH COLUMBIA,VANCOUVER GEN HOSP,DIV ANAT PATOL,VANCOUVER V5Z 1M9,BC,CANADA. WASHINGTON UNIV,MED CTR,DEPT PATHOL,ST LOUIS,MO 63130. RP WOLBER, RA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL & LAB MED,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 23 TC 83 Z9 83 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD AUG PY 1991 VL 96 IS 2 BP 243 EP 247 PG 5 WC Pathology SC Pathology GA FZ711 UT WOS:A1991FZ71100017 PM 1713741 ER PT J AU ZIMMERMAN, SW AHRENS, E JOHNSON, CA CRAIG, W LEGGETT, J OBRIEN, M OXTON, L ROECKER, EB ENGESETH, S AF ZIMMERMAN, SW AHRENS, E JOHNSON, CA CRAIG, W LEGGETT, J OBRIEN, M OXTON, L ROECKER, EB ENGESETH, S TI RANDOMIZED CONTROLLED TRIAL OF PROPHYLACTIC RIFAMPIN FOR PERITONEAL DIALYSIS-RELATED INFECTIONS SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE RIFAMPIN; PERITONEAL DIALYSIS; CATHETER INFECTION; PERITONITIS ID AUREUS NASAL CARRIAGE; STAPHYLOCOCCUS-AUREUS; EXIT-SITE; CAPD C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,SCH PHARM & BIOSTAT,MADISON,WI 53705. NR 20 TC 88 Z9 88 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD AUG PY 1991 VL 18 IS 2 BP 225 EP 231 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA GA470 UT WOS:A1991GA47000012 PM 1867179 ER PT J AU OBERLEY, TD OBERLEY, LW SLATTERY, AF ELWELL, JH AF OBERLEY, TD OBERLEY, LW SLATTERY, AF ELWELL, JH TI IMMUNOHISTOCHEMICAL LOCALIZATION OF GLUTATHIONE-S-TRANSFERASE AND GLUTATHIONE-PEROXIDASE IN ADULT SYRIAN-HAMSTER TISSUES AND DURING KIDNEY DEVELOPMENT SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID ANTIOXIDANT ENZYMES; CELL; EPITHELIUM AB Tissues from adult Syrian hamsters were studied with immunoperoxidase techniques using polyclonal antibodies to glutathione-S-transferase (rat liver and human placental enzymes) and human erythrocyte glutathione peroxidase. Most tissues immunostained similarly with these antibodies. Most notable was the cytoplasmic staining of mesenchyme tissues, especially smooth muscle, by all three antibodies. Epithelial cells stained distinctively, but usually less intensely than mesenchyme. Epithelial cells from all levels of the gastrointestinal tract, respiratory epithelium, transitional epithelium, and epidermis all showed strong staining with these antibodies. Other epithelial cell types were usually positive but showed less dramatic staining. Most epithelial tissues showed both nuclear and cytoplasmic staining; some also showed cell-surface (eg, cilia) staining. The role of these enzymes in cell differentiation of a stable organ was studied by immunostaining the kidney during its development. Early stroma (13- and 15-day fetuses) of the kidney (metanephric mesenchyme) showed strong cell-surface staining for glutathione transferases and moderate staining for glutathione peroxidase; renal tubules (which are epithelial cells) at this stage were negative for these markers. As renal tubules differentiated, first cytoplasm and then nuclei stained moderately, suggesting that glutathione-S-transferases and glutathione peroxidase are markers of both mesenchymal cells, including embryonic mesenchyme, and terminal differentiation of at least some epithelial cells. C1 UNIV WISCONSIN,DEPT PATHOL,MADISON,WI 53706. UNIV IOWA,RADIAT RES LAB,IOWA CITY,IA 52242. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SECT,LAB SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA-41267] NR 25 TC 33 Z9 33 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD AUG PY 1991 VL 139 IS 2 BP 355 EP 369 PG 15 WC Pathology SC Pathology GA GA982 UT WOS:A1991GA98200012 PM 1714242 ER PT J AU BURSTEN, SL STEVENSON, F TORRANO, F LOVETT, DH AF BURSTEN, SL STEVENSON, F TORRANO, F LOVETT, DH TI MESANGIAL CELL ACTIVATION BY BACTERIAL-ENDOTOXIN - INDUCTION OF RAPID CYTOSKELETAL REORGANIZATION AND GENE-EXPRESSION SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; PHOSPHATIDIC-ACID; STIMULATION; ACTIN; LIPOPOLYSACCHARIDE; TRANSCRIPTION; ARCHITECTURE; COLLAGENASE; FIBROBLASTS; PROTEINS AB Cultured glomerular mesangial cells (MC) respond to low concentrations of bacterial endotoxin (ET) by secreting prostaglandins and interleukin-1. To evaluate further the nature of ET-induced mesangial cell activation, the authors evaluated the effects of this agent on MC morphology and cytoskeletal organization. Bacterial ET, in concentrations as low as 1 ng/ml, induced reversible membrane ruffling, cellular rounding, and extension of many filopodia and lamellopodia. Augmented fluid-phase pinocytosis occurred in parallel, as determined by transmission electron microscopy and tritiated sucrose uptake. These cellular morphologic and functional changes were associated with an extensive, but reversible, depolymerization of actin microfilaments. Actin gene expression was also modified by ET. At 4 to 6 hours after ET exposure, Northern blot analysis showed a twofold to fourfold increase in actin mRNA levels. In situ hybridizations of ET-stimulated cells at the light and electron microscopic levels demonstrated a markedly asymmetric distribution of actin mRNA, which was localized in the cellular periphery at filopodial and lamellopodial extensions, presumably sites of new actin protein synthesis. It is concluded that ET effects on MC are distinct from the nonspecific lytic or 'toxic' actions described for other cell types. Endotoxin induces a global activation of this cell type associated with major changes in membrane structure, cytoskeletal organization, and gene expression, which resemble in many respects the responses to peptide mitogens. C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO VET ADM MED CTR,DEPT MED,DIV NEPHROL,111J MED SERV,SAN FRANCISCO,CA 94143. UNIV WASHINGTON,SEATTLE VET ADM MED CTR,DEPT MED,SEATTLE,WA 98195. NR 25 TC 31 Z9 32 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD AUG PY 1991 VL 139 IS 2 BP 371 EP 382 PG 12 WC Pathology SC Pathology GA GA982 UT WOS:A1991GA98200013 PM 1867323 ER PT J AU GLASS, WF RAMPT, E GARONI, JA FENTON, JW KREISBERG, JI AF GLASS, WF RAMPT, E GARONI, JA FENTON, JW KREISBERG, JI TI REGULATION OF MESANGIAL CELL-ADHESION AND SHAPE BY THROMBIN SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE UROKINASE; SINGLE-CHAIN UROKINASE; STRESS FIBERS; ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE; SMOOTH MUSCLE CELL ID PLASMINOGEN-ACTIVATOR INHIBITOR; TRANSFORMED CHICK FIBROBLASTS; HUMAN ALPHA-THROMBIN; GROWTH FACTOR-BETA; PRO-UROKINASE; EXTRACELLULAR-MATRIX; SARCOMA-CELLS; FIBRONECTIN; RECEPTOR; BINDING AB Adenosine 3',5'-cyclic monophosphate (cAMP) elevation in cultured rat mesangial cells causes urokinase-dependent adhesion loss, stress-fiber fragmentation, and shape change. Thrombin cleaves single-chain urokinase (scu-PA), causing its inactivation, but not two-chain u-PA [tcu-plasminogen activator (PA)] or tissue-type PA. We tested the ability of thrombin to inhibit the effects of cAMP elevation in mesangial cells and inactivate cell-associated scu-PA. In an assay of trypsin-sensitive adhesion, 65.9% of control cells and 5.5% of cells treated with isoproterenol + methylisobutylxanthine (IM) remained adherent. In the presence of 0.01, 0.1, 1.0, and 10.0 unit/ml thrombin, 20.9, 46.6, 50.4, and 53.3%, respectively, of IM-treated cells remained attached. Thrombin also inhibited stress-fiber fragmentation and shape change. The effects of thrombin were blocked by hirudin or antithrombin III plus heparin. Direct zymography in gels containing gelatin and plasminogen revealed loss of a closely spaced pair of PA bands with thrombin treatment (1.0 unit/ml). Hirudin blocked the loss. alpha-Thrombin inactivated by diisopropyl fluorophosphate neither inhibited shape change nor caused loss of the PA bands; however, gamma-thrombin was nearly as active as native alpha-thrombin in both regards. Pretreatment of the cells with as little as 1.0 unit/ml thrombin for 1.0 min caused marked inhibition of shape change and near total loss of the slower migrating u-PA band (of the doublet). The faster migrating band was inhibited less. The results indicate that the slower migrating band represents scu-PA; the nature of the faster migrating band is less certain. Thrombin reversed the adhesion loss and shape change caused by 8-(4-chlorophenylthio)-cAMP and MIX. Thus physiological concentrations of thrombin rapidly inactivate mesangial cell scu-PA and inhibit and reverse cAMP-stimulated adhesion loss and shape change. Although inhibition of urokinase-dependent hydrolysis of extracellular matrix protein is apparently one mechanism by which thrombin regulates mesangial cell shape and adhesion, these observations are consistent with the possibility that cleavage of receptor-bound scu-PA by thrombin regulates these processes through signal transduction as well. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201. RP GLASS, WF (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK-29787] NR 43 TC 16 Z9 16 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 1991 VL 261 IS 2 BP F336 EP F344 PN 2 PG 9 WC Physiology SC Physiology GA GC252 UT WOS:A1991GC25200098 PM 1652208 ER PT J AU ANWAR, A KOHN, SR DUNN, JF HYMER, TK KENNEDY, GT CRAWFORD, MH OROURKE, RA KATZ, MS AF ANWAR, A KOHN, SR DUNN, JF HYMER, TK KENNEDY, GT CRAWFORD, MH OROURKE, RA KATZ, MS TI ALTERED BETA-ADRENERGIC-RECEPTOR FUNCTION IN SUBJECTS WITH SYMPTOMATIC MITRAL-VALVE PROLAPSE SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Article DE MITRAL VALVE PROLAPSE; BETA-ADRENERGIC RECEPTOR; LYMPHOCYTE; ISOPROTERENOL; ADENYLATE CYCLASE; GUANINE NUCLEOTIDE-BINDING PROTEIN ID PLASMA-CATECHOLAMINE LEVELS; HUMAN-LYMPHOCYTES; DYNAMIC EXERCISE; BINDING; HEART; RADIOIMMUNOASSAY; ADRENOCEPTORS; AFFINITY; DENSITY AB Individuals with mitral valve prolapse (MVP) frequently show symptoms of a hyperadrenergic state. Beta-adrenergic receptor characteristics were compared in the lymphocytes of subjects with symptomatic MVP and control subjects during rest and exercise. At rest, the proportion of receptors binding agonist with high affinity, as determined from isoproterenol competition for (-)[I-125]-iodopindolol binding sites, was greater in MVP subjects than in controls. With exercise, the proportion of high-affinity receptors in MVP subjects decreased to control levels. Isoproterenol stimulation of lymphocyte 3',5'-cyclic adenosine monophosphate (cyclic AMP) also was greater in MVP subjects than in controls at rest, but not during exercise. Plasma catecholamine concentrations in MVP subjects were normal during both rest and exercise. Unlike exercise, isoproterenol infusion elicited clinical manifestations of increased adrenergic responsiveness in MVP subjects. The beta-receptor in exercised MVP subjects exhibited unusually high affinity agonist binding (i.e. a lower dissociation constant K(H) than in either the same subjects at rest or exercised controls) and also abnormal coupling to the stimulatory guanine nucleotide-binding regulatory protein (G(S)) of adenylate cyclase, as reflected by the inability of guanine nucleotide to convert the receptor to a low-affinity state. These findings suggest that functional alteration of the beta-adrenergic receptor, in the absence of abnormal plasma catecholamine levels, might contribute to the hyperadrenergic state of MVP subjects at rest. However, desensitization of high affinity beta-receptors or altered receptor-G(S) coupling might preserve normal adrenergic responsiveness during exercise. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. FU NHLBI NIH HHS [2T32HL07350]; NIA NIH HHS [R01AG03168] NR 37 TC 16 Z9 16 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9629 J9 AM J MED SCI JI Am. J. Med. Sci. PD AUG PY 1991 VL 302 IS 2 BP 89 EP 97 DI 10.1097/00000441-199108000-00004 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA GA234 UT WOS:A1991GA23400004 PM 1654743 ER PT J AU BADR, MS SKATRUD, JB SIMON, PM DEMPSEY, JA PULEO, DS LOOKABAUGH, JD AF BADR, MS SKATRUD, JB SIMON, PM DEMPSEY, JA PULEO, DS LOOKABAUGH, JD TI EFFECT OF HYPERCAPNIA ON TOTAL PULMONARY RESISTANCE DURING WAKEFULNESS AND DURING NREM SLEEP SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID UPPER AIRWAY-RESISTANCE; ANESTHETIZED DOGS; PRESSURE-FLOW; MUSCLE; OCCLUSION; DIAPHRAGM; RESPONSES; PATHOGENESIS; GENIOGLOSSAL; VENTILATION AB We investigated the effect of different levels of hypercapnia on total pulmonary resistance (RL) in 13 subjects ranging from nonsnorers with low RL to snorers with high RL and dynamic narrowing of the upper airway during inspiration. Added CO2 was adjusted to achieve a steady-state increase in PET(CO2) of +2, +4, or +6 mm Hg. RL was measured at peak inspiratory flow (RL(pf)), at maximal resistance within breath (RL(max)), and at 10 equally spaced points within inspiration in several trials. During wakefulness, hypercapnia was associated with decreased RL(max). During steady state +6 mm Hg hypercapnia, RL(max) decreased by 30% (p < 0.01). During NREM sleep, low levels of hypercapnia did not affect RL. However, +6 mm Hg hypercapnia was associated with decreased RL(max) in six of eight subjects (p = 0.07), especially in subjects with high RL(max) during room air breathing. The effects of hypercapnia on RL(pf) paralleled its effect on RL(max). We conclude that (1) the decrease in RL during awake hypercapnia suggests an increase in upper airway dimensions and stiffness, (2) the absence of increased RL during low level NREM hypercapnia (despite the increase in inspiratory flows and collapsing pressures) also suggests an increase in upper airway dimensions and stiffness, and (3) upper airway dilating muscles appear to be recruited in a coordinated fashion with inspiratory muscles in normal humans during NREM sleep. The implications of these findings in patients with obstructive sleep apnea are not clear at this point. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,JOHN RANKIN LAB PREVENT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT PREVENT MED,MADISON,WI 53706. FU NHLBI NIH HHS [P01 HL-42242-01] NR 38 TC 41 Z9 42 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD AUG PY 1991 VL 144 IS 2 BP 406 EP 414 PG 9 WC Respiratory System SC Respiratory System GA GA251 UT WOS:A1991GA25100030 PM 1859068 ER PT J AU SIMON, PM BASNER, RC WEINBERGER, SE FENCL, V WEISS, JW SCHWARTZSTEIN, RM AF SIMON, PM BASNER, RC WEINBERGER, SE FENCL, V WEISS, JW SCHWARTZSTEIN, RM TI ORAL MUCOSAL STIMULATION MODULATES INTENSITY OF BREATHLESSNESS INDUCED IN NORMAL SUBJECTS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID BREATHING PATTERN; VENTILATORY RESPONSE; AIRWAY ANESTHESIA; CO2 INHALATION; HUMANS; RECEPTORS; LIDOCAINE; ROUTE; DRIVE AB Patients with chronic obstructive pulmonary disease (COPD) often report an increase in breathlessness when they breathe through a mouthpiece. We hypothesized that stimulation of receptors in the oral mucosa modulates the sensation of breathlessness. We studied 10 normal naive volunteers in whom breathlessness was induced by having them breathe for 4 min with an inspiratory resistive load (18 cm H2O/L/s) while breathing was stimulated by CO2 inhalation (end-tidal PCO2 maintained at 55 mm Hg). Initially, subjects breathed with a tight-fitting face mask and inspiratory flow was displayed on a storage oscilloscope. In subsequent trials, the subjects were asked to match this trace, which controlled ventilation and the pattern of breathing. Subjects performed eight trials, four with the tight-fitting mask only (M) an four with a mouthpiece and the mask (MM). M and MM were alternated; the initial condition was chosen at random. Following each of the trials, subjects rated the intensity of their breathlessness by choosing a number from a modified Borg scale. On the average, subjects were more breathless while breathing with the mask and mouthpiece than with the mask alone (mean ratings of breathlessness 6.6 +/- 1.1 and 5.6 +/- 1.8 units, p < 0.01). Six subjects repeated the protocol on 2 additional days: 1 day with inhalation of warm (34-degrees-C), humidified air and 1 day after topical application of 4% lidocaine to the oral mucosa. Both these interventions abolished the differences in breathlessness between mask and mouthpiece intensity of breathlessness. C1 BETH ISRAEL HOSP,CHARLES A DANA RES INST,330 BROOKLINE AVE,BOSTON,MA 02215. BETH ISRAEL HOSP,HARVARD THORNDIKE LAB,BOSTON,MA 02215. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. HARVARD UNIV,SCH MED,BOSTON,MA 02115. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. FU NHLBI NIH HHS [HL-19170, HL-07633] NR 21 TC 17 Z9 17 U1 0 U2 3 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD AUG PY 1991 VL 144 IS 2 BP 419 EP 422 PG 4 WC Respiratory System SC Respiratory System GA GA251 UT WOS:A1991GA25100032 PM 1859070 ER PT J AU BROOKS, BR AF BROOKS, BR TI THE ROLE OF AXONAL-TRANSPORT IN NEURODEGENERATIVE DISEASE SPREAD - A METAANALYSIS OF EXPERIMENTAL AND CLINICAL POLIOMYELITIS COMPARES WITH AMYOTROPHIC-LATERAL-SCLEROSIS SO CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Article ID PATHOGENESIS; INFECTION; MICE AB ALS symptom spread results from local spread of the neuronal degeneration because contiguous areas are more quickly involved than non-contiguous areas. Local spread to contiguous areas of motor neuron dysfunction is faster at the brainstem, cervical and lumbar regions than spread to non-continguous areas. The time for caudal-rostral symptomatic spread of ALS to involve a distant region is a function of the distance of that region from the site of onset. The time for spread to the bulbar region is shorter following arm onset than leg onset. Spread to non-contiguous areas is faster within the spinal cord than from the spinal cord to the bulbar region. These kinetics are consistent with axonal transport of the etiological agent in a manner similar to spread of poliovirus in poliomyelitis patients. Spread from the bulbar region to the spinal cord, on the other hand, occurs faster than symptom spread from the limb region to the bulbar region in limb onset patients. This rapid limb involvement following bulbar onset is more dramatic in males compared with females. Females with leg onset, on the other hand, show more rapid involvement of the opposite leg, either arm or bulbar structures than males. Gender effects may determine the course of ALS depending on the original site of onset. C1 MDA MIDWEST REG ALS TREATMENT & RES PROGRAM,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT NEUROL,AMYOTROPH LATERAL SCLEROSIS CLIN RES CTR,MADISON,WI 53706. RP BROOKS, BR (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SECT,2500 OVERLOOK TERRACE B-6112,MADISON,WI 53705, USA. NR 9 TC 30 Z9 30 U1 0 U2 5 PU CANADIAN J NEUROL SCI INC PI CALGARY PA PO BOX 4220, STATION C EDITORIAL & SUBSCRIPTION SERV, CALGARY AB T2T 5N1, CANADA SN 0317-1671 J9 CAN J NEUROL SCI JI Can. J. Neurol. Sci. PD AUG PY 1991 VL 18 IS 3 SU S BP 435 EP 438 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA GD625 UT WOS:A1991GD62500018 PM 1718581 ER PT J AU DEJONG, DM PATE, JL KIRKLAND, TN TAYLOR, CE BAKER, PJ TAKAYAMA, K AF DEJONG, DM PATE, JL KIRKLAND, TN TAYLOR, CE BAKER, PJ TAKAYAMA, K TI LIPOPOLYSACCHARIDELIKE IMMUNOLOGICAL PROPERTIES OF CELL-WALL GLYCOPROTEINS ISOLATED FROM CYTOPHAGA-JOHNSONAE SO INFECTION AND IMMUNITY LA English DT Article ID III PNEUMOCOCCAL POLYSACCHARIDE; ANTIBODY-RESPONSE; OUTER-MEMBRANE; CAPNOCYTOPHAGA-OCHRACEA; LIPID-A; CHEMICAL CHARACTERIZATION; SALMONELLA-TYPHIMURIUM; LYMPHOCYTE MITOGEN; MASS-SPECTROMETRY; ESCHERICHIA-COLI AB Glycoproteins (GP) previously shown to be involved in the gliding motility of Cytophaga johnsonae were examined for biological activities characteristic of lipopolysaccharide (LPS). These integral membrane proteins activated 70Z/3 pre-B cells to synthesize immunoglobulin M, induced B cells to synthesize non-antigen-specific polyclonal immunoglobulin, induced macrophages to produce tumor necrosis factor, and modulated the antibody response to type III pneumococcal polysaccharide in the absence of thymus-derived (T) lymphocytes. Except for the GP activity in the 70Z/3 assay, all activities of the GP were comparable to or greater than those of LPS. No LPS was detected in the preparations of GP used or in the phenol-water extracts of C. johnsonae. The mechanism by which these GP exerted their biological activities was distinct from that of LPS, since LPS-resistant C3H/HeJ mice responded to GP. Furthermore, biologically inactive diphosphoryl lipid A obtained from nontoxic LPS of Rhodopseudomonas sphaeroides (an analog of toxic lipid A), which is an antagonist of LPS, did not block the induction of tumor necrosis factor by GP in macrophages. These results showed that the cell surface GP from C. johnsonae are potent LPS-like activators of B cells and macrophages. We suggest that these GP might be good candidates for use in developing an effective adjuvant system. C1 UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. UNIV CALIF SAN DIEGO,DEPT PATHOL & MED,SAN DIEGO,CA 92103. VET AFFAIRS MED CTR,DIV INFECT DIS,SAN DIEGO,CA 92161. NIAID,TWINBROOK II RES FACIL,IMMUNOGENET LAB,ROCKVILLE,MD 20852. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. FU NIGMS NIH HHS [GM-36054] NR 47 TC 4 Z9 4 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 1991 VL 59 IS 8 BP 2631 EP 2637 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FY331 UT WOS:A1991FY33100018 PM 1855983 ER PT J AU PETRIDES, AS GROOP, LC RIELY, CA DEFRONZO, RA AF PETRIDES, AS GROOP, LC RIELY, CA DEFRONZO, RA TI EFFECT OF PHYSIOLOGICAL HYPERINSULINEMIA ON GLUCOSE AND LIPID-METABOLISM IN CIRRHOSIS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INSULIN RESISTANCE; HYPERINSULINEMIA; GLUCOSE; FREE FATTY ACID CIRRHOSIS ID DEPENDENT DIABETES-MELLITUS; FREE FATTY-ACIDS; INSULIN RESISTANCE; ALCOHOLIC CIRRHOSIS; HEPATIC CIRRHOSIS; LIVER-CIRRHOSIS; HUMANS; TURNOVER; MUSCLE; NIDDM AB Insulin secretion and insulin sensitivity were evaluated in eight clinically stable cirrhotic patients and in 12 controls. OGTT was normal in cirrhotics but plasma insulin response was increased approximately twofold compared with controls. Subjects received a three-step (0.1, 0.5, 1.0 mU/kg.min) euglycemic insulin clamp with indirect calorimetry, [6-H-3]-glucose, and [1-C-14]-palmitate. During the two highest insulin infusion steps glucose uptake was impaired (3.33 +/- 0.31 vs. 5.06 +/- 0.40 mg/kg.min, P < 0.01, and 6.09 +/- 0.50 vs. 7.95 +/- 0.52 mg/kg.min, P < 0.01). Stimulation of glucose oxidation by insulin was normal; in contrast, nonoxidative glucose disposal (i.e., glycogen synthesis) was markedly reduced. Fasting (r = -0.553, P < 0.01) and glucose-stimulated (r = -0.592, P < 0.01) plasma insulin concentration correlated inversely with the severity of insulin resistance. Basal hepatic glucose production was normal in cirrhotics and suppressed normally with insulin. In postabsorptive state, plasma FFA conc (933 +/- 42 vs. 711 +/- 44-mu-mol/liter, P < 0.01) and FFA turnover (9.08 +/- 1.20 vs. 6.03 +/- 0.53-mu-mol/kg.min, P < 0.01) were elevated in cirrhotics despite basal hyperinsulinemia; basal FFA oxidation was similar in cirrhotic and control subjects. With low-dose insulin infusion, plasma FFA oxidation and turnover failed to suppress normally in cirrhotics. During the two higher insulin infusion steps, all parameters of FFA metabolism suppressed normally. In summary, stable cirrhotic patients with normal glucose tolerance exhibit marked insulin resistance secondary to the impaired nonoxidative glucose disposal. Our results suggest that chronic hyperinsulinism may be responsible for the insulin resistance observed in cirrhosis. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. HEINRICH HEINE UNIV DUSSELDORF,DEPT MED,DIV GASTROENTEROL & HEPATOL,DUSSELDORF,GERMANY. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK24092] NR 71 TC 115 Z9 117 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD AUG PY 1991 VL 88 IS 2 BP 561 EP 570 DI 10.1172/JCI115340 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GA276 UT WOS:A1991GA27600030 PM 1864966 ER PT J AU HARRIS, HW EICHBAUM, EB KANE, JP RAPP, JH AF HARRIS, HW EICHBAUM, EB KANE, JP RAPP, JH TI DETECTION OF ENDOTOXIN IN TRIGLYCERIDE-RICH LIPOPROTEINS INVITRO SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article DE LPDP = LIPOPROTEIN-DEFICIENT PLASMA; PBS = PHOSPHATE-BUFFERED SALINE SOLUTION; VLDL = VERY-LOW-DENSITY LIPOPROTEIN ID HIGH-DENSITY LIPOPROTEINS; SPIN-LABELED PHOSPHOLIPIDS; TUMOR NECROSIS FACTOR; BACTERIAL LIPOPOLYSACCHARIDE; CHROMOGENIC SUBSTRATE; CHYLOMICRON REMNANTS; MOLECULAR MONOLAYERS; PHYSICAL INTERACTION; LIMULUS TEST; PLASMA AB Numerous investigations have been performed in which volunteers have received infusions of triglyceride-rich lipoproteins without apparent screening of the infusates for bacterial endotoxin. This study was designed to examine the capacity of triglyceride-rich lipoproteins to mask their endotoxin content in vitro as measured by a chromogenic modification of the standard Limulus assay. Lipoproteins and lipoprotein-deficient plasma were isolated from normal human plasma by sequential ultracentrifugation under apyrogenic conditions. Individual lipoproteins and a synthetic lipid emulsion were suspended in 10% lipoprotein-deficient plasma. Samples were then incubated at 37-degrees-C for 4 hours with increasing concentrations of E. coli (055:B5) endotoxin and assayed for detectable endotoxin activity. The capacity to inhibit detection of endotoxin in 10% lipoprotein-deficient plasma was significantly increased (10 to 100 times) by the addition of VLDL (1.0 mg triglyceride/ml), chylomicrons (1.0 mg triglyceride/ml), or the synthetic lipid emulsion (2.5 mg triglycerides/ml). These data demonstrate that triglyceride-rich lipoproteins, and the synthetic lipid emulsion, can markedly inhibit the detection of endotoxin by the Limulus assay in vitro. In addition to the potential of harm to experimental subjects, infusion of endotoxin could vitiate kinetic studies by direct alteration of lipoprotein metabolism and by inducing changes in hepatic blood flow. Thus experimental protocols that involve the infusion of humans with triglyceride-rich lipoproteins should include detailed testing for the presence of endotoxin. C1 SAN FRANCISCO VET AFFAIRS MED CTR,DEPT SURG,SAN FRANCISCO,CA. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94143. FU NHLBI NIH HHS [HL07737, HL14237, HL41470] NR 42 TC 26 Z9 27 U1 2 U2 2 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 1991 VL 118 IS 2 BP 186 EP 193 PG 8 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA GA411 UT WOS:A1991GA41100010 PM 1856581 ER PT J AU WINOGRAD, CH GERETY, MB CHUNG, M GOLDSTEIN, MK DOMINGUEZ, F VALLONE, R AF WINOGRAD, CH GERETY, MB CHUNG, M GOLDSTEIN, MK DOMINGUEZ, F VALLONE, R TI SCREENING FOR FRAILTY - CRITERIA AND PREDICTORS OF OUTCOMES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID GERIATRIC CONSULTATION SERVICE; CONTROLLED TRIAL; EVALUATION UNIT; CLINICAL-TRIAL; SYSTEM; TEAM AB Objective: To determine the reliability of rapid screening by clinically derived geriatric criteria in predicting outcomes of elderly hospitalized patients. Design: Prospective cohort study of 985 patients screened at the time of hospital admission and followed for 1 year with respect to the outcomes of mortality, hospital readmission, and nursing home utilization. Setting: Palo Alto Veterans Affairs Medical Center, a tertiary care teaching hospital. Subjects: Male patients 65 years of age and older admitted to the Medical and Surgical services during the period from October 1, 1985 through September 30, 1986. Results: Patients were grouped by specific screening criteria into three groups of increasing frailty: Independent, Frail, and Severely Impaired. Each criterion focused on a geriatric condition and was designed to serve as a marker for frailty. Increasing frailty was significantly correlated with increasing length of hospital stay (P < 0.0001), nursing home utilization (P < 0.0001), and mortality (P < 0.0001). Multivariate analyses revealed that the clinical groups were more predictive of mortality and nursing home utilization than were age or Diagnosis-Related Groups (DRGs). Rehospitalization was unrelated to age, clinical group, or DRG, suggesting that utilization may not be driven by the clinical factors measured in this study. Conclusions: Rapid clinical screening using specific geriatric criteria is effective in identifying frail older subjects at risk for mortality and nursing home utilization. Our findings suggest that geriatric syndromes are more predictive of adverse outcomes than diagnosis per se. This well operationalized screening process is inexpensive as well as effective and could easily be introduced into other hospital settings. C1 STANFORD UNIV,MED CTR,SCH MED,DEPT MED,DIV ENDOCRINOL GERONTOL & METAB,STANFORD,CA 94305. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,AMER FEDERAT AGING RES,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV BRITISH COLUMBIA,UNIV HOSP,DEPT MED,DIV GERIATR MED,VANCOUVER V6T 1W5,BC,CANADA. ASHTON TATE CORP,DEPT SOFTWARE RES,SUNNYVALE,CA. RP WINOGRAD, CH (reprint author), VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,3801 MIRANDA AVE,PALO ALTO,CA 94304, USA. FU NIA NIH HHS [K08 AG00246] NR 18 TC 223 Z9 228 U1 3 U2 16 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 AUG PY 1991 VL 39 IS 8 BP 778 EP 784 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA GA273 UT WOS:A1991GA27300006 PM 1906492 ER PT J AU PANG, XP HERSHMAN, JM PEKARY, AE AF PANG, XP HERSHMAN, JM PEKARY, AE TI PLASMA DISAPPEARANCE AND ORGAN DISTRIBUTION OF RECOMBINANT HUMAN TUMOR-NECROSIS-FACTOR-ALPHA IN RATS SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID THYROID CELLS; FACTOR TNF; CACHECTIN; PHARMACOKINETICS; METABOLISM; INDUCTION; MICE AB The potential use of TNF as a therapeutic agent requires knowledge of the rate and mechanisms of its plasma and tissue clearance and its cellular localization. We have explored these issues using a male Sprague-Dawley rat model and a specific radioimmunoassay for human TNF that does not cross-react with rodent TNF. Unlabeled and I-125-labeled TNF were administered by intracardiac injection. A biexponential clearance was observed with t1/2 (beta-phase, metabolic) of 280 min for TCA-precipitable I-125-labeled TNF and t1/2 (beta-phase) of 30 min for unlabeled TNF. The Sephadex G-75 profile for I-125-labeled TNF obtained 2 min and 4 h after intracardiac injection did not differ significantly except for an increase in the amount of free I-125 at 4 h compared to 2 min. Scatchard plot analysis suggests that I-125 labeling alters significantly the binding of TNF to its receptors on FRTL-5 cells. I-125-labeled TNF uptake by 18 different tissues was corrected for the I-125-labeled TNF in the vascular space by simultaneous injection with I--131 or Tc-99m-labeled albumin. The I-125-labeled TNF tissue/plasma ratio was greater than 1.0 in adrenal, pituitary, lung, spleen, liver, and kidney. Most of these tissues have previously been shown to have TNF receptors and to experience the greatest endothelial damage in response to TNF administration. C1 UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,WADSWORTH DIV,ENDOCRINE RES LAB,LOS ANGELES,CA 90073. NR 23 TC 19 Z9 19 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0277-6766 J9 LYMPHOKINE CYTOK RES JI Lymphokine Cytokine Res. PD AUG PY 1991 VL 10 IS 4 BP 301 EP 306 PG 6 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA GD560 UT WOS:A1991GD56000010 PM 1932374 ER PT J AU DEYKIN, D AF DEYKIN, D TI MEMORANDUM ON A GOVERNMENT JUG SO MEDICAL CARE LA English DT Article; Proceedings Paper CT 7TH ANNUAL MEETING OF THE VETERANS AFFAIRS HEALTH SERVICES RESEARCH AND DEVELOPMENT SERVICE : QUALITY OF CARE CY MAY 23-25, 1991 CL ARLINGTON, VA SP VET AFFAIRS HLTH SERV RES & DEV SERV C1 US DEPT VET AFFAIRS,HLTH SERV RES & DEV SERV,WASHINGTON,DC. US DEPT VET AFFAIRS,COOPERAT STUDIES PROGRAM,WASHINGTON,DC. 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 0025-7079 J9 MED CARE JI Med. Care PD AUG PY 1991 VL 29 IS 8 SU S BP AS5 EP AS7 PG 3 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GD431 UT WOS:A1991GD43100002 ER PT J AU STRUMWASSER, I PARANJPE, NV UDOW, M SHARE, D WISGERHOF, M RONIS, DL BARTZACK, C SAAD, AN AF STRUMWASSER, I PARANJPE, NV UDOW, M SHARE, D WISGERHOF, M RONIS, DL BARTZACK, C SAAD, AN TI APPROPRIATENESS OF PSYCHIATRIC AND SUBSTANCE-ABUSE HOSPITALIZATION - IMPLICATIONS FOR PAYMENT AND UTILIZATION MANAGEMENT SO MEDICAL CARE LA English DT Article DE PSYCHIATRY; PROSPECTIVE PAYMENT SYSTEMS; SUBSTANCE ABUSE; UTILIZATION REVIEW; APPROPRIATENESS; COST CONTAINMENT; HOSPITALIZATION; UNNECESSARY HOSPITALIZATION; INAPPROPRIATE CARE ID DIAGNOSIS-RELATED GROUPS; EVALUATION PROTOCOL; TRIAL; CARE AB A study was conducted to determine the frequency with which hospitalized psychiatric and substance abuse patients actually required treatment on an inpatient basis. A total of 539 patient records were examined using a standardized utilization review instruments adopted or developed by Blue Cross and Blue Shield of Michigan for determining the appropriateness of hospitalization. Physicians reviewed nurse assessments of the appropriateness of hospitalization for accuracy. Overall, 38% of the inpatient days of care incurred by these patients were unnecessary because the care could have been provided on an outpatient basis. Since outpatient care of psychiatric patients is less restrictive and less expensive, and may be as effective as inpatient care for some patients, these findings point to an important inefficiency in the provision of psychiatric care. Sources of this problem and potential remedies are discussed. Three strategies for reducing the amount of unnecessary hospitalization are: increased utilization review and management efforts, the inclusion of preadmission review, the development and inclusion of psychiatric care in prospective payment reimbursement systems, and the development of psychiatric and substance abuse case management programs. C1 US DEPT VET AFFAIRS,HLTH SERV RES & DEV PROGRAM,ANN ARBOR,MI. BLUE CROSS & BLUE SHIELD MICHIGAN,DETROIT,MI. RP STRUMWASSER, I (reprint author), MICHIGAN HLTH CARE EDUC & RES FDN,600 LAFAYETTE E,MAIL CODE B243,DETROIT,MI 48226, USA. NR 25 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD AUG PY 1991 VL 29 IS 8 SU S BP AS77 EP AS90 PG 14 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GD431 UT WOS:A1991GD43100008 ER PT J AU WELCH, CE GROVER, PL AF WELCH, CE GROVER, PL TI AN OVERVIEW OF QUALITY ASSURANCE SO MEDICAL CARE LA English DT Review DE APPROPRIATENESS OF CARE MODELS; HOSPITAL-BASED MORTALITY MODELS; QUALITY ASSESSMENT; QUALITY ASSURANCE; SEVERITY OF ILLNESS MEASUREMENT SYSTEMS ID APPROPRIATENESS EVALUATION PROTOCOL; INTENSIVE-CARE UNIT; MEDICAL-CARE; HEALTH-CARE; DEATH RATES; PATIENT SATISFACTION; HOSPITAL QUALITY; AMBULATORY CARE; APACHE-II; SEVERITY AB This paper provides an overview of quality assurance models currently in use. A review of extant literature indicated that: 1) a universally acceptable definition of quality assurance was lacking; 2) hospital-based mortality models were imperfect; 3) appropriateness of care models were closely allied with industrial models of quality assurance (e.g., quality control processes); 4) Joint Commission on Accreditation of Healthcare Organizations (JCAHO) requirements were burdensome; and 5) few validated models of quality assurance were readily available. This overview builds on the identification of the basic tenets and primary problems of "quality assurance" by discussing a number of the responses to the apparent problems that have been undertaken. Among these recent efforts to promote a national agenda for the field of quality assurance are the Health Care Financing Administration's (HCFA) Quality of Care Research Symposium (1987); the Office of Technology Assessment's (OTA) comprehensive review of Quality-of-Care indicators (1988); the Agency for Health Care Policy and Research's (AHCPR) medical treatment effectiveness research program (1990); and the Institute of Medicine's (IOM) 10-year implementation strategy for quality assurance activities in the Medicare program (1990). The results of these programs have been encouraging. However, many difficulties remain unresolved and the proliferation of program-based quality assurance efforts must continue to be scrutinized. In addition, the research indicates that the quest for quality cannot be divorced from the need to continually refine guidelines for the practice of medical care in the United States. C1 US DEPT VET AFFAIRS,HLTH SERV RES & DEV SERV,SPECIAL PROJECTS OFF,PERRY POINT,MD. NR 139 TC 11 Z9 11 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD AUG PY 1991 VL 29 IS 8 SU S BP AS8 EP AS28 PG 21 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GD431 UT WOS:A1991GD43100003 ER PT J AU GAMBARANA, C ORDWAY, GA HAUPTMANN, M TEJANIBUTT, S FRAZER, A AF GAMBARANA, C ORDWAY, GA HAUPTMANN, M TEJANIBUTT, S FRAZER, A TI CENTRAL ADMINISTRATION OF 1-ISOPROTERENOL INVIVO INDUCES A PREFERENTIAL REGULATION OF BETA-2-ADRENOCEPTORS IN THE CENTRAL-NERVOUS-SYSTEM OF THE RAT SO BRAIN RESEARCH LA English DT Article DE BETA-ADRENOCEPTOR; DOWN-REGULATION; ISOPROTERENOL; 6-HYDROXYDOPAMINE; NOREPINEPHRINE; ANTIDEPRESSANT ID BETA-ADRENERGIC RECEPTORS; QUANTITATIVE AUTORADIOGRAPHY; BETA-1-ADRENOCEPTOR BINDING; BETA-2-ADRENERGIC RECEPTORS; ADRENOCEPTOR SUBTYPES; SELECTIVE REGULATION; CLENBUTEROL; 6-HYDROXYDOPAMINE; AGONIST; BRAIN AB 1-Isoproterenol has equal affinity for beta-1- and beta-2-adrenoceptors and is a full agonist at both subtypes. However, when infused in vivo into the rat brain, it has been shown to induce a preferential reduction of central beta-2-adrenoceptors. To investigate this phenomenon further, in the present study rats were infused centrally with higher doses of 1-isoproterenol (15 or 45-mu-g/h). Furthermore, isoproterenol was infused into rats lesioned neonatally with 6-hydroxydopamine (6-OHDA). Subtypes of beta-adrenoceptors were measured by quantitative autoradiography of the binding of [I-125]iodopindolol ([I-125]IPIN). In sham lesioned rats, infusions of isoproterenol at both doses caused comparable reductions in the density of [I-125]IPIN binding sites in many brain regions. The binding to beta-2-adrenoceptors was decreased in a larger number of brain areas than the binding to beta-1-adrenoceptors and the magnitude of the reduction was greater for beta-2- than for beta-1-adrenoceptors. However, isoproterenol at these doses did produce greater effects on the beta-1-subtype than those found previously with a lower dose. Treatment with 6-OHDA induced significant increases in the binding of [I-125]IPIN to both beta-1- and beta-2-adrenoceptors in cerebral cortical and hippocampal areas, indicating that endogenous norepinephrine may regulate both subtypes in these regions. Even in the 6-OHDA-lesioned rats, the binding of [I-125]IPIN to beta-2-adrenoceptors was reduced to a greater extent that the binding to beta-1-adrenoceptors. Thus, these studies demonstrate that the non-selective beta-adrenergic agonist isoproterenol induces a preferential regulation of beta-2-adrenoceptors, even at relatively high doses and in norepinephrine-depleted animals. C1 VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHARMACOL,PHILADELPHIA,PA 19104. FU NIMH NIH HHS [MHO 9497, MH 29094, MH 14654] NR 37 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUL 26 PY 1991 VL 555 IS 1 BP 141 EP 148 DI 10.1016/0006-8993(91)90870-2 PG 8 WC Neurosciences SC Neurosciences & Neurology GA FZ606 UT WOS:A1991FZ60600019 PM 1657295 ER PT J AU SZERLIP, HM AF SZERLIP, HM TI RENAL-DOSE DOPAMINE - FACT AND FICTION SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material ID FAILURE; INFUSION RP SZERLIP, HM (reprint author), PHILADELPHIA VET AFFAIRS MED CTR,MED SERV 3,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 17 TC 44 Z9 46 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JUL 15 PY 1991 VL 115 IS 2 BP 153 EP 154 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FW091 UT WOS:A1991FW09100013 PM 2058863 ER PT J AU MA, XL BARAONA, E LASKER, JM LIEBER, CS AF MA, XL BARAONA, E LASKER, JM LIEBER, CS TI EFFECTS OF ETHANOL-CONSUMPTION ON BIOACTIVATION AND HEPATOTOXICITY OF N-NITROSODIMETHYLAMINE IN RATS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID ALCOHOL-CONSUMPTION; NITROGEN-DIOXIDE; HUMAN-LIVER; DIMETHYLNITROSAMINE; CYTOCHROME-P-450; CARCINOGENESIS; DEMETHYLATION; DENITROSATION; NITROSAMINES; PURIFICATION AB To study the effects of ethanol on the hepatotoxicity of N-nitrosodimethylamine (NDMA), 5 mg NDMA/kg body weight was injected intraperitoneally 3 times a week for 6 weeks into rats pair-fed liquid diets containing 36% of energy either as ethanol or as additional carbohydrates. Another group of rats was pair-fed with the same diets but injected with saline instead of NDMA. Co-administration of ethanol and NDMA produced much higher elevations of serum alanine and aspartate aminotransferase and glutamic dehydrogenase activities than the administration of either agent alone. The combined treatment also slightly increased focal necrosis, whereas other liver lesions (steatosis and fibrosis) and the functional impairment of mitochondrial respiration were not affected significantly. Microsomal low K(m) NDMA demethylation, as well as NDMA denitrosation, were inhibited markedly by incubation with an antibody against P450IIE1, suggesting the involvement of this alcohol-inducible P450 in both NDMA bioactivation reactions. The addition of ethanol inhibited P450-dependent demethylation and denitrosation of NDMA in liver microsomes, whereas both activities were enhanced markedly by chronic ethanol administration. At ethanol concentrations similar to those prevailing in the blood of alcohol-fed animals at the time of NDMA administration, hepatic microsomal demethylation and denitrosation remained significantly higher in ethanol-fed rats given NDMA than in controls. Our results suggest that bioactivation plays a critical role in the hepatotoxicity of NDMA and its aggravation by chronic alcohol consumption. C1 BRONX VET AFFAIRS MED CTR,LIVER DIS & NUTR SECT,BRONX,NY. BRONX VET AFFAIRS MED CTR,ALCOHOL RES CTR,BRONX,NY. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. FU NIAAA NIH HHS [AA-03508, AA-05934] NR 43 TC 11 Z9 11 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD JUL 15 PY 1991 VL 42 IS 3 BP 585 EP 591 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FY958 UT WOS:A1991FY95800018 PM 1859464 ER PT J AU DORN, GW AF DORN, GW TI TISSUE-SPECIFIC AND SPECIES-SPECIFIC DIFFERENCES IN LIGAND-BINDING TO THROMBOXANE-A2 RECEPTORS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PLATELETS; VASCULAR SMOOTH MUSCLE ID SMOOTH-MUSCLE CELLS; ACUTE MYOCARDIAL-INFARCTION; CARBOCYCLIC THROMBOXANE-A2; HUMAN-PLATELETS; BLOOD-VESSELS; ANTAGONIST; AGONIST; ACTIVATION; MECHANISM; ARTERIES AB The ligand binding site of vascular smooth muscle (VSM) and platelet thromboxane A2 (TxA2) receptors was characterized in humans and rabbits using the TxA2 mimetic [I-125]BOP. Vessel contraction and platelet aggregation studies demonstrated that unlabeled I-BOP and the prostaglandin H2 (PGH2) mimetic U-46619 were potent agonists in rabbit aortas, human saphenous veins, and washed human and rabbit platelets. [I-125]BOP bound saturably to a single site on cultured vascular smooth muscle (VSM) cells from rabbit aortas and human saphenous veins with dissociation constants (K(d)) of 392 +/- 8 (n = 5) and 390 +/- 120 pM (n = 6) and binding capacities (B(max)) of 5,322 +/- 200 and 2,017 +/- 322 sites/cell, respectively. [I-125]BOP also bound saturably to one site on rabbit platelets (K(d) = 415 +/- 15 pM, B(max) = 594 +/- 43 sites/platelets, n = 4) but, in agreement with previous studies, to two sites on human platelets (high-affinity K(d) = 118 +/- 24 pM, B(max) = 121 +/- 33 sites/platelet; low-affinity K(d) = 1.1 +/- 0.47 nM, B(max) 232 +/- 23 sites/platelet, n = 4). [I-125]BOP was displaced from its binding site on rabbit and human VSM and platelets by stable TxA2/PGH2 analogues possessing either agonist or antagonist activity but not by other prostaglandins. The rank orders of the binding inhibition constants (IC50) for the TxA2/PGH2 analogues were compared among the four tissues and were highly correlated (r = 0.963) in VSM and platelets from rabbits but not humans (r = 0.699), suggesting that human VSM TxA2 receptors may be distinct from platelet TxA2 receptors. The IC50 rank order was also highly correlated (r = 0.935) between human and rabbit platelets. However, the human and rabbit VSM IC50 rank orders differed significantly (r = 0.466), suggesting that VSM TxA2 receptors are dissimilar in these species. Collectively, these receptor binding studies strongly suggest the existence of TxA2 receptors that are both tissue and species specific. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78229. VET AFFAIRS MED CTR,CINCINNATI,OH 45267. RP DORN, GW (reprint author), UNIV CINCINNATI,COLL MED,DEPT MED CARDIOL,231 BETHESDA AVE,ML 542,CINCINNATI,OH 45267, USA. NR 33 TC 32 Z9 32 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 1991 VL 261 IS 1 BP R145 EP R153 PN 2 PG 9 WC Physiology SC Physiology GA FY357 UT WOS:A1991FY35700059 PM 1830459 ER PT J AU CARDOZO, C EDELMAN, J JAGIRDAR, J LESSER, M AF CARDOZO, C EDELMAN, J JAGIRDAR, J LESSER, M TI LIPOPOLYSACCHARIDE-INDUCED PULMONARY VASCULAR SEQUESTRATION OF POLYMORPHONUCLEAR LEUKOCYTES IS COMPLEMENT INDEPENDENT SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID DISSEMINATED INTRAVASCULAR COAGULATION; LUNG INJURY; GRANULOCYTE-ADHERENCE; COBRA VENOM; ENDOTOXIN; NEUTROPHIL; RATS; ACTIVATION; ALVEOLITIS; DEPLETION AB Lipopolysaccharide (LPS) injected intravenously produces leukopenia and sequestration of polymorphonuclear leukocytes (PMN) in the pulmonary vascular bed. To evaluate the role of complement in this process, we used C5-sufficient (B10.D2/nSn) and C5-deficient (B10.D2/oSn) mice and Sprague-Dawley rats depleted of complement with Naja naja cobra venom factor (CVF). We found a comparable increase in the number of PMN in lung tissue of C5-sufficient and C5-deficient mice given Escherichia coli LPS (0127:B8, 3 mg/kg), revealing that LPS acts independently of C5 and its biologically active fragments. Intravenous injection of LPS (3 mg/kg) into rats caused significant intravascular complement activation as assessed by serum CH50 and resulted in an almost 10-fold increase in numbers of PMN in lung tissue. Pretreatment of rats with CVF (50 U) did not reduce LPS-induced PMN sequestration, suggesting that the process is independent of C3. As reported previously, we found large numbers of PMN in bronchoalveolar lavage samples of rats 24 h after injection of LPS (3 mg/kg). Complement depletion did not prevent LPS-induced migration of PMN. No PMN migration occurred 2, 6, 12, 24, or 48 h after injection of CVF alone, indicating that complement activation is not sufficient to cause PMN migration. In contrast to our findings in rats, no PMN migrated into airspaces of C5-sufficient and C5-deficient mice 24 or 48 h after injection of LPS (3 to 20 mg/kg). C1 BRONX VET AFFAIRS MED CTR,PULM SECT,130 W KINGSBRIDGE RD,BRONX,NY 10468. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT PATHOL,NEW YORK,NY 10029. NYU MED CTR,NEW YORK,NY 10016. UNIV PENN,DIV CARDIOVASC PULM,PHILADELPHIA,PA 19104. NR 41 TC 21 Z9 21 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 JUL PY 1991 VL 144 IS 1 BP 173 EP 178 PG 6 WC Respiratory System SC Respiratory System GA FW296 UT WOS:A1991FW29600032 PM 2064126 ER PT J AU FANTIN, B LEGGETT, J EBERT, S CRAIG, WA AF FANTIN, B LEGGETT, J EBERT, S CRAIG, WA TI CORRELATION BETWEEN INVITRO AND INVIVO ACTIVITY OF ANTIMICROBIAL AGENTS AGAINST GRAM-NEGATIVE BACILLI IN A MURINE INFECTION MODEL SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID EXPERIMENTAL PNEUMOCOCCUS INFECTION; PHARMACOKINETIC PARAMETERS; BACTERICIDAL ACTIVITY; THIGH-INFECTION; MICE; THERAPY; PHARMACODYNAMICS; ANTIBIOTICS; BACTEREMIA; GENTAMICIN AB We studied the relationship between in vitro susceptibility tests (MICs, MBCs) and in vivo activity of tobramycin, pefloxacin, ceftazidime, and imipenem against 15 gram-negative bacilli from five different species in a murine thigh infection model. Complete dose-response curves were determined for each antimicrobial agent against each strain, and three parameters of in vivo activity were defined: maximal attainable antimicrobial effect (i.e., reduction in log10 CFU per thigh compared with untreated controls) at 24 h (E(max)), total dose required to reach 50% of maximal effect (P50), and total dose required to achieve a bacteriostatic effect (static dose). Pefloxacin demonstrated the greatest E(max) (P < 0.05). Tobramycin was the most potent antimicrobial agent, as indicated by its having the lowest static dose/MIC ratio (P < 0.002). Log10 P50S and static doses correlated significantly with log10 MICs or MBS for the 15 strains of each antibiotic (P < 0.01) except imipenem (P < 0.50). The greater potency of imipenem against the three Pseudomonas aeruginosa strains than against strains of the family Enterobacteriaceae (P < 0.01) explained this lack of correlation. A longer duration of postantibiotic effect for imipenem against P. aeruginosa (P = 0.02) contributed to its increased potency against these strains. We conclude that in vitro susceptibility tests correlated well with in vivo activity in this animal model and that variations in potency among the four antimicrobial agents could be explained by differences in pharmacokinetics or pharmacodynamic activity. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53792. UNIV WISCONSIN,DEPT MED,MADISON,WI 53792. NR 37 TC 64 Z9 65 U1 1 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JUL PY 1991 VL 35 IS 7 BP 1413 EP 1422 PG 10 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA FV098 UT WOS:A1991FV09800027 PM 1929302 ER PT J AU RICHLIE, DG WINTERS, S PROCHAZKA, AV AF RICHLIE, DG WINTERS, S PROCHAZKA, AV TI DYSLIPIDEMIA IN VETERANS - MULTIPLE RISK-FACTORS MAY BREAK THE BANK SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID CORONARY HEART-DISEASE; CHOLESTEROL LEVELS; MORTALITY; TRIAL AB The National Cholesterol Education Program guidelines for treatment of high cholesterol levels especially target patients who have multiple risk factors for coronary heart disease. Veterans have an increased prevalence of smoking, are predominantly male, and may have higher rates of other risk factors than other groups; therefore, they may require more aggressive screening and treatment for dyslipidemias. To assess the prevalence of cardiac risk factors, current cholesterol screening practices, and the potential impact of the National Cholesterol Education Program guidelines on the Veterans Affairs health care system, we reviewed 185 randomly selected charts of outpatients who were actively receiving follow-up at the Denver (Colo) Veterans Affairs Medical Center. The patients had an average age of 58.3 years and 99.5% were male. Of these patients, 60% had a serum cholesterol level checked within the last 999 days. Nearly all patients (84%) had two or more risk factors noted. The mean cholesterol level was 5.85 mmol/L (226 mg/dL), with 72% of patients having levels above 5.20 mmol/L (200 mg/dL) and 36.1% having levels above 6.20 mmol/L (240 mg/dL). Of patients who had their cholesterol level checked, 69% (77/111) would require lipoprotein analysis by National Cholesterol Education Program guidelines (cholesterol, greater-than-or equal-to 6.20 mmol/L [greater-than-or-equal-to 240 mg/dL] or 5.15 to 6.20 mmol/L [200 to 239 mg/dL] with two or more risk factors), yet only 16% (l2/77) had lipoprotein analyses done. Extrapolating from these data, the Denver Veteran Affairs Medical Center, which cares for 28 000 patients, has more than 19 000 patients who would need lipoprotein analysis to meet current guidelines. Full evaluation and subsequent treatment of dysilpidemias in veterans would require tremendous financial and manpower commitments. C1 UNIV COLORADO,HLTH SCI CTR,DIV GEN INTERNAL MED,DENVER,CO 80262. RP RICHLIE, DG (reprint author), DENVER VET AFFAIRS MED CTR,DIV AMBULATORY CARE,1055 CLERMONT,DENVER,CO 80220, USA. NR 17 TC 16 Z9 16 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD JUL PY 1991 VL 151 IS 7 BP 1433 EP 1436 DI 10.1001/archinte.151.7.1433 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA FW295 UT WOS:A1991FW29500025 PM 2064496 ER PT J AU SCHWESINGER, WH PAGE, CP SIRINEK, KR LEVINE, BA AUST, JB AF SCHWESINGER, WH PAGE, CP SIRINEK, KR LEVINE, BA AUST, JB TI BILIARY PANCREATITIS - OPERATIVE OUTCOME WITH A SELECTIVE APPROACH SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 98TH ANNUAL MEETING OF THE WESTERN SURGICAL ASSOC CY NOV 12, 1990 CL SCOTTSDALE, AZ SP W SURG ASSOC ID ACUTE GALLSTONE PANCREATITIS; SURGICAL-MANAGEMENT; SURGERY; DIAGNOSIS; TIME AB To evaluate the efficacy of a selective approach to biliary pancreatitis, we reviewed the outcomes in 276 consecutive patients undergoing operations for this diagnosis during a 7-year period. Initial conservative therapy resulted in elective operations in 63% and urgent operations in 37%. Only 10 patients (3.6%) required primary pancreatic operations, 50% of them as emergencies. The proportion of common duct surgical explorations fell from 70% of those operated immediately after hospital admission to 20% by the third hospital day. Overall mortality was 1.8% but was increased to 30% in patients having an initial pancreatic operation. We conclude that a selective approach to biliary pancreatitis allows the operation to be performed electively in most patients and is associated with a low mortality and an acceptable length of stay. Most common duct stones pass spontaneously permitting cholecystectomy alone. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP SCHWESINGER, WH (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT SURG,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 23 TC 24 Z9 24 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD JUL PY 1991 VL 126 IS 7 BP 836 EP 840 PG 5 WC Surgery SC Surgery GA FV562 UT WOS:A1991FV56200006 PM 1854243 ER PT J AU GIBBONS, WJ LEVINE, SM BRYAN, CL SEGARRA, J CALHOON, JH TRINKLE, JK JENKINSON, SG AF GIBBONS, WJ LEVINE, SM BRYAN, CL SEGARRA, J CALHOON, JH TRINKLE, JK JENKINSON, SG TI CARDIOPULMONARY EXERCISE RESPONSES AFTER SINGLE LUNG TRANSPLANTATION FOR SEVERE OBSTRUCTIVE LUNG-DISEASE SO CHEST LA English DT Article ID EMPHYSEMA; HEART; STANDARDS AB The purpose of this study was to characterize cardiovascular and ventilatory responses to exercise in single lung transplantation (SLT) recipients with nonseptic, severe obstructive lung disease (SLT-OB). We also investigated whether the hyperinlfated native lung in SLT-OB recipients could limit normal increases in tidal volume by mechanically constraining the transplanted lung, resulting in ventilation-perfusion imbalance in the lung graft. Data from six SLT-OB recipients (five women, one man) and six age-matched SLT recipients (two women, four men) with severe interstitial lung disease (SLT-IN) were compared. Resting arterial O2 and CO2 tensions were normal and comparable between the SLT groups. Spirometry results were reduced but comparable between SLT groups. Total lung capacity was significantly larger in patients with SLT-OB than in patients with SLT-IN. Diffusion capacity was not different between SLT groups when differences in alveolar volume were accounted for. Quantitative perfusion to the lung graft was comparable between the SLT groups, but quantitative ventilation was greater in patients with SLT-OB than in patients with SLT-IN. Maximum exercise capacity following SLT-OB was decreased, but was comparable to that of SLT-IN recipients. None of the SLT-OB recipients reached predicted maximum minute ventilation and only one experienced mild arterial O2 desaturation, suggesting peripheral muscle abnormalities from corticosteroid use and deconditioning as limiting factors rather than a ventilatory limitation. Tidal volumes at end exercise in the SLT-OB recipients were normal. Our quantitative lung scan and exercise testing data suggest that ventilation-perfusion imbalance and resulting gas exchange abnormalities from lung graft constraint and compression do not occur at rest or with exercise after SLT for obstructive lung disease. C1 AUDIE L MURPHY MEM VET ADM MED CTR,PULM SECT 111E,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78221. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. FU PHS HHS [H-30556] NR 24 TC 42 Z9 42 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD JUL PY 1991 VL 100 IS 1 BP 106 EP 111 DI 10.1378/chest.100.1.106 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA FV610 UT WOS:A1991FV61000023 PM 2060328 ER PT J AU HARRITY, P PATEL, A BIANCO, J SUBRAMANIAN, R AF HARRITY, P PATEL, A BIANCO, J SUBRAMANIAN, R TI IMPROVED DIAGNOSIS AND CHARACTERIZATION OF POSTINFARCTION LEFT-VENTRICULAR PSEUDOANEURYSM BY CARDIAC MAGNETIC-RESONANCE-IMAGING SO CLINICAL CARDIOLOGY LA English DT Article DE MAGNETIC RESONANCE IMAGING; PSEUDOANEURYSM; LEFT VENTRICLE; MYOCARDIAL INFARCTION ID ACUTE MYOCARDIAL-INFARCTION; ANEURYSMS; RUPTURE AB A patient with a ruptured left ventricular pseudoaneurysm complicating an acute posteroinferior myocardial infarction is described. Left ventricular pseudoaneurysms are a rare complication of acute myocardial infarction, usually occurring with inferior and/or posterior infarction. In contrast to true aneurysms, pseudoaneurysms are much more likely to rupture, regardless of size, causing hemopericardium and death. Therefore, once the diagnosis has been confirmed, prompt surgical resection is the current accepted treatment. The most accurate noninvasive diagnostic method has been echocardiography, with recent reports suggesting improved diagnosis with color flow Doppler echocardiography. Ventriculography confirms the diagnosis with more accurate anatomic detail, but is an invasive procedure. In our patient, two-dimensional and color Doppler echocardiography could not demonstrate the suspected pseudoaneurysm, which was demonstrated by ventriculography. However, magnetic resonance imaging (MRI) demonstrated the pseudoaneurysm, showing detailed anatomy not obvious on ventriculography. Before surgery could be performed, the patient died and was autopsied. Heart sections corresponding to MRI planes confirmed the MRI findings. A review of the literature has revealed no similar reports using MRI in the diagnosis of postinfarction pseudoaneurysms. Major advantages of MRI are generation of three-dimensional soft tissue images noninvasively, and generation of tissue contrast by rapid imaging sequences, obviating the need for contrast injection. Major disadvantages of MRI are the high cost of instrumentation, nonportability, and a requirement for patient immobility during the study. In cases of suspected pseudoaneurysm with equivocal echocardiography findings, MRI could provide early diagnosis, leading to early surgical intervention and increased patient survival. C1 UNIV WISCONSIN HOSP,DEPT RADIOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT CARDIOL,MADISON,WI 53705. NR 11 TC 23 Z9 24 U1 0 U2 0 PU CLINICAL CARDIOLOGY PUBL CO PI MAHWAH PA PO BOX 832, MAHWAH, NJ 07430-0832 SN 0160-9289 J9 CLIN CARDIOL JI Clin. Cardiol. PD JUL PY 1991 VL 14 IS 7 BP 603 EP 606 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FV022 UT WOS:A1991FV02200012 PM 1747971 ER PT J AU TAKAHASHI, LK TURNER, JG KALIN, NH AF TAKAHASHI, LK TURNER, JG KALIN, NH TI DEVELOPMENT OF STRESS-INDUCED RESPONSES IN PREWEANLING RATS SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article ID ULTRASONIC VOCALIZATIONS; RATTUS-NORVEGICUS; NEONATAL RAT; ALBINO-RATS; SHOCK; PUPS; CORTICOTROPIN; PITUITARY; BEHAVIOR; ONTOGENY AB This study examined in postnatal Days 7, 14, and 21 male rats the effects of social isolation and social isolation with administration of brief foot shocks on the development of stress-induced behavioral and pituitary-adrenal hormone responses. Day 21 rats appeared similar to adult rats in their responses to the two test conditions. That is, exposure to either isolation or to shock increased both pituitary-adrenal hormone secretion and tail-flick latencies but only administration of shock potentiated freezing and ultrasonic vocalizations. Younger rats differed from Day 21 rats in their responses to the two test conditions. In both tests, Day 7 rats produced the highest number of ultrasounds, which may be due to a significant decrease in body temperature. In contrast, in Day 14 pups, exposure to shock significantly reduced isolation-induced ultrasonic vocalizations. Additional age-dependent differences were found in the analgesic responses of Days 7 and 14 rats. Day 7 rats exposed to stress became consistently hyperalgesic whereas Day 14 rats showed only a short-lasting analgesic response. Although in Days 7 and 14 rats exposure to the two stress conditions produced significant elevations in pituitary-adrenal hormone concentrations, plasma levels were lower than those measured in Day 21 rats. To summarize, preweanling rats exhibit varied age-dependent responses when exposed to different stress environments. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,MADISON,WI 53706, USA. FU NIMH NIH HHS [MH-43986] NR 35 TC 22 Z9 22 U1 1 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0012-1630 J9 DEV PSYCHOBIOL JI Dev. Psychobiol. PD JUL PY 1991 VL 24 IS 5 BP 341 EP 360 DI 10.1002/dev.420240504 PG 20 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA GM919 UT WOS:A1991GM91900003 PM 1661243 ER PT J AU HEATHER, DJ HOWELL, L MONTANA, M HOWELL, M HILL, R AF HEATHER, DJ HOWELL, L MONTANA, M HOWELL, M HILL, R TI EFFECT OF A BULK-FORMING CATHARTIC ON DIARRHEA IN TUBE-FED PATIENTS SO HEART & LUNG LA English DT Article AB Diarrhea is a significant complication for the patient being tube-fed. The purpose of this study was to observe whether giving a bulk-forming cathartic to patients receiving enteral nutrition via nasogastric or nasoduodenal tube would result in firmer stools for these patients. Forty-nine patients in a large medical center were randomly assigned to either a control or an experimental group. During the 6-day study period 1 teaspoon (5 ml) of psyllium preparation was administered through the feeding tube three times a day. Data were analyzed by using the Mann-Whitney U test for nonparametric data. The hypothesis that giving a bulk-forming cathartic would lead to firmer stools was supported at an alpha level of less than 0.01. The results of this study suggest that use of a bulk-forming cathartic in tube-fed patients will significantly reduce the diarrhea associated with this type of feeding. C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 0 TC 17 Z9 17 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0147-9563 J9 HEART LUNG JI Heart Lung PD JUL PY 1991 VL 20 IS 4 BP 409 EP 413 PG 5 WC Cardiac & Cardiovascular Systems; Nursing; Respiratory System SC Cardiovascular System & Cardiology; Nursing; Respiratory System GA FZ436 UT WOS:A1991FZ43600015 PM 1906447 ER PT J AU SULLIVAN, G WELLS, KB LEAKE, B AF SULLIVAN, G WELLS, KB LEAKE, B TI QUALITY-OF-LIFE OF SERIOUSLY MENTALLY-ILL PERSONS IN MISSISSIPPI SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Note C1 UNIV CALIF LOS ANGELES,DEPT GEN INTERNAL MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,ROBERT WOOD JOHNSON CLIN SCHOLARS PROGRAM,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT,BRENTWOOD,CA. RP SULLIVAN, G (reprint author), RAND CORP,1700 MAIN ST,SANTA MONICA,CA 90406, USA. NR 9 TC 64 Z9 64 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 JUL PY 1991 VL 42 IS 7 BP 752 EP 755 PG 4 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA FU493 UT WOS:A1991FU49300021 PM 1885191 ER PT J AU DUGGER, KO GALGIANI, JN AMPEL, NM SUN, SH MAGEE, DM HARRISON, J LAW, JH AF DUGGER, KO GALGIANI, JN AMPEL, NM SUN, SH MAGEE, DM HARRISON, J LAW, JH TI AN IMMUNOREACTIVE APOGLYCOPROTEIN PURIFIED FROM COCCIDIOIDES-IMMITIS SO INFECTION AND IMMUNITY LA English DT Article ID SUBMAXILLARY-GLAND APOMUCIN; TUBE PRECIPITIN; WALL FRACTION; ANTIGEN; ANTIBODY; PROTEIN; INFECTION; RESPONSES; PURIFICATION; RESISTANCE AB Deglycosylation of glycoproteins in a lysate of spherules of Coccidioides immitis has permitted purification and partial characterization of a proline-rich pronase-sensitive antigen. Moreover, soluble antigen specifically stimulated lymphocytes from persons with dermal delayed-type hypersensitivity to coccidiodial antigens. When related to reference coccidioidin by tandem two-dimensional immunoelectrophoresis, the antigen fused in the anodal region with a specific reference antigen (antigen 2). It did not show identity with coccidiodial antigens used in conventional serologic assays. Although immunoblots of the purified protein with monospecific rabbit and serum showed a single antigen at 33 kDa, the parent spherule lysate bound the same antibody in a broad band between 70 and > 200 kDa, which could be explained by microheterogeneity of glycosylation. Immunoelectron microscopy using affinity-purified human antibodies localized the antigen to the cell wall and internal septa of spherules. These findings suggest that the apoglycoprotein may be important in human immune responses to coccidioidal infection. C1 VET AFFAIRS MED CTR,MED SERV,TUCSON,AZ 85723. VET AFFAIRS MED CTR,RES SERV,SAN ANTONIO,TX 78284. UNIV ARIZONA,DEPT BIOCHEM,TUCSON,AZ 85724. VET AFFAIRS MED CTR,MED SERV,TUCSON,AZ 85723. UNIV ARIZONA,COLL MED,DEPT MED,TUCSON,AZ 85724. NR 48 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 1991 VL 59 IS 7 BP 2245 EP 2251 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FT922 UT WOS:A1991FT92200004 PM 2050396 ER PT J AU MAGEE, DM WILLIAMS, DM WING, EJ BLEICKER, CA SCHACHTER, J AF MAGEE, DM WILLIAMS, DM WING, EJ BLEICKER, CA SCHACHTER, J TI PRODUCTION OF COLONY-STIMULATING FACTORS DURING PNEUMONIA CAUSED BY CHLAMYDIA-TRACHOMATIS SO INFECTION AND IMMUNITY LA English DT Article ID LISTERIA-MONOCYTOGENES; GAMMA INTERFERON; PROGENITOR CELLS; MICE; MOUSE; INFECTION; IMMUNITY; GROWTH; AGENT AB The colony-stimulating factors (CSFs) are cytokines involved in the production, differentiation, and activation of host phagocytes. During murine infection with Chlamydia trachomatis (MoPn), plasma CSF levels increased in euthymic (nu/+) and athymic (nu/nu) BALB/c mice. Levels declined later in infection, with the nu/+ mice resolving the infection but the nu/nu mice succumbing by day 16. Either live or heat-killed Chlamydia organisms could induce CSF increases on day 7 postchallenge in nu/+ mice; however, by day 14, only mice challenged with live organims maintained high plasma levels. CSFs were also produced by spleen cells of nu/+ and nu/nu mice in response to Chlamydia antigen. Spleen cell CSF production was detectable by days 3 to 5 postinfection. In nu/+ mice, spleen cell CSF production was elevated throughout the rest of the time course but in nu/nu mice fell significantly at day 14. Like the plasma CSF activity (CSA) production, spleen cell CSA production on day 7 was seen in mice challenged with either live or heat-killed Chlamydia organisms, but on day 14 only nu/+ mice challenged with live organisms maintained significant CSA production. To further characterize the T-cell dependence of CSA production, spleen cells of nu/+ mice were depleted of T cells or T-cell subsets before producing supernatants. On day 14 postinfection, the CD4+ lymphocyte was the major producer of CSFs. Additionally, there were different types of CSFs secreted by nu/+ and nu/nu mice as determined by the ability of spleen cell supernatants to support the granulocyte-macrophage CSF/interleukin 3-dependent cell line FDCP-1. Supernatants from nu/+ mice had 4 to 8 times the level of FDCP-1 CSF activity of the supernatants from nu/nu mice. These results support the evidence that nu/+ mice were producing some CSFs by T-cell-dependent mechanisms. This is the first report of CSF production in vivo during Chlamydia infection. Furthermore, we show that CSFs are produced by both T-cell-dependent and T-cell-independent mechanisms. The capacity of the CSFs to increase the production and effector function of phagocytes may be important to host defenses. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV INFECT DIS,SAN ANTONIO,TX 78284. UNIV PITTSBURGH,SCH MED,DEPT MED,PITTSBURGH,PA 15213. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94132. RP MAGEE, DM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [AI 24141, AI 22380] NR 24 TC 13 Z9 13 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 1991 VL 59 IS 7 BP 2370 EP 2375 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FT922 UT WOS:A1991FT92200022 PM 1828791 ER PT J AU HAFFNER, SM KATZ, MS DUNN, JF AF HAFFNER, SM KATZ, MS DUNN, JF TI INCREASED UPPER-BODY AND OVERALL ADIPOSITY IS ASSOCIATED WITH DECREASED SEX-HORMONE BINDING GLOBULIN IN POSTMENOPAUSAL WOMEN SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE SEX HORMONE BINDING GLOBULIN; BODY FAT DISTRIBUTION ID DEPENDENT DIABETES-MELLITUS; HIGH-DENSITY LIPOPROTEIN-2; FAT DISTRIBUTION; CARDIOVASCULAR-DISEASE; TISSUE DISTRIBUTION; INSULIN RESISTANCE; CENTRALIZED ADIPOSITY; POSTHEPARIN PLASMA; MEXICAN-AMERICANS; HDL-CHOLESTEROL AB An unfavorable body fat distribution is associated with many metabolic abnormalities including a high prevalence and incidence of noninsulin dependent diabetes mellitus and decreased high density lipoprotein cholesterol and increased triglyceride levels. One mechanism for the effect of body fat distribution on metabolic variables may be through sex hormones. We examined the relationship of body mass index (BMI), ratio of subscapular-to-triceps skinfold ratio (centrality index) and ratio of waist-to-hip ratio (WHR) to sex hormone binding globulin (SHBG) (an in vivo measure of androgenicity) in 101 postmenopausal Mexican-American and non-Hispanic white women from the San Antonio Heart Study,a population based study of diabetes and cardiovascular disease. SHBG was significantly correlated with BMI (r = -0.440,P < 0.001), WHR (r = -0.255, P < 0.01) and centrality index (r = -0.210,P < 0.05). In a multiple linear regression analysis, SHBG remained significantly associated with BMI (P < 0.001) and WHR (P < 0.05) but not with age, ethnicity or centrality index. This work suggests that in postmenopausal women overall adiposity and an unfavorable body fat distribution are associated with increased androgenicity as measured by a lower SHBG concentration. Our finding may help to explain the association of body fat distribution with diabetes and cardiovascular risk factors in older women. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. 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 ENDOCRINOL & METAB,SAN ANTONIO,TX 78284. RP HAFFNER, SM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN EPIDEMIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU NCRR NIH HHS [RR-01346]; NHLBI NIH HHS [HL-24799] NR 54 TC 101 Z9 101 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD JUL PY 1991 VL 15 IS 7 BP 471 EP 478 PG 8 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA FV207 UT WOS:A1991FV20700005 PM 1894424 ER PT J AU KOMADINA, KH DUNCAN, CA BRYAN, CL JENKINSON, SG AF KOMADINA, KH DUNCAN, CA BRYAN, CL JENKINSON, SG TI PROTECTION FROM HYPERBARIC OXIDANT STRESS BY ADMINISTRATION OF BUTHIONINE SULFOXIMINE SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE GLUTATHIONE; GAMMA GLUTAMYL CYSTEINE SYNTHASE; HYPERBARIC OXYGEN TOXICITY ID OXYGEN-TOXICITY; GLUTATHIONE DEPLETION; REDUCED GLUTATHIONE; HYPEROXIA; INHIBITION; METABOLISM; INVIVO; CELLS; RATS AB To explore the role of glutathione in protecting rats from hyperbaric hyperoxia, we administered buthionine sulfoximine (BSO) to block gamma-glutamyl cysteine synthase activity and decrease tissue glutathione synthesis. We then exposed these animals and their vehicle-treated matched controls to 100% oxygen at 4 ATA or room air at 1 ATA. After BSO treatment, glutathione concentrations in air-exposed controls decreased 62% in lung, 76% in liver, 28% in brain, and 62% in plasma. Paradoxically, BSO-treated rats were protected from hyperbaric hyperoxia. The BSO-treated animals seized significantly later and had a markedly prolonged time of survival compared with the vehicle-treated controls. We conclude that BSO treatment protects rats from hyperbaric hyperoxia, despite its effects of lowering plasma and tissue glutathione concentrations. This protection may be related to a direct effect of the compound in decreasing free radical-mediated tissue injury, increasing tissue antioxidant defenses, or increasing seizure threshold. C1 AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT,111E,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,LUNG METAB UNIT,SAN ANTONIO,TX 78284. FU NHLBI NIH HHS [HL-30556] NR 29 TC 10 Z9 10 U1 0 U2 2 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 1991 VL 71 IS 1 BP 352 EP 358 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA FV262 UT WOS:A1991FV26200051 PM 1680846 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R FERRARI, MM AF SILVA, JA LEONG, GB WEINSTOCK, R FERRARI, MM TI MISIDENTIFIED POLITICAL FIGURES - AN UNDERAPPRECIATED DANGER SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; MISIDENTIFICATION SYNDROMES; POLITICAL FIGURES; VIOLENCE ID CAPGRAS SYNDROME; PSYCHIATRIC-PATIENTS; DELUSIONS; VIOLENCE; SERVICE AB A series of twelve patients is presented in which each patient suffered from one or more misidentification syndromes and also misidentified one or more political figures. The fact that misidentification syndromes have been associated with physical violence and that the majority of the patients studied had a history of physical violence suggests that these individuals could pose a significant danger of physical harm to others, including political figures. Persons who threaten political figures should be evaluated for misidentification syndromes. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,STUDENT PSYCHOL SERV,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. NR 38 TC 10 Z9 10 U1 1 U2 1 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 1991 VL 36 IS 4 BP 1170 EP 1178 PG 9 WC Medicine, Legal SC Legal Medicine GA FY039 UT WOS:A1991FY03900027 PM 1919476 ER PT J AU LICHTENSTEIN, MJ PINCUS, T AF LICHTENSTEIN, MJ PINCUS, T TI RHEUMATOID-ARTHRITIS IDENTIFIED IN POPULATION BASED CROSS-SECTIONAL STUDIES - LOW PREVALENCE OF RHEUMATOID-FACTOR SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE RHEUMATOID ARTHRITIS; RHEUMATOID FACTOR; EPIDEMIOLOGY ID SIGNIFICANT RADIOGRAPHIC DAMAGE; 1ST 2 YEARS; WORK DISABILITY; FOLLOW-UP; DISEASE; MORTALITY; QUESTIONNAIRE; PROGNOSIS; CRITERIA; TIME AB All 5 cross sectional population based studies which included evaluation of all subjects for both rheumatoid factor (RF) and rheumatoid arthritis (RA) were reviewed. RF was found in only 19-33% of individuals who met the 1958 ARA criteria for RA. Many individuals identified in these studies met criteria for only "probable" or "possible" RA according to the 1958 criteria, and might not meet the 1987 criteria. However, RF was found in only 26-60% of subjects who met criteria for "definite" RA in the studies that included this information. Population based studies of RA often have been interpreted as applicable to clinical RA patients, which may explain in part different views of RA as both a mild and a progressive disease. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT MED,DIV RHEUMATOL & IMMUNOL,T-3219 MED CTR N,NASHVILLE,TN 37232. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM-21393] NR 45 TC 44 Z9 44 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 JUL PY 1991 VL 18 IS 7 BP 989 EP 993 PG 5 WC Rheumatology SC Rheumatology GA FY159 UT WOS:A1991FY15900010 PM 1920334 ER PT J AU PRESTI, CF WALLING, AD MONTEMAYOR, I CAMPBELL, JM CRAWFORD, MH AF PRESTI, CF WALLING, AD MONTEMAYOR, I CAMPBELL, JM CRAWFORD, MH TI INFLUENCE OF EXERCISE-INDUCED MYOCARDIAL-ISCHEMIA ON THE PATTERN OF LEFT-VENTRICULAR DIASTOLIC FILLING - A DOPPLER ECHOCARDIOGRAPHIC STUDY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; PACING-INDUCED ISCHEMIA; RADIONUCLIDE ANGIOGRAPHY; FLOW VELOCITY; HYPERTROPHIC CARDIOMYOPATHY; ANGIOPLASTY; RELAXATION; REST; PERFORMANCE; DYSFUNCTION AB Previous studies using Doppler echocardiography to evaluate left ventricular diastolic filling have shown that myocardial ischemia induced by coronary balloon angioplasty or atrial pacing results in a decrease in the left ventricular inflow peak early (E) to peak atrial (A) velocity ratio. To investigate the effects of exercise-induced ischemia on Doppler-derived filling variables, 20 patients with coronary artery disease and exercise-induced electrocardiographic changes and regional wall motion abnormalities determined by two-dimensional echocardiography were evaluated and compared with 20 patients without evidence of exercise-induced ischemia. Doppler echocardiography was performed at rest and immediately after exercise before the resolution of exercise-induced wall motion abnormalities. Peak E and A velocities increased from rest to postexercise in both the ischemic and nonischemic groups, although the ischemic group demonstrated a greater increase in peak E velocity (from 68 +/- 15 cm/s at rest to 88 +/- 22 cm/s after exercise) than the nonischemic group (70 +/- 13 to 77 +/- 18 cm/s) (p < 0.05 for the difference in response between groups). Accompanying these changes was a slight increase in the peak E/A velocity ratio in the ischemic group (1.04 +/- 0.28 at rest to 1.13 +/- 0.42 after exercise) versus a decrease in the nonischemic group (1.07 +/- 0.30 to 0.90 +/- 0.28) (p < 0.05 intergroup difference). Within the ischemic group, the change from rest to postexercise in peak E/A velocity ratio was related to changes in left ventricular wall motion score (r = 0.61, p = 0.004) and inversely to changes in left ventricular ejection fraction (r = -0.61, p = 0.004) but not to changes in heart rate (r = -0.30, p = NS). This study demonstrates that during exercise-induced ischemia, early diastolic filling is not blunted but is instead maintained. This observation correlates with changes in left ventricular systolic function, suggesting that exercise-induced ischemia may lead to greater increases in left atrial pressure, which augments peak E velocity and results in pseudonormalization of the diastolic Doppler velocity profile. C1 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 37 TC 40 Z9 40 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 JUL PY 1991 VL 18 IS 1 BP 75 EP 82 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FU815 UT WOS:A1991FU81500013 PM 2050945 ER PT J AU CUMMINGS, JL AF CUMMINGS, JL TI BEHAVIORAL COMPLICATIONS OF DRUG-TREATMENT OF PARKINSONS-DISEASE SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID BROMOCRIPTINE-INDUCED MANIA; L-DOPA; LEVODOPA THERAPY; PSYCHOSIS; HYPERSEXUALITY; HALLUCINATIONS; CLOZAPINE; SYMPTOMS; DISTURBANCES; MESULERGINE AB A variety of neuropharmacologic agents, including anticholinergic drugs, amantadine hydrochloride, levodopa, selegiline, bromocriptine, and pergolide, are now available for the treatment of Parkinson's disease. Of patients treated with dopaminergic agents, 30% develop visual hallucinations, 10% exhibit delusions, 10% have euphoria, 1% have mania, 10% to 15% experience increased anxiety, 15% have confusional periods, and a few exhibit altered sexual behaviour. Anticholinergic drugs have a greater tendency to produce confusional states than dopaminergic compounds. Elderly patients and those with underlying dementia are most likely to have untoward side effects with anti-parkinsonism treatment. Dosage reduction is the optimum management strategy, although anti-psychotic agents may be necessary in patients with delusions, and lithium may help control drug-induced mania. Dopaminergic agents share the property of stimulation of D2 dopamine receptors, and this action may play an essential role in mediating their neuropsychiatric effects. C1 UNIV CALIF LOS ANGELES,DEPT NEUROL & PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT BEHAV SCI,LOS ANGELES,CA 90024. RP CUMMINGS, JL (reprint author), W LOS ANGLES VET AFFAIRS MED CTR,BEHAV NEUROSCI SECT,PSYCHIAT SERV,NEUROBEHAV UNIT,BLDG 256B,LOS ANGELES,CA 90073, USA. NR 89 TC 127 Z9 127 U1 0 U2 4 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 JUL PY 1991 VL 39 IS 7 BP 708 EP 716 PG 9 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA FU969 UT WOS:A1991FU96900012 PM 2061539 ER PT J AU SACHDEVA, AK ZAREN, HA SIGEL, B AF SACHDEVA, AK ZAREN, HA SIGEL, B TI SURGICAL-TREATMENT OF PEPTIC-ULCER DISEASE SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID PROXIMAL GASTRIC-VAGOTOMY; BLEEDING GASTRODUODENAL ULCERS; PERFORATED DUODENAL-ULCER; UPPER GASTROINTESTINAL HEMORRHAGE; HIGHLY SELECTIVE VAGOTOMY; CONTROLLED TRIAL; SIMPLE CLOSURE; PYLORIC-STENOSIS; HEATER PROBE; MANAGEMENT C1 MED COLL PENN,SURG EDUC,PHILADELPHIA,PA 19129. VET AFFAIRS MED CTR,SURG SERV,PHILADELPHIA,PA. RP SACHDEVA, AK (reprint author), MED COLL PENN,DEPT SURG,3300 HENRY AVE,PHILADELPHIA,PA 19129, USA. NR 56 TC 16 Z9 16 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD JUL PY 1991 VL 75 IS 4 BP 999 EP 1012 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA FX347 UT WOS:A1991FX34700016 PM 2072800 ER PT J AU MITTLER, JC AF MITTLER, JC TI TESTICULAR AUTOREGULATION - POSSIBLE ROLE FOR 7-ALPHA-HYDROXYLATED ANDROGENS SO MEDICAL HYPOTHESES LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; LUTEINIZING-HORMONE; MALE-RAT; SEMINIFEROUS TUBULES; GONADOTROPIN-SECRETION; INTERSTITIAL-TISSUE; IN-VITRO; HYPOPHYSECTOMIZED RATS; ANTERIOR-PITUITARY; RHESUS-MONKEY AB Pituitary FSH secretion appears to be supported by a tactor distinct from the gonadotropin-releasing hormone (Gn-RH). The ratio of FSH to LH is positively correlated with testicular steroid 5 alpha -reductase activity and negatively correlated with testicular steroid 7 alpha- hydroxylase under various experimental conditions. Literature describing interactions among the above and other factors is reviewed here. C1 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT MED,NEWARK,NJ 07103. RP MITTLER, JC (reprint author), US DEPT VET AFFAIRS,MED CTR,MED SERV,E ORANGE,NJ 07019, USA. NR 85 TC 1 Z9 1 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD JUL PY 1991 VL 35 IS 3 BP 184 EP 191 DI 10.1016/0306-9877(91)90231-M PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FW619 UT WOS:A1991FW61900004 PM 1943861 ER PT J AU DUMITRU, D KALANTRI, A DIERSCHKE, B AF DUMITRU, D KALANTRI, A DIERSCHKE, B TI SOMATOSENSORY EVOKED-POTENTIALS OF THE MEDIAL AND LATERAL PLANTAR AND CALCANEAL NERVES SO MUSCLE & NERVE LA English DT Article DE SOMATOSENSORY EVOKED POTENTIALS; PLANTAR NERVE; TARSAL TUNNEL; ELECTRODIAGNOSIS; CALCANEAL NERVE ID TARSAL TUNNEL-SYNDROME; NERVOUS-SYSTEM; CONDUCTION; STIMULATION; NEUROPATHY; DIAGNOSIS AB The ideal electrodiagnostic procedure to assess possible plantar neuropathies continues to elude investigators. Motor studies are rarely abnormal, pure sensory studies may be difficult to obtain, needle electromyography can demonstrate membrane instability in normal feet. Mixed nerve plantar studies may be more diagnostically valuable than the other techniques but they also have shortcomings. In this report, a technique utilizing somato-sensory evoked potentials to assess the medial and lateral plantar and calcaneal nerves is demonstrated. Normative data with respect to latencies, amplitudes, and side-to-side differences are presented. Two illustrative cases are also discussed in which the more standard techniques to evaluate plantar neuropathies fail to do so, but the SEP methodology suggests compromise of the intrinsic foot nerves. C1 AUDIE L MURPHY MEM VET ADM MED CTR,REHABIL SERV,SAN ANTONIO,TX. ORTHOPAED SURG ASSOCIATES,DAVENPORT,IA. RP DUMITRU, D (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PHYS MED & REHABIL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 34 TC 11 Z9 11 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD JUL PY 1991 VL 14 IS 7 BP 665 EP 671 DI 10.1002/mus.880140710 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FT153 UT WOS:A1991FT15300009 PM 1656250 ER PT J AU SMALL, GW EBELING, SC MATSUYAMA, SS HEYMAN, A REISNER, EG RENVOIZE, EB SULKAVA, R AF SMALL, GW EBELING, SC MATSUYAMA, SS HEYMAN, A REISNER, EG RENVOIZE, EB SULKAVA, R TI VARIABLE ASSOCIATION OF HLA-A2 IN MEN WITH EARLY-ONSET ALZHEIMER-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Note DE ALZHEIMER DISEASE; HLA ANTIGENS; AGE AT ONSET ID ANTIGENS AB In the present study, we attempted to replicate the finding of an increased frequency of HLA-A2 in men with early-onset (less-than-or-equal-to 60 years) Alzheimer disease (AD). HLA data obtained on 167 patients (including 19 men with early-onset AD) from three geographic regions (North Carolina. Great Britain, and Finland) failed to replicate the result. A recent prospective study from Oregon, however, confirmed the association. Studies demonstrating the association suggest its presence in sporadic rather than familial AD. These results indicate a variable HLA/AD association, with some factor such as geographic region or disease familiality contributing to this variability. C1 WAYNE STATE UNIV,DETROIT,MI 48202. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. DUKE UNIV,DURHAM,NC 27706. UNIV HELSINKI,SF-00100 HELSINKI 10,FINLAND. UNIV LEEDS,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. RP SMALL, GW (reprint author), UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. FU NIMH NIH HHS [1R29 MH46424] NR 11 TC 12 Z9 12 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD JUL-AUG PY 1991 VL 12 IS 4 BP 375 EP 377 DI 10.1016/0197-4580(91)90026-G PG 3 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA GB995 UT WOS:A1991GB99500026 PM 1961374 ER PT J AU NEWMAN, LH SALTZMAN, B AF NEWMAN, LH SALTZMAN, B TI IDENTIFYING RISK-FACTORS IN DEVELOPMENT OF CLINICALLY SIGNIFICANT POST-SHOCK-WAVE LITHOTRIPSY SUBCAPSULAR HEMATOMAS SO UROLOGY LA English DT Article ID EXTRACORPOREAL; COMPLICATIONS AB A retrospective study of 1,012 shock-wave lithotripsy treatments was performed to identify and analyze the risk factors for the development of six clinically significant post-extracorporeal shock-wave lithotripsy (ESWL) subcapsular hematomas. The patients studied had clinical signs and symptoms that on evaluation were confirmed as originating from a subcapsular hematoma. Common factors identified which we believe may put patients at increased risk for the development of subcapsular hematoma included hypertension, diabetes mellitus, coronary artery disease, and obesity. C1 BRONX VET AFFAIRS MED CTR,NEW YORK,NY. RP NEWMAN, LH (reprint author), MT SINAI MED CTR,SCH MED,DEPT UROL,5 E 98TH ST,NEW YORK,NY 10029, USA. NR 12 TC 36 Z9 40 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD JUL PY 1991 VL 38 IS 1 BP 35 EP 38 DI 10.1016/0090-4295(91)80009-V PG 4 WC Urology & Nephrology SC Urology & Nephrology GA FW772 UT WOS:A1991FW77200008 PM 1866855 ER PT J AU MAHLER, ME CUMMINGS, JL AF MAHLER, ME CUMMINGS, JL TI BEHAVIORAL NEUROLOGY OF MULTIINFARCT DEMENTIA SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article ID CEREBRAL BLOOD-FLOW; ALZHEIMERS-DISEASE; VASCULAR DEMENTIA; PERSONALITY ALTERATIONS; MULTIINFARCT DEMENTIA; BINSWANGER TYPE; MOOD DISORDERS; LANGUAGE; STROKE; PERFORMANCE AB Multi-infarct dementia (MID) is a heterogeneous entity in which a variety of cerebrovascular disorders leads to intellectual impairment. A variety of patterns of behavioral changes may be observed in MID, depression, psychosis, and personality change are common. The neurobehavioral syndromes of MID are determined by the specific arteries involved and the location and extent of tissue infarction. C1 W LOS ANGELES VET AFFAIRS MED CTR, NEUROBEHAV UNIT B111, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEH SCI, LOS ANGELES, CA 90024 USA. NR 52 TC 29 Z9 29 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD SUM PY 1991 VL 5 IS 2 BP 122 EP 130 DI 10.1097/00002093-199100520-00009 PG 9 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA GU430 UT WOS:A1991GU43000009 PM 2059404 ER PT J AU WARPINSKI, JR BUSH, RK AF WARPINSKI, JR BUSH, RK TI LATEX HYPERSENSITIVITY SO AMERICAN JOURNAL OF MEDICINE LA English DT Letter C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP WARPINSKI, JR (reprint author), INTERMT ALLERGY & ASTHMA CLIN,SALT LAKE CITY,UT, USA. NR 4 TC 2 Z9 2 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 JUN PY 1991 VL 90 IS 6 BP 769 EP 769 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FR832 UT WOS:A1991FR83200024 PM 2042700 ER PT J AU CHIANG, YY TAKEBAYASHI, S OBERLEY, TD AF CHIANG, YY TAKEBAYASHI, S OBERLEY, TD TI INVITRO ANALYSIS OF EXTRACELLULAR-MATRIX PRODUCTION BY PORCINE GLOMERULAR MESANGIAL AND VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID LAMININ; FIBRONECTIN; CULTURE; GROWTH; MODULATION; COMPONENTS; NEURONS AB Proliferation potential and extracellular matrix production were compared in cultured porcine glomerular mesangial cells and arterial and venous smooth muscle cells. Mesangial and arterial smooth muscle cells proliferated more rapidly than venous smooth muscle cells. In immunofluorescence studies, mesangial and arterial smooth muscle cells stained strongly for collagen types I, III, and V; venous smooth muscle showed weaker staining for collagens III and V. Total collagen synthesis in cultured mesangial and arterial smooth muscle cells was lower than in venous smooth muscle cells. Electrophoretic analysis showed type I collagen predominated in all cell types, although levels were highest in mesangial and arterial smooth muscle cells. Collagen V (alpha-3) occurred only in venous smooth muscle cells. Mesangial and arterial smooth muscle cells showed cell-bound fibronectin and laminin, which also were secreted into the medium. Venous smooth muscle cells secreted fibronectin, but all laminin was cell bound. The findings suggest a strong similarity between mesangial and arterial smooth muscle cells. C1 UNIV WISCONSIN,DEPT PATHOL,MADISON,WI 53706. FUKUOKA UNIV,DEPT PATHOL 2,FUKUOKA 81401,JAPAN. RP CHIANG, YY (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 39 TC 12 Z9 12 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1991 VL 138 IS 6 BP 1349 EP 1358 PG 10 WC Pathology SC Pathology GA FR746 UT WOS:A1991FR74600007 PM 2053592 ER PT J AU RONDINELLI, RD MURPHY, JR WILSON, DH MILLER, CC AF RONDINELLI, RD MURPHY, JR WILSON, DH MILLER, CC TI PREDICTORS OF FUNCTIONAL OUTCOME AND RESOURCE UTILIZATION IN INPATIENT REHABILITATION SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article DE FUNCTIONAL; REHABILITATION; RESOURCE AB Consecutive patients (n = 1,289) discharged from two inpatient rehabilitation facilities were prospectively examined to determine the extent to which rehabilitative outcomes, functionally based progress, and associated resource utilization (in terms of rehabilitation length of stay) can be concomitantly predicted using the Tufts/New England Medical Center functional assessment tool and bivariate and multivariate statistical comparisons. A high percentage (> 50%) of statistically significant associations between the predictor variables and seven outcome measures were seen. The R2s corresponding to these associations were generally small and resistant to enhancement by commonly accepted statistical manipulations. Consequently, they are, in general, of limited predictive value for determining functional prognosis or resource utilization among rehabilitation inpatients. Although functionally based predictors appear to be the best predictors of functional progress, their effectiveness as predictors of other domains (eg, discharge outcome and rehabilitation length of stay) is variable. The implication is that a prospective payment system using such an array of predictors and directed primarily at cost containment is likely to overlook potentially important gains in functional progress and patient outcome. Furthermore, the functionally based predictors, taken individually, varied in effectiveness as predictors among facilities, and, taken collectively, they varied in effectiveness as predictors for different diagnostic groupings within a facility. The inconsistency of predictions according to the various domains appears to further limit their application to a prospective payment model. C1 DENVER VET AFFAIRS MED CTR,INFORMAT RESOURCES MANAGEMENT SERV,DENVER,CO. UNIV COLORADO,SCH MED,DEPT PREVENT MED,DENVER,CO 80202. RP RONDINELLI, RD (reprint author), ROSE MED CTR,DEPT PM&R,4567 E 9TH AVE,DENVER,CO 80220, USA. NR 11 TC 23 Z9 23 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 JUN PY 1991 VL 72 IS 7 BP 447 EP 453 PG 7 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA FP702 UT WOS:A1991FP70200001 PM 1905529 ER PT J AU MCCORMICK, ML OBERLEY, TD ELWELL, JH OBERLEY, LW SUN, Y LI, JJ AF MCCORMICK, ML OBERLEY, TD ELWELL, JH OBERLEY, LW SUN, Y LI, JJ TI SUPEROXIDE-DISMUTASE AND CATALASE LEVELS DURING ESTROGEN-INDUCED RENAL TUMORIGENESIS, IN RENAL TUMORS AND THEIR AUTONOMOUS VARIANTS IN THE SYRIAN-HAMSTER SO CARCINOGENESIS LA English DT Article ID OXYGEN RADICALS; KIDNEY; TRANSFORMATION; PROMOTION; ENZYMES; INVITRO; CELLS AB Antioxidant enzyme levels were determined in kidneys during estrogen-induced cortical renal tumorigenesis in male Syrian hamsters. The activity of these enzymes in renal tumors were compared to those in the kidney cortex of untreated male castrated hamsters of different ages and in age-matched animals treated with diethylstilbestrol (DES) for varying periods. A transient increase in kidney Mn superoxide dismutase (MnSOD) and total SOD activity was seen after 1.5 and 3.1 months of DES treatment compared to untreated controls. However, after 4.4 months of DES exposure the activities of these antioxidant enzymes fell below untreated levels. The level of MnSOD and CuZnSOD was 3- to 10-fold lower compared to castrated male renal cortical values in DES-induced primary, serially transplanted and in autonomous renal tumour variants. Catalase activity declined steadily at 1.5 to 4.4 months of DES treatment. Low levels of catalase activity were found in all tumors examined. In general, Western blot analysis of immunoreactive proteins confirmed these findings, indicating that the low enzyme activities were due to low levels of enzyme proteins. Immunohistochemistry of the earliest tumor foci exhibited negligible antioxidant enzyme activity. The levels of these antioxidant enzymes were similar in all tumors surveyed, both primary and autonomous variants and in newborn kidneys, and they were about 10-fold lower than in normal kidney cortex or isolated proximal tubules. C1 UNIV MINNESOTA,SCH MED,DEPT PHARMACOL,MINNEAPOLIS,MN 55417. WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,MADISON,WI 53705. UNIV IOWA,RADIAT RES LAB,IOWA CITY,IA 52242. UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53705. VET ADM MED CTR,HORMONAL CARCINOGENESIS LAB,MINNEAPOLIS,MN 55417. FU NCI NIH HHS [CA 22009, CA 41267] NR 29 TC 38 Z9 38 U1 0 U2 2 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 JUN PY 1991 VL 12 IS 6 BP 977 EP 983 DI 10.1093/carcin/12.6.977 PG 7 WC Oncology SC Oncology GA FQ426 UT WOS:A1991FQ42600006 PM 2044204 ER PT J AU GOODFRIEND, TL BALL, DL WEINBERGER, MH MOORE, TJ WEDER, AB EGAN, BM AF GOODFRIEND, TL BALL, DL WEINBERGER, MH MOORE, TJ WEDER, AB EGAN, BM TI SALT LOADS RAISE PLASMA FATTY-ACIDS AND LOWER INSULIN SO HYPERTENSION LA English DT Article; Proceedings Paper CT 44TH ANNUAL FALL CONF AND SCIENTIFIC SESSION OF THE COUNCIL FOR HIGH BLOOD PRESSURE RESEARCH CY SEP 12-15, 1990 CL BALTIMORE, MD SP COUNCIL HIGH BLOOD PRESSURE RES DE BLOOD PRESSURE; SODIUM-DEPENDENT HYPERTENSION; INSULIN; NOREPINEPHRINE ID LIQUID-CHROMATOGRAPHIC ANALYSIS; BLOOD-PRESSURE; IDENTIFICATION; EPINEPHRINE; ALDOSTERONE; INHIBITORS; POTASSIUM; DIETS; TRIAL; RAT AB Some fatty acids are potent inhibitors of angiotensin binding and aldosterone production in adrenal glomerulosa cells and thereby may be involved in regulating salt and water balance. To study the possible regulation of fatty acids by salt, we measured the levels of unesterified fatty acids in plasma from patients subjected to extremes of dietary salt intake and saline infusion. Insulin and catecholamines, two known regulators of plasma fatty acids, also were measured. Infusion of 2 1 saline over 4 hours caused the levels of most unesterified fatty acids to rise. Total unesterified fatty acids rose 60-100%. A high salt diet caused a smaller rise in total unesterified fatty acids (approximately 33%). In both instances, oleic and palmitoleic acids showed the greatest proportionate increases, whereas stearic acid was relatively unaffected. When salt loads were administered by either intravenous or dietary routes, plasma insulin levels fell by approximately 50%. Plasma norepinephrine increased after saline infusion but not during a high salt diet. Postsaline levels of fatty acids correlated inversely with postsaline levels of aldosterone, supporting a possible role for fatty acids as physiological regulators of the adrenal glomerulosa. A rise in plasma fatty acids and fall in insulin in response to salt loads could act in concert to increase sodium excretion, constituting a physiological mechanism contributing to salt and water balance. C1 UNIV WISCONSIN,SCH MED,MADISON,WI 53706. INDIANA UNIV,SCH MED,INDIANAPOLIS,IN 46202. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48104. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NHLBI NIH HHS [HL-36568, HL-37717, HL-18575] NR 28 TC 24 Z9 24 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JUN PY 1991 VL 17 IS 6 SU S BP 958 EP 964 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FR814 UT WOS:A1991FR81400020 PM 2045176 ER PT J AU RO, JY BUCKNER, CK BRENDEL, JK FISHLEDER, RI GRAZIANO, FM AF RO, JY BUCKNER, CK BRENDEL, JK FISHLEDER, RI GRAZIANO, FM TI INFLUENCE OF INDOMETHACIN AND L-CYSTEINE ON HISTAMINE AND PEPTIDOLEUKOTRIENE RELEASE FROM SUPERFUSED TRACHEAS TAKEN FROM GUINEA-PIGS PASSIVELY SENSITIZED WITH IGG1 AND IGE ANTIBODIES SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID ARACHIDONIC-ACID METABOLISM; SLOW-REACTING SUBSTANCE; IMMUNOLOGICAL RELEASE; INDUCED CONTRACTION; MEDIATOR RELEASE; MAST-CELLS; HUMAN LUNG; ANAPHYLAXIS; INVITRO; ANTIGEN AB We have previously reported differences in mediator release during equivalent levels of antigen (Ag)-induced smooth muscle contraction of guinea pig pulmonary tissues after passive sensitization with IgG1 versus IgE antibodies (Abs). In the present study, we have examined the influence of indomethacin (5 x 10(-6) mol/L) and L-cysteine (3 or 10 mmol/L) on mediator release from superfused trachea taken from guinea pigs passively sensitized with IgG1 or IgE Ab 1 day before in vitro studies. Tissues were challenged with Ag (oxazolone-human serum albumin conjugate), and contractions and superfusate histamine and peptidoleukotrienes were monitored at discrete time intervals thereafter. Superfusate mediator contents were determined by spectrophotofluorimetry (histamine) and RAST (peptidoleukotrienes). The profiles of peptidoleukotrienes were examined with high-pressure liquid chromatography. At equivalent levels of contraction, significantly less histamine and peptidoleukotrienes were found in superfusate samples after sensitization with IgE Abs. None of the drug pretreatments significantly altered Ag-induced histamine release after IgG1 or IgE sensitization. Indomethacin resulted in an increase in total measurable peptidoleukotrienes found only after IgG1 receptor activation, but it did prolong tracheal contractions with both Abs. L-cysteine, 10 mmol/L, resulted in an increase in total measurable superfusate peptidoleukotriene content under all experimental conditions. The percentage increase in peptidoleukotriene content from that found without drug pretreatment was larger in the case of IgE compared to IgG1 sensitization. During early time periods, after Ag challenge, measurable peptidoleukotriene levels in superfusate samples were similar for both Abs in the presence of L-cysteine, 10 mmol/L. These data suggest that there is a differential pattern of peptidoleukotriene metabolism after activation of IgG1 versus IgE receptors in guinea pig trachea. C1 UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NHLBI NIH HHS [HL 33237, HL 28585]; NIAID NIH HHS [AI 00652] NR 37 TC 15 Z9 15 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JUN PY 1991 VL 87 IS 6 BP 1150 EP 1160 DI 10.1016/0091-6749(91)92161-S PG 11 WC Allergy; Immunology SC Allergy; Immunology GA FR066 UT WOS:A1991FR06600015 PM 1710633 ER PT J AU FANTIN, B EBERT, S LEGGETT, J VOGELMAN, B CRAIG, WA AF FANTIN, B EBERT, S LEGGETT, J VOGELMAN, B CRAIG, WA TI FACTORS AFFECTING DURATION OF INVIVO POSTANTIBIOTIC EFFECT FOR AMINOGLYCOSIDES AGAINST GRAM-NEGATIVE BACILLI SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID DOSING INTERVALS; THIGH-INFECTION; MICE C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,ROOM D-3224,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. NR 11 TC 41 Z9 41 U1 1 U2 1 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD JUN PY 1991 VL 27 IS 6 BP 829 EP 836 DI 10.1093/jac/27.6.829 PG 8 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA FT015 UT WOS:A1991FT01500016 PM 1938689 ER PT J AU OLDENDORF, WH AF OLDENDORF, WH TI SATURATION OF AMINO-ACID-UPTAKE BY HUMAN BRAIN-TUMOR DEMONSTRATED BY SPECT SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP OLDENDORF, WH (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,B-151C,LOS ANGELES,CA 90024, USA. NR 4 TC 6 Z9 6 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JUN PY 1991 VL 32 IS 6 BP 1229 EP 1230 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FP827 UT WOS:A1991FP82700016 PM 2045938 ER PT J AU SHAPIRO, SM BERSOHN, MM LAKS, MM AF SHAPIRO, SM BERSOHN, MM LAKS, MM TI IN SEARCH OF THE HOLY-GRAIL - THE STUDY OF DIASTOLIC VENTRICULAR-FUNCTION BY THE USE OF DOPPLER ECHOCARDIOGRAPHY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CONGESTIVE HEART-FAILURE; CANINE LEFT-VENTRICLE; CARDIOMYOPATHY; RELAXATION C1 UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,W LOS ANGELES VET AFFAIRS MED CTR,TORRANCE,CA 90509. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. NR 11 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN PY 1991 VL 17 IS 7 BP 1517 EP 1519 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FQ229 UT WOS:A1991FQ22900011 PM 2033183 ER PT J AU CLARK, MA OZGUR, LE CONWAY, TM DISPOTO, J CROOKE, ST BOMALASKI, JS AF CLARK, MA OZGUR, LE CONWAY, TM DISPOTO, J CROOKE, ST BOMALASKI, JS TI CLONING OF A PHOSPHOLIPASE-A2-ACTIVATING PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANTISENSE DNA; LEUKOTRIENE; ARACHIDONIC ACID ID BOVINE ENDOTHELIAL-CELLS; DIGLYCERIDE LIPASE; HUMAN-PLATELETS; CULTURED-CELLS; RELEASE; PHOSPHOLIPASES; BRADYKININ; LEUKOTRIENE-D4; COMPLEMENTARY; ARACHIDONATE AB Recently we have described the isolation and biochemical characterization of a phospholipase A2-activating protein (PLAP). We have cloned this protein and found it to be expressed as a 2.5-kilobase mRNA. The steady-state levels of PLAP mRNA are induced in smooth muscle and endothelial cells following treatment with leukotriene D4. The increased message levels coincide with increased amounts of PLAP. Synthetic antisense DNA was used to block the synthesis of PLAP and this treatment effectively blocked the activation of phospholipase A2 and the increased generation of prostanoids in smooth muscle and endothelial cells treated with leukotriene D4. C1 WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. SCHERING PLOUGH CORP,RES,BLOOMFIELD,NJ 07003. MED COLL PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19129. RP CLARK, MA (reprint author), SK&F LABS,KING OF PRUSSIA,PA 19479, USA. NR 40 TC 131 Z9 132 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN PY 1991 VL 88 IS 12 BP 5418 EP 5422 DI 10.1073/pnas.88.12.5418 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FR448 UT WOS:A1991FR44800073 PM 2052621 ER PT J AU WILLIAMS, WV KIEBEREMMONS, T WEINER, DB RUBIN, DH GREENE, MI AF WILLIAMS, WV KIEBEREMMONS, T WEINER, DB RUBIN, DH GREENE, MI TI CONTACT RESIDUES AND PREDICTED STRUCTURE OF THE REOVIRUS TYPE 3-RECEPTOR INTERACTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ANTIRECEPTOR ANTIBODY; MAMMALIAN REOVIRUS; CELL RECEPTORS; HEMAGGLUTININ; ATTACHMENT; BINDING; GLYCOPROTEINS; INHIBITION; IDIOTYPE; DOMAINS AB Sequence similarity between the reovirus type 3 hemagglutinin (HA3) and a anti-idiotypic monoclonal antibody (87.92.6) has been shown to define the site of interaction with a neutralizing (idiotypic) monoclonal antibody (9B.G5) and the cellular receptor for the virus. A synthetic peptide (V(L) peptide) derived from the anti-idiotypic sequence inhibits viral binding to the receptor. In this study, variants of the V(L) peptide were utilized to probe specific amino acid residues involved in binding the neutralizing antibody and the receptor. These studies indicate that the - OH groups of several residues are involved in contacting the reovirus type 3 receptor, including Tyr49, Ser50, Ser52, and Thr53 in the anti-idiotypic sequence, corresponding to Tyr326, Ser327, Ser329, and Ser325 in HA3, respectively. In contrast, only Ser50 of the anti-idiotypic sequence, corresponding to Ser327 of HA3, significantly altered neutralizing antibody binding. Additional studies implicate sialic acid as a potential reovirus type 3 receptor on some cells. This includes inhibition of binding of reovirus type 3 and 87.92.6 to L cells by heavily sialylated glycoproteins. Sialic acid was therefore utilized as a candidate receptor to analyze potential interaction schemes with HA3/87.92.6. Sequence similarity to other immunoglobulin structures with similar sequences allowed modeling of the three-dimensional structure of these epitopes. These structures, in combination with peptide studies, allow the development of a model of the interaction of these epitopes with sialic acid, which serves as a reovirus type 3 receptor. These models reveal that similar amino acid residues and side-chain geometries may be utilized by the reovirus type 3 and influenza hemagglutinins in their interactions with cell-surface receptors. C1 UNIV PENN,SCH MED,DEPT PATHOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MICROBIOL,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,DEPT MED,PHILADELPHIA,PA. WISTAR INST,PHILADELPHIA,PA 19104. RP WILLIAMS, WV (reprint author), UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104, USA. RI Weiner, David/H-8579-2014 NR 22 TC 36 Z9 36 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1991 VL 266 IS 14 BP 9241 EP 9250 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FM038 UT WOS:A1991FM03800087 PM 1709165 ER PT J AU GOUELI, SA HANTEN, JA AHMED, K AF GOUELI, SA HANTEN, JA AHMED, K TI MODULATION OF COFACTOR REQUIREMENT FOR THE ACTIVATION OF PROTEIN-KINASE-C BY HEPARIN - POSSIBLE EFFECT AT THE REGULATORY DOMAIN SO FEBS LETTERS LA English DT Article DE PROTEIN KINASE-C; HEPARIN; PHOSPHORYLATION; REGULATORY DOMAIN ID PURIFICATION; SUBSTRATE; ISOZYMES; CALCIUM AB Heparin was found to stimulate the phosphorylation of histone H1 but not protamine sulfate catalyzed by Ca2+/phospholipid-dependent protein kinase (protein kinase C or PKC). The effect of heparin on histone H1 phosphorylation appeared to be due to an increase in phosphatidylserine affinity of PKC activation in the presence of heparin. This effect of heparin was abolished when trypsinized, cofactor-independent, PKC was employed to phosphorylate histone H1. These studies suggest that heparin acts at the regulatory domain of PKC, and emphasize the importance of the negative charge in influencing the accessibility of the substrate to PKC action. C1 US DEPT VET AFFAIRS,MED CTR,1 VET DR,MINNEAPOLIS,MN 55417. UNIV MINNESOTA,SCH MED,CELLULAR & MOLEC BIOCHEM LAB 151,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. FU NCI NIH HHS [CA-15062, R01 CA015062] NR 13 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAY 6 PY 1991 VL 282 IS 2 BP 445 EP 448 DI 10.1016/0014-5793(91)80533-9 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FM908 UT WOS:A1991FM90800054 PM 2037060 ER PT J AU CLINKINGBEARD, C LAWRENCE, D SHENKER, Y AF CLINKINGBEARD, C LAWRENCE, D SHENKER, Y TI EFFECT OF VARYING POTASSIUM INTAKE ON ATRIAL NATRIURETIC HORMONE-INDUCED SUPPRESSION OF ALDOSTERONE SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Note DE ATRIAL NATRIURETIC HORMONE; ALDOSTERONE; POTASSIUM INTAKE; RENIN-ANGIOTENSIN SYSTEM AB To further assess the mechanism of atrial natriuretic hormone (ANH) induced suppression of aldosterone, we infused 0.5 pmol/kg/min Ser-Tyr28 human ANH over 2 h under three dietary conditions: low salt (LS), low potassium (LK), and high potassium (HK). The diets were consumed for 3 days before each study day. After 3 days of LK diet, blood pressure was slightly higher than under the other conditions. Serum potassium on LK was significantly lower than on HK (3.8 +/- 0.1 upsilon 4.3 +/- 0.2). The ANH infusion did not cause any changes in blood pressure or urinary sodium and potassium excretion. Urine volume increased with ANH infusion under all diet conditions. Plasma renin activity and plasma angiotensin II levels were significantly lower on LK than on LS or HK, probably reflecting sodium retention. Increase in plasma ANH levels of about 75% (well within normal range) suppressed all hormonal parameters on LS and HK diets, but had no significant effect on LK diet. The pattern of aldosterone changes closely followed the changes in the renin-angiotensin system. We conclude that under various physiologic conditions ANH suppresses aldosterone predominantly through suppression of renin. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705. FU NCRR NIH HHS [RR-03186]; NIDDK NIH HHS [R29-DK-39444] NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD MAY PY 1991 VL 4 IS 5 BP 456 EP 459 PN 1 PG 4 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FK921 UT WOS:A1991FK92100012 PM 1829901 ER PT J AU TITUS, MND GALL, NG YERXA, EJ ROBERSON, TA MACK, W AF TITUS, MND GALL, NG YERXA, EJ ROBERSON, TA MACK, W TI CORRELATION OF PERCEPTUAL PERFORMANCE AND ACTIVITIES OF DAILY LIVING IN STROKE PATIENTS SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE ASSESSMENT PROCESS; OCCUPATIONAL THERAPY; CEREBROVASCULAR DISORDERS; PERCEPTUAL DISORDERS; SELF CARE ID CONSTRUCTIONAL APRAXIA; CEREBRAL LESIONS; REHABILITATION C1 AUDIE L MURPHY MEM VET ADM MED CTR,REHABIL MED,SAN ANTONIO,TX 78284. UNIV SO CALIF,DEPT OCCUPAT THERAPY,LOS ANGELES,CA 90089. NO CALIF CTR REHABIL,SACRAMENTO,CA. UNIV SO CALIF,DEPT PREVENT MED,LOS ANGELES,CA 90089. RP TITUS, MND (reprint author), SAN ANTONIO WARM SPRINGS REHABIL HOSP,OCCUPAT THERAPY,5101 MED DR,SAN ANTONIO,TX 78229, USA. NR 56 TC 32 Z9 32 U1 0 U2 1 PU AMER OCCUPATION THERAPY ASSN PI ROCKVILLE PA 1383 PICCARD DRIVE PO BOX ROCKVILLE, MD 20850-4375 SN 0272-9490 J9 AM J OCCUP THER JI Am. J. Occup. Ther. PD MAY PY 1991 VL 45 IS 5 BP 410 EP 418 PG 9 WC Rehabilitation SC Rehabilitation GA FH399 UT WOS:A1991FH39900004 PM 2048622 ER PT J AU YOST, RW GRAUVICKEL, SJ CANTWELL, R BOMALASKI, JS HUDSON, AP AF YOST, RW GRAUVICKEL, SJ CANTWELL, R BOMALASKI, JS HUDSON, AP TI YEAST MITOCHONDRIA (SACCHAROMYCES-CEREVISIAE) CONTAIN CA2+-INDEPENDENT PHOSPHOLIPASE-A1 AND PHOSPHOLIPASE-A2 ACTIVITIES - EFFECT OF RESPIRATORY STATE SO BIOCHEMISTRY INTERNATIONAL LA English DT Article ID ENZYME-ACTIVITIES; RAT-HEART; PURIFICATION; HYDROLYSIS; LIPIDS; DNA C1 MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. MED COLL PENN,DEPT MICROBIOL IMMUNOL,PHILADELPHIA,PA 19129. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. RP YOST, RW (reprint author), DEPT VET AFFAIRS MED CTR,RES SERV,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIAMS NIH HHS [AR39382] NR 29 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 0158-5231 J9 BIOCHEM INT PD MAY PY 1991 VL 24 IS 2 BP 199 EP 208 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GC121 UT WOS:A1991GC12100001 PM 1930243 ER PT J AU FIELDS, SM KOELLER, JM AF FIELDS, SM KOELLER, JM TI IDARUBICIN - A 2ND-GENERATION ANTHRACYCLINE SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Article ID PHASE-II TRIAL; ADVANCED BREAST-CANCER; CELL LUNG-CANCER; ACUTE MYELOID-LEUKEMIA; NON-LYMPHOBLASTIC-LEUKEMIA; ADVANCED COLORECTAL-CARCINOMA; INTERMEDIATE-DOSE CYTARABINE; ACUTE MYELOGENOUS LEUKEMIA; COOPERATIVE GROUP GIMEMA; RELAPSED ACUTE LEUKEMIAS AB Because of its in vitro activity in leukemic cell lines and Phase I studies of acute leukemia, Phase II and III clinical trials with idarubicin hydrochloride were conducted in patients with acute lymphocytic leukemia or acute nonlymphocytic leukemia. In the Phase III comparative trials between the combinations of idarubicin and cytarabine and daunorubicin hydrochloride and cytarabine, the idarubicin/cytarabine combination resulted in significantly greater complete remission rates and longer overall survival in two of three studies conducted in the US. As a result, the Food and Drug Administration approved intravenous idarubicin with a Class 1A rating in September 1990 for use in combination with other antileukemic drugs (e.g., cytarabine) for the treatment of acute myelogenous leukemia in adults. The recommended dose of idarubicin is 12 mg/m2 daily for three days by slow intravenous injection in combination with cytarabine. Although idarubicin causes myelosuppression similar to that described with daunorubicin, the incidence of cardiotoxicity in animal models is lower. Idarubicin also has the advantages of oral administration, but the oral formulation of the drug remains investigational. The use of idarubicin in pediatric patients also remains to be established. C1 UNIV TEXAS,HLTH SCI CTR,DIV PHARM,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. UNIV TEXAS,CLIN,AUSTIN,TX 78712. AUDIE L MURPHY MEM VET ADM MED CTR,ONCOL CLIN,SAN ANTONIO,TX 78284. NR 103 TC 13 Z9 13 U1 0 U2 2 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD MAY PY 1991 VL 25 IS 5 BP 505 EP 517 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FL571 UT WOS:A1991FL57100013 PM 2068836 ER PT J AU GOODFRIEND, TL BALL, DL ELLIOTT, ME MORRISON, AR EVENSON, MA AF GOODFRIEND, TL BALL, DL ELLIOTT, ME MORRISON, AR EVENSON, MA TI FATTY-ACIDS ARE POTENTIAL ENDOGENOUS REGULATORS OF ALDOSTERONE SECRETION SO ENDOCRINOLOGY LA English DT Article ID LIQUID-CHROMATOGRAPHIC ANALYSIS; ANGIOTENSIN-II; GLOMERULOSA CELLS; HYPERTENSION; RECEPTORS; CORTICOSTERONE AB Adrenal glomerulosa cells washed with delipidated albumin produced increased amounts of aldosterone in response to angiotensin-II (AII) or (Bu)2cAMP. Albumin treatment also increased binding of I-125-labeled AII to high affinity binding sites on adrenal cells. Lipid extracts of albumin solutions that were used to wash cells inhibited AII binding and aldosterone responses by washed glomerulosa cells. Chromatographic fractionation and mass spectroscopic analysis indicated that the inhibitors removed from cells by albumin were long chain fatty acids. Exogenous fatty acids not only inhibited AII binding, but they inhibited basal aldosterone production and increments in aldosterone caused by AII or dbcAMP, suggesting an effect on postreceptor steps in aldosteronogenesis. The most potent and most abundant fatty acids removed from adrenal cells were oleic, linoleic, and arachidonic. These fatty acids inhibited at micromolar concentrations in the absence of albumin and at somewhat higher concentrations in its presence. Cells that had been washed, then inhibited by exogenous oleic acid in vitro, were restored to their enhanced responsiveness by a second albumin wash, making it unlikely that cell damage is the mechanism of inhibition by fatty acids. Responses of fasciculata cells were not potentiated by albumin washes, and cortisol production was less sensitive than aldosterone production to exogenous fatty acids. Binding of ANP to glomerulosa cells was not affected by albumin or fatty acids. These results combined with clinical correlations make it plausible that unesterified fatty acids are naturally occurring regulators of the adrenal glomerulosa. Insulin's ability to lower plasma levels of fatty acids may be one way that it causes sodium retention. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,MADISON,WI 53705. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERR,MADISON,WI 53705, USA. NR 27 TC 40 Z9 40 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAY PY 1991 VL 128 IS 5 BP 2511 EP 2519 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FJ396 UT WOS:A1991FJ39600040 PM 2019263 ER PT J AU SCHENKER, S MADDREY, WC AF SCHENKER, S MADDREY, WC TI SUBLIMINAL DRUG-DRUG INTERACTIONS - USERS AND THEIR PHYSICIANS TAKE NOTICE SO HEPATOLOGY LA English DT Editorial Material ID ACETAMINOPHEN-INDUCED HEPATOTOXICITY; CHRONIC ETHANOL-CONSUMPTION; CARBON-TETRACHLORIDE; LIVER-INJURY; ALCOHOL; RAT; CYTOCHROME-P-450; POTENTIATION; TOXICITY; METABOLISM C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SW MED SCH,DALLAS,TX 75235. RP SCHENKER, S (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07514] NR 39 TC 5 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD MAY PY 1991 VL 13 IS 5 BP 995 EP 998 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FM340 UT WOS:A1991FM34000029 PM 2030003 ER PT J AU ROZENTAL, JM LEVINE, RL MEHTA, MP KINSELLA, TJ LEVIN, AB ALGAN, O MENDOZA, M HANSON, JM SCHRADER, DA NICKLES, RJ AF ROZENTAL, JM LEVINE, RL MEHTA, MP KINSELLA, TJ LEVIN, AB ALGAN, O MENDOZA, M HANSON, JM SCHRADER, DA NICKLES, RJ TI EARLY CHANGES IN TUMOR METABOLISM AFTER TREATMENT - THE EFFECTS OF STEREOTAXIC RADIOTHERAPY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Note DE STEREOTAXIC RADIOTHERAPY; PET; GLIOMA METABOLISM; BRAIN TUMOR ID POSITRON EMISSION TOMOGRAPHY; NERVOUS-SYSTEM TUMORS; CEREBRAL BLOOD-FLOW; GLUCOSE-METABOLISM; BRAIN-TUMOR; LINEAR-ACCELERATOR; MALIGNANT GLIOMAS; PET; CHEMOTHERAPY; PROGNOSIS AB Four patients with intracranial neoplasms, two with malignant gliomas and two with brain metastases, were treated with stereotactic radiotherapy. Patients received between 15 and 27.5 Gray of photon irradiation to the central tumor target point; the 80% isodose line covered the periphery of the tumor as determined by contrast enhanced computed tomography. Patients underwent a sequence of three Positron Emission Tomographic scans using [F-18]-fluorodeoxyglucose (PET-FDG)-a baseline scan the day before treatment, and follow-up scans 1 and 7 days after treatment. Ratios between the maximal tumor regional cerebral metabolic rate for glucose (rCMRGlu) (T*) and the contralateral remote white matter rCMRGlu (RW), that is, the glucose uptake ratio (T*/RW), were calculated. The percent change in ratios relative to each patient's baseline scan were calculated. Ratios increased 25% to 42% 1 day post-radiotherapy, then decreased to between 10% above and 12% below the baseline value 7 days post-radiotherapy. The T*/RW increased acutely after stereotactic radiotherapy in a fashion similar to that previously described following chemotherapy with a complex multi-drug regimen. A common metabolic pathway may underlie the increase in T*/RW after these different treatments. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT NEUROL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT NEUROL SURG,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT RADIOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT HUMAN ONCOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT MED PHYS,MADISON,WI 53706. RP ROZENTAL, JM (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV 127,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. OI mehta, minesh/0000-0002-4812-5713 FU NCI NIH HHS [CA14520, CA47785]; NCRR NIH HHS [RR03186] NR 48 TC 45 Z9 46 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY PY 1991 VL 20 IS 5 BP 1053 EP 1060 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FL424 UT WOS:A1991FL42400020 PM 2022505 ER PT J AU CRAIG, WA REDINGTON, J EBERT, SC AF CRAIG, WA REDINGTON, J EBERT, SC TI PHARMACODYNAMICS OF AMIKACIN INVITRO AND IN MOUSE THIGH AND LUNG INFECTIONS SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID TOBRAMYCIN; EFFICACY; MURINE; INVIVO; MICE C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. MERITER HOSP,DEPT PHARM,MADISON,WI 53715. RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705, USA. NR 13 TC 155 Z9 155 U1 2 U2 7 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 1991 VL 27 SU C BP 29 EP 40 PG 12 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA FP055 UT WOS:A1991FP05500006 PM 1830302 ER PT J AU PECHERE, JC CRAIG, WA MEUNIER, F AF PECHERE, JC CRAIG, WA MEUNIER, F TI ONCE DAILY DOSING OF AMINOGLYCOSIDE - ONE-STEP FORWARD SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID NETILMICIN; GENTAMICIN; APPENDICITIS; COMBINATION; INFECTIONS; TOBRAMYCIN; KINETICS C1 UNIV GENEVA,MED CTR,DEPT MICROBIOL,CH-1211 GENEVA 4,SWITZERLAND. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. INST JULES BORDET,INFECT DIS UNIT,B-1000 BRUSSELS,BELGIUM. INST JULES BORDET,MICROBIOL LAB,B-1000 BRUSSELS,BELGIUM. NR 23 TC 26 Z9 27 U1 0 U2 0 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 1991 VL 27 SU C BP 149 EP 152 PG 4 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA FP055 UT WOS:A1991FP05500018 PM 1856144 ER PT J AU ANDERSON, RJ BRECKON, R DIXON, BS AF ANDERSON, RJ BRECKON, R DIXON, BS TI ATP RECEPTOR REGULATION OF ADENYLATE-CYCLASE AND PROTEIN-KINASE-C ACTIVITY IN CULTURED RENAL LLC-PK1 CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PURINOCEPTORS; VASOPRESSIN; ADENOSINE TRIPHOSPHATE; CYCLIC AMP ID CORTICAL COLLECTING TUBULE; SIGNAL TRANSDUCTION SYSTEMS; PHOSPHOLIPASE-C; PHOSPHOINOSITIDE TURNOVER; P2Y-PURINERGIC RECEPTOR; GUANINE-NUCLEOTIDES; VASOPRESSIN ACTION; CYCLIC-AMP; ADENOSINE; TRANSPORT AB In cultured intact LLC-PK1 renal epithelial cells, a nonhydrolyzable ATP analogue, ATP-gamma-S, inhibits AVP-stimulated cAMP formation. In LLC-PK1 membranes, several ATP analogues inhibit basal, GTP-, forskolin-, and AVP-stimulated adenylate cyclase activity in a dose-dependent manner. The rank order potency of inhibition by ATP analogues suggests that a P2y type of ATP receptor is involved in this inhibition. The compound ATP-gamma-S inhibits agonist-stimulated adenylate cyclase activity in solubilized and in isobutylmethylxanthine (IBMX) and quinacrine pretreated membranes, suggesting that ATP-gamma-S inhibition occurs independent of AVP and A1 adenosine receptors and of phospholipase A2 activity. The ATP-gamma-S inhibition of AVP-stimulated adenylate cyclase activity is not affected by pertussis toxin but is attenuated by GDP-beta-S, suggesting a possible role for a pertussis toxin insensitive G protein in the inhibition. Exposure of intact LLC-PK cells to ATP-gamma-S results in a significant increase in protein kinase C activity. However, neither of two protein kinase C inhibitors (staurosporine and H-7) prevents ATP-gamma-S inhibition of AVP-stimulated adenylate cyclase activity, suggesting that this inhibition occurs by a protein kinase C independent mechanism. These findings suggest the presence of functional P2y purinoceptors coupled to two signal transduction pathways in cultured renal epithelial cells. The effect of P2y purinoceptors to inhibit AVP-stimulated adenylate cyclase activity may be mediated, at least in part, by a pertussis toxin insensitive G protein. C1 DENVER VET AFFAIRS MED CTR,MED SERV,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. NR 37 TC 39 Z9 39 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAY PY 1991 VL 87 IS 5 BP 1732 EP 1738 DI 10.1172/JCI115191 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FK453 UT WOS:A1991FK45300035 PM 1850760 ER PT J AU LEONG, GB ETH, S SILVA, JA AF LEONG, GB ETH, S SILVA, JA TI THE TARASOFF DILEMMA IN CRIMINAL COURT SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; JURISPRUDENCE; PRIVACY; DOCTOR-PATIENT PRIVILEGE; DUTY TO PROTECT; TESTIMONY; DANGEROUSNESS; CONFIDENTIALITY; PRIVILEGE; ETHICS; PSYCHOTHERAPY AB The duty to protect, or Tarasoff duty, has been conceptualized as arising solely in the context of a clinical setting. A recent California Supreme Court ruling in People nu. Clark adds legal, clinical, and ethical dilemmas to the oftentimes contentious Tarasoff issue. Though the Tarasoff issue is but a minor legal point in Clark, a possible consequence of Clark is that a Tarasoff warning could be deemed nonconfidential and admissible in a criminal trial. Psychoterapists could therefore be testifying in criminal courts as prosecution witnesses. While the possibility of a chilling effect on patients' disclosure of violent ideation in the context of psychotherapy first caused apprehension after the California Supreme Court's 1976 decision in Tarasoff nu. Regents of the University of California, this same Court's ruling in People nu. Clark some 14 years later may ensure that this fear finally becomes realized. C1 UNIV CALIF LOS ANGELES,SCH MED,PSYCHIAT,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,PSYCHIAT,LOS ANGELES,CA 90033. RP LEONG, GB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,B116A12,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 8 TC 8 Z9 8 U1 0 U2 1 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 MAY PY 1991 VL 36 IS 3 BP 728 EP 735 PG 8 WC Medicine, Legal SC Legal Medicine GA FP610 UT WOS:A1991FP61000019 PM 1856640 ER PT J AU SCHULMAN, KA KINOSIAN, BP JACOBSON, TA GLICK, H EISENBERG, J AF SCHULMAN, KA KINOSIAN, BP JACOBSON, TA GLICK, H EISENBERG, J TI FORMULARY POLICY FOR CHOLESTEROL REDUCTION SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Letter RP SCHULMAN, KA (reprint author), HOSP UNIV PENN, PHILADELPHIA VET AFFAIRS MED CTR, DEPT MED, PHILADELPHIA, PA 19104 USA. OI Jacobson, Terry/0000-0002-9926-2179 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0884-8734 EI 1525-1497 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD MAY-JUN PY 1991 VL 6 IS 3 BP 266 EP 266 DI 10.1007/BF02598978 PG 1 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA FM057 UT WOS:A1991FM05700017 ER PT J AU SEBREE, L BIANCO, JA SUBRAMANIAN, R WILSON, MA SWANSON, D HEGGE, J TSCHUDY, J PYZALSKI, R AF SEBREE, L BIANCO, JA SUBRAMANIAN, R WILSON, MA SWANSON, D HEGGE, J TSCHUDY, J PYZALSKI, R TI DISCORDANCE BETWEEN ACCUMULATION OF C-14 DEOXYGLUCOSE AND TL-201 IN REPERFUSED MYOCARDIUM SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE REPERFUSION; ACUTE; NECROSIS; DEOXYGLUCOSE ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLUCOSE-UTILIZATION; ISCHEMIC CELL-DEATH; BLOOD-FLOW; CORONARY-OCCLUSION; CANINE MYOCARDIUM; WAVEFRONT PHENOMENON; METABOLIC OXIDATION; CARDIAC METABOLISM; ARTERY OCCLUSION C1 UNIV WISCONSIN, HOSP & CLIN, DEPT RADIOL, E1-382, 600 HIGHLAND AVE, MADISON, WI 53792 USA. UNIV WISCONSIN, HOSP & CLIN, DEPT PATHOL, MADISON, WI 53792 USA. UNIV WISCONSIN, HOSP & CLIN, DEPT MED, MADISON, WI 53792 USA. UNIV WISCONSIN, HOSP & CLIN, DEPT SURG, MADISON, WI 53792 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53792 USA. FU NHLBI NIH HHS [R01HL33514] NR 55 TC 31 Z9 31 U1 1 U2 1 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 MAY PY 1991 VL 23 IS 5 BP 603 EP 616 PG 14 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA FT298 UT WOS:A1991FT29800008 PM 1886139 ER PT J AU GUENTER, PA SETTLE, RG PERLMUTTER, S MARINO, PL DESIMONE, GA ROLANDELLI, RH AF GUENTER, PA SETTLE, RG PERLMUTTER, S MARINO, PL DESIMONE, GA ROLANDELLI, RH TI TUBE FEEDING-RELATED DIARRHEA IN ACUTELY ILL PATIENTS SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID VOLATILE FATTY-ACIDS; CLOSTRIDIUM-DIFFICILE; PREVENTION; PECTIN AB Acutely ill patients received tube feeding for an average of 15.8 days and, on average, 35% of those days were spent in the intensive care unit (ICU). Patients were prospectively assigned either a fiber-free formula (FFF-OSMOLITE HN, Ross; n = 50) or a fiber-supplemented (soy polysaccharide 14.4 g/L) formula (FSF = JEVITY, Ross; n = 50). Diarrhea was defined as three or more loose or watery stools per day and occurred in 30% of all patients. Diarrhea developed in 29 (41%) of the 71 patients who received antibiotics during, or within 2 weeks prior to, the feeding period, whereas only 1 (3%) of the 29 patients not receiving antibiotics developed diarrhea (p < 0.005); and this patient developed diarrhea on the day of death. Among the 30 patients with diarrhea, stool Clostridium difficile (CD) toxin was positive in 15 (50%), negative in 11 (37%), and was not measured in four. The mean serum albumin was significantly lower in patients with diarrhea (2.43) than in those without diarrhea (2.75) (p = 0.043). There were no significant differences in age, sex, diagnoses, number of feeding days, and percent ICU days between patients with and without diarrhea. While not statistically significant, patients who received FSF were observed to have a lower incidence of diarrhea, a lower percentage of diarrhea days per total feeding days, and a lower frequency of positive CD toxin assays than patients who received FFF. In this patient population, antibiotic usage was the factor most strongly associated with diarrhea during tube feedings. C1 UNIV PENN,GRAD HOSP,SCH MED,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP GUENTER, PA (reprint author), UNIV PENN,GRAD HOSP,SCH NURSING,PHILADELPHIA,PA 19104, USA. NR 23 TC 87 Z9 95 U1 0 U2 6 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 1991 VL 15 IS 3 BP 277 EP 280 DI 10.1177/0148607191015003277 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA FP831 UT WOS:A1991FP83100007 PM 1650854 ER PT J AU ORDWAY, GA GAMBARANA, C TEJANIBUTT, SM ARESO, P HAUPTMANN, M FRAZER, A AF ORDWAY, GA GAMBARANA, C TEJANIBUTT, SM ARESO, P HAUPTMANN, M FRAZER, A TI PREFERENTIAL REDUCTION OF BINDING OF I-125 IODOPINDOLOL TO BETA-1 ADRENOCEPTORS IN THE AMYGDALA OF RAT AFTER ANTIDEPRESSANT TREATMENTS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID ADRENERGIC-RECEPTOR BINDING; BEHAVIORAL DESPAIR TEST; SEROTONIN UPTAKE; CEREBRAL-CORTEX; QUANTITATIVE AUTORADIOGRAPHY; BETA-2-ADRENERGIC RECEPTORS; SELECTIVE INHIBITOR; MONOAMINE-OXIDASE; BRAIN; IMIPRAMINE AB This study utilized quantitative receptor autoradiography to examine the effects of repeated administration of antidepressants to rats on the binding of the beta adrenoceptor antagonist, I-125-iodopindolol (I-125-IPIN) to either beta-1 or beta-2 adrenoceptors in various regions of brain. Antidepressants were selected to represent various chemical and pharmacological classes including tricyclic compounds (desipramine and protriptyline), monoamine oxidase inhibitors (clorgyline, phenelzine and tranylcypromine), atypical antidepressants (mianserin and trazodone) and selective inhibitors of the uptake of serotonin (citalopram and sertraline). Additionally, rats were treated with various psychotropic drugs that lack antidepressant efficacy (cocaine, deprenyl, diazepam and haloperidol). Repeated treatment of rats with desipramine, protriptyline, clorgyline, phenelzine, tranylcy-promine or mianserin reduced the binding of I-125-IPIN to beta-1 adrenoceptors in many brain areas. Only in the basolateral and lateral nuclei of the amygdala did all six of these antidepressants significantly reduce I-125-IPIN binding to beta-1 adrenoceptors. In these amygdaloid nuclei, the magnitude of the reduction in the binding of I-125-IPIN caused by each of these drugs was comparable to or greater than the reduction in binding produced in any other region of brain. Reductions of binding of I-125-IPIN after antidepressant treatments were not consistently observed in the cortex, the area of brain examined most often in homogenate binding studies. Only the monoamine oxidase inhibitors caused reductions in the binding of I-125-IPIN to beta-2 adrenoceptors, and this effect was generally localized to the amygdala and hypothalamus. Repeated treatment of rats with citalopram, sertraline, or trazodone or with drugs lacking clinical antidepressant efficacy caused no significant effects on the binding of I-125-IPIN to either subtype of beta adrenoceptor in any region of brain. These results demonstrate that amygdaloid beta-1 adrenoceptors are particularly susceptible to regulation by certain antidepressant treatments and implicate the amygdala as an important site of action for antidepressants with pharmacological activity on noradrenergic neurons. C1 VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHARMACOL,PHILADELPHIA,PA 19104. FU NIMH NIH HHS [MH29094, MH09497, MH14654] NR 65 TC 90 Z9 90 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 MAY PY 1991 VL 257 IS 2 BP 681 EP 690 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FM161 UT WOS:A1991FM16100022 PM 1674532 ER PT J AU COLLINS, JF ANZUETO, AA PETERS, JI DELOSSANTOS, R GONZALEZ, DC JOHANSON, WG SEIDENFELD, JJ COALSON, JJ JENKINSON, SG AF COLLINS, JF ANZUETO, AA PETERS, JI DELOSSANTOS, R GONZALEZ, DC JOHANSON, WG SEIDENFELD, JJ COALSON, JJ JENKINSON, SG TI ELASTASE ACTIVITY IN BRONCHOALVEOLAR LAVAGE FLUID FROM OXYGEN-EXPOSED, PSEUDOMONAS-INFECTED BABOONS SO LUNG LA English DT Article DE ARDS; ELASTASE; ACUTE LUNG INJURY; BRONCHOALVEOLAR LAVAGE ID RESPIRATORY-DISTRESS SYNDROME; OXIDIZED ALPHA-1-PROTEINASE INHIBITOR; DIFFUSE ALVEOLAR DAMAGE; NOSOCOMIAL PNEUMONIA; ELASTOLYTIC ACTIVITY; NEUTROPHIL ELASTASE; HUMAN-LEUKOCYTE; LUNG INJURY; MYELOPEROXIDASE; PATHOGENESIS AB The adult respiratory distress syndrome is a major cause of morbidity and mortality in critical care patients. Lung injury in this syndrome is frequently associated with lung infection. The combined insults result in an influx of neutrophils and damage to the pulmonary epithelium. We investigated whether active neutrophil elastolytic activity was present in the bronchoalveolar fluid in baboons with mild or moderate hyperoxic lung injury and infection. Group A (N = 7) was exposed for 6 days to FIO2 = 0.8 and then inoculated by intratracheal bolus with Pseudomonas aeruginosa strain DGI-R130 (PA); the FIO2 was reduced to 0.5. Group B (N = 6) was exposed to similar concentrations of inspired oxygen but inoculated with buffered saline. Antibiotics included parenteral penicillin and topical gentamicin and polymyxin B. All 3 were given continuously in group B but stopped 24 h prior to PA inoculation in group A. Bronchoalveolar lavage fluid was collected 1 week before oxygen administration, when the FIO2 was reduced (day 6 or 7) and prior to necropsy (day 11). Hemodynamic, pulmonary function, microbiological, and biochemical variables were studied. Injured, infected animals (group A) had significant elevations of mean pulmonary artery pressure and decreases in total lung capacity and PaO2 compared both to baseline and to group B at day 11. At autopsy, group A had significant increases of bronchoalveolar lavage fluid (BALF) neutrophils and bacterial pathogens. Elastase levels in BALF (equal to 0 at baseline) rose to 136 +/- 98 ng/ml in group A vs. 6 +/- 14 ng/ml in group B. The elastase was inhibited by inhibitors of serine proteases including ones specific for neutrophil elastase. On Sephacryl S-300 chromatography the elastase activity eluted near human alpha-macroglobulin and separated from other proteolytic activity. These studies demonstrate a significant level of elastase in BALF from injured, infected baboons compared to injured, uninfected animals. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. SW FDN BIOMED RES,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NHLBI NIH HHS [HL-23578] NR 38 TC 6 Z9 6 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0341-2040 J9 LUNG JI Lung PD MAY-JUN PY 1991 VL 169 IS 3 BP 165 EP 179 DI 10.1007/BF02714152 PG 15 WC Respiratory System SC Respiratory System GA FR159 UT WOS:A1991FR15900004 PM 1895779 ER PT J AU KAWAMURA, J MEYER, JS AF KAWAMURA, J MEYER, JS TI HEADACHES DUE TO CEREBROVASCULAR-DISEASE SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID FIBROMUSCULAR DYSPLASIA; CAROTID ENDARTERECTOMY; CEREBELLAR HEMORRHAGE; DISSECTION; STROKE C1 DEPT VET AFFAIRS MED CTR,CEREBROVASC RES LABS,2002 HOLCOMBE BLVD,HOUSTON,TX 77211. BAYLOR UNIV,DEPT NEUROL,HOUSTON,TX 77030. NR 29 TC 13 Z9 13 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAY PY 1991 VL 75 IS 3 BP 617 EP 630 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA FJ960 UT WOS:A1991FJ96000009 PM 2020217 ER PT J AU ROZENTAL, JM AF ROZENTAL, JM TI POSITRON EMISSION TOMOGRAPHY (PET) AND SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY (SPECT) OF BRAIN-TUMORS SO NEUROLOGIC CLINICS LA English DT Article ID MAGNETIC-RESONANCE SPECTROSCOPY; CEREBRAL GLUCOSE-UTILIZATION; 8-DRUGS-IN-ONE-DAY CHEMOTHERAPY; LINEAR-ACCELERATOR; MALIGNANT GLIOMAS; METABOLIC CHANGES; CANCER-THERAPY; ADULT PATIENTS; BLOOD-FLOW; TC-99M-HMPAO C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. UNIV WISCONSIN HOSP,DEPT NEUROL,MADISON,WI 53792. UNIV WISCONSIN HOSP,DEPT NEUROSURG,MADISON,WI 53792. NR 75 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD MAY PY 1991 VL 9 IS 2 BP 287 EP 305 PG 19 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FM843 UT WOS:A1991FM84300004 PM 1944100 ER PT J AU BRAND, JG TEETER, JH KUMAZAWA, T HUQUE, T BAYLEY, DL AF BRAND, JG TEETER, JH KUMAZAWA, T HUQUE, T BAYLEY, DL TI TRANSDUCTION MECHANISMS FOR THE TASTE OF AMINO-ACIDS SO PHYSIOLOGY & BEHAVIOR LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL SYMP ON UMAMI CY OCT 07-10, 1990 CL SICILY, ITALY DE CHEMICAL SENSES; TASTE; GLUTAMATE; RECEPTORS; ION CHANNEL ID ICTALURUS-PUNCTATUS; RECEPTOR-SITES; CATFISH; BINDING; SENSATION; CELLS; SPECIFICITY; GLUTAMATE; MEMBRANES; TISSUE AB Amino acids are important taste stimuli for a variety of animals. One animal model, the channel catfish, I. punctatus, possesses sensitive taste receptor systems for several amino acids. Neurophysiological and biochemical receptor binding studies suggest the presence of at least three receptor pathways: one is a relatively nonspecific site(s) responsive to short-chain neutral amino acids such as L-alanine (L-ALA); another is responsive to the basic amino acid L-arginine (L-ARG); still another is a low affinity site for L-proline (L-PRO). Several possible transduction pathways are available in the taste system of this animal model for these amino acids. One of these, formation of inositol trisphosphate (IP3) and cyclic AMP (cAMP), is mediated by GTP-binding regulatory proteins, while another involves ion channels directly activated by stimuli. L-ALA is a potent stimulus to cAMP and IP3 accumulation, while L-ARG at low concentrations is without effect. On the other hand, L-ARG and L-PRO, but not L-ALA, are able to activate stimulus-specific and cation-selective channels in taste epithelial membranes reconstituted in phospholipid bilayers at the tips of patch pipettes. Preliminary studies using mouse taste tissue demonstrate that monosodium-L-glutamate (MSG) did not enhance production of IP3 or cAMP. However, in reconstitution experiments using taste epithelium of mouse, conductance changes due to MSG are observed. The specificity of this channel(s) and its uniqueness have yet to be determined. C1 UNIV PENN,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP BRAND, JG (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. FU NIDCD NIH HHS [DC-00356, DC-00327] NR 26 TC 41 Z9 43 U1 0 U2 3 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 MAY PY 1991 VL 49 IS 5 BP 899 EP 904 DI 10.1016/0031-9384(91)90201-X PG 6 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA FP005 UT WOS:A1991FP00500011 PM 1679559 ER PT J AU SILVA, JA LEONG, GB SHANER, AL AF SILVA, JA LEONG, GB SHANER, AL TI THE SYNDROME OF INTERMETAMORPHOSIS SO PSYCHOPATHOLOGY LA English DT Article ID CAPGRAS SYNDROME; MISIDENTIFICATION SYNDROMES; CONTRIBUTORS AB A series of 15 patients suffering from the syndrome of intermetamorphosis or its variants is discussed in terms of this misidentification syndrome's historical, classification, diagnostic, and psychosocial aspects. One case is presented in detail. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. RP SILVA, JA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED CTR,PSYCHIAT SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 38 TC 16 Z9 16 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD MAY-JUN PY 1991 VL 24 IS 3 BP 158 EP 165 PG 8 WC Psychiatry SC Psychiatry GA GL243 UT WOS:A1991GL24300006 PM 1754646 ER PT J AU TAKAYAMA, K DATTA, AK AF TAKAYAMA, K DATTA, AK TI STRUCTURE-TO-FUNCTION RELATIONSHIP OF MYCOBACTERIAL CELL-ENVELOPE COMPONENTS SO RESEARCH IN MICROBIOLOGY LA English DT Article; Proceedings Paper CT 6TH INTERNATIONAL SYMP ON THE GENETICS OF INDUSTRIAL MICROORGANISMS CY AUG 12-18, 1990 CL STRASBOURG, FRANCE ID TUMOR NECROSIS FACTOR; MYCOLIC ACID SYNTHESIS; HUMAN MACROPHAGES; AVIUM COMPLEX; FACTOR-ALPHA; TUBERCULOSIS; WALL; INHIBITION; ETHAMBUTOL; INFECTION C1 UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. RP TAKAYAMA, K (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705, USA. FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 37 TC 6 Z9 7 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2508 J9 RES MICROBIOL JI Res. Microbiol. PD MAY PY 1991 VL 142 IS 4 BP 443 EP 448 DI 10.1016/0923-2508(91)90118-T PG 6 WC Microbiology SC Microbiology GA FN625 UT WOS:A1991FN62500015 PM 1871431 ER PT J AU DRAPER, P BARROW, W LANEELLE, G DAFFE, M NIKAIDO, H TAKAYAMA, K HOFFNER, SE SVENSON, SB RASTOGI, N AF DRAPER, P BARROW, W LANEELLE, G DAFFE, M NIKAIDO, H TAKAYAMA, K HOFFNER, SE SVENSON, SB RASTOGI, N TI RECENT OBSERVATIONS CONCERNING STRUCTURE AND FUNCTION RELATIONSHIPS IN THE MYCOBACTERIAL CELL-ENVELOPE - ELABORATION OF A MODEL IN TERMS OF MYCOBACTERIAL PATHOGENICITY, VIRULENCE AND DRUG-RESISTANCE - DISCUSSION SO RESEARCH IN MICROBIOLOGY LA English DT Discussion DE MYCOBACTERIUM; CELL MEMBRANE; CELL WALL; DRUG RESISTANCE; VIRULENCE; FORUM ID AVIUM C1 TEXAS COLL OSTEOPATH MED,DEPT MICROBIOL & IMMUNOL,FT WORTH,TX 76107. CNRS,CTR RECH BIOCHIM GENET CELLULAIRES,F-31062 TOULOUSE,FRANCE. UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. NATL BACTERIOL LAB,DIV MYCOBACTERIOL,S-10521 STOCKHOLM,SWEDEN. NATL BACTERIOL LAB,DEPT VACCINE & DEV PROD,S-10521 STOCKHOLM,SWEDEN. INST PASTEUR,UNITE TUBERCULOSE & MYCOBACTERIES,F-75724 PARIS 15,FRANCE. RP DRAPER, P (reprint author), NATL INST MED RES,MILL HILL,LONDON NW7 1AA,ENGLAND. NR 9 TC 1 Z9 1 U1 0 U2 2 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2508 J9 RES MICROBIOL JI Res. Microbiol. PD MAY PY 1991 VL 142 IS 4 BP 477 EP 481 PG 5 WC Microbiology SC Microbiology GA FN625 UT WOS:A1991FN62500019 ER PT J AU KAHN, RS DAVIDSON, M GABRIEL, S DUMONT, K DUBIE, CR MOORE, C APTER, S SIEVER, L DAVIS, KL AF KAHN, RS DAVIDSON, M GABRIEL, S DUMONT, K DUBIE, CR MOORE, C APTER, S SIEVER, L DAVIS, KL TI SEROTONIN RECEPTOR SENSITIVITY IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR, MT SINAI HOSP, DEPT PSYCHIAT, BRONX, NY 10468 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 EI 1573-2509 J9 SCHIZOPHR RES JI Schizophr. Res. PD MAY-JUN PY 1991 VL 4 IS 3 BP 347 EP 348 PG 2 WC Psychiatry SC Psychiatry GA FD743 UT WOS:A1991FD74300174 ER PT J AU FABER, R COSTELLO, R MITZEL, H SCHNEIDER, S AF FABER, R COSTELLO, R MITZEL, H SCHNEIDER, S TI DIMENSIONALITY OF A NEUROPSYCHIATRIC SOFT SIGN BATTERY SO SCHIZOPHRENIA 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 ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD MAY-JUN PY 1991 VL 4 IS 3 BP 382 EP 383 DI 10.1016/0920-9964(91)90317-K PG 2 WC Psychiatry SC Psychiatry GA FD743 UT WOS:A1991FD74300229 ER PT J AU ABBOUD, HE AF ABBOUD, HE TI RESIDENT GLOMERULAR CELLS IN GLOMERULAR INJURY - MESANGIAL CELLS SO SEMINARS IN NEPHROLOGY LA English DT Article ID REACTIVE OXYGEN METABOLITES; GROWTH-FACTOR; PROLIFERATIVE GLOMERULONEPHRITIS; RAT; INFLAMMATION; GLOMERULOSCLEROSIS; PROTEOGLYCANS; PROGRESSION; EXPRESSION; INDUCTION C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV RENAL,SAN ANTONIO,TX. RP ABBOUD, HE (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK 33665] NR 56 TC 30 Z9 31 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9295 J9 SEMIN NEPHROL JI Semin. Nephrol. PD MAY PY 1991 VL 11 IS 3 BP 304 EP 311 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA FK642 UT WOS:A1991FK64200009 PM 2057645 ER PT J AU KAWAMURA, J MEYER, JS TERAYAMA, Y WEATHERS, S AF KAWAMURA, J MEYER, JS TERAYAMA, Y WEATHERS, S TI LEUKOARAIOSIS CORRELATES WITH CEREBRAL HYPOPERFUSION IN VASCULAR DEMENTIA SO STROKE LA English DT Article DE CEREBRAL BLOOD FLOW; LEUKOENCEPHALOPATHY; DEMENTIA ID WHITE MATTER LUCENCIES; SCAN LEUKO-ARAIOSIS; BLOOD-FLOW; RISK-FACTORS; NEUROLOGIC FINDINGS; NORMAL INDIVIDUALS; LESIONS; ATROPHY; COGNITION AB Leukoaraiosis quantified by computerized densitometric measurements of reduced Hounsfield numbers was correlated with local cerebral blood flow on the same computed tomographic images of 35 patients with multi-infarct dementia and 16 age-matched elderly normal volunteers. The ratio for area of frontal leukoaraiosis to total area of parenchyma among the patients was significantly greater than that among the normal volunteers (5.8 +/- 2.3% compared with 3.1 +/- 1.3%, p < 0.001). Severity of leukoaraiosis around the frontal horns of the lateral ventricles correlated significantly with severity of leukoaraiosis of the centrum semiovale adjacent to the bodies of the lateral ventricles. Cerebral blood flow values for all representative cerebral regions except the parietal white matter were reduced among the patients compared with the normal volunteers. Multivariate regression analysis revealed that reduced cerebral perfusion in the putamen and thalamus correlated significantly with the severity of leukoaraiosis. Cerebral hypoperfusion in territories supplied by deep penetrating arteries may contribute to the pathogenesis of leukoaraiosis. C1 DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,2002 HOLCOMBE BLVD,HOUSTON,TX 77211. BAYLOR UNIV,DEPT NEUROL,HOUSTON,TX 77030. BAYLOR UNIV,DEPT RADIOL,HOUSTON,TX 77030. NR 27 TC 86 Z9 91 U1 1 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD MAY PY 1991 VL 22 IS 5 BP 609 EP 614 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA FL344 UT WOS:A1991FL34400008 PM 2028490 ER PT J AU ROSS, NS ARON, DC AF ROSS, NS ARON, DC TI HORMONAL EVALUATION OF PATIENTS WITH AN INCIDENTALLY DISCOVERED ADRENAL MASS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID CUSHINGS-SYNDROME; TUMORS C1 VET AFFAIRS MED CTR,CLEVELAND,OH 44106. RP ROSS, NS (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 18 PY 1991 VL 324 IS 16 BP 1135 EP 1136 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FG912 UT WOS:A1991FG91200018 ER PT J AU FLESCHER, E FOSSUM, D GRAY, PJ FERNANDES, G HARPER, MJK TALAL, N AF FLESCHER, E FOSSUM, D GRAY, PJ FERNANDES, G HARPER, MJK TALAL, N TI ASPIRIN-LIKE DRUGS PRIME HUMAN T-CELLS - MODULATION OF INTRACELLULAR CALCIUM CONCENTRATIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID BLOOD MONONUCLEAR-CELLS; RABBIT BLASTOCYSTS; MEMBRANE FLUIDITY; ARACHIDONIC-ACID; ANTIGEN RECEPTOR; IL-2 PRODUCTION; PROSTAGLANDIN; LYMPHOCYTES; ACTIVATION; INTERLEUKIN-2 AB Aspirin-like drugs (ALD) enhance T cell proliferation by suppressing PG production in monocytes. Normal human T cells do not produce any eicosanoids. Therefore we studied whether ALD would affect purified T cells directly. We found that ALD enhanced the proliferation and IL-2 production of T cells in the absence of monocytes. This effect did not depend on arachidonic acid metabolism as no lipoxygenase products and only nonsuppressive levels of cyclooxygenase products were detected in T cell cultures. Several possible mechanisms of the ALD effect were ruled out including 1) enhanced mitogen binding, 2) induction of activation markers (IL-2R, transferrin receptor, HLA-DR) on the cell surface, 3) down-regulation of suppressor cells. ALD caused a rise in [Ca2+]i which appeared to reflect an influx of Ca2+ from the extracellular milieu and was more pronounced in CD4+ cells. The rise in intracellular levels of Ca2+, that is considered a necessary second messenger for T cell activation, may prime these cells for an enhanced response to mitogens. In addition, ALD increased T cell membrane fluidity but only at higher concentrations than those found to enhance proliferation. The pharmacologic effect of ALD on T cells presents a possible new immunoenhancing potential of these drugs and may have therapeutic use in immunosuppressed individuals. C1 UNIV TEXAS,HLTH SCI CTR,DEPT OBSTET & GYNECOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG03417]; NICHD NIH HHS [HD14048]; NIDCR NIH HHS [R01 DE09311-01] NR 37 TC 64 Z9 64 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 1991 VL 146 IS 8 BP 2553 EP 2559 PG 7 WC Immunology SC Immunology GA FG729 UT WOS:A1991FG72900010 PM 1901879 ER PT J AU QURESHI, N TAKAYAMA, K MEYER, KC KIRKLAND, TN BUSH, CA CHEN, L WANG, R COTTER, RJ AF QURESHI, N TAKAYAMA, K MEYER, KC KIRKLAND, TN BUSH, CA CHEN, L WANG, R COTTER, RJ TI CHEMICAL-REDUCTION OF 3-OXO AND UNSATURATED GROUPS IN FATTY-ACIDS OF DIPHOSPHORYL LIPID-A FROM THE LIPOPOLYSACCHARIDE OF RHODOPSEUDOMONAS-SPHAEROIDES - COMPARISON OF BIOLOGICAL PROPERTIES BEFORE AND AFTER REDUCTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; COMPLETE STRUCTURAL DETERMINATION; NUCLEAR MAGNETIC-RESONANCE; SALMONELLA-TYPHIMURIUM; MASS-SPECTROMETRY; ESCHERICHIA-COLI; MACROPHAGES; MUTANT; PURIFICATION; DESORPTION AB Unlike the diphosphoryl lipid A (DPLA) derived from toxic lipopolysaccharide of Escherichia coli and Salmonella strains, the DPLA from nontoxic lipopolysaccharide of Rhodopseudomonas sphaeroides ATCC 17023 is biologically inactive. This could be due to the presence of 3-oxotetradecanoic and DELTA-7-tetradecenoic acids. These two fatty acids in R. sphaeroides DPLA were catalytically reduced in platinum oxide/H-2 to the 3-hydroxy and saturated fatty acids, respectively. The biologically active E. coli DPLA was also treated with platinum oxide/H-2, but as expected, the reduction step did not change the structure. These two preparations were then compared with the untreated samples for biological activity in three select in vitro assays. Over a range of 0.01-100 ng/ml, both normal and reduced DPLA from R. sphaeroides were inactive in priming phorbol myristate acetate-stimulated superoxide anion release in human alveolar macrophages. Over a range of 10-10(3) ng/ml, both samples failed to induce tumor necrosis factor in the RAW 264.7 murine macrophage cell line. The reduced DPLA marginally activated 70Z/3 pre-B cells at concentrations of 0.1-30-mu-g/ml. In every case, both normal and platinum oxide/H-2-treated E. coli DPLA were biologically active. These results indicate that the lack of biological activity of R. sphaeroides DPLA is not due to the presence of 3-oxo and unsaturated fatty acids, but rather to one or more of the following: (i) presence of only five fatty acyl groups (compared to six in active lipid A); (ii) presence of 3-hydroxydecanoic acids (rather than 3-hydroxytetradecanoic, in active lipid A); (iii) greater variation in size of the fatty acids. C1 UNIV WISCONSIN,SCH MED,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. VET ADM MED CTR,DIV INFECT DIS,SAN DIEGO,CA 92161. UNIV CALIF SAN DIEGO,DEPT PATHOL & MED,LA JOLLA,CA 92093. UNIV MARYLAND,DEPT CHEM & BIOCHEM,CATONSVILLE,MD 21228. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. RP QURESHI, N (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705, USA. RI Wang, Rong/A-8721-2009 FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 28 TC 65 Z9 68 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 APR 5 PY 1991 VL 266 IS 10 BP 6532 EP 6538 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300079 PM 2007601 ER PT J AU HENDERSON, GI BASKIN, GS FROSTO, TA SCHENKER, S AF HENDERSON, GI BASKIN, GS FROSTO, TA SCHENKER, S TI INTERACTIVE EFFECTS OF ETHANOL AND CAFFEINE ON RAT FETAL HEPATOCYTE REPLICATION AND EGF RECEPTOR EXPRESSION SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article ID AMINO-ACID-UPTAKE; PROTEIN-KINASE; GROWTH-FACTOR; ALCOHOL; PREGNANCY; TRANSPORT; EXPOSURE; PHOSPHORYLATION; CONSUMPTION; INHIBITION AB This study reports on the interactive effects of ethanol and caffeine on growth of rat fetal hepatocytes. Exposure of cultured rat fetal hepatocytes (RFH) to ethanol in concentrations above 1 mg/ml, causes a blockade of EGF-dependent cell replication along with an overexpression of surface EGF receptors (EGF-R). However, RFHs exposed for 24 hours to ethanol at a concentration of 1 mg/ml alone had little effect on cell replication. Caffeine, when combined with this concentration of alcohol, progressively impaired RFH growth by up to 100%. Caffeine alone up to 10-mu-g/ml, on the other hand, caused a progressive increase in RFH replication associated with a 69% enhancement of DNA synthesis. Caffeine concentrations in excess of 50-mu-g/ml had no effect on replicative capacity. Concomitant caffeine exposure had no effect on the ethanol-related increase in cell DNA content, yet it caused a further enhancement of the cell protein accrual induced by ethanol alone. Caffeine (10-mu-g/ml) alone had no effect on EGF-R expression, while ethanol (2 mg/ml) increased it by almost 200%. Addition of caffeine to ethanol reduced this enhanced EGF binding by 45%. Scatchard analysis indicated that no treatment altered ligand affinity for the receptor, but that the alterations in binding caused by ethanol and the caffeine/ethanol combination reflected changes in binding capacity, in both low and high affinity components. It is concluded that (1) ethanol blocks EGF-mediated replication accompanied by a reduction in DNA synthesis, (2) caffeine alone at low concentrations has the opposite effect and can actually potentiate the EGF-mediated mitogenic response, (3) caffeine in combination with ethanol acts synergistically to reduce RFH replication. We suggest that the ethanol-induced perturbation of the EGF-R may be due to an altered cAMP kinase that plays a regulatory role in EFG-R expression. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,DIV GASTROENTEROL & NUTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP HENDERSON, GI (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 36 TC 10 Z9 10 U1 0 U2 1 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 APR PY 1991 VL 15 IS 2 BP 175 EP 180 DI 10.1111/j.1530-0277.1991.tb01850.x PG 6 WC Substance Abuse SC Substance Abuse GA FG761 UT WOS:A1991FG76100005 PM 2058791 ER PT J AU LAWRENCE, DL SHENKER, Y AF LAWRENCE, DL SHENKER, Y TI EFFECT OF HYPOXIC EXERCISE ON ATRIAL-NATRIURETIC-FACTOR AND ALDOSTERONE REGULATION SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE ALDOSTERONE REGULATION; PHYSICAL ACTIVITY; HORMONE STIMULATION; PLASMA RENIN ACTIVITY AB To evaluate the possible physiologic role of atrial natriuretic factor (ANF) in the observed dissociation of aldosterone secretion from the renin-angiotensin system during hypoxic exercise, 12 untrained men, ages 18 to 24, were studied on two separate days for 30 min during hypoxic (16% 0(2)) and normoxic (room air exercise on a bicycle ergometer. Workloads were adjusted to produce individual heart rates that remained within 70 to 75% of their previously measured maximum. Hemoglobin saturation decreased during hypoxia from 98 +/- 0.1% to 90 +/- 0.4% (P < .01). Plasma aldosterone levels increased significantly (P < .01) under both breathing conditions, yet were on average 36% lower during hypoxia than during normoxia (P < .001). Plasma ANF levels increased during exercise under both conditions (P < .01), yet levels were 45% greater during hypoxia than during normoxia (P < .001). Plasma renin activity, adrenocorticotropic hormone, cortisol, potassium, and systolic blood pressure increased during exercise on both study days (P < .01, compared to basal level), and showed no difference between normoxic and hypoxic conditions. Plasma pH was slightly higher during hypoxic exercise (P < .05, compared to normoxia). We conclude that acute hypoxemia is a potent enhancing stimulus for ANF release during dynamic exercise and that ANF is probably a contributing factor in the dissociation of aldosterone secretion from the renin-angiotensin system under these conditions. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705. FU NCRR NIH HHS [RR-03186]; NIDDK NIH HHS [1-R29-DK-38444] NR 0 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD APR PY 1991 VL 4 IS 4 BP 341 EP 347 PN 1 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FG949 UT WOS:A1991FG94900009 PM 1829370 ER PT J AU HICKEY, R HOFFMAN, J RAMAMURTHY, S AF HICKEY, R HOFFMAN, J RAMAMURTHY, S TI A COMPARISON OF ROPIVACAINE 0.5-PERCENT AND BUPIVACAINE 0.5-PERCENT FOR BRACHIAL-PLEXUS BLOCK SO ANESTHESIOLOGY LA English DT Article DE ANESTHETIC TECHNIQUES, BRACHIAL PLEXUS BLOCK; ANESTHETICS, LOCAL, BUPIVACAINE; ROPIVACAINE ID LIDOCAINE; TOXICITY; AGENT AB This study compared the effectiveness of 0.5% ropivacaine and 0.5% bupivacaine for brachial plexus block. Forty-eight patients received a subclavian perivascular brachial plexus block for upper-extremity surgery. One group (n = 24) received ropivacaine 0.5% (175 mg) and a second group (n = 24) received bupivacaine 0.5% (175 mg), both without epinephrine. Onset times for analgesia and anesthesia in each of the C5 through T1 brachial plexus dermatomes did not differ significantly between groups. Duration of analgesia and anesthesia was long (mean duration of analgesia, 13-14 h; mean duration of anesthesia, 9-11 h) and also did not differ significantly between groups. Motor block was profound, with shoulder paralysis as well as hand paresis developing in all of the patients in both groups. Two patients in each group required supplemental blocks before surgery. Ropivacaine 0.5% and bupivacaine 0.5% appeared equally effective in providing brachial plexus anesthesia. C1 MED CTR HOSP,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP HICKEY, R (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT ANESTHESIOL,SAN ANTONIO,TX 78284, USA. NR 11 TC 77 Z9 79 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD APR PY 1991 VL 74 IS 4 BP 639 EP 642 DI 10.1097/00000542-199104000-00002 PG 4 WC Anesthesiology SC Anesthesiology GA FE106 UT WOS:A1991FE10600002 PM 2008942 ER PT J AU SHARKEY, PK RINALDI, MG DUNN, JF HARDIN, TC FETCHICK, RJ GRAYBILL, JR AF SHARKEY, PK RINALDI, MG DUNN, JF HARDIN, TC FETCHICK, RJ GRAYBILL, JR TI HIGH-DOSE ITRACONAZOLE IN THE TREATMENT OF SEVERE MYCOSES SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; KETOCONAZOLE THERAPY; FUNGAL-INFECTIONS; SYNDROME AIDS; INVITRO; ENZYMES AB Eight patients with systemic mycoses and with prior treatment failures were treated with itraconazole (600 mg/day) for a mean duration of 5.5 months. All six patients without AIDS experienced improvement or stabilization of their fungal infections while receiving high-dose itraconazole, although two patients later experienced treatment failures, one by relapse and one by progression, on lower doses. Treatment failures also occurred in the two patients with AIDS and cryptococcal meningitis. The failures were associated with low serum itraconazole concentrations (< 2.5-mu-g/ml) in both patients. All other patients had mean trough levels in serum above 5-mu-g/ml. One patient who was improving on 600 mg/day developed a progressive infection after reduction of the dose to 400 mg/day. Side effects included reversible adrenal insufficiency in one patient; severe hypokalemia, mild diastolic hypertension, and rhabdomyolysis in one patient; mild hypokalemia and hypertension in four other patients; and breast tenderness in one patient. The mean decrease in serum potassium during treatment was statistically significant (P = 0.05). Selected patients with severe systemic mycoses may benefit from prolonged high-dose itraconazole treatment. However, 600 mg/day may be approaching the upper limits of acceptable dosing for long-term treatment. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP SHARKEY, PK (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. FU NCRR NIH HHS [MO1-RR-01346] NR 40 TC 90 Z9 94 U1 0 U2 1 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 APR PY 1991 VL 35 IS 4 BP 707 EP 713 PG 7 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA FF789 UT WOS:A1991FF78900018 PM 1648887 ER PT J AU ALLENDOERFER, R MARQUIS, AJ RINALDI, MG GRAYBILL, JR AF ALLENDOERFER, R MARQUIS, AJ RINALDI, MG GRAYBILL, JR TI COMBINED THERAPY WITH FLUCONAZOLE AND FLUCYTOSINE IN MURINE CRYPTOCOCCAL MENINGITIS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; AMPHOTERICIN-B; CEREBROSPINAL-FLUID; KETOCONAZOLE; COMBINATION; PENETRATION; INFECTIONS AB To assess the possible beneficial effects of combined therapy (fluconazole and flucytosine) in the treatment of cryptococcal meningitis in the immunocompromised host, we compared therapy with fluconazole and flucytosine, individually and combined, in the experimental murine model. BALB/c athymic (nu/nu) mice were infected intracerebrally with 150 to 300 CFU of Cryptococcus neoformans. In mortality studies, treatment was initiated 24 h postinfection and continued for 10 to 14 days with either fluconazole (1 to 15 mg/kg of body weight per day), flucytosine (60 to 120 mg/kg/8 h), both drugs, or 0.3% Noble agar (control). Combined therapy delayed mortality significantly when compared with controls and single-drug regimens. This was observed over a broad range of doses. Quantitative determinations of CFU in brain tissue demonstrated a significantly lower burden of C. neoformans in mice receiving combined therapy. The results indicate that combined therapy with fluconazole and flucytosine is superior to single-drug therapy. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP ALLENDOERFER, R (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. NR 22 TC 63 Z9 63 U1 1 U2 4 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 APR PY 1991 VL 35 IS 4 BP 726 EP 729 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA FF789 UT WOS:A1991FF78900021 PM 2069378 ER PT J AU OBERLEY, TD GONZALEZ, A LAUCHNER, LJ OBERLEY, LW LI, JJ AF OBERLEY, TD GONZALEZ, A LAUCHNER, LJ OBERLEY, LW LI, JJ TI CHARACTERIZATION OF EARLY KIDNEY LESIONS IN ESTROGEN-INDUCED TUMORS IN THE SYRIAN-HAMSTER SO CANCER RESEARCH LA English DT Article ID SUPEROXIDE-DISMUTASE ACTIVITY; RENAL TUMOR; CARCINOGENESIS; TISSUES; CELL AB Syrian hamsters were treated with diethylstilbestrol (DES), a potent estrogen and kidney carcinogen, or ethinyl estradiol (EE), a strong estrogen but weak carcinogen, for 1-9 months. At monthly intervals their kidneys were studied using light, immunoperoxidase, and electron microscopic techniques. At 5 months, DES-treated animals exhibited interstitial lesions composed of small round cells with a high nuclear:cytoplasmic ratio. Immunoperoxidase and ultrastructural studies showed these cells to be similar to cells in fully formed tumors at 9 months. Early lesions in EE-treated animals (seen as early as 1 month) were dissimilar; these lesions appeared in the deep cortex adjacent to the renal pelvis, where proximal tubules underwent hyperplastic changes, showing columnar cells with large nuclei, occasional mitoses, and sloughing of apical cytoplasm. Cells in early lesions of EE-treated animals did not resemble the fully developed tumor in either immunoperoxidase or ultrastructural features; although with longer treatment these tubular lesions progressed to dysplasia (3-5 months) and severe dysplasia/carcinoma in situ (7 months), they did not form grossly visible tumors during the 9-month study. Both early lesions identified were specific, inasmuch as they were not observed in control animals and animals treated with beta-dienestrol and 17-alpha-estradiol (noncarcinogenic weak estrogens). Animals given a combination of DES and EE showed tubular hyperplasia but not interstitial lesions; this finding was of particular interest because hamsters given this combination of estrogens do not develop gross renal tumors. These results strongly implicate the primitive interstitial cell in the hamster kidney as the cell of origin of the DES-induced neoplasm. C1 UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53706. WASHINGTON STATE UNIV,COLL PHARM,HORMONAL CARCINOGENESIS LAB,PULLMAN,WA 99164. UNIV IOWA,COLL MED,RADIAT RES LAB,IOWA CITY,IA 52242. VET AFFAIRS MED CTR,PATHOL SERV,SALT LAKE CITY,UT 84121. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA-22008, CA-41267] NR 24 TC 51 Z9 51 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1991 VL 51 IS 7 BP 1922 EP 1929 PG 8 WC Oncology SC Oncology GA FE041 UT WOS:A1991FE04100027 PM 2004377 ER PT J AU ALCANTARA, O SUNVISON, R BOLDT, DH AF ALCANTARA, O SUNVISON, R BOLDT, DH TI DIFFERENTIAL REGULATION OF PROTEIN-KINASE-C ISOFORMS BY IRON IN HEMATOPOIETIC-CELL LINES 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 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A269 EP A269 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300743 ER PT J AU BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G DIEHL, AK AF BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G DIEHL, AK TI AMBULATORY CARE IN THE 3RD YEAR CLERKSHIP - EFFECT ON CAREER CHOICE - A RANDOMIZED TRIAL 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 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A614 EP A614 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302723 ER PT J AU BAUER, RL AF BAUER, RL TI CHARACTERISTICS OF FALLS AND FALLERS - AGE-RELATED-CHANGES 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 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A409 EP A409 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301516 ER PT J AU HAFFNER, SM BAUER, RL AF HAFFNER, SM BAUER, RL TI RELATIONSHIP OF FASTING INSULIN TO BONE-DENSITY IN NONDIABETIC WOMEN 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. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A447 EP A447 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301746 ER PT J AU MCCORMICK, ML OBERLEY, LW OBERLEY, TD CIHLA, HP BRITIGAN, BE AF MCCORMICK, ML OBERLEY, LW OBERLEY, TD CIHLA, HP BRITIGAN, BE TI ASSOCIATION OF MANGANESE SUPEROXIDE-DISMUTASE WITH THE PLASMA-MEMBRANE OF HUMAN NEUTROPHILS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,DEPT MED,IOWA CITY,IA 52240. VET ADM MED CTR,DEPT RADIOL,IOWA CITY,IA 52240. UNIV WISCONSIN,MADISON,WI 53706. VET ADM MED CTR,RES SERV,IOWA CITY,IA 52240. UNIV IOWA,COLL MED,IOWA CITY,IA 52242. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT ANESTHESIOL,MADISON,WI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A353 EP A353 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301191 ER PT J AU MULROW, CD TULEY, MR AGUILAR, C AF MULROW, CD TULEY, MR AGUILAR, C TI SUSTAINED BENEFITS OF HEARING-AIDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,AMBULATORY CARE & GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A593 EP A593 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302597 ER PT J AU SCHEURICH, JW WRAY, NP AF SCHEURICH, JW WRAY, NP TI SUBJECTIVE ASSESSMENT OF ILLNESS SEVERITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 BAYLOR UNIV,HOUSTON VET ADM MED CTR,GEN MED SECT,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A608 EP A608 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302688 ER PT J AU FLESCHER, E FOSSUM, D TALAL, N AF FLESCHER, E FOSSUM, D TALAL, N TI POLYAMINE-DEPENDENT PRODUCTION OF LYMPHOCYTOTOXIC LEVELS OF AMMONIA BY HUMAN PERIPHERAL-BLOOD MONOCYTES SO IMMUNOLOGY LETTERS LA English DT Article DE MACROPHAGE; CYTOTOXICITY; OXIDASE; POLYAMINE; AMMONIA ID OXIDASE; OXIDATION; INVITRO; CELLS AB The activity of polyamine oxidase down-regulates IL-2 production in cultures of peripheral blood mononuclear cells. Monocytes are the main source of this enzymatic activity which generates ammonia. We therefore assessed the production of ammonia by human monocytes. We report that human peripheral blood monocytes produce and secrete ammonia and that this activity peaks after 2 days of incubation in vitro. Ammonia production can be suppressed by inhibiting polyamine biosynthesis and polyamine oxidation; thus, the activity of polyamine oxidase in human monocytes generates ammonia. Ammonia production could serve as a measure of polyamine oxidase activity in human monocytes. The levels of ammonia produced in our system reduce human lymphocyte viability. Therefore, ammonia can be added to the list of macrophage products having cytotoxic and immunosuppressive potential. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP FLESCHER, E (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 [R01 DEO9311-01] NR 15 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD APR PY 1991 VL 28 IS 1 BP 85 EP 90 DI 10.1016/0165-2478(91)90131-S PG 6 WC Immunology SC Immunology GA FH787 UT WOS:A1991FH78700013 PM 2071175 ER PT J AU DASHEIFF, RM AF DASHEIFF, RM TI SUDDEN UNEXPECTED DEATH IN EPILEPSY - A SERIES FROM AN EPILEPSY SURGERY PROGRAM AND SPECULATION ON THE RELATIONSHIP TO SUDDEN CARDIAC DEATH SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Article DE SUDDEN UNEXPECTED DEATH; SEIZURES; EPILEPSY SURGERY ID EPILEPTOGENIC ACTIVITY; UNEXPLAINED DEATH; AUTONOMIC DYSFUNCTION; NEURAL DISCHARGE; ARRHYTHMIAS; SEIZURES AB Sudden unexpected death represents a significant cause of mortality in people with epilepsy. It derives this significance not because it is the most frequent cause of death but because it is apparently a direct consequence of a seizure. The implication is that epilepsy is an inherently lethal disorder. Seven patients who were studied in an epilepsy surgery program died a sudden unexpected death. This incidence of sudden unexpected death was five times higher than the 1-2/1,000 per year reported in the general epilepsy population. Sudden unexpected death shares some of the characteristics associated with sudden cardiac death, which kills 300,000 people in the United States each year. A cardiac arrhythmia, usually ventricular fibrillation, is the most common terminal event for sudden cardiac death and is the leading candidate as the mechanism for sudden unexpected death. Despite this knowledge, little is known on how to identify a high-risk group of patients for sudden death or how these deaths might be prevented. C1 US DEPT VET AFFAIRS,NEUROL SERV,PITTSBURGH,PA. UNIV PITTSBURGH,CTR EPILEPSY,JOHNSTOWN,PA 15902. US DEPT VET AFFAIRS,SCH MED,DEPT NEUROL,PITTSBURGH,PA. US DEPT VET AFFAIRS,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA. NR 44 TC 127 Z9 128 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0736-0258 J9 J CLIN NEUROPHYSIOL JI J. Clin. Neurophysiol. PD APR PY 1991 VL 8 IS 2 BP 216 EP 222 DI 10.1097/00004691-199104000-00010 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FK455 UT WOS:A1991FK45500010 PM 2050822 ER PT J AU ELLIOTT, ME JONES, HM TOMASKO, S GOODFRIEND, TL AF ELLIOTT, ME JONES, HM TOMASKO, S GOODFRIEND, TL TI SPHINGOSINE INHIBITS ANGIOTENSIN-STIMULATED ALDOSTERONE SYNTHESIS SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article ID ADRENAL GLOMERULOSA CELLS; PROTEIN-KINASE-C; CALCIUM; BINDING; CYTOCHROME-P-450; PHOSPHORYLATION; SPHINGANINE; POTASSIUM; PATHWAY; CORTEX AB Sphingosine and other protein kinase C inhibitors were tested for their ability to inhibit aldosterone synthesis by bovine adrenal glomerulosa cells. Sphingosine inhibited angiotensin (AII)-stimulated aldosterone synthesis (IC50 of 5-mu-M). At doses that totally blocked steroidogenesis, sphingosine did not affect protein synthesis or [I-125]AII binding to cells. Sphingosine also inhibited dibutyryl cyclic AMP (dbcAMP)-stimulated aldosterone synthesis. Sphingosine inhibited pregnenolone synthesis from cholesterol, but not the conversion of progesterone or 20-alpha-hydroxycholesterol to aldosterone. These results suggest that sphingosine inhibits steroidogenesis at a locus close to that where stimulation occurs by AII and dbcAMP. Other protein kinase C inhibitors were tested. Retinal, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), and staurosporine inhibited aldosterone synthesis stimulated by AII and dbcAMP. Retinal and H-7 also inhibited progesterone conversion to aldosterone, and retinal blocked [I-125]AII binding. Staurosporine was more specific, inhibiting AII-stimulated aldosteronogenesis at concentrations which had little effect on conversion of progesterone to aldosterone. Because they inhibited dbcAMP stimulation, none of the inhibitors was sufficiently specific to use as a probe of the role of protein kinase C. The IC50 of sphingosine suggests that this or related products of lipid hydrolysis could act as endogenous regulators of adrenal cell function. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,MADISON,WI 53705. RP ELLIOTT, ME (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,HYPERTENS RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 28 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 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD APR PY 1991 VL 38 IS 4 BP 475 EP 481 DI 10.1016/0960-0760(91)90335-3 PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA FL602 UT WOS:A1991FL60200009 PM 1851631 ER PT J AU MEYER, JS AF MEYER, JS TI DOES DIASCHISIS HAVE CLINICAL CORRELATES SO MAYO CLINIC PROCEEDINGS LA English DT Editorial Material ID CEREBRAL BLOOD-FLOW; BEHAVIORAL ACTIVATION C1 BAYLOR UNIV,NEUROL,HOUSTON,TX 77030. RP MEYER, JS (reprint author), BAYLOR UNIV,DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,HOUSTON,TX 77030, USA. NR 9 TC 13 Z9 13 U1 0 U2 0 PU MAYO CLINIC PROCEEDINGS PI ROCHESTER PA 660 SIEBENS BLDG MAYO CLINIC, ROCHESTER, MN 55905 SN 0025-6196 J9 MAYO CLIN PROC JI Mayo Clin. Proc. PD APR PY 1991 VL 66 IS 4 BP 430 EP 432 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FH269 UT WOS:A1991FH26900011 PM 2013993 ER PT J AU GERBING, DW TULEY, MR AF GERBING, DW TULEY, MR TI THE 16PF RELATED TO THE 5-FACTOR MODEL OF PERSONALITY - MULTIPLE-INDICATOR MEASUREMENT VERSUS THE A-PRIORI SCALES SO MULTIVARIATE BEHAVIORAL RESEARCH LA English DT Article ID NATURAL-LANGUAGE; QUESTIONNAIRES; GOODNESS; FIT AB This article examines the Sixteen Personality Factor Inventory (16PF; Cattell, Eber, & Tatsuoka, 1970) in terms of recent methodological and substantive developments: restricted (confirmatory) factor analysis and the five-factor model of personality as operationalized by the NEO-PI (NEO Personality Inventory). A multiple-indicator measurement model of the 16PF was constructed and analyzed with a restricted factor analysis and then cross-validated with a confirmatory analysis on a new sample. The relations of the a priori 16PF scales and the derived scales with the NEO-PI were investigated with comparative canonical correlation analyses. Both the a priori and derived 16PF scales demonstrated strong relationships to the NEO-PI scales, with the canonical correlations for the a priori scales slightly larger. These findings lead to the conclusion that the original 16PF remains robust in the context of these more recent developments. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP GERBING, DW (reprint author), PORTLAND STATE UNIV,SCH BUSINESS ADM,SBA MGMT,PORTLAND,OR 97207, USA. NR 36 TC 17 Z9 18 U1 3 U2 5 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0027-3171 J9 MULTIVAR BEHAV RES JI Multivariate Behav. Res. PD APR PY 1991 VL 26 IS 2 BP 271 EP 289 DI 10.1207/s15327906mbr2602_5 PG 19 WC Mathematics, Interdisciplinary Applications; Social Sciences, Mathematical Methods; Psychology, Experimental; Statistics & Probability SC Mathematics; Mathematical Methods In Social Sciences; Psychology GA GD732 UT WOS:A1991GD73200006 PM 26828255 ER PT J AU SILVA, JA LEONG, GB FERRARI, MM AF SILVA, JA LEONG, GB FERRARI, MM TI POSTTRAUMATIC-STRESS-DISORDER IN BURN PATIENTS SO SOUTHERN MEDICAL JOURNAL LA English DT Article C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90033. RP SILVA, JA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV,B116A WARD 206A,LOS ANGELES,CA 90073, USA. NR 8 TC 9 Z9 9 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 APR PY 1991 VL 84 IS 4 BP 530 EP 531 DI 10.1097/00007611-199104000-00035 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FG629 UT WOS:A1991FG62900035 PM 2014448 ER PT J AU TAKAYAMA, K OLSEN, M DATTA, P HUNTER, RL AF TAKAYAMA, K OLSEN, M DATTA, P HUNTER, RL TI ADJUVANT ACTIVITY OF NONIONIC BLOCK COPOLYMERS .5. MODULATION OF ANTIBODY ISOTYPE BY LIPOPOLYSACCHARIDES, LIPID-A AND PRECURSORS SO VACCINE LA English DT Article DE ADJUVANT; LIPOPOLYSACCHARIDE; LIPID-A; COPOLYMER; ISOTYPE ID DELAYED-TYPE HYPERSENSITIVITY; T-CELL CLONE; SALMONELLA-TYPHIMURIUM; POLYMER SURFACTANTS; ESCHERICHIA-COLI; STRUCTURAL DETERMINATION; POLYSACCHARIDE CHAIN; SUBCLASS RESPONSES; IMMUNE-RESPONSES; DEFICIENT MUTANT AB Non-ionic block copolymers and lipopolysaccharides are both effective immunological adjuvants which are thought to act via distinct mechanisms. We hypothesized that they might produce synergistic effects when used together. We prepared a series of lipopolysaccharide (LPS) preparations ranging from the smallest precursor, lipid X through complete LPS with O-polysaccharide chains. Three preparations with reduced toxicity, monophosphoryl lipid A, partially hydrolysed Ra-LPS and LPS of Rhodopseudomonas sphaeroides were also utilized. All LPS preparations except the smallest were effective adjuvants for inducing early antibody responses to trinitrophenyl-conjugated hen egg albumin (TNP-HEA) when injected in squalane-in-water emulsions with copolymer L141. Only the larger LPS preparations induced sustained antibody responses. By itself, emulsions of copolymer L141 induced a predominant IgG1 antibody isotype response with lesser amounts of IgG2a and IgG2b. Surprisingly, all of the LPS preparations tested increased the proportion of IgG2 isotypes even though some had little effect on overall titres. The detoxified Ra-LPS (Ra-detox) was the most effective preparation for both increasing antibody titres and inducing the desirable IgG2a and IgG2b isotypes. These results demonstrate that the combination of LPS and block polymer adjuvants can produce synergistic effects without unacceptable toxicities. C1 EMORY UNIV,DEPT PATHOL,762 WMB,ATLANTA,GA 30322. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL LAB,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 55 TC 54 Z9 54 U1 0 U2 1 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0264-410X J9 VACCINE JI Vaccine PD APR PY 1991 VL 9 IS 4 BP 257 EP 265 DI 10.1016/0264-410X(91)90109-J PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FF564 UT WOS:A1991FF56400008 PM 2058268 ER PT J AU LEHRER, RI ROSENMAN, M HARWIG, SSSL JACKSON, R EISENHAUER, P AF LEHRER, RI ROSENMAN, M HARWIG, SSSL JACKSON, R EISENHAUER, P TI ULTRASENSITIVE ASSAYS FOR ENDOGENOUS ANTIMICROBIAL POLYPEPTIDES SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE ANTIBIOTIC; RADIAL DIFFUSION ASSAY; POLYACRYLAMIDE; ESCHERICHIA; FUNGI; SALMONELLA ID PURIFICATION; NEUTROPHILS; DEFENSINS AB We developed two sensitive methods for identifying antimicrobial molecules in leukocytes and other tissues. One method uses a gel overlay technique and was designed to identify antimicrobial polypeptides in samples subjected to polyacrylamide gel electrophoresis. The other, a radial diffusion assay, allows multiple fractions obtained by chromatographic procedures to be tested for antimicrobial activity conveniently. When we used E. coli ML-35p or Salmonella typhimurium 14028S as test organisms in the radial diffusion assay, we routinely detected 5-10 ng of rabbit defensin NP-1 in 5-mu-l of sample. With minor modifications, both methods can be applied to other organisms, including Gram-positive bacteria, several Candida species and Cryptococcus neoformans. C1 W LOS ANGELES VET ADM HOSP,LOS ANGELES,CA 90073. RP LEHRER, RI (reprint author), UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT MED,CHS 37-062,LOS ANGELES,CA 90024, USA. FU NIAID NIH HHS [AI 22839, AI 25693, AI 29595] NR 11 TC 488 Z9 544 U1 1 U2 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD MAR 21 PY 1991 VL 137 IS 2 BP 167 EP 173 DI 10.1016/0022-1759(91)90021-7 PG 7 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA FD419 UT WOS:A1991FD41900003 PM 1901580 ER PT J AU SHUSTER, E AF SHUSTER, E TI NAZI SCIENCE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP SHUSTER, E (reprint author), VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 21 PY 1991 VL 324 IS 12 BP 845 EP 845 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FC442 UT WOS:A1991FC44200011 ER PT J AU ELLIOTT, ME JONES, HM GOODFRIEND, TL AF ELLIOTT, ME JONES, HM GOODFRIEND, TL TI EFFECTS OF CALMIDAZOLIUM AND OTHER CALMODULIN ANTAGONISTS ON ADRENAL GLOMERULOSA CELLS SO BIOCHEMICAL PHARMACOLOGY LA English DT Note ID DEPENDENT PROTEIN-KINASE; ANGIOTENSIN-II; ALDOSTERONE SYNTHESIS; ZONA GLOMERULOSA; CALCIUM; STEROIDOGENESIS; INOSITOL; PHOSPHODIESTERASE; CYCLOHEXIMIDE; INHIBITION C1 UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT INTERNAL MED,MADISON,WI 53706. RP ELLIOTT, ME (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,HYPERTENS RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 26 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 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 15 PY 1991 VL 41 IS 6-7 BP 1083 EP 1086 DI 10.1016/0006-2952(91)90219-U PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FD172 UT WOS:A1991FD17200033 PM 2009077 ER PT J AU ALCANTARA, O JAVORS, M BOLDT, DH AF ALCANTARA, O JAVORS, M BOLDT, DH TI INDUCTION OF PROTEIN-KINASE-C MESSENGER-RNA IN CULTURED LYMPHOBLASTOID T-CELLS BY IRON-TRANSFERRIN BUT NOT BY SOLUBLE IRON SO BLOOD LA English DT Article ID LYMPHOCYTES-T; RECEPTOR EXPRESSION; GENE-EXPRESSION; PHORBOL ESTERS; ACTIVATION; PROLIFERATION; LINES; INTERLEUKIN-2; HETEROGENEITY; METABOLISM C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV HEMATOL,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 PSYCHIAT,SAN ANTONIO,TX 78284. NR 36 TC 32 Z9 32 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1991 VL 77 IS 6 BP 1290 EP 1297 PG 8 WC Hematology SC Hematology GA FB731 UT WOS:A1991FB73100022 PM 2001452 ER PT J AU SCHILLER, JH STORER, BE WITT, PL ALBERTI, D TOMBES, MB ARZOOMANIAN, R PROCTOR, RA MCCARTHY, D BROWN, RR VOSS, SD REMICK, SC GREM, JL BORDEN, EC TRUMP, DL AF SCHILLER, JH STORER, BE WITT, PL ALBERTI, D TOMBES, MB ARZOOMANIAN, R PROCTOR, RA MCCARTHY, D BROWN, RR VOSS, SD REMICK, SC GREM, JL BORDEN, EC TRUMP, DL TI BIOLOGICAL AND CLINICAL EFFECTS OF INTRAVENOUS TUMOR-NECROSIS-FACTOR-ALPHA ADMINISTERED 3 TIMES WEEKLY SO CANCER RESEARCH LA English DT Article ID INTERFERON-GAMMA; PHASE-I; CELL-LINES; TRANSFORMED-CELLS; HUMAN LYMPHOTOXIN; CANCER-PATIENTS; MURINE TUMORS; FACTOR TNF; MACROPHAGES; EXPRESSION AB Tumor necrosis factor (TNF) is a cytokine with pleiotropic biological and antitumor effects in vitro and in mouse models. The immunological effects of the molecule as a single agent, however, have not been well studied clinically. We conducted a Phase I trial of TNF in 53 patients with advanced malignancies in order to determine the biological and clinical effects of TNF when administered as a 30-min i.v. infusion three times/week. Dose levels of TNF ranged from 5 to 275-mu-g/m2; doses of TNF were escalated between patient groups. The most common clinical toxicities of TNF consisted of rigors, anorexia, headache, and fatigue. Dose-limiting toxicity consisted of hypotension, fatigue, and nausea. Four patients treated at the maximally tolerated dose of 225-mu-g/m2 received dexamethasone to determine whether the toxicities of TNF could be ameliorated. No significant differences in hypotension or subjective symptomatology were observed in those patients receiving dexamethasone and those who did not or between injections in which dexamethasone was administered and when it was not. One patient with colorectal carcinoma treated with 50-mu-g/m2 had a partial response lasting about 9 months. Biological responses were evaluated in 8 patients treated at the maximally tolerated dose before therapy and 24 h afterward. TNF significantly (P < 0.05 for all) enhanced serum beta-2-microglobulin, serum neopterin, and serum interleukin-2 receptor (Tac antigen) levels. Indoleamine 2,3-dioxygenase activity was also increased 24 h following the administration of TNF, although this increase was only of borderline statistical significance (P = 0.07). TNF did not enhance granulocyte bactericidal activity. The expression of cell surface proteins on monocytes, including HLA-DR, HLA-DQ, beta-2-microglobulin, and the Fc receptor, and serum interleukin-1 activity also were not significantly increased by the administration of TNF. Thus, in humans TNF caused biological response modulation with evidence of HLA Class I (beta-2-microglobulin) increase and T-cell (Tac antigen) and monocyte (neopterin) activation. C1 UNIV WISCONSIN,DEPT HUMAN ONCOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. RP SCHILLER, JH (reprint author), UNIV WISCONSIN,CTR CLIN CANC,ROOM K4 666 CSC,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [P30-CA14520, N01 CM57735]; NCRR NIH HHS [N01-RR03186] NR 47 TC 89 Z9 95 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1991 VL 51 IS 6 BP 1651 EP 1658 PG 8 WC Oncology SC Oncology GA FB576 UT WOS:A1991FB57600013 PM 1998956 ER PT J AU DENEKE, SM AF DENEKE, SM TI ARSENITE EFFECTIVE INDUCER OF CYSTINE TRANSPORT AND CELLULAR GLUTATHIONE (GSH) IN BOVINE PULMONARY-ARTERY ENDOTHELIAL-CELLS (BPAEC) SO FASEB JOURNAL 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 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1188 EP A1188 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001569 ER PT J AU FREYALDENHOVEN, AM KATZ, MS AF FREYALDENHOVEN, AM KATZ, MS TI PARATHYROID-HORMONE AND DIRECT ACTIVATORS OF PROTEIN-KINASE-C INDUCE PHOSPHORYLATION OF COMMON SUBSTRATES IN CLONAL OSTEOBLAST-LIKE CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 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 15 PY 1991 VL 5 IS 5 BP A1066 EP A1066 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000864 ER PT J AU ORSON, FM THOMAS, DW MCSHAN, WM KESSLER, DM HOGAN, ME AF ORSON, FM THOMAS, DW MCSHAN, WM KESSLER, DM HOGAN, ME TI TRIPLEX FORMING OLIGONUCLEOTIDE MODULATION OF IL2R-ALPHA MESSENGER-RNA TRANSCRIPTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 BAYLOR UNIV,CTR BIOTECHNOL,DEPT VET AFFAIRS MED CTR,HOUSTON,TX 77030. 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 15 PY 1991 VL 5 IS 5 BP A970 EP A970 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000312 ER PT J AU SUBRAMANIAN, R VOLOVSEK, A COURSIN, D HO, YS AF SUBRAMANIAN, R VOLOVSEK, A COURSIN, D HO, YS TI ENHANCED POSTISCHEMIC RECOVERY OF CARDIAC-FUNCTION IN HEARTS OF RATS EXPOSED TO 85-PERCENT 02 SO FASEB JOURNAL LA English DT Meeting Abstract C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT ANESTHESIOL,MADISON,WI 53706. DUKE UNIV,MED CTR,DEPT PULM MED,DURHAM,NC 27710. 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 15 PY 1991 VL 5 IS 5 BP A1283 EP A1283 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002125 ER PT J AU WARPINSKI, JR FOLGERT, J COHEN, M BUSH, RK AF WARPINSKI, JR FOLGERT, J COHEN, M BUSH, RK TI ALLERGIC REACTION TO LATEX - A RISK FACTOR FOR UNSUSPECTED ANAPHYLAXIS SO ALLERGY PROCEEDINGS LA English DT Article AB Allergic reactions to latex, including anaphylaxis may be a problem in certain individuals exposed to latex. Four atopic patients with symptoms of rhinitis, asthma, anaphylaxis, and/or urticaria upon contact with latex products were studied. The patients showed IgE binding to latex RAST disks ranging from 1.0 to 27.3 times the negative control. Latex products (gloves, balloons, and condoms) directly bound IgE from all four patients. Eluted proteins from the latex products inhibited IgE binding to commercial latex RAST disks. SDS-PAGE demonstrated multiple latex protein bands by Coomassie Blue staining between 14 and 66 kD. Immunoblotting showed specific IgE binding to latex proteins at 30 and 66 kD. These results indicate that latex-allergic patients have IgE directed against specific latex proteins. Allergy to latex can pose a substantial health risk to susceptible individuals. RP WARPINSKI, JR (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705, USA. NR 0 TC 46 Z9 46 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 MAR-APR PY 1991 VL 12 IS 2 BP 95 EP 102 DI 10.2500/108854191779011846 PG 8 WC Allergy SC Allergy GA FK469 UT WOS:A1991FK46900006 PM 2060787 ER PT J AU FLESCHER, E TALAL, N AF FLESCHER, E TALAL, N TI DO VIRUSES CONTRIBUTE TO THE DEVELOPMENT OF SJOGREN SYNDROME SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID EPSTEIN-BARR VIRUS; SYSTEMIC LUPUS-ERYTHEMATOSUS; SALIVARY-GLAND BIOPSIES; INFECTION; COMPLEX; MICE; DNA C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. NR 24 TC 58 Z9 59 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 MAR PY 1991 VL 90 IS 3 BP 283 EP 285 DI 10.1016/0002-9343(91)90566-G PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FC488 UT WOS:A1991FC48800001 PM 1848393 ER PT J AU FLETCHER, EC GOODNIGHTWHITE, S MUNAFO, D MILLER, CC LUCKETT, R QIAN, W AF FLETCHER, EC GOODNIGHTWHITE, S MUNAFO, D MILLER, CC LUCKETT, R QIAN, W TI RATE OF OXYHEMOGLOBIN DESATURATION IN OBSTRUCTIVE VERSUS NONOBSTRUCTIVE APNEA SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID SATURATION; SLEEP AB Preapneic thoracic gas volume (Vtg), arterial saturation (Sa(O2)), and mixed venous oxygen saturation (SvBAR(O2)), have been shown to influence the rate of Sa(O2) fall (dSa(O2)/dt) during apnea. We asked the following question: does tissue oxygen consumption (tV(O2)) affect the dSa(O2)/dt during apnea? We attempted to answer this question by comparing dSa(O2)/dt during obstructive apneas (high tVO2) with dSa(O2)/dt during nonobstructive apneas (low tVO2) in six adult baboons. Fiberoptic central venous and arterial catheters were used for continuous monitoring of SvBAR(O2), Sa(O2), and cardiac output. A sapphire-bearing turbine monitored minute ventilation and airflow cessation. A Respitrace(R) and esophageal pressures were used to assess relative differences in Vtg. Obstructive apneas (30, 45, and 60-s) were created by clamping an indwelling cuffed endotracheal tube at end-expiration. Nonobstructive apneas were created by paralyzing the animals with atracurium and interrupting ventillation for periods equivalent to those of the obstructed apneas. The ventillator was adjusted to duplicate the respiratory rate, tidal volume, and relative Vtg of the spontaneously breathing animal. Mean tVO2 during spontaneous breathing was 110 ml/min (Fick method) and decreased to 90 ml/min during paralysis (p < 0.05). The dSa(O2)/dt for the three apnea durations (mean, all animals), obstructive versus nonobstructed were: 0.85 and 0.74%/s (n = 6), 0.87 and 0.75%/s (n = 6), and 0.60 and 0.48%/s (n = 4), respectively. The dSa(O2)/dt was significantly lower during the nonobstructive apneas. We conclude that differences in VO2 during apnea may affect the dSa(O2)/dt and that for the same duration apnea, central apneas may show less desaturation than obstructive apneas where vigorous muscular efforts at overcoming obstruction are common. C1 BAYLOR UNIV,HOUSTON,TX 77030. RP FLETCHER, EC (reprint author), HOUSTON VET AFFAIRS MED CTR,DEPT MED 3I,PULM DIS SECT,UAMC,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 10 TC 8 Z9 9 U1 0 U2 1 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 MAR PY 1991 VL 143 IS 3 BP 657 EP 660 PG 4 WC Respiratory System SC Respiratory System GA FA931 UT WOS:A1991FA93100034 PM 2001079 ER PT J AU BUCKNER, CK RO, J BRENDEL, J FISHLEDER, RI WILL, JA CONKLIN, R GRAZIANO, FM AF BUCKNER, CK RO, J BRENDEL, J FISHLEDER, RI WILL, JA CONKLIN, R GRAZIANO, FM TI STUDIES OF DESENSITIZATION AND CROSS-DESENSITIZATION TO IMMUNOLOGICAL AND NONIMMUNOLOGIC STIMULI THAT EVOKE CONTRACTION AND HISTAMINE-RELEASE IN SUPERFUSED GUINEA-PIG TRACHEA SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID HUMAN BASOPHILS; MEDIATOR RELEASE; SMOOTH-MUSCLE; MAST-CELLS; ANTIGEN; ACTIVATION; SECRETION AB This study examined the possibility that there is cross-desensitization between immunologic and nonimmunologic stimuli that evoke contraction and histamine release (HR) in the isolated guinea pig trachea. Compound 48/80 and D-tubocurarine were found to cause homologous and heterologous desensitization for both contraction and HR from superfused trachea. Specific antigen challenge of trachea obtained from animals sensitized with either IgG1 (ovalbumin [OA]) or IgE (oxazolone-human serum albumin [OX-HSA]) also resulted in homologous desensitization for both contraction and HR. However, in experiments with animals sensitized with both IgGl and IgE antibodies, prechallenge with OA resulted in cross-desensitization to OX-HSA, whereas the reverse sequence was ineffective in eliciting this phenomenon. This may be related to the type of desensitization produced by each antigen (specific versus nonspecific) or to heterogeneity of mast cells in the tissue. Prechallenge of the trachea with compound 48/80 or D-tubocurarine failed to alter subsequent effects of antigen after active sensitization with OA or passive sensitization with either IgGl or IgE antibodies. Small but statistically significant decreases in tracheal responses to D-tubocurarine were observed after antigen prechallenge to activate both IgGl and IgE antibodies. This is the first study to demonstrate a cross-desensitization between compound 48/80 and D-tubocurarine and the first to examine cross-desensitization with IgGl and IgE antibodies in the guinea pig trachea. The overall conclusion is that there is no major overlap in the desensitization mechanisms between immunologic and nonimmunologic stimuli in the guinea pig trachea. C1 UNIV WISCONSIN HOSP & CLIN,SCH MED,600 HIGHLAND AVE,MADISON,WI 53792. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT VET SCI,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NHLBI NIH HHS [HL33237] NR 24 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 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD MAR PY 1991 VL 87 IS 3 BP 655 EP 661 DI 10.1016/0091-6749(91)90384-Z PG 7 WC Allergy; Immunology SC Allergy; Immunology GA FB801 UT WOS:A1991FB80100008 PM 1706369 ER PT J AU JENKINSON, SG ROBERTS, RJ DELEMOS, RA LAWRENCE, RA COALSON, JJ KING, RJ NULL, DM GERSTMANN, DR AF JENKINSON, SG ROBERTS, RJ DELEMOS, RA LAWRENCE, RA COALSON, JJ KING, RJ NULL, DM GERSTMANN, DR TI ALLOPURINOL-INDUCED EFFECTS IN PREMATURE BABOONS WITH RESPIRATORY-DISTRESS SYNDROME SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE GLUTATHIONE; OXYGEN TOXICITY ID LUNG INJURY; OXYGEN-TOXICITY; TISSUE-INJURY; FREE-RADICALS; RAT LUNGS; SURFACTANT; REPERFUSION; OXYPURINOL; INHIBITOR; HYPEROXIA AB To test the hypothesis that administration of allopurinol could modify the response to prolonged hyperoxia in premature baboons (140 days gestation) with respiratory distress syndrome, we evaluated physiological, pathological, and lung biochemical parameters in groups of premature baboons treated with mechanical ventilation and exposed to various amounts of oxygen for 6 days. Three groups of experimental animals were studied, including animals that received oxygen as needed to maintain arterial oxygen between 60 and 80 Torr [inspiratory O2 concentration- (FI(o2)) PRN], animals that received 100% oxygen continuously but also received allopurinol intravenously at a dose of 10 mg.kg-1.day-1 (FI(o2) -1.0 + allopurinol), and animals that received 100% oxygen continuously and the vehicle for allopurinol administration (FI(o2) -1.0). Pathological examinations of the experimental animals showed evidence of lung injury in both 100% oxygen-exposed groups, but the allopurinol-treated animals had findings more compatible with the FI(o2) - PRN group, with relatively few macrophages or polymorphonuclear lymphocytes being present in lung tissue. Lungs of animals treated with allopurinol were also more distensible and had a trend toward decreased lung water compared with the FI(o2) -1.0 group. Allopurinol-treated animals were able to induce lung glutathione concentrations and glutathione-related and antioxidant enzyme activities compared with the normoxic control (FI(o2) - PRN) group. Ventilator pressure requirements were also decreased in the allopurinol-treated animals compared with the FI(o2) -1.0 controls after 42 h. These data suggest that treatment of hyperoxia-exposed premature baboons with allopurinol for the first 6 days of life results in significant changes in lung responses and antioxidant defenses compared with vehicle-treated baboons exposed to 100% oxygen for the same time period. C1 SW FDN BIOMED RES,SAN ANTONIO,TX 78284. UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA 22908. RP JENKINSON, SG (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY VET ADM HOSP,DEPT MED,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. RI Vinnikova, Lydmila/P-5860-2015; Pshenishnyuk, George /E-8554-2016; Ignatenkov, Oleksandr/J-1429-2016 OI Vinnikova, Lydmila/0000-0002-6106-1785; Pshenishnyuk, George /0000-0002-9915-5576; Ignatenkov, Oleksandr/0000-0002-0770-3847 FU NHLBI NIH HHS [HL-36536, HL-30556] NR 33 TC 19 Z9 19 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 1991 VL 70 IS 3 BP 1160 EP 1167 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA FA971 UT WOS:A1991FA97100027 PM 2032982 ER PT J AU KURIHARA, N CIVIN, C ROODMAN, GD AF KURIHARA, N CIVIN, C ROODMAN, GD TI OSTEOTROPIC FACTOR RESPONSIVENESS OF HIGHLY PURIFIED POPULATIONS OF EARLY AND LATE PRECURSORS FOR HUMAN MULTINUCLEATED CELLS EXPRESSING THE OSTEOCLAST PHENOTYPE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID BONE-MARROW CULTURES; PARATHYROID-HORMONE; 1,25-DIHYDROXYVITAMIN-D3 CAUSES; PROGENITOR CELLS; INVITRO; GENERATION; RESORPTION; BLOOD AB Recently we have adapted human long-term bone marrow cultures to form multinucleated cells (MNC) that express the osteoclast phenotype and used semisolid culture techniques to identify early (bipotent) and late (unipotent) mononuclear precursors for these MNC. The early precursor can form both osteoclast-like MNC and macrophage polykaryons; the late precursor forms only osteoclast-like MNC. In this study we examined the effects of osteotropic hormones and cytokines of MNC formation from highly purified populations of these early or late mononuclear precursor cells. MNC expressing the osteoclast phenotype were identified by their cross-reactivity with the 23c6 monoclonal antibody, which preferentially identifies osteoclasts. 1,25-(OH)2D3 (10(-8) M), IL-1-beta (10 u/ml), and IL-6 (100 pg/ml) stimulated formation of 23c6-positive MNC from highly purified populations of early or late precursor cells. In contrast, PTH (50 ng/ml) did not act directly on late precursor cells but only stimulated 23c6-positive MNC formation from early precursors. These results show that (1) 1,25-(OH)2D3, IL-1-beta, and IL-6 can stimulate 23c6-positive MNC formation from a highly enriched population of early and late precursors, and (2) PTH does not act on late precursors but may act indirectly on the late precursors. 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,SAN ANTONIO,TX 78284. JOHNS HOPKINS UNIV,CTR ONCOL,BALTIMORE,MD 21218. FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM 35188] NR 24 TC 105 Z9 105 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 MAR PY 1991 VL 6 IS 3 BP 257 EP 261 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GN785 UT WOS:A1991GN78500006 PM 2035352 ER PT J AU LEVINE, RL DOBKIN, JA ROZENTAL, JM SATTER, MR NICKLES, RJ AF LEVINE, RL DOBKIN, JA ROZENTAL, JM SATTER, MR NICKLES, RJ TI BLOOD-FLOW REACTIVITY TO HYPERCAPNIA IN STRICTLY UNILATERAL CAROTID DISEASE - PRELIMINARY-RESULTS SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID CEREBRAL-CIRCULATION; STENOSIS; ARTERY; PERFUSION; OCCLUSION; ISCHEMIA; STROKE; BYPASS; RCBF AB To show a relationship between degree of carotid arterial stenosis and cerebral blood flow reactivity (RES%) to induced hypercapnia, fluorine-18-fluoromethane and positron emission tomography (PET) was used to study 18 patients with carotid distribution transient ischaemic attacks (TIA), all free of stroke, who had angiographic-proven unilateral arterial disease. Non-involved carotid arteries were either normal or had non-stenotic plaque. Either normal arteries or non-stenotic ulcerations in the symptomatic carotid arteries were present in five of 18 (28%), ipsilateral carotid stenosis from 50-99% was present in eight of 18 (44%), and ipsilateral internal carotid occlusion was present in five of 18 (28%) patients. In comparison with 14 normal controls, all patients with symptomatic middle cerebral artery (MCA) flow territories had significantly lower mean (SEM) RES% [5.0 (0.2) vs 4.0 (0.9), p < 0.04]. Symptomatic anterior borderzone (ABZ) RES% was also significantly lower [4.6 (0.4) vs 3.3 (0.9), p < 0.04], than controls. In patient subgroup comparisons, the 50-99% stenosis subgroup clearly had the lowest MCA RES% [3.4 (0.2)] as well as the lowest ABZ RES% [2.8 (0.4)] on their symptomatic sides. Age, expired pCO2, mean arterial blood pressure, serum glucose, serum haematocrit and number, type and estimated duration of TIAs were not significantly different between subgroups. Linear regression showed a significant relationship between RES% and both measured percentage-stenosis (p = 0.04) and residual luminal diameter (p = 0.05) in symptomatic MCA territories. This approached significance in symptomatic ABZ regions. This preliminary data set suggests that unilateral carotid stenosis can and does result in impaired CO2 reactivity following hypercapnia. The relative normality of CO2 reactivity in those with carotid occlusion is discussed. C1 UNIV WISCONSIN HOSP & CLIN,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED PHYS,MADISON,WI 53705. NR 25 TC 28 Z9 28 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD MAR PY 1991 VL 54 IS 3 BP 204 EP 209 DI 10.1136/jnnp.54.3.204 PG 6 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA FB085 UT WOS:A1991FB08500004 PM 1903147 ER PT J AU YOSHIKAWA, TT AF YOSHIKAWA, TT TI ELIMINATION OF TUBERCULOSIS FROM THE UNITED-STATES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Editorial Material RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE,WASHINGTON,DC, USA. NR 13 TC 3 Z9 3 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 MAR PY 1991 VL 39 IS 3 BP 312 EP 314 PG 3 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA FC070 UT WOS:A1991FC07000015 PM 2005348 ER PT J AU PATTON, JP NASH, DB ABRUTYN, E AF PATTON, JP NASH, DB ABRUTYN, E TI URINARY-TRACT INFECTION - ECONOMIC-CONSIDERATIONS SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID SINGLE-DOSE THERAPY; COST-BENEFIT-ANALYSIS; TRIMETHOPRIM-SULFAMETHOXAZOLE; NOSOCOMIAL INFECTIONS; ACUTE DYSURIA; SIGNIFICANT BACTERIURIA; PERIODIC INSTILLATIONS; EXCRETORY UROGRAPHY; ANTIBIOTIC-THERAPY; RANDOMIZED TRIAL C1 UNIV PENN,LEONARD DAVIS INST HLTH ECON,GEN INTERNAL MED SECT,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. VET AFFAIRS MED CTR,PHILADELPHIA,PA. NR 94 TC 102 Z9 107 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAR PY 1991 VL 75 IS 2 BP 495 EP 513 PG 19 WC Medicine, General & Internal SC General & Internal Medicine GA EZ546 UT WOS:A1991EZ54600017 PM 1996046 ER PT J AU KANE, MA KELLEY, K ROSS, SE PORTANOVA, LB AF KANE, MA KELLEY, K ROSS, SE PORTANOVA, LB TI ISOLATION OF A GASTRIN RELEASING PEPTIDE RECEPTOR FROM NORMAL RAT PANCREAS SO PEPTIDES LA English DT Article DE GASTRIN RELEASING PEPTIDE; BOMBESIN; RECEPTOR ID BOMBESIN-LIKE PEPTIDES; SWISS 3T3 CELLS; GASTROINTESTINAL-TRACT; CROSS-LINKING; IMMUNOREACTIVITY; BINDING; IDENTIFICATION; LOCALIZATION; MEMBRANES; GROWTH AB The presence of a putative GRP receptor on rat pancreatic particulate membranes was demonstrated by covalent cross-linking to I-125-gastrin releasing peptide (GRP), which revealed a radioactive band with M(r) = 80-90 kDa on reduced SDS-PAGE. Fresh rat pancreatic membranes contained a GRP receptor which was solubilized with Triton X-100 as assessed by its failure to sediment at 100,000 x g for one hour and its ability to pass through a 0.22-mu filter. When I-125-GRP binding was studied using Sephadex G50 gel filtration chromatography to separate bound from unbound ligand, substantial amounts of I-125-GRP binding were observed in rat crude solubilized pancreatic membranes, but essentially no specific binding was observed until the crude solubilized membranes were fractionated by ammonium sulfate precipitation. Specific I-125-GRP binding was 500, 700 and 1400 fmol/mg protein, respectively, in the 0-25%, 25-50% and 50-80% saturated ammonium sulfate fractions (I-125-I-GRP concentration = 1 nM). Specific binding was temperature dependent, saturable and of high affinity (K(D) = 2.3 nM). A unique 70 kDa band was visualized by silver staining of the SDS-PAGE of eluates of GRP(14-27) affinity gels compared with eluates of control affinity gels incubated with the 25-50% (NH4)2 SO4 fraction. The lower M(r) than that observed with covalent cross-linking may represent the binding subunit of a larger receptor protein. This ligand-affinity isolated protein is thus a good candidate for the GRP receptor, or the binding subunit of it, from normal rat pancreas. C1 UNIV COLORADO,CTR CANC,DENVER,CO 80220. RP KANE, MA (reprint author), UNIV COLORADO,HLTH SCI CTR,DENVER VET AFFAIRS MED CTR,MED ONCOL SECT,111F,1055 CLERMONT ST,DENVER,CO 80220, USA. FU PHS HHS [R29-44763] NR 35 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 0196-9781 J9 PEPTIDES JI Peptides PD MAR-APR PY 1991 VL 12 IS 2 BP 207 EP 213 DI 10.1016/0196-9781(91)90001-6 PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA FE045 UT WOS:A1991FE04500001 PM 1648710 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R AF SILVA, JA LEONG, GB WEINSTOCK, R TI MISIDENTIFICATION SYNDROME AND MALE PSEUDOCYESIS SO PSYCHOSOMATICS LA English DT Article ID PERSPECTIVE; SELF C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. RP SILVA, JA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV,B116A WARD 206A,LOS ANGELES,CA 90073, USA. NR 23 TC 12 Z9 12 U1 1 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SPR PY 1991 VL 32 IS 2 BP 228 EP 230 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA FE052 UT WOS:A1991FE05200016 PM 2027947 ER PT J AU AAGAARD, J MADSEN, PO AF AAGAARD, J MADSEN, PO TI BACTERIAL PROSTATITIS - NEW METHODS OF TREATMENT SO UROLOGY LA English DT Article ID FLUID; PH AB Four different clinical categories of prostatitis are recognized at present: acute bacterial prostatitis, chronic bacterial prostatitis, nonbacterial prostatitis, and prostatodynia. Treatment results of chronic bacterial prostatitis have, in the past, been rather poor. In addition to local factors (e.g., prostatic calculi), the poor results may well be due, in part, to lack of penetration of the various drugs used into the prostatic tissue and fluid, mostly because of unfavorable lipid solubility, degree of ionization, protein binding, and unfavorable pH gradients from the plasma to prostatic fluid. All of these factors determine the diffusion of a drug into prostatic tissue and fluid. The minimum inhibitory concentrations (MIC) of the various drugs used and the concentration of the drugs actually obtained in the prostate, combined with the influence of pH, inoculum size, and effect of prostatic fluid and prostatic extract on MIC, are important factors in determining at least the theoretical efficacy of various drugs in the treatment of chronic bacterial prostatitis. The new fluoroquinolones have excellent penetration into both animal and human prostates and very low MIC for the infecting organisms and should, from a theoretical standpoint, be ideal in the treatment of chronic bacterial prostatitis. Few clinical studies have been done, and only prospective, randomized clinical trials will determine the relative efficacy of the various quinolones in the treatment of chronic bacterial prostatitis. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI 53706. NR 12 TC 8 Z9 8 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD MAR PY 1991 VL 37 IS 3 SU S BP 4 EP 8 DI 10.1016/0090-4295(91)80088-O PG 5 WC Urology & Nephrology SC Urology & Nephrology GA FC424 UT WOS:A1991FC42400002 PM 2003343 ER PT J AU KLEYMAN, TR KRAEHENBUHL, JP ERNST, SA AF KLEYMAN, TR KRAEHENBUHL, JP ERNST, SA TI CHARACTERIZATION AND CELLULAR-LOCALIZATION OF THE EPITHELIAL NA+ CHANNEL - STUDIES USING AN ANTI-NA+ CHANNEL ANTIBODY RAISED BY AN ANTIIDIOTYPIC ROUTE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MEDULLARY COLLECTING DUCT; TOAD URINARY-BLADDER; SODIUM-CHANNEL; MONOCLONAL-ANTIBODIES; BASOLATERAL MEMBRANE; AMILORIDE ANTIBODIES; APICAL MEMBRANE; KIDNEY-CELLS; RECEPTOR; TRANSPORT AB Amiloride-sensitive Na+ channels are expressed at the apical membrane of high resistance, Na+-transporting epithelial. The specific interaction of amiloride with this transport protein suggested the feasibility of raising anti-Na+ channel antibodies by an antiidiotypic approach designed to generate antibodies directed against the amiloride-binding domain on the channel. Antiidiotypic monoclonal antibody RA6.3 mimicked the effect of amiloride by inhibiting Na+ transport across A6 cell monolayers when applied to the apical cell surface. Inhibition of transport required pretreatment of the apical cell surface with trypsin in the presence of amiloride in order to enhance accessibility of the antibody to the amiloride-binding site. This antibody specifically immunoprecipitated a large 750,000-700,000 Da protein from [S-35]methionine-labeled A6 cell cultures, which was resolved further under reducing conditions as a set of polypeptides with apparent molecular masses of 260,000-230,000, 180,000, 140,000-110,000, and 70,000 Da. The antibody recognized the 140,000-Da subunit, known to contain the amiloride-binding domain, on immunoblots of purified A6 cell Na+ channel. Immunoprecipitation of apical or basolateral plasma membrane proteins selectively labeled with I-125 demonstrated that expression of the oligomeric Na+ channel was restricted to the apical plasma membrane. Immunocytochemical localization in A6 cultures revealed apical membrane as well as cytosolic immunoreactive sites. Immunostaining was also observed at or near the basolateral plasma membrane. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. SWISS INST EXPTL CANC RES,CH-1066 EPALINGES,SWITZERLAND. UNIV MICHIGAN,DEPT ANAT & CELL BIOL,ANN ARBOR,MI 48109. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. UNIV LAUSANNE,DEPT BIOCHEM,CH-1000 LAUSANNE 17,SWITZERLAND. RP KLEYMAN, TR (reprint author), UNIV PENN,DEPT MED,RENAL SECT,700 CLIN RES BLDG,PHILADELPHIA,PA 19104, USA. FU NCRR NIH HHS [RR05385]; NIDDK NIH HHS [DK27559] NR 43 TC 57 Z9 57 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1991 VL 266 IS 6 BP 3907 EP 3915 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200084 PM 1847393 ER PT J AU BAILEY, H MULCAHY, RT TUTSCH, KD ROZENTAL, JM ALBERTI, D ARZOOMANIAN, RZ TOMBES, MB TRUMP, DL WILDING, G AF BAILEY, H MULCAHY, RT TUTSCH, KD ROZENTAL, JM ALBERTI, D ARZOOMANIAN, RZ TOMBES, MB TRUMP, DL WILDING, G TI A PHASE-I STUDY OF SR-2508 AND CYCLOPHOSPHAMIDE ADMINISTERED BY INTRAVENOUS-INJECTION SO CANCER RESEARCH LA English DT Article ID HYPOXIC CELL RADIOSENSITIZER; SENSITIZER MISONIDAZOLE; TRIAL; CHEMOTHERAPY; PHARMACOKINETICS; NITROIMIDAZOLES; ENHANCEMENT; MELPHALAN; CANCER; PLUS AB SR-2508, a less lipophilic and neurotoxic analogue of the nitroimidazole, misonidazole, has exhibited significant chemosensitization properties in preclinical studies with alkylating agents. A phase I trial was carried out to assess toxicity and possible pharmacological interactions of the combination of short infusions of SR-2508 and cyclophosphamide (CP). Patients were randomly assigned to receive either CP alone followed in 3 wk by CP + SR-2508, or CP + SR-2508 followed by CP alone. All additional courses were CP + SR-2508. The maximum tolerated dose of the combination was determined by dose escalation of SR-2508 while the dose of CP remained fixed, initially 1.0 g/m2, and then a second maximum tolerated dose was determined with CP at 1.6 g/m2. One hundred seventeen evaluable courses were administered to 39 patients, the majority of whom had received prior treatment. Somewhat unexpectedly, reversible grade 4 granulocytopenia was the dose-limiting toxicity occurring in four of five evaluable first combination courses at level 6 (SR-2508, 11.3 g/m2; CP, 1.0 g/m2), the initial maximum tolerated dose. SR-2508 enhanced CP-induced myelosuppression as exhibited by the significant difference (p < 0.001) between the 27 paired courses (CP versus CP + SR-2508) for WBC nadirs over levels 1 to 6. The neurotoxicity encountered was similar to that seen in past clinical trials, being reversible, mild, and usually peripheral in nature. There was one treatment-related death (neutropenic sepsis) on study. No other significant toxicity was seen. SR-2508 exhibited linear pharmacokinetics over the dose range studied. The SR-2508 area under the concentration-time curve increased linearly with dose (r = 0.858; p < 0.001). No other parameters were dose related. Neither drug appeared to affect the pharmacokinetics of the other, and CP pharmacokinetic values were consistent with those from prior studies. Due to the interaction noted between the two agents and the preclinical data suggesting preferential enhancement of antitumor efficacy under this combination, phase II study appears warranted. C1 UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53792. UNIV WISCONSIN,DEPT NEUROL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NCI NIH HHS [CA42325, N01-CM57735] NR 30 TC 11 Z9 11 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1991 VL 51 IS 4 BP 1099 EP 1104 PG 6 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700007 PM 1825475 ER PT J AU BAILEY, H TUTSCH, KD ARZOOMANIAN, RZ TOMBES, MB ALBERTI, D BRUGGINK, J WILDING, G AF BAILEY, H TUTSCH, KD ARZOOMANIAN, RZ TOMBES, MB ALBERTI, D BRUGGINK, J WILDING, G TI PHASE-I CLINICAL-TRIAL OF FAZARABINE AS A 24-HOUR CONTINUOUS INFUSION SO CANCER RESEARCH LA English DT Article ID LYMPHOBLASTIC CELLS MOLT-4; NSC 281272; ARABINOSYL-5-AZACYTOSINE; 1-BETA-D-ARABINOFURANOSYL-5-AZACYTOSINE; 5-AZACYTIDINE; DNA; METABOLISM; XENOGRAFTS; KINETICS; LEUKEMIA AB A phase I trial of fazarabine (ara-AC, 1-beta-D-arabinofuranosyl-5-azacytosine, NSC 281272) administered as a 24-h continuous infusion was performed in 24 adults with solid tumor malignancies. The majority of patients had received prior marrow-suppressive therapy. Level 7 (54.5 mg/m2/h for 24 h) was the maximum tolerated dose since during 6 evaluable first courses, 2 episodes of grade 4 granulocytopenia and 3 episodes of grade 3 occurred. Moderate thrombocytopenia also occurred at level 7 with 3 episodes of grade 1 and 1 episode of grade 4 thrombocytopenia during 6 first course treatments. Minimal myelosuppression, principally leukpenia, was seen prior to level 7. The nadir WBC through 47 courses had a linear relationship with plasma steady-state concentrations of ara-AC. The only other toxicity noted was moderate nausea/vomiting, which did not appear to be dose related. Plasma steady-state concentrations of ara-AC were reached in all patients within 4-6 h and ranged from 1.1-mu-M (11 mg/m2/h for 24 h) to 7.5-mu-M (54.5 mg/m2/h for 24 h). The mean total body clearance of ara-AC for 47 courses, levels 1-7, was 592 +/- 147 (SD) ml/min/m2 which is similar to prior pharmacokinetic data from the 24-h and 72-h infusion trials of the Pediatric and Medicine Branches, respectively. There were no objective disease responses during the trial. The recommended adult phase II dose for a 24-h infusion of ara-AC is 45-50 mg/m2/h. C1 UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NCI NIH HHS [N01-CM57735] NR 15 TC 11 Z9 12 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1991 VL 51 IS 4 BP 1105 EP 1108 PG 4 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700008 PM 1705165 ER PT J AU LEHMANN, LS RODRIGUEZ, L AF LEHMANN, LS RODRIGUEZ, L TI CLOZAPINE AND THE MANDATORY MONITORING-SYSTEM SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP LEHMANN, LS (reprint author), US DEPT VET AFFAIRS,WASHINGTON,DC 20420, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 14 PY 1991 VL 324 IS 7 BP 490 EP 490 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EX363 UT WOS:A1991EX36300011 ER PT J AU BERSOHN, MM VEMURI, R SCHUIL, DW WEISS, RS PHILIPSON, KD AF BERSOHN, MM VEMURI, R SCHUIL, DW WEISS, RS PHILIPSON, KD TI EFFECT OF TEMPERATURE ON SODIUM-CALCIUM EXCHANGE IN SARCOLEMMA FROM MAMMALIAN AND AMPHIBIAN HEARTS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE RECONSTITUTION; SARCOLEMMAL VESICLE; SODIUM-CALCIUM ION EXCHANGE; (DOG HEART); (FROG HEART); (RABBIT HEART) ID RAT-BRAIN; MEMBRANES; VESICLES; TRANSPORT AB We have investigated temperature dependence of Ca2+ uptake by the cardiac sarcolemmal Na+ -Ca2+ exchanger from dog, rabbit and bullfrog. In native rabbit sarcolemmal vesicles, Ca2+ affinity of the Na+ -Ca2+ exchanger is unchanged from 7 to 37-degrees-C; however, the initial velocity of Ca2+ uptake declines much more steeply below 22-degrees-C than above 22-degrees-C. In native dog sarcolemma, the temperature dependence of Na+-Ca2+ exchange velocity is similar to that of native rabbit. However, in frog heart the velocity of Na+-Ca2+ exchange declines much more slowly with decreasing temperature at both temperature ranges. Reconstitution of the Na+-Ca2+ exchanger into artificial lipid vesicles consisting of either asolectin or phosphatidylserine, phosphatidylcholine, and cholesterol has little effect on temperature dependence of Na+-Ca2+ exchange velocity in any of the three species. We conclude that the lesser temperature sensitivity of the cardiac sarcolemmal Na+-Ca2+ exchanger of a poikilothermic species is at least partly an intrinsic property of the transport protein. C1 SEPULVEDA VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHYSIOL,LOS ANGELES,CA 90024. RP BERSOHN, MM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,CARDIOL SECT W111E,LOS ANGELES,CA 90073, USA. FU NHLBI NIH HHS [HL27821] NR 17 TC 39 Z9 39 U1 1 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD FEB 11 PY 1991 VL 1062 IS 1 BP 19 EP 23 DI 10.1016/0005-2736(91)90329-7 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EZ980 UT WOS:A1991EZ98000004 PM 1998706 ER PT J AU LINDGRENFURMAGA, EM SCHUNA, AA WOLFF, NL GOODFRIEND, TL AF LINDGRENFURMAGA, EM SCHUNA, AA WOLFF, NL GOODFRIEND, TL TI COST OF SWITCHING HYPERTENSIVE PATIENTS FROM ENALAPRIL MALEATE TO LISINOPRIL SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE COSTS; DOSAGE; ECONOMICS; ENALAPRIL MALEATE; EQUIVALENCY, THERAPEUTIC; HYPERTENSION; HYPOTENSIVE AGENTS; LISINOPRIL ID MK421; MK521 AB The costs and potential savings associated with switching patients in a hypertension clinic from enalapril maleate to lisinopril were analyzed. Patients taking enalapril were randomized to receive lisinopril or to continue taking enalapril. For the 47 patients randomized, data were collected for 25 patients switched to an equal milligram dosage of lisinopril and for 21 patients who continued to receive a constant dosage of enalapril. To maintain blood pressure control, it was necessary to double the dosage of lisinopril in five patients (20%) and halve it in one patient (4%), while the enalapril dosage was doubled in two patients (9.5%). The total direct cost of switching patients to lisinopril was $66.33 per patient. The annual drug cost savings per patient for switching to lisinopril would be $52.08, $46.80, and $120.24 for therapy with one 5-, 10-, and 20-mg tablet per day, respectively. A patient would have to receive 15, 17, or 7 months of therapy with 5-, 10-, or 20-mg tablets of lisinopril, respectively, before a net cost savings would be realized. In the evaluation of a less expensive therapeutic alternative, the total cost of switching must be considered. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PHARM SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,HLTH SERV RES,MADISON,WI 53705. UNIV WISCONSIN,DEPT PREVENT MED,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. RP LINDGRENFURMAGA, EM (reprint author), UNIV ILLINOIS,COLL PHARM,DEPT PHARM PRACTICE,MC 886,ROOM 244,833 S WOOD ST,CHICAGO,IL 60680, USA. NR 8 TC 19 Z9 19 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD FEB PY 1991 VL 48 IS 2 BP 276 EP 279 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV467 UT WOS:A1991EV46700023 PM 1848392 ER PT J AU KINTZEL, PE KENNEDY, PE AF KINTZEL, PE KENNEDY, PE TI STABILITY OF AMPHOTERICIN-B IN 5-PERCENT DEXTROSE INJECTION AT CONCENTRATIONS USED FOR ADMINISTRATION THROUGH A CENTRAL VENOUS LINE SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE ADDITIVES; AMPHOTERICIN-B; ANTIFUNGALS; CONCENTRATION; DEXTROSE; INCOMPATIBILITIES; INJECTIONS; STABILITY; STORAGE; TEMPERATURE; VEHICLES AB The stability of amphotericin B in 5% dextrose injection was studied at concentrations used for administration through a central venous line. Amphotericin B 60, 80, and 100 mg was diluted in 50 mL of 5% dextrose injection; final mean +/- S.D. concentrations after adjustment for total volume were 0.92 +/- 0.01, 1.20 +/- 0.03, and 1.40 +/- 0.03 mg/mL, respectively. For each concentration, six admixtures were prepared; of these, three were stored at 25-degrees-C and three at 6-degrees-C. Amphotericin B concentration was tested at 0, 4, 12, 24, and 36 hours by stability-indicating high-performance liquid chromatography. The admixtures were inspected visually at each time point for precipitation, turbidity, gas formation, and color change, and the pH was measured. Concentrations of amphotericin B remained within 3% of initial concentrations at each time point at both storage temperatures. No precipitation, turbidity, gas formation, or color change was observed, and no changes in pH were measured. Amphotericin B in 5% dextrose injection was stable at concentrations of 0.92, 1.20, and 1.40 mg/mL when stored at 6 and 25-degrees-C for up to 36 hours. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NIH,WARREN G MAGNUSON CLIN CTR,PHARMACEUT DEV SERV,ANALYT LAB,BETHESDA,MD 20892. RP KINTZEL, PE (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 7 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD FEB PY 1991 VL 48 IS 2 BP 283 EP 285 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV467 UT WOS:A1991EV46700025 PM 2003501 ER PT J AU KLEYMAN, TR ZEBROWITZ, JR AF KLEYMAN, TR ZEBROWITZ, JR TI DISTINCT EPITOPES ON AMILORIDE .2. VARIABLY RESTRICTED EPITOPES DEFINED BY MONOCLONAL ANTI-AMILORIDE ANTIBODIES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE EPITHELIAL SODIUM CHANNEL; SODIUM-HYDROGEN EXCHANGER; AMILORIDE ANTIBODIES ID SODIUM-TRANSPORT; RECEPTOR; ANALOGS; INHIBITION; EXCHANGE; HORMONE; PROBE AB Specific regions of amiloride appear to participate in binding to receptors on amiloride-sensitive transport proteins. Previous studies characterizing epitopes on amiloride recognized by anti-amiloride antibodies have demonstrated that antibodies recognize specific domains on amiloride and that these epitopes are determined, in part, by the site on amiloride used to couple to carrier protein. The 3,5-diaminopyrazinyl and guanidinocarbonyl moieties were identified as distinct epitopes. Since Na+-selective transport proteins are sensitive to changes of the halide on the amiloride molecule, additional monoclonal anti-amiloride antibodies were raised to determine whether the C-6 halo group of amiloride could be identified as an important site for drug-antibody binding. The epitopes recognized by a series of three monoclonal antibodies raised against amiloride coupled to rabbit serum albumin through its C-5 NH2-group were defined. Two antibodies recognize extensive regions on the amiloride molecule, including both the acylguanidino and pyrazinyl groups. In addition, both antibodies are sensitive to changes in the C-6 halo group on amiloride. A third antibody was relatively insensitive to changes in the halide in the C-6 position of the pyrazine ring of amiloride and recognized a more restricted epitope on amiloride. C1 UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP KLEYMAN, TR (reprint author), UNIV PENN,DEPT MED,RENAL & ELECTROLYTE SECT,700 CRB,PHILADELPHIA,PA 19104, USA. NR 20 TC 4 Z9 4 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 1991 VL 260 IS 2 BP C271 EP C276 PN 1 PG 6 WC Physiology SC Physiology GA EY855 UT WOS:A1991EY85500013 PM 1705099 ER PT J AU SILVA, JA LEONG, GB LONGHITANO, M BOTELLO, TE AF SILVA, JA LEONG, GB LONGHITANO, M BOTELLO, TE TI DELUSION OF FETAL DUPLICATION IN A CAPGRAS PATIENT SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Note AB A case of Capgras syndrome in a pregnant patient is described. In addition to perceiving living family members as impostors, she believed that there was a double or twin of her fetus. She conceptualized her "twins" differently than the way she viewed doubles of family members. Her fetus may represent the youngest "person" to have been duplicated. The relationship of Capgras syndrome to misidentification phenomena is discussed. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90089. UNIV SO CALIF,INST PSYCHIAT LAW & BEHAV SCI,LOS ANGELES,CA 90089. NR 19 TC 2 Z9 2 U1 1 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 FEB PY 1991 VL 36 IS 1 BP 46 EP 47 PG 2 WC Psychiatry SC Psychiatry GA FA896 UT WOS:A1991FA89600008 PM 2029683 ER PT J AU CARNES, M GOODMAN, BM LENT, SJ AF CARNES, M GOODMAN, BM LENT, SJ TI HIGH-RESOLUTION SPECTRAL-ANALYSIS OF PLASMA ADRENOCORTICOTROPIN REVEALS A MULTIFACTORIAL FREQUENCY STRUCTURE SO ENDOCRINOLOGY LA English DT Article ID HUMAN PITUITARY INVITRO; INTRINSIC PULSATILITY; EPISODIC SECRETION; HORMONE-SECRETION; ACTH; CORTICOTROPIN; RELEASE; DECONVOLUTION; OSCILLATIONS; ALGORITHMS AB Time series of plasma ACTH concentrations were analyzed with a high resolution spectral analysis program based on digital Fourier transforms. Both coherent signal and stochastic aspects of the time series were analyzed. Samples were collected at 2- and 15-min intervals in control rats and rats immunoneutralized against CRH. The individual and composite spectral distributions revealed significant structure at both the higher and lower ranges of frequencies studied, with multiple periodicities between 4-220 min in both groups. CRH immunoneutralization consistently reduced the amplitude by 82% and compressed the frequency distribution for waveforms with periods longer than 15 min by 23%. A systematic break in the slopes of the background continua occurred between 10 and 15 min in the 2-min time series. This break was unaffected by CRH immunoneutralization. Digital Fourier transform analysis of our ACTH time series suggests a system with a more complex high frequency structure than has previously been appreciated. Our analyses suggest a biological system with the following characteristics: 1) both a fast and a slow response to a fairly constant unspecified fast forcing; 2) the slow response is initiated by the fast response and represents an imperfect integration due to feedback processes; 3) CRH alters the ability of the fast forcing to elicit a slow response without altering the fast response or ACTH clearance; and 4) this alteration consists of both amplitude and frequency modulation in the signal output. This view of ACTH secretion suggest an adaptive and energy-efficient system. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,CTR SPACE SCI & ENGN,MADISON,WI 53706. RP CARNES, M (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED SERV,GERIATR SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NIDDK NIH HHS [DK-40759] NR 46 TC 13 Z9 13 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD FEB PY 1991 VL 128 IS 2 BP 902 EP 910 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300038 PM 1846594 ER PT J AU WILLIAMS, JH DRINKA, TJK GREENBERG, JR FARRELLHOLTAN, J EUHARDY, R SCHRAM, M AF WILLIAMS, JH DRINKA, TJK GREENBERG, JR FARRELLHOLTAN, J EUHARDY, R SCHRAM, M TI DEVELOPMENT AND TESTING OF THE ASSESSMENT OF LIVING SKILLS AND RESOURCES (ALSAR) IN ELDERLY COMMUNITY-DWELLING VETERANS SO GERONTOLOGIST LA English DT Article DE FUNCTIONAL; INSTRUMENTAL ACTIVITIES OF DAILY LIVING; EVALUATION ID GERIATRICS; BURDEN; INDEX C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIATR SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705. DIVINE SAVIOR HOSP,PORTAGE,WI. UNIV WISCONSIN,SCH SOCIAL WORK,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. NR 25 TC 34 Z9 34 U1 4 U2 5 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD FEB PY 1991 VL 31 IS 1 BP 84 EP 91 PG 8 WC Gerontology SC Geriatrics & Gerontology GA FJ237 UT WOS:A1991FJ23700012 PM 2007479 ER PT J AU GOODFRIEND, TL AF GOODFRIEND, TL TI ANGIOTENSINS - A FAMILY THAT GROWS FROM WITHIN SO HYPERTENSION LA English DT Editorial Material DE ANGIOTENSINS; ANGIOTENSIN CONVERTING ENZYME INHIBITORS; RENIN-ANGIOTENSIN SYSTEM ID II RECEPTOR SUBTYPES C1 UNIV WISCONSIN,DEPT PHARMACOL & INTERNAL MED,MADISON,WI 53706. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705, USA. NR 10 TC 14 Z9 14 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD FEB PY 1991 VL 17 IS 2 BP 139 EP 140 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW658 UT WOS:A1991EW65800003 PM 1991646 ER PT J AU OCONNOR, PJ MORGAN, WP KOLTYN, KF RAGLIN, JS TURNER, JG KALIN, NH AF OCONNOR, PJ MORGAN, WP KOLTYN, KF RAGLIN, JS TURNER, JG KALIN, NH TI AIR-TRAVEL ACROSS 4 TIME ZONES IN COLLEGE SWIMMERS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE BLOOD PRESSURE; HEART RATE; MOOD; MUSCLE SORENESS; PERCEIVED EXERTION; SALIVARY CORTISOL ID SALIVARY CORTISOL-LEVELS; CIRCADIAN-RHYTHMS; HUMAN-PERFORMANCE; JET-LAG; EXERCISE; SLEEP AB Eighteen female and 22 male college swimmers were flown across four time zones in east-to-west (E-W) and west-to-east (W-E) directions. A pre- and postflight paced swim of 182.9 m at an intensity equal to 90% of the swimmers' maximal velocity was completed, and salivary cortisol, heart rate (HR), and rated perceived exertion were measured. Blood pressure, HR, muscle soreness, and mood were also assessed at rest on the day before and on the day after travel. Because training volumes for both females and males were greater (P < 0.001) in the week before W-E than E-W travel, the W-E and E-W data were analyzed separately. Two-way repeated-measures analyses of variance revealed that pre- and postexercise cortisol decreased after E-W travel and increased after W-E travel in comparison to preflight values. Resting and exercise HR responses to air travel were small in magnitude, and their significance depended on the direction of travel. Effort sense was not altered by air travel, but significant (P < 0.001) improvements in mood and reductions in muscle soreness were observed after E-W and W-E travel for both genders. It was concluded that 1) female and male college swimmers have similar responses to air travel and 2) air travel across four time zones during heavy swim training does not have negative physiological, perceptual, or affective consequences. C1 UNIV WISCONSIN,SPORT PSYCHOL LAB,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,MADISON,WI 53706. INDIANA UNIV,DEPT KINESIOL,BLOOMINGTON,IN 47405. RP OCONNOR, PJ (reprint author), ARIZONA STATE UNIV,EXERCISE & SPORT RES INST,PEBE 210,TEMPE,AZ 85287, USA. NR 29 TC 30 Z9 30 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 FEB PY 1991 VL 70 IS 2 BP 756 EP 763 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA EX526 UT WOS:A1991EX52600037 PM 2022567 ER PT J AU FERNANDEZCHECA, JC GARCIARUIZ, C OOKHTENS, M KAPLOWITZ, N AF FERNANDEZCHECA, JC GARCIARUIZ, C OOKHTENS, M KAPLOWITZ, N TI IMPAIRED UPTAKE OF GLUTATHIONE BY HEPATIC MITOCHONDRIA FROM CHRONIC ETHANOL-FED RATS - TRACER KINETIC-STUDIES INVITRO AND INVIVO AND SUSCEPTIBILITY TO OXIDANT STRESS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE COMPARTMENTALIZATION; TRANSPORT; OXIDANT STRESS; GLUTATHIONE ESTER; CELL DEATH; TERT-BUTYLHYDROPEROXIDE ID HEPATOCYTIC GLUTATHIONE; EFFLUX; LIVER; INHIBITION; METABOLISM; DEPLETION; CELLS AB Isolated hepatocytes incubated with [S-35]-methionine were examined for the time-dependent accumulation of [S-35]-glutathione (GSH) in cytosol and mitochondria, the latter confirmed by density gradient purification. In GSH-depleted and -repleted hepatocytes, the increase of specific activity of mitochondrial GSH lagged behind cytosol, reaching nearly the same specific activity by 1-2 h. However, in hepatocytes from ethanol-fed rats, the rate of increase of total GSH specific radioactivity in mitochondria was markedly suppressed. In in vivo steady-state experiments, the mass transport of GSH from cytosol to mitochondria and vice versa was 18 nmol/min per g liver, indicating that the half-life of mitochondrial GSH was approximately 18 min in controls. The fractional transport rate of GSH from cytosol to mitochondria, but not mitochondria to cytosol, was significantly reduced in the livers of ethanol-fed rats. Thus, ethanol-fed rats exhibit a decreased mitochondrial GSH pool size due to an impaired entry of cytosol GSH into mitochondria. Hepatocytes from ethanol-fed rats exhibited a greater susceptibility to the oxidant stress-induced cell death from tert-butylhydroperoxide. Incubation with glutathione monoethyl ester normalized the mitochondrial GSH and protected against the increased susceptibility to t-butylhydroperoxide, which was directly related to the lowered mitochondrial GSH pool size in ethanol-fed cells. C1 US DEP VET AFFAIRS,OUTPATIENT CLIN,LOS ANGELES,CA 90033. RP FERNANDEZCHECA, JC (reprint author), UNIV SO CALIF,SCH MED,DIV GASTROINTESTINAL & LIVER DIS,2025 ZONAL AVE,LAC 11221,LOS ANGELES,CA 90033, USA. RI Garcia-Ruiz, Carmen/L-8211-2014; Fernandez-Checa, Jose Carlos/L-8342-2014 OI Garcia-Ruiz, Carmen/0000-0002-2652-6102; Fernandez-Checa, Jose Carlos/0000-0003-3422-2990 FU NIDDK NIH HHS [DK30312] NR 38 TC 197 Z9 198 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 397 EP 405 DI 10.1172/JCI115010 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500004 PM 1991826 ER PT J AU ROZENTAL, JM LEVINE, RL NICKLES, RJ AF ROZENTAL, JM LEVINE, RL NICKLES, RJ TI CHANGES IN GLUCOSE-UPTAKE BY MALIGNANT GLIOMAS - PRELIMINARY-STUDY OF PROGNOSTIC-SIGNIFICANCE SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE MALIGNANT GLIOMA; PET SCAN; TUMOR BIOENERGETICS; PATIENT PROGNOSIS ID MAGNETIC-RESONANCE SPECTROSCOPY; POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLIOMAS; 8-DRUGS-IN-ONE-DAY CHEMOTHERAPY; ADULT PATIENTS; BRAIN-TUMOR; DEXAMETHASONE; RADIOTHERAPY; METABOLISM; PET AB Sequential positron emission tomographic scans with [F-18]-2-fluorodeoxyglucose (PET-FDG) were performed on 14 patients with malignant gliomas. All patients had prior brain irradiation. Five patients received adjuvant eight-drugs-in-one-day chemotherapy (experimental subjects) and 9 did not (control subjects). Ratios between the maximal tumor regional cerebral metabolic rate for glucose (rCMRGlu) and the contralateral white matter rCMRGlu, the glucose uptake ratio, were determined. Percent changes in the ratio 1 day after chemotherapy in experimental subjects, and 30 days after the baseline scan in controls, were of prognostic significance. In both groups, patients with the largest percent changes in rCMRGlu had the shortest survival. In contrast, the baseline glucose uptake ratio did not predict length of survival. C1 UNIV WISCONSIN,SCH MED,DEPT NEUROL,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,DEPT RADIOL,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,DEPT MED PHYS,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT NEUROL SURG,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,DEPT RADIOL,MADISON,WI 53706. RP ROZENTAL, JM (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL & RES SERV,NEUROL SERV 127,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA14520]; NCRR NIH HHS [RR03186] NR 30 TC 33 Z9 34 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD FEB PY 1991 VL 10 IS 1 BP 75 EP 83 DI 10.1007/BF00151248 PG 9 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA ER691 UT WOS:A1991ER69100007 PM 2022974 ER PT J AU OLDENDORF, WH STOLLER, BE AF OLDENDORF, WH STOLLER, BE TI RAT-BRAIN FREE GLUCOSE AND LACTATE MEASUREMENT BY A NOVEL METHOD USING BISECTING DECAPITATION-EXTRUSION AND ENZYME DENATURATION AT 5 SECONDS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE BRAIN FREE GLUCOSE; BRAIN LACTATE; ASPIRATION-EXTRUSION SYRINGE; BISECTING DECAPITATION; HEAT DENATURATION; UREA DENATURATION AB This study investigates a novel method as a means for animal decapitation with rapid brain removal and enzyme denaturation. Briefly, the rat head is simultaneously decapitated and bisected. Either half of the in situ brain is aspirated under -250 mm Hg pressure into a modified small plastic syringe and then extruded through a needle as a fine strand into a relatively large volume of 2 M urea at 95-degrees-C. After cooling, sonication, and centrifugation of the brain homogenate, the supernatant is measured enzymatically for brain free glucose and lactate concentration. Enzyme denaturation is effected within 4-6 s. The results are in good agreement with published values for glucose and lactate using other rapid enzyme inactivation techniques. C1 UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. RP OLDENDORF, WH (reprint author), W LOS ANGELES VET ADM,RES SERV,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 9 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD FEB PY 1991 VL 56 IS 2 BP 611 EP 614 DI 10.1111/j.1471-4159.1991.tb08193.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA ET732 UT WOS:A1991ET73200034 PM 1988559 ER PT J AU HENSLER, JG ORDWAY, GA GAMBARANA, C ARESO, P FRAZER, A AF HENSLER, JG ORDWAY, GA GAMBARANA, C ARESO, P FRAZER, A TI SEROTONERGIC NEURONS DO NOT INFLUENCE THE REGULATION OF BETA-ADRENOCEPTORS INDUCED BY EITHER DESIPRAMINE OR ISOPROTERENOL SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID RAT CEREBRAL-CORTEX; ADRENERGIC-RECEPTOR-BINDING; QUANTITATIVE AUTORADIOGRAPHY; DOWN-REGULATION; BRAIN CORTEX; ANTIDEPRESSANTS; CLENBUTEROL; AGONIST; SLICES; SITES AB It has been suggested that 5-hydroxytryptamine (serotonin)-containing neurons influence the regulation of central beta adrenoceptors caused by antidepressants. [H-3]Dihydroalprenolol ([H-3]DHA) was the radioligand used in these previous studies to measure beta adrenoceptors. In this study, we compared the binding characteristics of [H-3]DHA with those of [I-125]iodopindolol ([I-125]IPIN) and used [I-125]IPIN to study effects of lesioning serotonergic nerves on the regulation of beta adrenoceptors. A comparison was made in homogenates prepared from rat frontal cortex of the specific binding of [H-3]DHA with that of [I-125-IPIN to beta adrenoceptors. Nonlinear regression analysis of saturation experiments of [H-3]DHA binding to cortical homogenates indicated that a two-component binding model fit the data significantly better than a one-component model. A dissociation constant value of 0.47 +/- 0.16 nM and a B(max) value of 62 +/- 7 fmol/mg protein were obtained for the high-affinity site. The low-affinity site was poorly defined. Rosenthal transformations of the saturation isotherms for [H-3]DHA binding were clearly curvilinear. By contrast, nonlinear regression analysis of saturation experiments of the binding of [I-125]IPIN indicated that the binding of this radioligand was described adequately by a one-component model and yielded a dissociation constant value of 147 +/- 10 pM with a B(max) of 80 +/- 5 fmol/mg protein. Rosenthal transformations of the [I-125]IPIN data were linear. From such data, it was inferred that [H-3]DHA binds to some site in addition to beta adrenoceptors, whereas [I-125]IPIN does not. In frontal cortical homogenates of rats treated with 5,7-dihydroxytryptamine (5,7-DHT), the density of specific binding sites for [H-3]DHA was significantly increased, whereas no increase in the specific binding of [I-125]IPIN was observed. Moreover, when [I-125]IPIN was used as the ligand to measure beta adrenoceptors, lesioning serotonergic neurons with 5,7-DHT did not prevent the down-regulation of beta adrenoceptors induced by chronic administration of desipramine. Furthermore, as assessed by quantitative autoradiography using [I-125]IPIN, the down-regulation of subtypes of beta adrenoceptors in different regions of brain, produced by chronic intraventricular infusion of the direct acting agonist isoproterenol, was not altered in rats pretreated with 5,7-DHT. We conclude that 5,7-DHT-induced lesioning of serotonergic neurons does not influence the down-regulation of beta adrenoceptors as a result of repeated administration of the tricyclic antidepressant desipramine or chronic infusion of the agonist isoproterenol when [I-125]IPIN is used as the radioligand to measure these receptors. Interestingly, treatment of rats with 5,7-DHT resulted in a significant reduction in the binding of [I-125]IPIN to beta1 adrenoceptors in nine of 13 areas of the brain examined and a significant reduction in beta-2 adrenoceptors in five of the areas, suggesting the presence of beta adrenoceptors on serotonergic neurons in many areas of the brain. C1 UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. RP HENSLER, JG (reprint author), DEPT VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT,151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIMH NIH HHS [MH 14654, MH 29094, MH 09834] NR 44 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD FEB PY 1991 VL 256 IS 2 BP 656 EP 664 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EY611 UT WOS:A1991EY61100037 PM 1847207 ER PT J AU ODELL, K MCNEIL, MR ROSENBEK, JC HUNTER, L AF ODELL, K MCNEIL, MR ROSENBEK, JC HUNTER, L TI PERCEPTUAL CHARACTERISTICS OF VOWEL AND PROSODY PRODUCTION IN APRAXIC, APHASIC, AND DYSARTHRIC SPEAKERS SO JOURNAL OF SPEECH AND HEARING RESEARCH LA English DT Article DE CONSONANT ARTICULATION; PERCEPTUAL ANALYSIS; APRAXIA OF SPEECH; ATAXIC DYSARTHRIA; CONDUCTION APHASIA ID SPEECH; COARTICULATION; PATTERNS C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,SPEECH PATHOL & AUDIOL SERV,MADISON,WI. UNIV WISCONSIN,DEPT AFRICAN LANGUAGES & LINGUIST,MADISON,WI 53706. RP ODELL, K (reprint author), UNIV WISCONSIN,DEPT COMMUNICAT DISORDERS,MADISON,WI 53706, USA. FU NICHD NIH HHS [5030 HD03352]; PHS HHS [N518797] NR 70 TC 52 Z9 53 U1 1 U2 4 PU AMER SPEECH-LANG-HEARING ASSN 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 FEB PY 1991 VL 34 IS 1 BP 67 EP 80 PG 14 WC Language & Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA FA503 UT WOS:A1991FA50300010 PM 2008083 ER PT J AU HENSLER, JG KOVACHICH, GB FRAZER, A AF HENSLER, JG KOVACHICH, GB FRAZER, A TI A QUANTITATIVE AUTORADIOGRAPHIC STUDY OF SEROTONIN-1A RECEPTOR REGULATION - EFFECT OF 5,7-DIHYDROXYTRYPTAMINE AND ANTIDEPRESSANT TREATMENTS SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE SEROTONIN-1A RECEPTOR; 5,7-DIHYDROXYTRYPTAMINE; MONOAMINE OXIDASE INHIBITORS; SEROTONIN UPTAKE INHIBITORS; HYPOTHERMIA; ANTIDEPRESSANTS ID MONOAMINE-OXIDASE INHIBITORS; CENTRAL NERVOUS-SYSTEM; STIMULATED ADENYLATE-CYCLASE; PUTATIVE 5-HT1A AGONISTS; DORSAL RAPHE NEURONS; RAT-BRAIN; ELECTROCONVULSIVE SHOCK; BINDING-SITES; FILM AUTORADIOGRAPHY; H-3 CYANOIMIPRAMINE AB There have been few studies investigating the effect of treatments that alter serotonergic neurotransmission on the density of serotonin1A (5-hydroxytryptamine1A [5-HT-1A]) receptors, even though lesioning serotonergic neurons has been reported to enhance certain responses thought to be due to activation of 5-HT1A receptors and repeated treatment of rats with different types of antidepressants can diminish 5-HT1A-mediated responses. Consequently, the binding of H-3-8-hydroxy-2-(di-n-propylamino)-tetralin (DPAT) to 5-HT1A receptors in serotonergic cell body and terminal field areas of rat brain was measured by quantitative autoradiography following either the lesioning of serotonergic neurons with 5,7-dihydroxytryptamine (5,7-DHT), or after chronic administration of monoamine oxidase inhibitors (MAOIs) (clorgyline, phenelzine, or tranylcypromine) or inhibitors of 5-HT uptake (citalopram or sertraline). Treatment of rats with 5,7-DHT did not cause any significant increase in binding of H-3-DPAT to 5-HT1A receptors in any area of the brain examined. There was no significant reduction in the binding of H-3-DPAT in terminal field areas of serotonergic innervation in rats treated with 5,7-DHT except in the CA2/CA3 region of the hippocampus (33% to 35% reduction). In the dorsal and median raphe nuclei, the specific binding of H-3-DPAT was reduced by treatment of rats with 5,7-DHT. In lesioned rats, the binding of H-3-cyanoimipramine (H-3-CN-IMI) to uptake sites for serotonin was essentially eliminated in all terminal field areas examined, as well as in the dorsal and median raphe nuclei. Repeated administration of clorgyline, phenelzine, tranylcypromine, citalopram, or sertraline produced an attenuation of the hypothermic response of rats to acute subcutaneous injection of the 5-HT1A-receptor-agonist DPAT. In spite of this change in 5-HT1A responsivity, these treatments caused in the same animals no consistent change in the binding of H-3-DPAT in either serotonergic cell body or terminal field areas. Of the five drugs studied that diminished DPAT-induced hypothermia, only phenelzine and clorgyline significantly reduced the binding of H-3-DPAT, and even then in only a few of the 12 areas of brain measured. As a result of treatment of rats with tranylcypromine there was a significant increase in the binding of H-3-DPAT in the CA2/CA3 region of the hippocampus. We find, therefore, little evidence that the changes in the sensitivity of 5-HT1A-mediated behavioral and electrophysiologic responses following treatment with 5,7-DHT or chronic administration of antidepressant drugs are a result of changes in the density of 5-HT1A receptors as measured by the binding of H-3-DPAT in discrete areas of the brain of the rat. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. RP HENSLER, JG (reprint author), VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIMH NIH HHS [MH 09834, MH 14654, MH 29024] NR 73 TC 175 Z9 175 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD FEB PY 1991 VL 4 IS 2 BP 131 EP 144 PG 14 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA EZ503 UT WOS:A1991EZ50300008 PM 2025379 ER PT J AU FARNETT, L MULROW, CD LINN, WD LUCEY, CR TULEY, MR AF FARNETT, L MULROW, CD LINN, WD LUCEY, CR TULEY, MR TI THE J-CURVE PHENOMENON AND THE TREATMENT OF HYPERTENSION - IS THERE A POINT BEYOND WHICH PRESSURE REDUCTION IS DANGEROUS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID CORONARY HEART-DISEASE; DIASTOLIC BLOOD-PRESSURE; MYOCARDIAL-INFARCTION; ELDERLY PATIENTS; FOLLOW-UP; MORTALITY; RISK; TRIAL; FRAMINGHAM; CARE AB We critically appraised the medical literature to evaluate whether there is a point beyond which blood pressure reduction in hypertensive subjects is no longer beneficial and possibly even deleterious. Thirteen studies that stratified cardiovascular outcomes by level of achieved blood pressure in treated hypertensive subjects who had been followed up for at least 1 year were critiqued by four independent reviewers. Data addressing population, protocol, and methodological characteristics were evaluated. Studies did not show a consistent J-shaped relationship between treated blood pressure and stroke, but they did demonstrate a consistent J-shaped relationship for cardiac events and diastolic blood pressure. The beneficial therapeutic threshold point was 85 mm Hg. We conclude that low treated diastolic blood pressure levels, ie, below 85 mm Hg, are associated with increased risk of cardiac events. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78248. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284. NR 41 TC 297 Z9 302 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 JAN 23 PY 1991 VL 265 IS 4 BP 489 EP 495 DI 10.1001/jama.265.4.489 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA ET377 UT WOS:A1991ET37700029 PM 1824642 ER PT J AU GROOP, LC RATHEISER, K LUZI, L MELANDER, A SIMONSON, DC PETRIDES, A BONADONNA, RC WIDEN, E DEFRONZO, RA AF GROOP, LC RATHEISER, K LUZI, L MELANDER, A SIMONSON, DC PETRIDES, A BONADONNA, RC WIDEN, E DEFRONZO, RA TI EFFECT OF SULFONYLUREA ON GLUCOSE-STIMULATED INSULIN-SECRETION IN HEALTHY AND NON-INSULIN-DEPENDENT DIABETIC SUBJECTS - A DOSE-RESPONSE STUDY SO ACTA DIABETOLOGICA LA English DT Article DE INSULIN; C-PEPTIDE; GLUCOSE; GLIPIZIDE; NON-INSULIN-DEPENDENT DIABETES-MELLITUS ID SULFONYLUREA THERAPY; NORMAL HUMANS; C-PEPTIDE; BETA-CELL; HYPERGLYCEMIA; GLYBURIDE; GLIPIZIDE; MELLITUS; DRUGS; SERUM AB The effect of a rapid-acting sulphonylurea, glipizide, on the dose-response relationship between the beta-cell response (insulin and C-peptide secretion) and the ambient plasma glucose concentration was examined in 12 healthy and 6 non-insulin-dependent diabetic subjects. The subjects participated in two sets of experiments which were performed in random order: (A) four hyperglycaemic clamp studies, during which the plasma glucose concentration was raised for 120 min by 1 (only in healthy subjects), 3, 7, and 17 mmol/l; and (B) the same four hyperglycaemic clamp studies preceded by ingestion of 5 mg glipizide. All subjects participated in a further study, in which glipizide was ingested and the plasma glucose concentration was maintained at the basal level. In control subjects in the absence of glipizide, the first-phase plasma insulin response (0-10 min) increased progressively with increasing plasma glucose concentration up to 10 mmol/l, above which it tended to plateau. Glipizide augmented the first-phase insulin response without changing the slope of the regression line relating plasma insulin to glucose concentrations. The second-phase plasma insulin response (20-120 min) increased linearly with increasing hyperglycaemia (r = 0.997). Glipizide alone increased the plasma insulin response by 180 pmol/l. A similar increase in plasma insulin response following glipizide was observed at each hyperglycaemic step, indicating that glipizide did not affect the sensitivity of the beta-cell to glucose. First-phase insulin secretion was reduced in the type 2 (non-insulin-dependent) diabetic patients, and was not influenced by glipizide. The dose-response curve relating second-phase insulin secretion to the ambient plasma glucose concentration was significantly (P < 0.001) flatter in the diabetic patients than in the control subjects. Glipizide alone increased the plasma insulin response by 60 pmol/l without changing the slope of the dose-response curve. It is concluded that, in both type 2 diabetic patients and healthy subjects: (A) sulphonylurea augments glucose-stimulated second-phase insulin secretion without changing the sensitivity of the beta-cell to glucose; (B) first-phase insulin secretion is reduced in non-insulin-dependent diabetic patients with fasting hyperglycaemia and is not influenced by sulphonylurea. C1 YALE UNIV,SCH MED,NEW HAVEN,CT 06510. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV LUND,DEPT PHARMACOL & TOXICOL,S-21401 MALMO,SWEDEN. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,SAN ANTONIO,TX 78284. RP GROOP, LC (reprint author), UNIV HELSINKI,DEPT MED 4,UNIONKATU 38,SF-00170 HELSINKI 17,FINLAND. RI Luzi, Livio/M-2696-2016 OI Luzi, Livio/0000-0003-3183-0552 FU FIC NIH HHS [F05-TWO-3451]; NCRR NIH HHS [RR 125]; NIADDK NIH HHS [AM-24092] NR 30 TC 26 Z9 26 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0940-5429 J9 ACTA DIABETOL JI Acta Diabetol. PY 1991 VL 28 IS 2 BP 162 EP 168 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GQ144 UT WOS:A1991GQ14400006 PM 1777653 ER PT J AU BESS, FH LICHTENSTEIN, MJ LOGAN, SA AF BESS, FH LICHTENSTEIN, MJ LOGAN, SA TI MAKING HEARING IMPAIRMENT FUNCTIONALLY RELEVANT - LINKAGES WITH HEARING DISABILITY AND HANDICAP SO ACTA OTO-LARYNGOLOGICA LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON HEARING IN THE AGED CY NOV 26-29, 1989 CL HELSINGOR, DENMARK SP COMMISS EUROPEAN COMMUNITIES C1 BILL WILKERSON HEARING & SPEECH CTR,NASHVILLE,TN. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP BESS, FH (reprint author), VANDERBILT UNIV,SCH MED,DIV HEARING & SPEECH SCI,1114 19TH AVE S,NASHVILLE,TN 37212, USA. NR 20 TC 3 Z9 3 U1 1 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6489 J9 ACTA OTO-LARYNGOL JI Acta Oto-Laryngol. PY 1991 SU 476 BP 226 EP 231 PG 6 WC Otorhinolaryngology SC Otorhinolaryngology GA FA468 UT WOS:A1991FA46800035 ER PT J AU MINTZ, J PHIPPS, CC ARRUDA, MJ GLYNN, SM SCHNEIDER, NG JARVIK, ME AF MINTZ, J PHIPPS, CC ARRUDA, MJ GLYNN, SM SCHNEIDER, NG JARVIK, ME TI COMBINED USE OF ALCOHOL AND NICOTINE GUM SO ADDICTIVE BEHAVIORS LA English DT Article ID CHEWING-GUM; SMOKING CESSATION; TRIAL C1 UNIV CALIF LOS ANGELES,BRENTWOOD DIV,W LOS ANGELES VET ADM MED CTR,LOS ANGELES,CA 90024. RP MINTZ, J (reprint author), UNIV CALIF LOS ANGELES,BRENTWOOD VET ADM HOSP 691 B117,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90073, USA. NR 14 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4603 J9 ADDICT BEHAV JI Addict. Behav. PY 1991 VL 16 IS 1-2 BP 1 EP 10 DI 10.1016/0306-4603(91)90034-F PG 10 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA EZ512 UT WOS:A1991EZ51200001 PM 2048453 ER PT J AU SCHWARDT, JD GOBRAN, SR NEUFELD, GR AUKBURG, SJ SCHERER, PW AF SCHWARDT, JD GOBRAN, SR NEUFELD, GR AUKBURG, SJ SCHERER, PW TI SENSITIVITY OF CO2 WASHOUT TO CHANGES IN ACINAR STRUCTURE IN A SINGLE-PATH MODEL OF LUNG AIRWAYS SO ANNALS OF BIOMEDICAL ENGINEERING LA English DT Article DE CONVECTION; DIFFUSION; PULMONARY GAS EXCHANGE; NUMERICAL MODEL; PHASE-III SLOPE ID GAS; DIFFUSION; PLATEAU AB A numerical solution of the convection-diffusion equation with an alveolar source term in a single-path model (SPM) of the lung airways simulates steady state CO2 washout. The SPM is used to examine the effects of independent changes in physiologic and acinar structure parameters on the slope and height of Phase III of the single-breath CO2 washout curve. The parameters investigated include tidal volume, breathing frequency, total cardiac output, pulmonary arterial CO2 tension, functional residual capacity, pulmonary bloodflow distribution, alveolar volume, total acinar airway cross sectional area, and gas-phase molecular diffusivity. Reduced tidal volume causes significant steepening of Phase III, which agrees well with experimental data. Simulations with a fixed frequency and tidal volume show that changes in bloodflow distribution, model airway cross section, and gas diffusivity strongly affect the slope of Phase III while changes in cardiac output and in pulmonary arterial CO2 tension strongly affect the height of Phase III. The paper also discusses differing explanations for the slope of Phase III, including sequential emptying, stratified inhomogeneity, and the issue of asymmetry, in the context of the SPM. C1 UNIV PENN,SCH ENGN & APPL SCI,DEPT BIOENGN,220 S 33RD ST,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT ANESTHESIA,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. FU NHLBI NIH HHS [HL-33891] NR 29 TC 38 Z9 38 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0090-6964 J9 ANN BIOMED ENG JI Ann. Biomed. Eng. PY 1991 VL 19 IS 6 BP 679 EP 697 DI 10.1007/BF02368076 PG 19 WC Engineering, Biomedical SC Engineering GA GY714 UT WOS:A1991GY71400003 PM 1781569 ER PT J AU DAVIDSON, M KAHN, RS POWCHIK, P WARNE, P LOSONCZY, MF KAMINSKY, R APTER, S JAFF, S DAVIS, KL AF DAVIDSON, M KAHN, RS POWCHIK, P WARNE, P LOSONCZY, MF KAMINSKY, R APTER, S JAFF, S DAVIS, KL TI CHANGES IN PLASMA HOMOVANILLIC-ACID CONCENTRATIONS IN SCHIZOPHRENIC-PATIENTS FOLLOWING NEUROLEPTIC DISCONTINUATION SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CATECHOLAMINE METABOLITES; DOPAMINE METABOLISM; DEBRISOQUIN; RAT; HALOPERIDOL; HVA AB Changes in plasma levels of the dopamine metabolite homovanillic acid have been reported to correlate with changes in the severity of schizophrenic symptoms during neuroleptic administration and after neuroleptic discontinuation. This study examined the effects of discontinuation of neuroleptic treatment on plasma homovanillic acid levels in 23 patients with chronic schizophrenia. It was hypothesized that clinical decompensation would be associated with increased plasma homovanillic acid levels. Plasma homovanillic acid was measured during administration of neuroleptic medication and during a subsequent 6-week drug-free period. Nine patients decompensated during the drug-free period and 14 patients did not. Following drug discontinuation, plasma homovanillic acid concentrations were higher in schizophrenic patients who decompensated than in those who did not. Furthermore, peak plasma homovanillic acid elevation after discontinuation of neuroleptic medication was significantly correlated with peak of Brief Psychiatric Rating Scale increases. The data suggest that, in some schizophrenic patients, symptomatic decompensation after discontinuation of neuroleptic treatment is associated with increases in dopamine turnover. RP DAVIDSON, M (reprint author), MT SINAI HOSP,SCH MED,BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,PSYCHIAT SERV 116A,BRONX,NY 10468, USA. NR 24 TC 56 Z9 56 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 1991 VL 48 IS 1 BP 73 EP 76 PG 4 WC Psychiatry SC Psychiatry GA ET378 UT WOS:A1991ET37800009 PM 1670618 ER PT J AU ROODMAN, GD KUEHL, TJ VANDEBERG, JL MUIRHEAD, DY AF ROODMAN, GD KUEHL, TJ VANDEBERG, JL MUIRHEAD, DY TI INUTERO BONE-MARROW TRANSPLANTATION OF FETAL BABOONS WITH MISMATCHED ADULT BABOON MARROW SO BLOOD CELLS LA English DT Article; Proceedings Paper CT 6TH ANNUAL SYMP ON MOLECULAR BIOLOGY OF HEMOPOIESIS - FRONTIERS IN BONE MARROW TRANSPLANTATION : FETAL HEMATOPOIESIS CY JUN, 1990 CL FARMINGTON, CT DE INUTERO; FETAL; BABOONS; BONE MARROW TRANSPLANTATION ID HEMATOPOIETIC STEM-CELLS; MOUSE FETUSES AB In utero bone marrow transplantation to fetuses offers the potential advantage of ameliorating the effects of genetic disorders by transplanting allogeneic hematopoietic stem cells into recipients who are immunoincompetent and require no preparative regimen. Therefore, we undertook studies to examine the feasibility of in utero bone marrow transplantation of unrelated allogeneic adult bone marrow into fetal baboons. Thirty-one baboon fetuses were transplanted between the ages of 60 and 160 days gestation (normal gestation, 182 days) with unrelated allogeneic adult bone marrow containing a different isozyme of glucose-phosphate isomerase (GPI). Approximately one third of the 80-day fetuses demonstrated engraftment 1 month after transplantation. Three of three of the initial chimeras died in utero 45 to 80 days after transplantation and the remaining chimeras lost their graft. Furthermore, 80-day fetal baboons were able to recognize donor cells, maternal cells, and other adult baboon peripheral blood cells in a mixed lymphocyte culture (MLC) reaction but still could engraft with allogeneic bone marrow. In contrast all nonchimeric animals survived to term. These data suggest that fetal transplantation of primates is feasible using techniques employed in these studies and that transplantation of younger fetuses who are immunocompetent should be attempted. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. SW FDN BIOMED RES,SAN ANTONIO,TX 78284. RP ROODMAN, GD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 8 TC 21 Z9 21 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 1991 VL 17 IS 2 BP 367 EP 375 PG 9 WC Hematology SC Hematology GA FN569 UT WOS:A1991FN56900016 PM 1833000 ER PT B AU COBURN, JW SALUSKY, IB NORRIS, KC GOODMAN, WG AF COBURN, JW SALUSKY, IB NORRIS, KC GOODMAN, WG BE MORII, H TI ORAL AND PARENTERAL CALCITRIOL FOR THE MANAGEMENT OF END-STAGE RENAL-DISEASE SO CALCIUM-REGULATING HORMONES I : ROLE IN DISEASE AND AGING SE CONTRIBUTIONS TO NEPHROLOGY LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON CALCIUM-REGULATING HORMONES, BODY FUNCTIONS AND KIDNEY CY JUL 11-13, 1990 CL NARA, JAPAN RP COBURN, JW (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,NEPHROL SECT W111L,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 21 Z9 21 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5371-4 J9 CONTRIB NEPHROL JI Contrib.Nephrol. PY 1991 VL 90 BP 166 EP 182 PG 17 WC Endocrinology & Metabolism; Pathology; Pharmacology & Pharmacy; Physiology; Urology & Nephrology SC Endocrinology & Metabolism; Pathology; Pharmacology & Pharmacy; Physiology; Urology & Nephrology GA BU27H UT WOS:A1991BU27H00025 PM 1959343 ER PT J AU LIU, AW WEISSBECKER, KA DELGADOESCUETA, A SERRATOSA, JM TREIMAN, L SPARKES, R PARK, MS AF LIU, AW WEISSBECKER, KA DELGADOESCUETA, A SERRATOSA, JM TREIMAN, L SPARKES, R PARK, MS TI LINKAGE STUDIES OF JUVENILE MYOCLONIC EPILEPSY SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,DEPT NEUROL,LOS ANGELES,CA 90024. LOUISIANA STATE UNIV,MED CTR,DEPT BIOCHEM & GENET,NEW ORLEANS,LA 70112. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,NEUROL & RES SERV,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED GENET,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,TISSUE TYPING LAB,LOS ANGELES,CA 90024. NR 2 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1913 EP 1914 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900175 ER PT J AU BONADONNA, RC DEFRONZO, RA AF BONADONNA, RC DEFRONZO, RA TI GLUCOSE-METABOLISM IN OBESITY AND TYPE-2 DIABETES SO DIABETES & METABOLISM LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON NON-INSULIN DEPENDENT DIABETES TODAY CY SEP 07-08, 1990 CL HELSINGOR, DENMARK DE NIDDM; OBESITY; INSULIN-RESISTANCE; INSULIN SECRETION; GLUCOSE METABOLISM ID BODY-FAT DISTRIBUTION; HUMAN SKELETAL-MUSCLE; HEPATIC GLYCOGEN FORMATION; AMINO-ACID METABOLISM; INVIVO INSULIN ACTION; RAT ADIPOSE-CELLS; MAGNETIC-RESONANCE SPECTROSCOPY; SYNTHASE PHOSPHATASE-ACTIVITY; TRANSPORTER MESSENGER-RNA; PANCREATIC BETA-CELLS AB The aim of this review is to provide a comprehensive summary of the subject of glucose metabolism in normal and obese subjects, and in those with type 2 diabetes. The following topics are discussed: - Glucose and insulin metabolism, including characterization of the role of various organs in maintaining glucose homeostasis in the basal state and after food. - The action of insulin and the concept of insulin resistance, its main characteristics as revealed by studies of glucose metabolism in liver and skeletal muscle, the two organs primarily involved. Changes in insulin secretion in obese subjects and in diabetics are reviewed. - Finally, the development of diabetes as a consequence of increasing insulin resistance in the obese diabetic subject is discussed. The principal features - insulin resistance, elevated free fatty acid levels and glucotoxicity - are emphasized. A possible explanation of how obesity leads to diabetes, emphasizing the role played by upper body fat distribution, is provided. C1 UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP BONADONNA, RC (reprint author), UNIV PISA,CNR,INST CLIN PHYSIOL,I-56100 PISA,ITALY. FU NCRR NIH HHS [MOI-RR-01346]; NIDDK NIH HHS [DK24092] NR 240 TC 39 Z9 40 U1 0 U2 1 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0338-1684 J9 DIABETES METAB JI Diabetes Metab. PY 1991 VL 17 IS 1BIS BP 112 EP 135 PG 24 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FP437 UT WOS:A1991FP43700008 PM 1936466 ER PT J AU WONG, M BRUCE, S JOSEPH, D LIVELY, H AF WONG, M BRUCE, S JOSEPH, D LIVELY, H TI ESTIMATING LEFT-VENTRICULAR EJECTION FRACTION FROM 2-DIMENSIONAL ECHOCARDIOGRAMS - VISUAL AND COMPUTER-PROCESSED INTERPRETATIONS SO ECHOCARDIOGRAPHY-A JOURNAL OF CARDIOVASCULAR ULTRASOUND AND ALLIED TECHNIQUES LA English DT Article DE DIGITAL ECHOCARDIOGRAPHY; EJECTION FRACTION; INTRAOBSERVER ERRORS AB Digital echocardiography makes computer-processed estimates of ejection fraction feasible for clinical use but increases physician reading time. The practicabilities were examined by three novice fellows and four experienced attendings. Ejection fraction was visually estimated from playback of videotape or cine-loop displays. Ejection fraction was also estimated from single tracings of endocardium, digitized and applied to biplane Simpson's rule, and expressed in whole units. Differences between fellows' and attendings' visual estimates were close to 0 +/- 6.4 median standard deviation. The 95% confidence intervals for reproducing visual and computer-processed ejection fractions ranged from 15% to 46% of mean ejection fraction; for comparing the two methods, from 7% to 36%. Intraobserver reading errors varied widely and with one observer, systematically, and were independent of experience, but dependent on the quality of signals. Computer-processed readings of ejection fraction should be reserved for images of reasonable quality and for confirming visually estimated ejection fractions between the lower limits of normal (45%-50%) to moderately severely depressed (25%-30%), when accuracy is clinically relevant or when a serial change is at the confidence limits of the reader and needs verification. RP WONG, M (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,CARDIOL SECT W111E,LOS ANGELES,CA 90073, USA. NR 0 TC 16 Z9 16 U1 0 U2 0 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 0742-2822 J9 ECHOCARDIOGR-J CARD JI Echocardiography-J. Cardiovasc. Ultrasound Allied Tech. PD JAN PY 1991 VL 8 IS 1 BP 1 EP 7 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EX710 UT WOS:A1991EX71000001 PM 10149242 ER PT J AU CALLAWAY, E AF CALLAWAY, E TI TOWARDS A PHARMACOLOGY OF INFORMATION-PROCESSING - DISCUSSION SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Discussion C1 SAN FRANCISCO VET ADM MED CTR,TIBURON,CA 94920. NR 4 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PY 1991 SU 42 BP 173 EP 176 PG 4 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA HB514 UT WOS:A1991HB51400019 ER PT J AU OBERLEY, TD ALLEN, RG SCHULTZ, JL LAUCHNER, LJ AF OBERLEY, TD ALLEN, RG SCHULTZ, JL LAUCHNER, LJ TI ANTIOXIDANT ENZYMES AND STEROID-INDUCED PROLIFERATION OF KIDNEY TUBULAR CELLS SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Note DE ANTIOXIDANT ENZYMES; LIPOSOMES; PROLIFERATION; CELL CULTURE; FREE RADICALS AB Diethylstilbestrol induces proliferation of Syrian hamster renal proximal tubular cells. By counting the number of cells in culture, we showed that liposomes containing superoxide dismutase or catalase suppressed diethylstibestrol-induced proliferation, whereas empty liposomes or liposomes containing inactivated superoxide dismutase did not. Liposomes containing antioxidant enzymes did not suppress proliferation of cells in control media or of cells treated with ethinyl estradiol. In the absence of liposomes, exogenous superoxide dismutase did not suppress diethylstilbestrol-induced proliferation. The decrease in cell number when diethylstilbestrol-treated cells were treated with antioxidant enzyme-containing liposomes was not due to decreased cell viability. Results were confirmed by measuring a correlate of cell proliferation immunohistochemically, using an antibody to proliferation cell nuclear antigen. A larger proportion of diethylstilbestrol-treated cells than of control cells showed nuclear immunostaining with this antibody. The number of cells immunostained in diethylstilbestrol-treated cultures was sharply decreased by the addition of superoxide dismutase- or catalase-containing liposomes. Our studies suggest a role for active oxygen species in diethylstilbestrol-induced proliferation of cultured proximal tubular cells. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SECT,LAB SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA 22008] NR 0 TC 19 Z9 19 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1991 VL 10 IS 1 BP 79 EP 83 DI 10.1016/0891-5849(91)90024-W PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA EY737 UT WOS:A1991EY73700012 PM 2050299 ER PT J AU STRONG, A WOLFF, H KINDER, S LUBISCHER, A AF STRONG, A WOLFF, H KINDER, S LUBISCHER, A TI DRUG ADMINISTRATION IN RELATION TO MEALS IN THE INSTITUTIONAL SETTING SO HEART & LUNG LA English DT Article AB To investigate adherence to literature recommendations for administration of five cardiovascular drugs in relation to mealtimes, data from records of 183 adult patients in two short-term and two long-term care settings were tabulated. Ninety-three percent of patients taking quinidine sulfate and 85% of patients taking the other four study drugs received one or more doses incorrectly. Findings show that timing recommendations for dosing in relation to meals are not considered in these institutions when drug administration schedules are established. The practice of arbitrary schedule selection could have serious consequences, including adverse physiologic and financial impact on the patient from loss of therapeutic effectiveness or development of drug toxicosis. Medication schedules need to be designed to achieve the greatest drug bioavailability. RP STRONG, A (reprint author), PORTLAND VET AFFAIRS MED CTR,ANP 111B,POB 1034,PORTLAND,OR 97207, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0147-9563 J9 HEART LUNG JI Heart Lung PD JAN PY 1991 VL 20 IS 1 BP 39 EP 44 PG 6 WC Cardiac & Cardiovascular Systems; Nursing; Respiratory System SC Cardiovascular System & Cardiology; Nursing; Respiratory System GA EW501 UT WOS:A1991EW50100009 PM 1988391 ER PT J AU CEBRA, JJ CUFF, CF RUBIN, DH AF CEBRA, JJ CUFF, CF RUBIN, DH TI RELATIONSHIP BETWEEN ALPHA/BETA T-CELL RECEPTOR/CD8+ PRECURSORS FOR CYTOTOXIC LYMPHOCYTES-T IN THE PEYER,MURINE PATCHES AND THE INTRAEPITHELIAL COMPARTMENT PROBED BY ORAL INFECTION WITH REOVIRUS SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID PEYERS PATCHES C1 VET AFFAIRS MED CTR,DEPT MED,PHILADELPHIA,PA. RP CEBRA, JJ (reprint author), UNIV PENN,DEPT BIOL,415 S UNIV AVE,PHILADELPHIA,PA 19104, USA. NR 4 TC 7 Z9 7 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 1991 VL 10 IS 3-4 BP 321 EP 323 DI 10.1007/BF02919715 PG 3 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600028 PM 1659604 ER PT J AU AAGAARD, J GASSER, T RHODES, P MADSEN, PO AF AAGAARD, J GASSER, T RHODES, P MADSEN, PO TI MICS OF CIPROFLOXACIN AND TRIMETHOPRIM FOR ESCHERICHIA-COLI - INFLUENCE OF PH, INOCULUM SIZE AND VARIOUS BODY-FLUIDS SO INFECTION LA English DT Article; Proceedings Paper CT 7TH SILS MARIA SYMP : PROSTATITIS CY 1990 CL SILS MARIA, SWITZERLAND SP BAYER ID INVITRO ACTIVITY; PROSTATIC FLUID AB The influence of pH, inoculum size, human urine and prostatic extract on the MICs of ciprofloxacin and trimethoprim for Escherichia coli was investigated. There was no influence by the bacterial inoculum size within wide ranges on either drug. An increase in pH had a variable influence on the MICs of trimethoprim for E. coli but lowered those of ciprofloxacin considerably. Human prostatic extract increased the trimethoprim MIC for E. coli but lowered those of ciprofloxacin as compared to Mueller Hinton broth. Human urine increased the MICs of both drugs for E. coli. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,TECH LAB,MADISON,WI 53705. KANTONSSPITAL,UROL ABT,CH-4004 BASEL,SWITZERLAND. RP AAGAARD, J (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 5 TC 8 Z9 8 U1 0 U2 2 PU MMW MEDIZIN VERLAG GMBH PI MUNICH 80 PA NEUMARKTER STRASSE 18, W-8000 MUNICH 80, GERMANY SN 0300-8126 J9 INFECTION JI Infection PY 1991 VL 19 SU 3 BP S167 EP S169 DI 10.1007/BF01643691 PG 3 WC Infectious Diseases SC Infectious Diseases GA FJ043 UT WOS:A1991FJ04300015 PM 2055655 ER PT J AU FRICK, J MADSEN, PO RUTISHAUSER NEAL FOWLER, JE WEIDNER, W SCHAEFFER, AJ BERGMAN GASSER, T PFAU, A NICKEL, JC ECHOLS BLENK, H RIEDASCH, G NABER, KG MARGET, W SVENSON KALLENIUS PHILPOTT, AC MADSEN, PO BAERT, L RUSKIN BUSCH AF FRICK, J MADSEN, PO RUTISHAUSER NEAL FOWLER, JE WEIDNER, W SCHAEFFER, AJ BERGMAN GASSER, T PFAU, A NICKEL, JC ECHOLS BLENK, H RIEDASCH, G NABER, KG MARGET, W SVENSON KALLENIUS PHILPOTT, AC MADSEN, PO BAERT, L RUSKIN BUSCH TI PROSTATITIS - (VII-SILS-MARIA SYMPOSIUM 1990) - DISCUSSIONS SO INFECTION LA English DT Discussion C1 UNIV ILLINOIS,COLL MED,DIV UROL,CHICAGO,IL 60680. UNIV GOTTINGEN,UROL KLIN,W-3400 GOTTINGEN,GERMANY. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. KANTONSSPITAL,UROL ABT,CH-4004 BASEL,SWITZERLAND. HADASSAH MED CTR,IL-91120 JERUSALEM,ISRAEL. QUEENS UNIV,KINGSTON GEN HOSP,DEPT UROL,KINGSTON K7L 2V7,ONTARIO,CANADA. LAB MED MIKROBIOL & IMMUNOL,W-8500 NURNBERG 90,GERMANY. UNIV HEIDELBERG,ZENTRUM CHIRURG,UROL ABT,W-6900 HEIDELBERG,GERMANY. ELISABETH HOSP,UROL KLIN,W-8440 STRAUBING,GERMANY. UNIV COLORADO,HLTH SCI CTR,DIV UROL,DENVER,CO 80262. WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SERV,MADISON,WI 53705. UNIV ZIEKENHUIS ST PETER,DEPT UROL,B-3000 LOUVAIN,BELGIUM. RP FRICK, J (reprint author), LANDESKRANKENANSTALTEN SALZBURG,UROL ABT,MULLNER HAUPTSTR 48,A-5020 SALZBURG,AUSTRIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MMW MEDIZIN VERLAG GMBH PI MUNICH 80 PA NEUMARKTER STRASSE 18, W-8000 MUNICH 80, GERMANY SN 0300-8126 J9 INFECTION JI Infection PY 1991 VL 19 SU 3 BP S178 EP S188 PG 11 WC Infectious Diseases SC Infectious Diseases GA FJ043 UT WOS:A1991FJ04300017 ER PT J AU MADSEN, PO AAGAARD, J AF MADSEN, PO AAGAARD, J TI PHARMACOKINETICS OF QUINOLONE DERIVATIVES IN THE PROSTATE SO INFECTION LA English DT Article; Proceedings Paper CT 7TH SILS MARIA SYMP : PROSTATITIS CY 1990 CL SILS MARIA, SWITZERLAND SP BAYER ID CHRONIC BACTERIAL PROSTATITIS; FLUID AB The pharmacokinetics of six quinolone derivatives were investigated in the human and dog prostate. The possible therapeutic applications of these findings are discussed. RP MADSEN, PO (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 7 TC 2 Z9 2 U1 0 U2 0 PU MMW MEDIZIN VERLAG GMBH PI MUNICH 80 PA NEUMARKTER STRASSE 18, W-8000 MUNICH 80, GERMANY SN 0300-8126 J9 INFECTION JI Infection PY 1991 VL 19 SU 3 BP S154 EP S156 DI 10.1007/BF01643687 PG 3 WC Infectious Diseases SC Infectious Diseases GA FJ043 UT WOS:A1991FJ04300011 PM 1647370 ER PT J AU KIRKLAND, TN QURESHI, N TAKAYAMA, K AF KIRKLAND, TN QURESHI, N TAKAYAMA, K TI DIPHOSPHORYL LIPID-A DERIVED FROM LIPOPOLYSACCHARIDE (LPS) OF RHODOPSEUDOMONAS-SPHAEROIDES INHIBITS ACTIVATION OF 70Z/3 CELLS BY LPS SO INFECTION AND IMMUNITY LA English DT Article ID NF-KAPPA-B; STRUCTURAL DETERMINATION; SALMONELLA-TYPHIMURIUM; TRANSCRIPTION; INDUCTION; PURIFICATION; ATCC-17023; PRECURSORS; LOCATION; MUTANT AB Diphosphoryl lipid A derived from nontoxic lipopolysaccharide (LPS) of Rhodopseudomonas sphaeroides ATCC 17023 did not stimulate the murine pre-B cell line 70Z/3 to synthesize surface immunoglobulin or kappa mRNA. However, it effectively blocked Escherichia coli LPS-induced activation of 70Z/3 cells in a concentration-dependent manner. This inhibition was specific only to cells activated by LPS, since it did not inhibit activation of 70Z/3 cells by gamma interferon. Maximal inhibitory effect occurred when the antagonist was added within 2 h before adding the LPS. These results strongly suggested that R. sphaeroides diphosphoryl lipid A is competing with E. coli LPS for physiological lipid A receptors on the 70Z/3 cells. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. VET ADM MED CTR,SAN DIEGO,CA 92161. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL LAB,MADISON,WI 53705. RP KIRKLAND, TN (reprint author), UNIV CALIF SAN DIEGO,DEPT PATHOL,LA JOLLA,CA 92093, USA. FU NIGMS NIH HHS [GM-36054] NR 26 TC 56 Z9 56 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1991 VL 59 IS 1 BP 131 EP 136 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP751 UT WOS:A1991EP75100020 PM 1898897 ER PT J AU QURESHI, N TAKAYAMA, K KURTZ, R AF QURESHI, N TAKAYAMA, K KURTZ, R TI DIPHOSPHORYL-LIPID-A OBTAINED FROM THE NONTOXIC LIPOPOLYSACCHARIDE OF RHODOPSEUDOMONAS-SPHAEROIDES IS AN ENDOTOXIN ANTAGONIST IN MICE SO INFECTION AND IMMUNITY LA English DT Note ID TUMOR NECROSIS FACTOR; PERFORMANCE LIQUID-CHROMATOGRAPHY; COMPLETE STRUCTURAL DETERMINATION; SALMONELLA-TYPHIMURIUM; ESCHERICHIA-COLI; PURIFICATION; ATCC-17023; INDUCTION; INTERLEUKIN-1; MECHANISMS AB Diphosphoryl lipid A (DPLA) obtained from the nontoxic lipopolysaccharide (LPS) of Rhodopseudomonas sphaeroides ATCC 17023 did not induce interleukin-1 release by murine peritoneal macrophages. However, it blocked this induction by toxic deep-rough chemotype LPS (ReLPS) from Escherichia coli D31m4. Previously, we obtained similar results on the induction of tumor necrosis factor (TNF) by macrophages. These results showed that DPLA is able to block in vitro the induction of two important mediators of gram-negative bacterial sepsis. We then wanted to determine whether DPLA could also block the induction of TNF by LPS in animals. Mice were treated with 100-mu-g of R. sphaeroides DPLA and challenged 60 min later with 1.0-mu-g of ReLPs from E. coli. The serum TNF level was measured after 60 min. Treatment of mice with this DPLA blocked the rapid and transient rise of TNF caused by ReLPS. This result suggested that R. sphaeroides DPLA might be able to protect animals against endotoxin shock caused by gram-negative bacterial infection. 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. FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 31 TC 106 Z9 107 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1991 VL 59 IS 1 BP 441 EP 444 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP751 UT WOS:A1991EP75100065 PM 1987057 ER PT J AU HARTSTEIN, AI WARD, TT AF HARTSTEIN, AI WARD, TT TI METHICILLIN-RESISTANT STAPHYLOCOCCUS-AUREUS SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Editorial Material C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP HARTSTEIN, AI (reprint author), OREGON HLTH SCI UNIV,DEPT MED,DIV INFECT DIS,L457,3181 SAM JACKSON PK RD,PORTLAND,OR 97201, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD JAN PY 1991 VL 12 IS 1 BP 9 EP 10 PG 2 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA FM812 UT WOS:A1991FM81200004 PM 1999646 ER PT J AU BENNETT, CL GRAF, L HUNTERYOUNG, N DALEY, J MAKADON, HJ AF BENNETT, CL GRAF, L HUNTERYOUNG, N DALEY, J MAKADON, HJ TI INTENSITY OF IN-HOSPITAL CARE FOR PERSONS WITH AIDS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE INTENSITY OF RESOURCE USE; TERMINAL CARE ID COSTS AB We evaluated the intensity of medical care for 30 consecutive AIDS patients at one hospital, using methodology based on the Delay Tool of Selker et al. Of 25 AIDS patients who survived hospitalization, 15 had at least one delay day in the hospital. Major factors associated with care that could have been provided at an alternative site included difficulty with skilled nursing facility placement in 20% of the patients, difficulty coordinating out-of-hospital care in 28%, and scheduling of outpatient surgical procedures in 12%. For the 15 patients who could have received some of their care at a lower intensity setting, a median of 7 hospital days could have been potentially saved with better coordination of outpatient care and increased availability of skilled nursing facilities. The five patients who died in hospital also used large amounts of resources and had long lengths of stay. Prior studies of non-AIDS patients revealed similar results, suggesting that, for reasons of quality of care, quality of life, and economics, policy-makers must develop managed care programs, skilled nursing facilities that accept AIDS patients, inpatient psychiatry facilities, and increased hospice availability. C1 UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET AFFAIRS MED CTR,DEPT GEN MED,LOS ANGELES,CA 90024. DEPT VET AFFAIRS,WESTERN REG SPECIAL STUDIES GRP,LOS ANGELES,CA. CLIN PARTNERS INC,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,DIV GEN MED & PRIMARY CARE,BOSTON,MA 02115. RP BENNETT, CL (reprint author), RAND CORP,1700 MAIN ST,SANTA MONICA,CA 90407, USA. RI Bennett, Charles/C-2050-2008 NR 8 TC 11 Z9 11 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. PY 1991 VL 4 IS 9 BP 856 EP 860 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GD597 UT WOS:A1991GD59700005 PM 1895205 ER PT J AU GROOP, LC SALORANTA, C SHANK, M BONADONNA, RC FERRANNINI, E DEFRONZO, RA AF GROOP, LC SALORANTA, C SHANK, M BONADONNA, RC FERRANNINI, E DEFRONZO, RA TI THE ROLE OF FREE FATTY-ACID METABOLISM IN THE PATHOGENESIS OF INSULIN RESISTANCE IN OBESITY AND NONINSULIN-DEPENDENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GLUCOSE-TOLERANCE; PLASMA-GLUCOSE; POSTRECEPTOR DEFECTS; LIPID OXIDATION; RECEPTOR; BINDING; INVIVO; MUSCLE; HYPERGLYCEMIA; CARBOHYDRATE AB To investigate the mechanisms of insulin resistance in obesity and noninsulin-dependent diabetes mellitus (NIDDM), we examined oxidative and nonoxidative pathways of free fatty acid (FFA) and glucose metabolism in 14 lean and 17 obese (with normal oral glucose tolerance) nondiabetic subjects and in 8 lean and 8 obese subjects with NIDDM. FFA and glucose metabolism were measured using the sequential insulin clamp technique in combination with indirect calorimetry and infusion of [3-H-3]glucose and [1-C-14]palmitate. Obesity was characterized by enlarged fat mass, which correlated positively with the plasma FFA concentration (r = 0.62; P < 0.01). FFA metabolism was less sensitive to insulin in obese than in lean nondiabetic subjects, but this defect could be overcome by increasing the plasma insulin concentration. NIDDM patients showed normal sensitivity to the inhibitory action of insulin FFA metabolism; however, maximal suppression by insulin was impaired. The combination of obesity and NIDDM was associated with a further enhancement of reesterification of FFA than observed in either condition alone. In both obesity and NIDDM, the dose-response curve for suppression of hepatic glucose production by insulin was impaired. While obesity was primarily characterized by reduced sensitivity to the stimulatory action of insulin on oxidative and nonoxidative pathways of glucose metabolism, resistance to the effect of insulin on glucose metabolism in NIDDM was characterized by a reduced maximal response. The combination of obesity and NIDDM further impaired the sensitivity of liver glucose output and glucose oxidation to insulin. The hypothesis is advanced that in uncomplicated obesity, increased availability and oxidation of FFA leads, by the FFA/glucose cycle, to the impairment in glucose utilization. In NIDDM, on the other hand, the defect in glucose utilization is primary, and the enhanced rate of FFA oxidation may represent a compensatory phenomenon. C1 UNIV PISA, CNR, INST CLIN PHYSIOL, I-56100 PISA, ITALY. UNIV PISA, MED CLIN 2, I-56100 PISA, ITALY. UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP GROOP, LC (reprint author), HELSINKI UNIV HOSP, DEPT MED, UNIONINKATU 38, SF-00170 HELSINKI, FINLAND. FU FIC NIH HHS [F05-TWO-3451]; NCRR NIH HHS [RR-125]; NIADDK NIH HHS [AM-24092] NR 53 TC 262 Z9 268 U1 0 U2 10 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 1991 VL 72 IS 1 BP 96 EP 107 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ518 UT WOS:A1991EQ51800017 PM 1986032 ER PT J AU TULEY, MR MULROW, CD MCMAHAN, CA AF TULEY, MR MULROW, CD MCMAHAN, CA TI ESTIMATING AND TESTING AN INDEX OF RESPONSIVENESS AND THE RELATIONSHIP OF THE INDEX TO POWER SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE RESPONSIVENESS; POWER; RELIABILITY; VALIDITY; SENSITIVITY TO CHANGE; EVALUATIVE INSTRUMENT ID HEALTH-STATUS AB Responsiveness has been proposed as a criterion, in addition to reliability and validity, to evaluate instruments that measure quality of life or functional status. The responsiveness index measures the change in a quality of life score due to a treatment relative to the variability of changes in that score within a stable control group. We derive the expected value, variance and distribution of the responsiveness index and give a large sample distribution for comparing the responsiveness of two different instruments. We also give the relationship between the responsiveness index and the power of a test of treatment effect. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX 78284. RP TULEY, MR (reprint author), JOHN L MCCLELLAN MEM VET ADM MED CTR,LITTLE ROCK HLTH SERV RES & DEV FIELD PROGRAM,LITTLE ROCK,AR 72205, USA. NR 11 TC 55 Z9 56 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. PY 1991 VL 44 IS 4-5 BP 417 EP 421 DI 10.1016/0895-4356(91)90080-S PG 5 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA FD427 UT WOS:A1991FD42700010 PM 2010785 ER PT J AU GROOP, LC BONADONNA, RC SHANK, M PETRIDES, AS DEFRONZO, RA AF GROOP, LC BONADONNA, RC SHANK, M PETRIDES, AS DEFRONZO, RA TI ROLE OF FREE FATTY-ACIDS AND INSULIN IN DETERMINING FREE FATTY-ACID AND LIPID OXIDATION IN MAN SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE FREE FATTY ACID; INSULIN; LIPID OXIDATION; GLUCOSE DISPOSAL ID GLUCOSE; RESISTANCE; VALIDATION; MUSCLE AB Plasma FFA oxidation (measured by infusion of C-14-palmitate) and net lipid oxidation (indirect calorimetry) are both inhibited by insulin. The present study was designed to examine whether these insulin-mediated effects on lipid metabolism resulted from a decline in circulating FFA levels or from a direct action of the hormone on FFA/lipid oxidation. Nine subjects participated in two euglycemic insulin clamps, performed with and without heparin. During each insulin clamp study insulin was infused at two rates, 4 and 20 mU/m2 . min for 120 min. The studies were performed with indirect calorimetry and 3-H-3-glucose and C-14-palmitate infusion. During the control study plasma FFA fell from 610 +/- 46 to 232 +/- 42 to 154 +/- 27 mu-mol/liter, respectively. When heparin was infused basal plasma FFA concentration remained constant. During the control study, FFA/lipid oxidation rates decreased in parallel with the fall in the plasma FFA concentration. During the insulin/heparin study, plasma C-14-FFA oxidation remained unchanged while net lipid oxidation decreased. In conclusion, when the plasma FFA concentration is maintained unchanged by heparin infusion, insulin has no direct effect on FFA turnover and disposal. These results thus suggest that plasma FFA oxidation is primarily determined by the plasma FFA concentrations, while net lipid oxidation is regulated by both the plasma FFA and the insulin level. C1 YALE UNIV,SCH MED,DEPT MED,DIV ENDOCRINOL DIABET,NEW HAVEN,CT 06504. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,SAN ANTONIO,TX 78284. VET ADM MED CTR,SAN ANTONIO,TX 78284. RP GROOP, LC (reprint author), HELSINKI UNIV HOSP,DEPT MED 4,UNIONINKATU 38,SF-00170 HELSINKI,FINLAND. FU FIC NIH HHS [FO5 TWO 3451]; NCRR NIH HHS [RR125]; NIADDK NIH HHS [AM 24092] NR 29 TC 154 Z9 154 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1991 VL 87 IS 1 BP 83 EP 89 DI 10.1172/JCI115005 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EQ976 UT WOS:A1991EQ97600013 PM 1985114 ER PT J AU WARFEL, AH CARDOZO, C YOO, OH ZUCKERFRANKLIN, D AF WARFEL, AH CARDOZO, C YOO, OH ZUCKERFRANKLIN, D TI CYSTATIN-C AND CATHEPSIN-B PRODUCTION BY ALVEOLAR MACROPHAGES FROM SMOKERS AND NONSMOKERS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE ANTIPROTEINASE; PROTEINASE; CYSTEINE PROTEINASES; INFLAMMATION; EMPHYSEMA; LUNGS ID BRONCHOALVEOLAR LAVAGE FLUID; ALPHA-1-PROTEINASE INHIBITOR; PERITONEAL-MACROPHAGES; PROTEINASE-INHIBITORS; CIGARETTE-SMOKING; DOWN-REGULATION; GAMMA-TRACE; NEUTROPHIL; ELASTASE; STIMULATION AB The capacity of alveolar macrophages (AM) obtained from smokers and nonsmokers to secrete cathespin B and its inhibitor cystatin C was examined because of the concept that an imbalance in the production of proteolytic enzymes and/or their inhibitors could be responsible for the lung damage seen in smokers. Quantitation of immunoprecipitates on Western blots showed that the amount of total cystatin C secreted into the culture medium by AM of smokers was significantly greater than the amount secreted by cells obtained from nonsmokers, whereas the difference between the amount of cathespin B secreted by the AM of smokers and that from nonsmokers did not appear significant. The cystatin C found in the medium conditioned by AM of nonsmokers appeared to be more heterogeneous in molecular size, presenting either as a single band of about 14 Kd or as a high-molecular-weight triplet of about 69 Kd, 63 Kd, and 57.3 Kd. Furthermore, in some cases there were single or doublet bands at 14 Kd as well as the high-molecular-weight triplets. In contrast, smokers AM-conditioned medium uniformly possessed both the low-and the high-molecular-weight cystatin C. Cathepsin B was not detected in Western blots at its reported molecular weights but was identified at the exact area occupied by the higher molecular weight cystatin C, i.e., at bands corresponding to 69 Kd, 63 Kd, and 57.3 Kd. Therefore, it is clear that in culture media of AM, cystatin C and cathepsin B are present as proteinase-antiproteinase complexes. The observation also suggests that in smokers an excess of cystatin C may be elaborated, which, if further substantiated, would show for the first time a likely role for this proteinase inhibitor in vivo. C1 NYU MED CTR, DEPT MED, 550 1ST AVE, NEW YORK, NY 10016 USA. BRONX VET ADM MED CTR, DIV PULM & CRIT CARE MED, NEW YORK, NY USA. CUNY MT SINAI SCH MED, NEW YORK, NY 10029 USA. FU NCI NIH HHS [CA16247]; NIADDK NIH HHS [AM-01431, AM-12274] NR 30 TC 29 Z9 29 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1991 VL 49 IS 1 BP 41 EP 47 PG 7 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA EP033 UT WOS:A1991EP03300006 PM 1984484 ER PT J AU ARESO, MP FRAZER, A AF ARESO, MP FRAZER, A TI EFFECT OF REPEATED ADMINISTRATION OF NOVEL STRESSORS ON CENTRAL BETA-ADRENOCEPTORS SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Note DE STRESS; BETA-ADRENOCEPTORS; AMYGDALA ID RAT-BRAIN; NORADRENALINE RELEASE; ADRENERGIC-RECEPTORS; QUANTITATIVE AUTORADIOGRAPHY; H-3 DIHYDROALPRENOLOL; LOCUS COERULEUS; SEROTONIN; REDUCTION; AMYGDALA; REGIONS AB Subtypes of beta adrenoceptors were measured in 17 different areas of brain in rats exposed for 12 days to novel stressors. Mild stress such as individual housing and handling caused no change in beta1 and beta2 adrenoceptors in comparison with that measured in rats that were group housed and never handled. Exposure of rats to more severe stressors did reduce significantly the binding of I-125-iodopindolol (I-125-IPIN) to beta1 adrenoceptors, but not beta2 adrenoceptors, only in the lateral and basolateral nuclei of the amygdala. C1 UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. RP ARESO, MP (reprint author), DEPT VET AFFAIRS MED CTR,ISIE,NEUROPSYCHOPHARMACOL UNIT,PHILADELPHIA,PA 19104, USA. FU NIMH NIH HHS [MH 29094] NR 36 TC 16 Z9 16 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1991 VL 86 IS 3 BP 229 EP 235 DI 10.1007/BF01250709 PG 7 WC Neurosciences SC Neurosciences & Neurology GA GQ473 UT WOS:A1991GQ47300008 PM 1685653 ER PT J AU OCONOR, LM WOODY, G YEH, HS MANNY, I DHOPESH, V AF OCONOR, LM WOODY, G YEH, HS MANNY, I DHOPESH, V TI METHADONE AND EDEMA SO JOURNAL OF SUBSTANCE ABUSE TREATMENT LA English DT Article DE METHADONE; EDEMA ID MAINTENANCE TREATMENT RP OCONOR, LM (reprint author), UNIV PENN,VET AFFAIRS MED CTR,DEPT PSYCHIAT,38TH & WOODLAND,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [DA0518603] NR 10 TC 8 Z9 8 U1 0 U2 0 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. PY 1991 VL 8 IS 3 BP 153 EP 155 DI 10.1016/0740-5472(91)90006-V PG 3 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA GJ353 UT WOS:A1991GJ35300006 PM 1960766 ER PT J AU YEAGER, RA AF YEAGER, RA TI COMPARISON OF EJECTION FRACTION AND GOLDMAN RISK FACTOR-ANALYSIS TO DIPYRIDAMOLE-THALLIUM-201 STUDIES IN THE EVALUATION OF CARDIAC MORBIDITY AFTER AORTIC-ANEURYSM SURGERY SO JOURNAL OF VASCULAR SURGERY LA English DT Letter ID THALLIUM C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97207. RP YEAGER, RA (reprint author), OREGON HLTH SCI UNIV,DEPT SURG,DIV VASC SURG,PORTLAND,OR 97201, USA. NR 6 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD JAN PY 1991 VL 13 IS 1 BP 173 EP 173 PG 1 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA EV211 UT WOS:A1991EV21100020 PM 1987389 ER PT J AU KALIN, NH SHELTON, SE TURNER, JG AF KALIN, NH SHELTON, SE TURNER, JG TI EFFECTS OF ALPRAZOLAM ON FEAR-RELATED BEHAVIORAL, HORMONAL, AND CATECHOLAMINE RESPONSES IN INFANT RHESUS-MONKEYS SO LIFE SCIENCES LA English DT Article ID CORTICOTROPIN-RELEASING-FACTOR; PITUITARY-ADRENAL ACTIVITY; BENZODIAZEPINE RECEPTORS; BRAIN CATECHOLAMINES; RAT-BRAIN; IMIPRAMINE; DIAZEPAM; DOPAMINE; PLASMA; CHLORDIAZEPOXIDE AB We tested the effects of various doses of the triazolobenzodiazepine alprazolam on behavioral, hormonal, and neurochemical responses of infant rhesus monkeys under three conditions of separation from their mothers: alone, in the presence of a human who stared at them, and in the presence of a human who avoided eye contact. Alprazolam affected stress-induced responses in all three of these classes. Unrelated to its effects on the stress response, alprazolam appears to reduce the function of brain dopamine systems. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP KALIN, NH (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [MH46729] NR 34 TC 18 Z9 18 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 1991 VL 49 IS 26 BP 2031 EP 2044 DI 10.1016/0024-3205(91)90646-S PG 14 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA GQ672 UT WOS:A1991GQ67200011 PM 1660955 ER PT J AU ASCH, DA PATTON, JP HERSHEY, JC AF ASCH, DA PATTON, JP HERSHEY, JC TI PROGNOSTIC INFORMATION VERSUS ACCURACY - ONCE MORE WITH MEANING - REPLY SO MEDICAL DECISION MAKING LA English DT Letter ID DECISION-MAKING C1 UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. HOSP UNIV PENN,GEN INTERNAL MED SECT,PHILADELPHIA,PA 19104. UNIV PENN,WHARTON SCH,PHILADELPHIA,PA 19104. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. NR 7 TC 9 Z9 9 U1 1 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 0272-989X J9 MED DECIS MAKING JI Med. Decis. Mak. PD JAN-MAR PY 1991 VL 11 IS 1 BP 45 EP 47 DI 10.1177/0272989X9101100108 PG 3 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA ER812 UT WOS:A1991ER81200008 PM 1827859 ER PT J AU FABER, R TRIMBLE, MR AF FABER, R TRIMBLE, MR TI ELECTROCONVULSIVE-THERAPY IN PARKINSONS-DISEASE AND OTHER MOVEMENT-DISORDERS SO MOVEMENT DISORDERS LA English DT Review DE ELECTROCONVULSIVE THERAPY; MOVEMENT DISORDERS; PARKINSONS DISEASE AB Early case reports note marked improvements in the signs of Parkinson' s disease (PD) in several patients with coexisting psychiatric disorders after treatment with electroconvulsive therapy (ECT). Studies since 1959 reveal improvement of parkinsonism in over half of PD patients receiving ECT, regardless of the presence or absence of psychiatric comorbidity. Drug-induced parkinsonism, tardive dystonia, and tardive dyskinesia have also been shown to improve with ECT administration; tic syndromes have achieved mixed results. In animals, ECT enhances dopamine-mediated effects and increases GABA concentrations in the CNS. Optimal parameters relevant to the antiparkinsonism effects of ECT require further study. RP FABER, R (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PSYCHIAT,7400 MERTON MINTER DR,SAN ANTONIO,TX 78284, USA. NR 0 TC 76 Z9 79 U1 1 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PY 1991 VL 6 IS 4 BP 293 EP 303 DI 10.1002/mds.870060405 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA GN705 UT WOS:A1991GN70500003 PM 1758447 ER PT J AU CHAUDHURI, TK AF CHAUDHURI, TK TI RADIONUCLIDE METHODS OF DETECTING ACUTE GASTROINTESTINAL-BLEEDING SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT SYMP AT THE 1989 ANNUAL CONF OF THE SOC OF NUCLEAR MEDICINE, INDIA : CURRENT TRENDS AND FUTURE PERSPECTIVES IN NUCLEAR MEDICINE CY DEC 17-20, 1989 CL LUCKNOW, INDIA SP INDO AMER SOC NUCL MED, SOC NUCL MED INDIA ID RED-BLOOD-CELLS AB It is clinically very important to localize the bleeding site in suspected patients. Current common diagnostic methods are endoscopic, angiographic, and radionuclidic. Of the noninvasive procedures, Tc-99m-RBC and Tc-99m-colloid methods have gained wide popularity. In our series of a comparative study, the RBC method has been shown to be more accurate than the colloid method. The Tc-99m-RBC method should be available as a routine emergency procedure in every large clinical center. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP CHAUDHURI, TK (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,NUCL MED SERV,SAN ANTONIO,TX 78284, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PY 1991 VL 18 IS 6 BP 655 EP 661 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GB121 UT WOS:A1991GB12100011 ER PT J AU ZUPANC, ML DOBKIN, JA PERLMAN, SB AF ZUPANC, ML DOBKIN, JA PERLMAN, SB TI I-123 IODOAMPHETAMINE SPECT BRAIN IMAGING IN ALTERNATING HEMIPLEGIA SO PEDIATRIC NEUROLOGY LA English DT Article ID COMPLICATED MIGRAINE; CHILDHOOD; FLUNARIZINE; CHILDREN; INFANCY AB Alternating hemiplegia of childhood is an unusual disorder characterized by early onset (occurring before 18 months of age); repeated attacks of hemiplegia involving both sides of the body; other paroxysmal phenomena, such as tonic stiffening, dystonic posturing, choreoathetoid movements, ocular motor abnormalities, and autonomic disturbances, in association with bouts of hemiplegia or occurring independently; and evidence of mental or neurologic deficits. A girl was examined because of left hemiplegia at the age of 16 months. The patient had begun exhibiting episodes of alternating hemiplegia at approximately 4 months of age. They consisted of tonic stiffening and dystonia of the right or left extremities, lasting from 30 min to several hours and followed by residual hemiparesis. They were invariably accompanied by ocular motor abnormalities. Magnetic resonance imaging, computed tomography, and angiography all were normal. Single proton emission computed tomography brain images during an acute episode of right hemiplegia demonstrated hypoperfusion of the left cerebral hemisphere. Following improvement of the hemiplegia, the patient was re-evaluated. The uptake of the radiotracer in the left hemisphere was increased. The scan did not demonstrate significant asymmetry in cerebral perfusion. C1 UNIV WISCONSIN HOSP & CLIN,DEPT NUCL MED,MADISON,WI. UNIV WISCONSIN HOSP,DEPT NEUROL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. NR 9 TC 31 Z9 32 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD JAN-FEB PY 1991 VL 7 IS 1 BP 35 EP 38 DI 10.1016/0887-8994(91)90103-R PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA EY978 UT WOS:A1991EY97800006 PM 1903036 ER PT J AU BUSH, RK AF BUSH, RK TI NOCTURNAL ASTHMA - MECHANISMS AND THE ROLE OF THEOPHYLLINE IN TREATMENT SO POSTGRADUATE MEDICAL JOURNAL LA English DT Article; Proceedings Paper CT SYMP ON OBSTRUCTIVE AIRWAYS DISEASE : A THERAPEUTIC PARADOX CY OCT 12-13, 1990 CL KILLARNEY, IRELAND ID SUSTAINED-RELEASE THEOPHYLLINE; HOUSE DUST; CORTISOL; THERAPY; NIGHT AB Asthma is characterized by airway inflammation and hyper-responsiveness. Clinically, these features are manifested by attacks of cough, wheezing, and dyspnoea. Nocturnal asthma symptoms are frequent; 39% of asthmatics awaken nightly, and 94% have nocturnal awakenings at least once a month. A number of mechanisms have been hypothesized to explain the phenomenon of nocturnal asthma, including exposure to dust mite allergen, late-phase allergic reactions, effects of posture and sleep stage on airway tone, gastro-oesophageal reflex, impaired mucociliary clearance, airway cooling, and changes in circadian rhythms of circulating hormones. While no single mechanism can explain these changes, circadian rhythms may be particularly relevant. Normal airway tone increases during sleep and is magnified in asthmatics. Bronchial responsiveness to histamine and allergen challenge increases during sleep and mast cell mediator release is enhanced. Circulating eosinophils increase, which may allow their ingress into pulmonary tissue. Decreases in plasma catecholamine and cortisol levels have also been observed. All of these may influence airway tone, inflammation, and responsiveness during sleep and produce the observed clinical picture. Inhaled sympathomimetics are frequently ineffective in preventing nocturnal symptoms due to their short duration of action. While corticosteroids, cromoglycate, and anticholinergics are effective, sustained-release theophylline is particularly advantageous for controlling nocturnal symptoms. Once-daily theophylline when dosed in the evening not only controls nocturnal symptoms and improves airflow during the early morning hours, but decreases airway responsiveness to histamine as well. The close association between airway inflammation, airway hyper-responsiveness, and nocturnal asthma symptoms makes further studies of the mechanism of action of theophylline especially interesting. C1 UNIV WISCONSIN,MADISON,WI 53706. RP BUSH, RK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 33 TC 7 Z9 7 U1 0 U2 2 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0032-5473 J9 POSTGRAD MED J JI Postgrad. Med. J. PY 1991 VL 67 SU 4 BP S20 EP S24 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA GG257 UT WOS:A1991GG25700004 PM 1758831 ER PT J AU LIVINGSTON, EH PASSARO, EP AF LIVINGSTON, EH PASSARO, EP TI RESUSCITATION - REVIVAL SHOULD BE THE 1ST PRIORITY SO POSTGRADUATE MEDICINE LA English DT Article AB Successful resuscitation requires prompt and appropriate response from medical personnel. Drs Livingston and Passaro describe the initial steps common to all resuscitative efforts and discuss often-observed maneuvers that should not be part of the initial management of critically ill patients. Their helpful ABCDEF mnemonic summarizes the steps needed for revival. RP LIVINGSTON, EH (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BLDG 115,ROOM 107,LOS ANGELES,CA 90073, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 0032-5481 J9 POSTGRAD MED JI Postgrad. Med. PD JAN PY 1991 VL 89 IS 1 BP 117 EP 122 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA ET943 UT WOS:A1991ET94300009 PM 1985304 ER PT J AU VANPUTTEN, T ARAVAGIRI, M MARDER, SR WIRSHING, WC MINTZ, J CHABERT, N AF VANPUTTEN, T ARAVAGIRI, M MARDER, SR WIRSHING, WC MINTZ, J CHABERT, N TI PLASMA FLUPHENAZINE LEVELS AND CLINICAL-RESPONSE IN NEWLY ADMITTED SCHIZOPHRENIC-PATIENTS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 30TH ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 29-JUN 01, 1990 CL KEY BISCAYNE, FL SP NIMH, DIV CLIN RES ID RADIOIMMUNOASSAY AB Seventy-two newly readmitted, drug-free men with the diagnosis of schizophrenia by DSM-III were assigned randomly to receive fluphenazine hydrochloride at 5 mg, 10 mg, or 20 mg daily for 4 weeks. Fluphenazine (FLU), fluphenazine sulfoxide, 7-hydroxyfluphenazine, and fluphenazine N-oxide were measured by highly specific and sensitive radioimmunoassays. Data were analyzed by logistic regression using the Clinical Global Impressions Disabling Side Effects and Global Improvement as the outcome measures. Disabling side effects were defined as "side effects that significantly interfered with patient's functioning" or "side effects that outweigh therapeutic effects" (National Institute of Mental Health 1985, p. 839). Higher plasma FLU levels (up to 4.23 ng/mL) were significantly (p = .015) associated with a higher rate of global improvement. However, close to 90 percent of these acute patients had disabling side effects at a plasma FLU level of 2.7 ng/mL. At least in the patient's view, these disabling side effects negated or compromised the improvement in psychosis. Fluphenazine N-oxide may be a toxic metabolite in that it was more powerfully associated with side effects than was the parent FLU. RP VANPUTTEN, T (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,BLDG 210C,LOS ANGELES,CA 90073, USA. NR 16 TC 15 Z9 16 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1991 VL 27 IS 2 BP 91 EP 96 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA GA037 UT WOS:A1991GA03700002 PM 1924666 ER PT J AU CRAIG, WA MCDONALD, P AF CRAIG, WA MCDONALD, P TI ANTIBIOTIC PHARMACOKINETICS, UPTAKE BY BACTERIA AND INTERACTION WITH PHAGOCYTOSIS - DISCUSSION OF SESSION-I SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Discussion RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1991 SU 74 BP 58 EP 59 PG 2 WC Infectious Diseases SC Infectious Diseases GA EZ469 UT WOS:A1991EZ46900008 ER PT J AU CRAIG, WA EBERT, SC AF CRAIG, WA EBERT, SC TI KILLING AND REGROWTH OF BACTERIA INVITRO - A REVIEW SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT SYMP ON PHARMACODYNAMICS OF ANTIBIOTICS : CONSEQUENCES FOR DOSING CY JUL 07-09, 1990 CL STOCKHOLM, SWEDEN SP ASTRA INFECT ID PSEUDOMONAS-AERUGINOSA; ANTIBACTERIAL ACTIVITY; STAPHYLOCOCCUS-AUREUS; ESCHERICHIA-COLI; MODEL; ANTIBIOTICS; AMPICILLIN; IMIPENEM; CIPROFLOXACIN; INTERMITTENT AB Minimum inhibitory and bactericidal concentrations do not describe the time course of a drug's antimicrobial activity against bacteria. Some antimicrobials exhibit concentration dependent killing over a wide range of concentrations (e.g. aminoglycosides and quinolones), while others show maximal killing at concentrations near the MIC (e.g. beta-lactams and glycopeptides). The aminoglycosides and quinolones can require high drug concentrations (about 10-fold higher than the MIC) to prevent the selection of resistant subpopulations of bacteria. Persistent suppression of bacterial growth after antimicrobial exposure is called the 'postantibiotic effect' (PAE) and varies in duration depending on the drug-organism combination, as well as the concentration and duration of drug exposure. Antimicrobials which are inhibitors of protein and nucleic acid synthesis exhibit prolonged PAEs with a large variety of bacteria. While beta-lactam antibiotics demonstrate PAEs with Gram-positive cocci, very short or no PAEs are observed with these drugs with Gram-negative bacilli. The only exception is that penem antibiotics can induce PAEs with some strains of Gram-negative bacilli, primarily Pseudomonas aeruginosa. Thus, the pharmacodynamic activity of an antimicrobial can vary markedly depending on the microorganism and the class of drug and its concentration. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 39 TC 3 Z9 4 U1 2 U2 2 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1991 SU 74 BP 63 EP 70 PG 8 WC Infectious Diseases SC Infectious Diseases GA EZ469 UT WOS:A1991EZ46900009 ER PT J AU LEGGETT, JE EBERT, S FANTIN, B CRAIG, WA AF LEGGETT, JE EBERT, S FANTIN, B CRAIG, WA TI COMPARATIVE DOSE-EFFECT RELATIONS AT SEVERAL DOSING INTERVALS FOR BETA-LACTAM, AMINOGLYCOSIDE AND QUINOLONE ANTIBIOTICS AGAINST GRAM-NEGATIVE BACILLI IN MURINE THIGH-INFECTION AND PNEUMONITIS MODELS SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT SYMP ON PHARMACODYNAMICS OF ANTIBIOTICS : CONSEQUENCES FOR DOSING CY JUL 07-09, 1990 CL STOCKHOLM, SWEDEN SP ASTRA INFECT ID KLEBSIELLA-PNEUMONIAE; COMPARATIVE EFFICACY; TOBRAMYCIN; MICE; GENTAMICIN AB Relatively few animal studies have investigated the influence of dosing regimens on the efficacy of antibiotics possessing different pharmacodynamic characteristics. We evaluated the impact of dosing interval on the relative efficacy and potency of beta-lactams, aminoglycosides, and ciprofloxacin against Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae in murine pneumonitis and thigh-infection models. We used a sigmoid dose-response model to determine the maximal bactericidal effect at 24 hours (E(max)) and the total dose required to achieve 50% of E(max) (P50) at several dosing intervals. P50S (a measure of drug potency, in mg/kg/day) for beta-lactams increased 14- to 73-fold with longer intervals in both models. Dosing interval had little impact on P50S for aminoglycosides or ciprofloxacin. E(max) varied among drugs but displayed no dependence on dosing interval. This method of analysis allows comparison of efficacy and dependence of potency on dosing regimen among different classes of antibiotics. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,SCH PHARM,MADISON,WI 53705. UNIV WISCONSIN,MADISON,WI 53706. NR 13 TC 0 Z9 2 U1 1 U2 5 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1991 SU 74 BP 179 EP 184 PG 6 WC Infectious Diseases SC Infectious Diseases GA EZ469 UT WOS:A1991EZ46900025 ER PT J AU CARS, O CRAIG, WA AF CARS, O CRAIG, WA TI PHARMACODYNAMICS OF ANTIBIOTICS - CONSEQUENCES FOR DOSING IN PATIENTS - DISCUSSION OF SESSION-IV SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Discussion C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP CARS, O (reprint author), UNIV HOSP UPPSALA,DEPT INFECT DIS,S-75185 UPPSALA,SWEDEN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1991 SU 74 BP 280 EP 281 PG 2 WC Infectious Diseases SC Infectious Diseases GA EZ469 UT WOS:A1991EZ46900038 ER PT J AU CARS, O CRAIG, WA AF CARS, O CRAIG, WA TI GENERAL DISCUSSION ON ANTIBIOTIC DOSING SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Discussion C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP CARS, O (reprint author), UNIV HOSP UPPSALA,DEPT INFECT DIS,S-75185 UPPSALA,SWEDEN. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1991 SU 74 BP 282 EP 283 PG 2 WC Infectious Diseases SC Infectious Diseases GA EZ469 UT WOS:A1991EZ46900039 ER PT J AU CRAIG, WA AF CRAIG, WA TI PHARMACODYNAMICS OF ANTIBIOTICS-CONSEQUENCES FOR DOSING - PROCEEDINGS OF A SYMPOSIUM HELD IN STOCKHOLM, JUNE 7-9, 1990 - SUMMARY AND FUTURE-DIRECTIONS SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Editorial Material RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1991 SU 74 BP 284 EP 286 PG 3 WC Infectious Diseases SC Infectious Diseases GA EZ469 UT WOS:A1991EZ46900040 ER PT J AU ENGDAHL, BE PAGE, WF MILLER, TW AF ENGDAHL, BE PAGE, WF MILLER, TW TI AGE, EDUCATION, MALTREATMENT, AND SOCIAL SUPPORT AS PREDICTORS OF CHRONIC DEPRESSION IN FORMER PRISONERS OF WAR SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY LA English DT Article ID PSYCHIATRIC-ILLNESS; FOLLOW-UP; STRESS DISORDER; PREVALENCE; SYMPTOMS; VETERANS; RELEASE; SCALE C1 US DEPT VETERANS AFFAIRS,MED CTR,LEXINGTON,KY. UNIV MINNESOTA,DEPT PSYCHOL,MINNEAPOLIS,MN 55455. NATL ACAD SCI,INST MED,MED FOLLOW UP AGCY,WASHINGTON,DC 20418. UNIV KENTUCKY,DEPT PSYCHIAT,LEXINGTON,KY 40506. RP ENGDAHL, BE (reprint author), US DEPT VET AFFAIRS,MED CTR 116B,MINNEAPOLIS,MN 55417, USA. OI Engdahl, Brian/0000-0001-5436-457X NR 29 TC 27 Z9 27 U1 1 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0933-7954 J9 SOC PSYCH PSYCH EPID JI Soc. Psychiatry Psychiatr. Epidemiol. PY 1991 VL 26 IS 2 BP 63 EP 67 DI 10.1007/BF00791528 PG 5 WC Psychiatry SC Psychiatry GA FE814 UT WOS:A1991FE81400002 PM 2047905 ER PT J AU SCHULMAN, KA KINOSIAN, B JACOBSON, TA GLICK, H WILLIAN, MK KOFFER, H EISENBERG, JM AF SCHULMAN, KA KINOSIAN, B JACOBSON, TA GLICK, H WILLIAN, MK KOFFER, H EISENBERG, JM TI REDUCING HIGH BLOOD CHOLESTEROL LEVEL WITH DRUGS - COST-EFFECTIVENESS OF PHARMACOLOGICAL MANAGEMENT SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article C1 UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,ROBERT WOOD JOHNSON FDN CLIN SCHOLARS PROGRAM,PHILADELPHIA,PA 19104. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. PHILADELPHIA ASSOC CLIN TRIALS,PHILADELPHIA,PA. NR 71 TC 89 Z9 89 U1 0 U2 2 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 DEC 19 PY 1990 VL 264 IS 23 BP 3025 EP 3033 DI 10.1001/jama.264.23.3025 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA EM763 UT WOS:A1990EM76300026 PM 2123013 ER PT J AU HERNANDEZMUNOZ, R CABALLERIA, J BARAONA, E UPPAL, R GREENSTEIN, R LIEBER, CS AF HERNANDEZMUNOZ, R CABALLERIA, J BARAONA, E UPPAL, R GREENSTEIN, R LIEBER, CS TI HUMAN GASTRIC ALCOHOL-DEHYDROGENASE - ITS INHIBITION BY H2-RECEPTOR ANTAGONISTS, AND ITS EFFECT ON THE BIOAVAILABILITY OF ETHANOL SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151G,130 W KINGSBRIDGE RD,BRONX,NY 10468. CUNY MT SINAI SCH MED,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY 10029. FU NIAAA NIH HHS [AA 03508] NR 24 TC 125 Z9 125 U1 0 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 1990 VL 14 IS 6 BP 946 EP 950 DI 10.1111/j.1530-0277.1990.tb01843.x PG 5 WC Substance Abuse SC Substance Abuse GA EN628 UT WOS:A1990EN62800028 PM 1982399 ER PT J AU KANG, HK THOMAS, TL AF KANG, HK THOMAS, TL TI NATIONAL SOURCES OF VITAL STATUS INFORMATION - EXTENT OF COVERAGE AND POSSIBLE SELECTIVITY IN REPORTING SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter RP KANG, HK (reprint author), US DEPT VET AFFAIRS,OFF ENVIRONM EPIDEMIOL,WASHINGTON,DC 20006, USA. NR 7 TC 5 Z9 5 U1 0 U2 0 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD DEC PY 1990 VL 132 IS 6 BP 1196 EP 1197 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA EN620 UT WOS:A1990EN62000020 PM 2260551 ER PT J AU ZHOU, WG WEI, C LEVINE, BA OLSON, MS AF ZHOU, WG WEI, C LEVINE, BA OLSON, MS TI EVIDENCE FOR PLATELET-ACTIVATING-FACTOR AS A LATE-PHASE MEDIATOR OF CHRONIC-PANCREATITIS IN THE RAT SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID GLYCERYL ETHER PHOSPHORYLCHOLINE; VASCULAR-PERMEABILITY; EXOCRINE CELLS; PAF; INFLAMMATION; NEUTROPHILS; ANTAGONIST; BN-52021; LIGATION; DAMAGE AB The role of platelet-activating factor (PAF) as a mediator of pancreatic inflammation was examined in the rat pancreatic duct ligation model of obstructive pancreatitis. Pancreatic generation of PAF, as measured by bioassay (ie, platelet[H-3]serotonin secretion), was determined at various times after induction of inflammation. Tissue levels of PAF in the normal pancreas averaged 600 +/- 49 pg/g, but PAF was not detectable during the initial 24 hours of pancreatitis, a time when the inflammatory reaction would be considered acute, that is, during the period of maximal serum amylase release and the development of interstitial edema. However a substantial increase in pancreatic PAF levels (12 times control levels) was observed 7 to 14 days after duct ligation during the late-phase response interval similar to the situation characteristic of chronic pancreatitis in which parenchymal atrophy, fibrosis, and pancreatic insufficiency evolve. One week after duct ligation when PAF levels peaked, an evaluation was made of the effects of PAF antagonists (BN52021 and WEB2170) on pancreatic lesions using Evan's blue extravasation, pancreatic myeloperoxidase (MPO) activity, and acid phosphatase activity in peritoneal lavage fluid. BN52021 or WEB2170 treatment was shown to reduce pancreatic damage and inflammation significantly. Long-term in vivo administration of exogenous PAF (20 mu-g/kg/hr for 7 days) exhibited a reduction of [H-3]thymidine uptake into and amylase release from pancreatic acini in vitro. Our observations 1) that pancreatic PAF levels increased significantly during the chronic phase of obstructive pancreatitis induced by duct ligation; 2) that inhibition of the action of PAF, through specific receptor antagonism, caused an attenuation of pancreatic lesions; and 3) that chronic administration of PAF resulted in decreased pancreatic regeneration and exocrine function are consistent with a pivotal role for PAF as a late-phase inflammatory mediator in chronic pancreatitis in rats. C1 UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,7703 FLOYD CURL DR,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. FU NIADDK NIH HHS [AM-19473] NR 44 TC 23 Z9 25 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD DEC PY 1990 VL 137 IS 6 BP 1501 EP 1508 PG 8 WC Pathology SC Pathology GA EP243 UT WOS:A1990EP24300025 PM 1701964 ER PT J AU HELFAND, M CRAPO, LM AF HELFAND, M CRAPO, LM TI SCREENING FOR THYROID-DISEASE - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 SANTA CLARA VALLEY MED CTR,SAN JOSE,CA 95128. RP HELFAND, M (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97207, USA. NR 5 TC 0 Z9 0 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD DEC 1 PY 1990 VL 113 IS 11 BP 897 EP 897 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EK558 UT WOS:A1990EK55800018 ER PT J AU SAWICKI, MP HOWARD, TJ DALTON, M STABILE, BE PASSARO, E AF SAWICKI, MP HOWARD, TJ DALTON, M STABILE, BE PASSARO, E TI THE DICHOTOMOUS DISTRIBUTION OF GASTRINOMAS SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 14TH ANNUAL SURGICAL SYMP OF THE ASSOC OF VETERANS AFFAIR SURGEONS CY MAY 07, 1990 CL CHARLESTON, SC SP ASSOC VETERANS AFFAIR SURGEONS C1 W LOS ANGELES VET AFFAIRS MED CTR,SURG SERV,LOS ANGELES,CA. VET ADM MED CTR,SURG SERV,SAN DIEGO,CA 92161. RP SAWICKI, MP (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,LOS ANGELES,CA 90024, USA. NR 21 TC 9 Z9 9 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD DEC PY 1990 VL 125 IS 12 BP 1584 EP 1587 PG 4 WC Surgery SC Surgery GA EL385 UT WOS:A1990EL38500014 PM 1978773 ER PT J AU FREEMAN, GL COLSTON, JT AF FREEMAN, GL COLSTON, JT TI EVALUATION OF LEFT-VENTRICULAR MECHANICAL RESTITUTION IN CLOSED-CHEST DOGS BASED ON SINGLE-BEAT ELASTANCE SO CIRCULATION RESEARCH LA English DT Article 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 25 TC 28 Z9 28 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 DEC PY 1990 VL 67 IS 6 BP 1437 EP 1445 PG 9 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA EM020 UT WOS:A1990EM02000014 PM 1700935 ER PT J AU BAUER, RL AF BAUER, RL TI ARE FALLERS FRAIL - AN ANALYSIS OF BONE-DENSITY IN FALLERS 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 1990 VL 38 IS 4 BP A1001 EP A1001 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900447 ER PT J AU BEER, WH HUDSON, J GUENTZEL, N JOHNSON, RF SCHENKER, S AF BEER, WH HUDSON, J GUENTZEL, N JOHNSON, RF SCHENKER, S TI ZINC TRANSPORT BY THE HUMAN PLACENTA, EFFECT OF ALCOHOL AND LIGAND 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. UNIV TEXAS,DEPT LIFE SCI,SAN ANTONIO,TX 78285. 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 1990 VL 38 IS 4 BP A939 EP A939 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900127 ER PT J AU FREYALDENHOVEN, AM KATZ, MS AF FREYALDENHOVEN, AM KATZ, MS TI EFFECTS OF PROTEIN-KINASE-C ACTIVATION ON HORMONE-SENSITIVE ADENYLATE-CYCLASE AND PROTEIN-PHOSPHORYLATION IN CLONAL OSTEOBLAST-LIKE 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 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 1990 VL 38 IS 4 BP A953 EP A953 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900206 ER PT J AU HARFORD, PH DENEKE, SM JENKINSON, SG AF HARFORD, PH DENEKE, SM JENKINSON, SG TI INCREASED CYSTINE UPTAKE AND GLUTATHIONE LEVELS IN CHINESE-HAMSTER OVARY CELLS EXPOSED TO DISULFIRAM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1990 VL 38 IS 4 BP A957 EP A957 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900228 ER PT J AU HENDERSON, GI ANTONY, A PEREZ, A JOHNSON, RF SCHENKER, S AF HENDERSON, GI ANTONY, A PEREZ, A JOHNSON, RF SCHENKER, S TI FOLATE TRANSPORT BY THE HUMAN PLACENTA - NORMAL TRANSPORT AND ROLE OF SHORT-TERM EXPOSURE TO ETHANOL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED GASTROINTESTINAL NUTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. INDIANA UNIV,DEPT MED HEMATOL ONCOL,INDIANAPOLIS,IN 46204. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1990 VL 38 IS 4 BP A940 EP A940 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900132 ER PT J AU JENKINS, OR TYDEN, HE FREEMAN, GL AF JENKINS, OR TYDEN, HE FREEMAN, GL TI IMPAIRED RESPONSE TO DOBUTAMINE FOLLOWING A SINGLE BRIEF CORONARY-OCCLUSION IN THE PRESENCE OF FLOW-LIMITING STENOSIS 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 1990 VL 38 IS 4 BP A965 EP A965 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900267 ER PT J AU LEVINE, SM BRYAN, CL CALHOON, JH ZAMORA, CA ANZUETO, A TRINKLE, JK JENKINSON, SG MURPHY, AL AF LEVINE, SM BRYAN, CL CALHOON, JH ZAMORA, CA ANZUETO, A TRINKLE, JK JENKINSON, SG MURPHY, AL TI REJECTION IN SINGLE LUNG-TRANSPLANT RECIPIENTS WITH PRIMARY PULMONARY-HYPERTENSION RESULTS IN SEVERE VENTILATION PERFUSION MISMATCH 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 1990 VL 38 IS 4 BP A984 EP A984 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900369 ER PT J AU MULROW, CD TULEY, MR AGUILAR, C AF MULROW, CD TULEY, MR AGUILAR, C TI SUSTAINED BENEFITS OF HEARING-AIDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1990 VL 38 IS 4 BP A936 EP A936 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900113 ER PT J AU PEACOCK, MD LAWRENCE, RA JENKINSON, SG AF PEACOCK, MD LAWRENCE, RA JENKINSON, SG TI THE EFFECTS OF GAMMA-GLUTAMYL TRANSPEPTIDASE INHIBITION ON GLUTATHIONE PROTECTION FROM HYPERBARIC-OXYGEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. 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 1990 VL 38 IS 4 BP A957 EP A957 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900226 ER PT J AU PRABHU, SD OROURKE, RA FREEMAN, GL AF PRABHU, SD OROURKE, RA FREEMAN, GL TI THE KINETICS OF DIASTOLIC RESTITUTION IN CLOSED-CHEST DOGS 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 1990 VL 38 IS 4 BP A965 EP A965 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900270 ER PT J AU SCHENKER, S COBURN, SP MAHUREN, JD JOHNSON, RF HENDERSON, GI AF SCHENKER, S COBURN, SP MAHUREN, JD JOHNSON, RF HENDERSON, GI TI PYRIDOXAL TRANSPORT BY HUMAN PLACENTA - NORMAL TRANSFER AND EFFECTS OF ALCOHOL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 FT WAYNE STATE DEV CTR,DEPT BIOCHEM,FT WAYNE,IN. UNIV TEXAS,HLTH SCI CTR,DEPT MED GASTROINTESTINAL NUTR,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 1990 VL 38 IS 4 BP A939 EP A939 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EN539 UT WOS:A1990EN53900129 ER PT J AU KURIHARA, N GLUCK, S ROODMAN, GD AF KURIHARA, N GLUCK, S ROODMAN, GD TI SEQUENTIAL EXPRESSION OF PHENOTYPE MARKERS FOR OSTEOCLASTS DURING DIFFERENTIATION OF PRECURSORS FOR MULTINUCLEATED CELLS FORMED IN LONG-TERM HUMAN MARROW CULTURES SO ENDOCRINOLOGY LA English DT Article C1 VET ADM MED CTR,RES SER,SAN ANTONIO,TX 78284. VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT CELL BIOL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PHYSIOL,ST LOUIS,MO 63110. JEWISH HOSP ST LOUIS,ST LOUIS,MO 63110. FU NIADDK NIH HHS [AM-35188]; NIAMS NIH HHS [AR-32087]; NIDDK NIH HHS [DK-38848] NR 32 TC 57 Z9 57 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 DEC PY 1990 VL 127 IS 6 BP 3215 EP 3221 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EL108 UT WOS:A1990EL10800077 PM 1701138 ER PT J AU LIEBER, CS DECARLI, LM MAK, KM KIM, CI LEO, MA AF LIEBER, CS DECARLI, LM MAK, KM KIM, CI LEO, MA TI ATTENUATION OF ALCOHOL-INDUCED HEPATIC-FIBROSIS BY POLYUNSATURATED LECITHIN SO HEPATOLOGY LA English DT Article ID CHRONIC ETHANOL-CONSUMPTION; ESSENTIAL FATTY-ACIDS; LIVER-INJURY; RAT-LIVER; INTESTINAL-ABSORPTION; TRANSITIONAL CELLS; AMINO-ACIDS; CIRRHOSIS; PHOSPHOLIPIDS; BABOON AB Characteristic features of alcoholic liver injury include fibrosis and striking membrane alterations, with associated phospholipid changes. To offset some of these abnormalities, a 10-yr study was conducted in baboons: 12 animals (eight females, four males) were fed a liquid diet supplemented with polyunsaturated lecithin (4.1 mg/kcal) for up to 8 yr, with either ethanol (50% of total energy) or isocaloric carbohydrate. They were compared with another group of 18 baboons fed an equivalent amount of the same diet (with or without ethanol), but devoid of lecithin. In the two groups, comparable increases in lipids developed in the ethanol-fed animals, but striking differences in the degree of fibrosis were seen. Whereas at least septal fibrosis (with cirrhosis in two) and transformation of their lipocytes into transitional cells developed in seven of the nine baboons fed the regular diet with ethanol, septal fibrosis did not develop in any animals fed lecithin (p < 0.005). They did not progress beyond the stage of perivenular fibrosis (sometimes associated with pericellular and perisinusoidal fibrosis) and had a significantly lesser activation of lipocytes to transitional cells. Furthermore, when three of these animals were taken off lecithin, but continued on the same amount of the ethanol-containing diet, they rapidly (within 18 to 21 mo) progressed to cirrhosis, accompanied by an increased transformation of their lipocytes to transitional cells. These results indicate that some component of lecithin exerts a protective action against the fibrogenic effects of ethanol. Because we have previously found the choline, in amounts present in lecithin, has no comparable action, the polyunsaturated phospholipids themselves might be responsible for the protective effect. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT 151-G,LIVER DIS & NUTR SECT,BRONX,NY 10468, USA. FU NIAAA NIH HHS [AA03508]; NIDDK NIH HHS [DK32810] NR 79 TC 120 Z9 123 U1 2 U2 4 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD DEC PY 1990 VL 12 IS 6 BP 1390 EP 1398 DI 10.1002/hep.1840120621 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA EQ625 UT WOS:A1990EQ62500020 PM 2258155 ER PT J AU SCHNENKER, S KAHN, SA AF SCHNENKER, S KAHN, SA TI HEPATOLOGY - WHAT A DIFFERENCE A DECADE MAKES SO HEPATOLOGY LA English DT Editorial Material C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. AMER ASSOC STUDY LIVER DIS,SAN ANTONIO,TX 78284. RP SCHNENKER, S (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD DEC PY 1990 VL 12 IS 6 BP 1436 EP 1439 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA EQ625 UT WOS:A1990EQ62500026 ER PT J AU LEE, JW MELCHER, GA RINALDI, MG PIZZO, PA WALSH, TJ AF LEE, JW MELCHER, GA RINALDI, MG PIZZO, PA WALSH, TJ TI PATTERNS OF MORPHOLOGICAL VARIATION AMONG ISOLATES OF TRICHOSPORON-BEIGELII SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. UNIV TEXAS,DEPT PATHOL,SAN ANTONIO,TX 78285. WILFORD HALL USAF MED CTR,INFECT DIS SECT,LACKLAND AFB,TX 78236. AUDIE L MURPHY MEM VET ADM MED CTR,LAB SERV,SAN ANTONIO,TX 78284. NR 12 TC 36 Z9 37 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 DEC PY 1990 VL 28 IS 12 BP 2823 EP 2827 PG 5 WC Microbiology SC Microbiology GA EJ459 UT WOS:A1990EJ45900049 PM 2280018 ER PT J AU SMITH, JG MAGEE, DM WILLIAMS, DM GRAYBILL, JR AF SMITH, JG MAGEE, DM WILLIAMS, DM GRAYBILL, JR TI TUMOR-NECROSIS-FACTOR-ALPHA PLAYS A ROLE IN HOST DEFENSE AGAINST HISTOPLASMA-CAPSULATUM SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT INFECT DIS 111F,INFECT DIS SECT,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. NR 32 TC 94 Z9 94 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 DEC PY 1990 VL 162 IS 6 BP 1349 EP 1353 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EK574 UT WOS:A1990EK57400019 PM 2230264 ER PT J AU NERY, EB LEE, KK CZAJKOWSKI, S DOONER, JJ DUGGAN, M ELLINGER, RF HENKIN, JM HINES, R MILLER, M OLSON, JW RAFFERTY, M SULLIVAN, T WALTERS, P WELCH, D WILLIAMS, A AF NERY, EB LEE, KK CZAJKOWSKI, S DOONER, JJ DUGGAN, M ELLINGER, RF HENKIN, JM HINES, R MILLER, M OLSON, JW RAFFERTY, M SULLIVAN, T WALTERS, P WELCH, D WILLIAMS, A TI A VETERANS-ADMINISTRATION COOPERATIVE STUDY OF BIPHASIC CALCIUM-PHOSPHATE CERAMIC IN PERIODONTAL OSSEOUS DEFECTS SO JOURNAL OF PERIODONTOLOGY LA English DT Article C1 VET ADM MED CTR,BATH,NY. VET ADM MED CTR,LEAVENWORTH,KS. VET ADM MED CTR,SAN ANTONIO,TX. VET ADM COOPERAT STUDY PROGRAM,CTR COORDINATING,PALO ALTO,CA. VET ADM MED CTR,MIAMI,FL 33125. VET ADM MED CTR,KANSAS CITY,MO 64128. VET ADM MED CTR,CLEVELAND,OH 44106. VET ADM MED CTR,LOUISVILLE,KY 40202. VET ADM MED CTR,BIRMINGHAM,AL 35233. VET ADM MED CTR,BROCKTON,MA 02401. VET ADM MED CTR W ROXBURY,BOSTON,MA 02132. RP NERY, EB (reprint author), CLEMENT J ZABLOCKI VET ADM,DENT RES SECT 151,MILWAUKEE,WI 53295, USA. NR 56 TC 33 Z9 33 U1 0 U2 0 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD DEC PY 1990 VL 61 IS 12 BP 737 EP 744 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA EM128 UT WOS:A1990EM12800004 PM 2269915 ER PT J AU MILLER, AL HATCH, JP PRIHODA, TJ AF MILLER, AL HATCH, JP PRIHODA, TJ TI DICHLOROACETATE INCREASES GLUCOSE USE AND DECREASES LACTATE IN DEVELOPING RAT-BRAIN SO METABOLIC BRAIN DISEASE LA English DT Article DE GLUCOSE; DICHLOROACETATE; BRAIN; DEVELOPMENT; LACTATE ID PYRUVATE-DEHYDROGENASE ACTIVITY; ISCHEMIC CELL-DAMAGE; LACTIC-ACIDOSIS; BLOOD-GLUCOSE; METABOLISM; HYPERCAPNIA; PHOSPHORYLATION; ACCUMULATION; MITOCHONDRIA; REPERFUSION AB Dichloroacetate (DCA) activates pyruvate dehydrogenase (PDH) by inhibiting PDH kinase. Neutralized DCA (100 mg/kg) or saline was intravenously administered to 20 to 25-day-old rats (50-75 g). Fifteen minutes later a mixture of [6-C-14]glucose and [H-3]fluorodeoxyglucose (FDG) was administered intravenously and the animals were sacrificed by microwave irradiation (2450 MHz, 8.0 kW, 0.6-0.8 sec) after 2 or 5 min. Brain regional rates of glucose use and metabolite levels were determined. DCA-treated rats had increased rates of glucose use in all regions studied (cortex, thalamus, striatum, and brain stem), with an average increase of 41%. Lactate levels were lower in all regions, by an average of 35%. There were no significant changes in levels of ATP, creatine phosphate, or glycogen in any brain region. Blood levels of lactate did not differ significantly between the DCA- and the saline-treated groups. Blood glucose levels were higher in the DCA group. In rats sacrified by freeze-blowing, DCA treatment caused lower brain levels of both lactate and pyruvate. These results cannot be explained by any systemic effect of DCA. Rather, it appears that in the immature rat, DCA treatment results in activation of brain PDH, increased metabolism of brain pyruvate and lactate, and a resulting increase in brain glycolytic rate. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,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 NICHD NIH HHS [HD 15053] NR 36 TC 6 Z9 6 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0885-7490 J9 METAB BRAIN DIS JI Metab. Brain Dis. PD DEC PY 1990 VL 5 IS 4 BP 195 EP 204 DI 10.1007/BF00997073 PG 10 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA FB708 UT WOS:A1990FB70800004 PM 2087218 ER PT J AU TEJANIBUTT, SM BRUNSWICK, DJ FRAZER, A AF TEJANIBUTT, SM BRUNSWICK, DJ FRAZER, A TI [H-3] NISOXETINE - A NEW RADIOLIGAND FOR NOREPINEPHRINE UPTAKE SITES IN BRAIN SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,NEUROPSYCHOPHARMACOL UNIT,PHILADELPHIA,PA 19104. RP TEJANIBUTT, SM (reprint author), VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [DA 05137] NR 10 TC 109 Z9 109 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD NOV 27 PY 1990 VL 191 IS 2 BP 239 EP 243 DI 10.1016/0014-2999(90)94155-Q PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EM858 UT WOS:A1990EM85800017 PM 2086242 ER PT J AU RAGO, R MITCHEN, J WILDING, G AF RAGO, R MITCHEN, J WILDING, G TI DNA FLUOROMETRIC ASSAY IN 96-WELL TISSUE-CULTURE PLATES USING HOECHST-33258 AFTER CELL-LYSIS BY FREEZING IN DISTILLED WATER SO ANALYTICAL BIOCHEMISTRY LA English DT Article C1 UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,K4-666 CSC 600 HIGHLAND AVE,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NCI NIH HHS [R29-CA50590, T321-CA 09614] NR 4 TC 341 Z9 342 U1 2 U2 19 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD NOV 15 PY 1990 VL 191 IS 1 BP 31 EP 34 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA EK227 UT WOS:A1990EK22700006 PM 1706565 ER PT J AU ROSS, NS ARON, DC AF ROSS, NS ARON, DC TI HORMONAL EVALUATION OF THE PATIENT WITH AN INCIDENTALLY DISCOVERED ADRENAL MASS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. VET AFFAIRS MED CTR,ENDOCRINOL SECT,CLEVELAND,OH. CASE WESTERN RESERVE UNIV,SCH MED,DEPT MED,DIV ENDOCRINOL & HYPERTENS,CLEVELAND,OH 44106. RP ROSS, NS (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINOL SECT,W111D,SAWTELLE & WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. FU NICHD NIH HHS [HD25299]; NIDDK NIH HHS [DK41527] NR 38 TC 255 Z9 258 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 15 PY 1990 VL 323 IS 20 BP 1401 EP 1405 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA EH546 UT WOS:A1990EH54600007 PM 2233907 ER PT J AU LEVINE, SM GIBBONS, WJ BRYAN, CL WALLING, AD BROWN, RW BAILEY, SR CRONIN, T CALHOON, JP TRINKLE, JK JENKINSON, SG AF LEVINE, SM GIBBONS, WJ BRYAN, CL WALLING, AD BROWN, RW BAILEY, SR CRONIN, T CALHOON, JP TRINKLE, JK JENKINSON, SG TI SINGLE LUNG TRANSPLANTATION FOR PRIMARY PULMONARY-HYPERTENSION SO CHEST LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CARDIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP LEVINE, SM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM CRIT CARE,PULM SECT 111E,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU PHS HHS [H-30556] NR 39 TC 86 Z9 87 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 1990 VL 98 IS 5 BP 1107 EP 1115 DI 10.1378/chest.98.5.1107 PG 9 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA EG259 UT WOS:A1990EG25900018 PM 2225954 ER PT J AU KOELLER, JM AF KOELLER, JM TI RATIONAL USE OF ANTIBIOTICS IN THE CRITICALLY ILL PATIENT SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP KOELLER, JM (reprint author), UNIV TEXAS,HLTH SCI CTR,AUSTIN,TX 78712, USA. NR 8 TC 1 Z9 1 U1 0 U2 1 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD NOV PY 1990 VL 24 IS 11 SU S BP S17 EP S19 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EL348 UT WOS:A1990EL34800004 PM 2270693 ER PT J AU FLESCHER, E FOSSUM, D BALLESTER, A MAIZEL, A SHARMA, S TALAL, N AF FLESCHER, E FOSSUM, D BALLESTER, A MAIZEL, A SHARMA, S TALAL, N TI CHARACTERIZATION OF B-CELL GROWTH IN SYSTEMIC LUPUS-ERYTHEMATOSUS - EFFECTS OF RECOMBINANT 12-KDA B-CELL GROWTH-FACTOR, INTERLEUKIN-4 AND TRANSFORMING GROWTH-FACTOR-BETA SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. BROWN UNIV,ROGER WILLIAMS GEN HOSP,DEPT PATHOL,PROVIDENCE,RI 02908. RP FLESCHER, E (reprint author), UNIV TEXAS,HLTH SCI CTR,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NCI NIH HHS [CA 45148, CA 46959] NR 47 TC 20 Z9 20 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD NOV PY 1990 VL 20 IS 11 BP 2425 EP 2430 DI 10.1002/eji.1830201110 PG 6 WC Immunology SC Immunology GA EM972 UT WOS:A1990EM97200009 PM 2253682 ER PT J AU WIEDERHOLD, ML SHARMA, JS DRISCOLL, BP HARRISON, JL AF WIEDERHOLD, ML SHARMA, JS DRISCOLL, BP HARRISON, JL TI DEVELOPMENT OF THE STATOCYST IN APLYSIA-CALIFORNICA .1. OBSERVATIONS ON STATOCONIAL DEVELOPMENT SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT SYMP CELEBRATING 30 YEARS OF RESEARCH AT THE EATON PEABODY LABORATORY, IN HONOR OF DR N YSS KIANGS 60TH BIRTHDAY : BASIC RESEARCH IN CA CLINICAL ENVIRONMENT CY JUL 05-07, 1989 CL MIT, ENDICOTT HOUSE, DEDHAM, MA HO MIT, ENDICOTT HOUSE C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP WIEDERHOLD, ML (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT OTOLARYNGOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 58 TC 17 Z9 17 U1 3 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1990 VL 49 IS 1-3 BP 63 EP 78 DI 10.1016/0378-5955(90)90095-7 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EL333 UT WOS:A1990EL33300006 PM 2292509 ER PT J AU LORR, M CAMPBELL, L STRACK, S LAMNIN, A AF LORR, M CAMPBELL, L STRACK, S LAMNIN, A TI PERSONALITY AND SYMPTOM DIMENSIONS OF THE MCMI-II - AN ITEM FACTOR-ANALYSIS SO JOURNAL OF CLINICAL PSYCHOLOGY LA English DT Article C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. US DEPT VET AFFAIRS,OUTPATIENT CLIN,LOS ANGELES,CA. UNIV MIAMI,CORAL GABLES,FL 33124. RP LORR, M (reprint author), CATHOLIC UNIV AMER,INST LIFE CYCLE,WASHINGTON,DC 20064, USA. NR 22 TC 7 Z9 7 U1 0 U2 0 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 NOV PY 1990 VL 46 IS 6 BP 749 EP 754 DI 10.1002/1097-4679(199011)46:6<749::AID-JCLP2270460608>3.0.CO;2-B PG 6 WC Psychology, Clinical SC Psychology GA EN009 UT WOS:A1990EN00900007 PM 2286665 ER PT J AU OBRIEN, WA KOYANAGI, Y NAMAZIE, A ZHAO, JQ DIAGNE, A IDLER, K ZACK, JA CHEN, ISY AF OBRIEN, WA KOYANAGI, Y NAMAZIE, A ZHAO, JQ DIAGNE, A IDLER, K ZACK, JA CHEN, ISY TI HIV-1 TROPISM FOR MONONUCLEAR PHAGOCYTES CAN BE DETERMINED BY REGIONS OF GP120 OUTSIDE THE CD4-BINDING DOMAIN SO NATURE LA English DT Article C1 YAMAGUCHI UNIV,SCH MED,DEPT VIROL & PARASITOL,UBE,YAMAGUCHI 755,JAPAN. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,DEPT MED,LOS ANGELES,CA 90024. ABBOTT LABS,DEPT 93D,ABBOTT PK,IL 60064. RP OBRIEN, WA (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,LOS ANGELES,CA 90073, USA. NR 40 TC 535 Z9 538 U1 1 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD NOV 1 PY 1990 VL 348 IS 6296 BP 69 EP 73 DI 10.1038/348069a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EF994 UT WOS:A1990EF99400065 PM 2172833 ER PT J AU DONAHOE, CP CARTER, MJ BLOEM, WD HIRSCH, GL LAASI, N WALLACE, CJ AF DONAHOE, CP CARTER, MJ BLOEM, WD HIRSCH, GL LAASI, N WALLACE, CJ TI ASSESSMENT OF INTERPERSONAL PROBLEM-SOLVING SKILLS SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article C1 CALIF STATE UNIV NORTHRIDGE,MARRIAGE & FAMILY COUNSELING,NORTHRIDGE,CA 91330. BATTLE CREEK VET ADM MED CTR,BATTLE CREEK,MI. UNIV CALIF DAVIS,SACRAMENTO MED CTR,MED CTR,CTR ALZHEIMERS,SACRAMENTO,CA 95817. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. RP DONAHOE, CP (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHOL TRAINING,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 21 TC 90 Z9 91 U1 0 U2 4 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD NOV PY 1990 VL 53 IS 4 BP 329 EP 339 PG 11 WC Psychiatry SC Psychiatry GA EH674 UT WOS:A1990EH67400001 PM 2263676 ER PT J AU SULLIVAN, G MARDER, SR LIBERMAN, RP DONAHOE, CP MINTZ, J AF SULLIVAN, G MARDER, SR LIBERMAN, RP DONAHOE, CP MINTZ, J TI SOCIAL SKILLS AND RELAPSE HISTORY IN OUTPATIENT SCHIZOPHRENICS SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article C1 UNIV CALIF LOS ANGELES,BRENTWOOD VET ADM HOSP,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHOL TRAINING,SAN ANTONIO,TX 78284. RP SULLIVAN, G (reprint author), UNIV CALIF LOS ANGELES,BRENTWOOD VET ADM REHABIL SERV,LOS ANGELES,CA 90024, USA. FU AHRQ HHS [1-T32-HS0007] NR 15 TC 32 Z9 32 U1 1 U2 4 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD NOV PY 1990 VL 53 IS 4 BP 340 EP 345 PG 6 WC Psychiatry SC Psychiatry GA EH674 UT WOS:A1990EH67400002 PM 2263677 ER PT J AU FINN, SE BAILEY, JM SCHULTZ, RT FABER, R AF FINN, SE BAILEY, JM SCHULTZ, RT FABER, R TI SUBJECTIVE UTILITY RATINGS OF NEUROLEPTICS IN TREATING SCHIZOPHRENIA SO PSYCHOLOGICAL MEDICINE LA English DT Article C1 NORTHWESTERN UNIV,DEPT PSYCHOL,EVANSTON,IL 60201. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP FINN, SE (reprint author), UNIV TEXAS,DEPT PSYCHOL,MEZES HALL 330,AUSTIN,TX 78712, USA. NR 14 TC 79 Z9 83 U1 0 U2 2 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD NOV PY 1990 VL 20 IS 4 BP 843 EP 848 PG 6 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA EL917 UT WOS:A1990EL91700013 PM 1980954 ER PT J AU FIELDS, S KOELLER, J TOPPER, RL GURITZ, G VONHOFF, D AF FIELDS, S KOELLER, J TOPPER, RL GURITZ, G VONHOFF, D TI LOCAL SOFT-TISSUE TOXICITY FOLLOWING CISPLATIN EXTRAVASATION SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV ONCOL 111J,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. NR 6 TC 10 Z9 10 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD OCT 17 PY 1990 VL 82 IS 20 BP 1649 EP 1650 DI 10.1093/jnci/82.20.1649 PG 2 WC Oncology SC Oncology GA EE244 UT WOS:A1990EE24400021 PM 2145441 ER PT J AU CUMMINGS, SR BROWNER, WS GRADY, D ETTINGER, B AF CUMMINGS, SR BROWNER, WS GRADY, D ETTINGER, B TI SHOULD PRESCRIPTION OF POSTMENOPAUSAL HORMONE-THERAPY BE BASED ON THE RESULTS OF BONE DENSITOMETRY SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material C1 US DEPT VET AFFAIRS,MED CTR,SAN FRANCISCO,CA 94121. KAISER FDN HOSP,DIV RES,OAKLAND,CA 94611. RP CUMMINGS, SR (reprint author), UNIV CALIF SAN FRANCISCO,MED CTR,BOX 0886,SAN FRANCISCO,CA 94143, USA. FU NIA NIH HHS [R01-AG05407] NR 27 TC 33 Z9 33 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD OCT 15 PY 1990 VL 113 IS 8 BP 565 EP 566 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA ED339 UT WOS:A1990ED33900001 PM 2119160 ER PT J AU DERWINSKI, EJ AF DERWINSKI, EJ TI COST OF VA MEDICAL-CARE SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP DERWINSKI, EJ (reprint author), US DEPT VET AFFAIRS,WASHINGTON,DC 20420, USA. NR 1 TC 0 Z9 0 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 OCT 15 PY 1990 VL 113 IS 8 BP 639 EP 640 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA ED339 UT WOS:A1990ED33900024 PM 2205143 ER PT J AU FRAZER, A HENSLER, JG AF FRAZER, A HENSLER, JG TI 5-HT1A RECEPTORS AND 5-HT1A-MEDIATED RESPONSES - EFFECT OF TREATMENTS THAT MODIFY SEROTONERGIC NEUROTRANSMISSION SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID MONOAMINE-OXIDASE INHIBITORS; CENTRAL NERVOUS-SYSTEM; RAT CEREBRAL-CORTEX; BETA-2 ADRENERGIC-RECEPTORS; DORSAL RAPHE NEURONS; STIMULATED ADENYLATE-CYCLASE; TRICYCLIC ANTI-DEPRESSANTS; ACID DIETHYLAMIDE BINDING; HIPPOCAMPAL CA1 NEURONS; QUANTITATIVE AUTORADIOGRAPHY C1 VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,PHILADELPHIA,PA 19104. RP FRAZER, A (reprint author), UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104, USA. NR 90 TC 54 Z9 56 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD OCT 15 PY 1990 VL 600 BP 460 EP 475 DI 10.1111/j.1749-6632.1990.tb16902.x PG 16 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EZ860 UT WOS:A1990EZ86000034 PM 2174665 ER PT J AU SCHENKER, S BECKER, HC RANDALL, CL PHILLIPS, DK BASKIN, GS HENDERSON, GI AF SCHENKER, S BECKER, HC RANDALL, CL PHILLIPS, DK BASKIN, GS HENDERSON, GI TI FETAL ALCOHOL SYNDROME - CURRENT STATUS OF PATHOGENESIS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Review C1 VET ADM MED CTR,CHARLESTON,SC. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. MED UNIV S CAROLINA,DEPT PSYCHIAT,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PHYSIOL,CHARLESTON,SC 29425. RP SCHENKER, S (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL & NUTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07514, AA07029] NR 184 TC 148 Z9 150 U1 1 U2 3 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 OCT PY 1990 VL 14 IS 5 BP 635 EP 647 DI 10.1111/j.1530-0277.1990.tb01220.x PG 13 WC Substance Abuse SC Substance Abuse GA EE700 UT WOS:A1990EE70000001 PM 2264590 ER PT J AU SHIAU, YF KELEMEN, RJ REED, MA AF SHIAU, YF KELEMEN, RJ REED, MA TI ACIDIC MUCIN LAYER FACILITATES MICELLE DISSOCIATION AND FATTY-ACID DIFFUSION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article C1 UNIV PENN,DEPT MED,GASTROINTESTINAL SECT,PHILADELPHIA,PA 19104. RP SHIAU, YF (reprint author), VET AFFAIRS MED CTR,GASTROINTESTINAL SECT,PHILADELPHIA,PA 19104, USA. FU NIDDK NIH HHS [R01-DK-39361-01] NR 23 TC 23 Z9 23 U1 0 U2 3 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 1990 VL 259 IS 4 BP G671 EP G675 PN 1 PG 5 WC Physiology SC Physiology GA EE020 UT WOS:A1990EE02000063 PM 2221076 ER PT J AU LICHTENSTEIN, MJ AF LICHTENSTEIN, MJ TI SCREENING FOR DISABILITY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP LICHTENSTEIN, MJ (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 5 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 OCT 1 PY 1990 VL 113 IS 7 BP 557 EP 557 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EA850 UT WOS:A1990EA85000014 ER PT J AU MUIRHEAD, DY KUEHL, TJ VANDEBERG, JL MENCHACA, EM DOWNS, MP ROODMAN, GD AF MUIRHEAD, DY KUEHL, TJ VANDEBERG, JL MENCHACA, EM DOWNS, MP ROODMAN, GD TI MIXED LYMPHOCYTE CULTURE REACTIVITY OF FETAL BABOONS - APPLICATION FOR INUTERO BONE-MARROW TRANSPLANTATION SO BONE MARROW TRANSPLANTATION LA English DT Article C1 SW FDN BIOMED RES,DEPT GENET,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. RP MUIRHEAD, DY (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284, USA. FU NCI NIH HHS [CA-40035]; NHLBI NIH HHS [HL31264]; NIAMS NIH HHS [AR31588] NR 8 TC 3 Z9 3 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 OCT PY 1990 VL 6 IS 4 BP 263 EP 267 PG 5 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA EE270 UT WOS:A1990EE27000008 PM 2150766 ER PT J AU FREEMAN, GL DORN, GW AF FREEMAN, GL DORN, GW TI BETA-ANTAGONISTIC EFFECTS OF METHOXAMINE - PHYSIOLOGICAL AND RECEPTOR STUDIES SO CIRCULATION 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 HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1990 VL 82 IS 4 SU S BP 217 EP 217 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EC764 UT WOS:A1990EC76400880 ER PT J AU FREEMAN, GL WIDMAN, LE CAMPBELL, JM COLSTON, JT AF FREEMAN, GL WIDMAN, LE CAMPBELL, JM COLSTON, JT TI ONSET OF PULSUS ALTERNANS IN CLOSED-CHEST DOGS SO CIRCULATION 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 HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1990 VL 82 IS 4 SU S BP 696 EP 696 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EC764 UT WOS:A1990EC76402770 ER PT J AU WIDMAN, L MEAD, C PIERCE, B AF WIDMAN, L MEAD, C PIERCE, B TI EXPERT COMPUTER RECOGNITION OF MALIGNANT ARRHYTHMIAS BY FREQUENCY-DOMAIN ECG ANALYSIS SO CIRCULATION 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 HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT PY 1990 VL 82 IS 4 SU S BP 753 EP 753 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EC764 UT WOS:A1990EC76402998 ER PT J AU MILLER, ML DANG, H TALAL, N AF MILLER, ML DANG, H TALAL, N TI ACCELERATED EXPRESSION OF ANTI-SM AND Y2 IDIOTYPE DIFFER IN DEPENDENCE ON T-CELL SUBSETS IN MRL/+ MICE SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,AUDIE L MURPHY VET ADM HOSP,HLTH SCI CTR,SAN ANTONIO,TX 78285. RP MILLER, ML (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 23 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD OCT PY 1990 VL 82 IS 1 BP 27 EP 32 PG 6 WC Immunology SC Immunology GA EA588 UT WOS:A1990EA58800006 PM 2119919 ER PT J AU JENCK, MA REYNOLDS, MS AF JENCK, MA REYNOLDS, MS TI ANTICONVULSANT DRUG-WITHDRAWAL IN SEIZURE-FREE PATIENTS SO CLINICAL PHARMACY LA English DT Editorial Material C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0278-2677 J9 CLIN PHARMACY PD OCT PY 1990 VL 9 IS 10 BP 781 EP 787 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA ED770 UT WOS:A1990ED77000006 PM 2242659 ER PT J AU WESER, E HARPER, A AF WESER, E HARPER, A TI INHIBITION OF POLYAMINE SYNTHESIS PREVENTS ADAPTATION TO SMALL-BOWEL RESECTION - REVERSAL BY ENTERAL OR PARENTERAL PUTRESCINE 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 OCT PY 1990 VL 38 IS 3 BP A862 EP A862 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EA235 UT WOS:A1990EA23500528 ER PT J AU BRITTAIN, E WITTES, J AF BRITTAIN, E WITTES, J TI THE RUN-IN PERIOD IN CLINICAL-TRIALS - THE EFFECT OF MISCLASSIFICATION ON EFFICIENCY SO CONTROLLED CLINICAL TRIALS LA English DT Article C1 NHLBI, DIV EPIDEMIOL & CLIN APPLICAT, BETHESDA, MD 20892 USA. NHLBI, BIOSTAT RES BRANCH, BETHESDA, MD 20892 USA. US DEPT VET AFFAIRS, COOPERAT STUDIES PROGRAM COORDINATING CTR, WASHINGTON, DC USA. NR 11 TC 23 Z9 23 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0197-2456 EI 1879-050X J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD OCT PY 1990 VL 11 IS 5 BP 327 EP 338 DI 10.1016/0197-2456(90)90174-Z PG 12 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA EM545 UT WOS:A1990EM54500003 PM 2289394 ER PT J AU SHIMIZU, M LASKER, JM TSUTSUMI, M LIEBER, CS AF SHIMIZU, M LASKER, JM TSUTSUMI, M LIEBER, CS TI IMMUNOHISTOCHEMICAL LOCALIZATION OF ETHANOL-INDUCIBLE P450IIE1 IN THE RAT ALIMENTARY-TRACT SO GASTROENTEROLOGY LA English DT Article C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,130 W KINGSBRIDGE RD,BRONX,NY 10468. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. FU NIAAA NIH HHS [AA-03508, AA-05934, AA-07842] NR 43 TC 104 Z9 105 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD OCT PY 1990 VL 99 IS 4 BP 1044 EP 1053 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA DY353 UT WOS:A1990DY35300021 PM 2203661 ER PT J AU BASKIN, G SCHENKER, S HENDERSON, GI AF BASKIN, G SCHENKER, S HENDERSON, GI TI TRANSFORMING GROWTH FACTOR-BETA-1 INHIBITS EPIDERMAL GROWTH-FACTOR (EGF) RECEPTOR-MEDIATED ENDOCYTOSIS AND DOWN-REGULATION SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,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. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1990 VL 12 IS 4 BP 916 EP 916 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ED299 UT WOS:A1990ED29900314 ER PT J AU BASKIN, G KUSHWAHA, A SCHENKER, S HENDERSON, GI AF BASKIN, G KUSHWAHA, A SCHENKER, S HENDERSON, GI TI EFFECT OF ETHANOL ON PROTEIN-KINASE-C ACTIVATION AND REGULATION OF EPIDERMAL GROWTH-FACTOR (EGF) ENDOCYTOSIS SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,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. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1990 VL 12 IS 4 BP 922 EP 922 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ED299 UT WOS:A1990ED29900339 ER PT J AU SPEEG, KV MALDONADO, AL AF SPEEG, KV MALDONADO, AL TI CROSS COMPETITION BETWEEN COLCHICINE AND ICG FOR BILIARY-SECRETION SO HEPATOLOGY 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 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1990 VL 12 IS 4 BP 1001 EP 1001 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ED299 UT WOS:A1990ED29900653 ER PT J AU TISCHLER, GL AF TISCHLER, GL TI UTILIZATION MANAGEMENT AND THE QUALITY OF CARE SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP TISCHLER, GL (reprint author), UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024, USA. NR 18 TC 20 Z9 20 U1 2 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD OCT PY 1990 VL 41 IS 10 BP 1099 EP 1102 PG 4 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA EB262 UT WOS:A1990EB26200009 PM 2242871 ER PT J AU BUSH, RK AF BUSH, RK TI OCCUPATIONAL ASTHMA FROM VEGETABLE GUMS SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Editorial Material C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. RP BUSH, RK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERR,MADISON,WI 53705, USA. NR 10 TC 5 Z9 5 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD OCT PY 1990 VL 86 IS 4 BP 443 EP 444 DI 10.1016/S0091-6749(05)80197-6 PN 1 PG 2 WC Allergy; Immunology SC Allergy; Immunology GA EG454 UT WOS:A1990EG45400001 PM 2229807 ER PT J AU SCHILLER, JH STORER, B PAULNOCK, DM BROWN, RR DATTA, SP WITT, PL BORDEN, EC AF SCHILLER, JH STORER, B PAULNOCK, DM BROWN, RR DATTA, SP WITT, PL BORDEN, EC TI A DIRECT COMPARISON OF BIOLOGICAL RESPONSE MODULATION AND CLINICAL SIDE-EFFECTS BY INTERFERON-BETA-SER, INTERFERON-GAMMA, OR THE COMBINATION OF INTERFERON-BETA-SER AND INTERFERON-GAMMA IN HUMANS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article C1 UNIV WISCONSIN,CTR CLIN CANC,DEPT MED MICROBIOL,MADISON,WI 53792. UNIV WISCONSIN,CTR CLIN CANC,DEPT STAT,MADISON,WI 53792. UNIV WISCONSIN,CTR CLIN CANC,DEPT MED,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP SCHILLER, JH (reprint author), UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,ROOM K4666,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [N01-CM47669] NR 34 TC 24 Z9 24 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT PY 1990 VL 86 IS 4 BP 1211 EP 1221 DI 10.1172/JCI114827 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EE199 UT WOS:A1990EE19900025 PM 2120284 ER PT J AU FREEMAN, GL COLSTON, JT AF FREEMAN, GL COLSTON, JT TI ROLE OF VENTRICULOVASCULAR COUPLING IN CARDIAC RESPONSE TO INCREASED CONTRACTILITY IN CLOSED-CHEST DOGS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP FREEMAN, GL (reprint author), UNIV TEXAS,HLTH SCI CTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 31 TC 15 Z9 15 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT PY 1990 VL 86 IS 4 BP 1278 EP 1284 DI 10.1172/JCI114835 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EE199 UT WOS:A1990EE19900033 PM 2212012 ER PT J AU WITTE, J LLOYD, M LORENZSONN, V KORSMO, H OLSEN, W AF WITTE, J LLOYD, M LORENZSONN, V KORSMO, H OLSEN, W TI THE BIOSYNTHETIC BASIS OF ADULT LACTASE DEFICIENCY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,GASTROENTEROL LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. FU NIADDK NIH HHS [5P30-AM-26659, AM-13927]; NIDDK NIH HHS [K08 DK 01789] NR 16 TC 48 Z9 48 U1 1 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT PY 1990 VL 86 IS 4 BP 1338 EP 1342 DI 10.1172/JCI114843 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EE199 UT WOS:A1990EE19900041 PM 2120287 ER PT J AU GALGIANI, JN SUN, SH CLEMONS, KV STEVENS, DA AF GALGIANI, JN SUN, SH CLEMONS, KV STEVENS, DA TI ACTIVITY OF CILOFUNGIN AGAINST COCCIDIOIDES-IMMITIS - DIFFERENTIAL INVITRO EFFECTS ON MYCELIA AND SPHERULES CORRELATED WITH INVIVO STUDIES SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article C1 VET ADM MED CTR,RES SERV,TUCSON,AZ 85723. UNIV ARIZONA,COLL MED,TUCSON,AZ 85721. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. SANTA CLARA VALLEY MED CTR,DEPT MED,SAN JOSE,CA 95128. INST MED RES,SAN JOSE,CA 95128. STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305. RP GALGIANI, JN (reprint author), VET ADM MED CTR,MED SERV 111,TUCSON,AZ 85723, USA. NR 19 TC 16 Z9 16 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 OCT PY 1990 VL 162 IS 4 BP 944 EP 948 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EA376 UT WOS:A1990EA37600024 PM 2144867 ER PT J AU KURIHARA, N ROODMAN, GD AF KURIHARA, N ROODMAN, GD TI INTERFERON-ALPHA AND INTERFERON-GAMMA INHIBIT INTERLEUKIN-1-BETA-STIMULATED OSTEOCLAST-LIKE CELL-FORMATION IN LONG-TERM HUMAN MARROW CULTURES SO JOURNAL OF INTERFERON RESEARCH LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV HEMATOL,SAN ANTONIO,TX 78284. NR 22 TC 39 Z9 39 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0197-8357 J9 J INTERFERON RES JI J. Interferon Res. PD OCT PY 1990 VL 10 IS 5 BP 541 EP 547 DI 10.1089/jir.1990.10.541 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EF709 UT WOS:A1990EF70900012 PM 2125633 ER PT J AU ROSS, RJ BALL, WA LEVITT, DR GRESCH, PJ MORRISON, AR AF ROSS, RJ BALL, WA LEVITT, DR GRESCH, PJ MORRISON, AR TI EFFECTS OF MONOAMINE REUPTAKE BLOCKADE ON PONTOGENICULOOCCIPITAL WAVE ACTIVITY SO NEUROPHARMACOLOGY LA English DT Note C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH VET MED,DEPT ANIM BIOL,PHILADELPHIA,PA 19104. RP ROSS, RJ (reprint author), VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. FU NIMH NIH HHS [F32-MH-09584-01, R01-MH42903] NR 11 TC 3 Z9 3 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3908 J9 NEUROPHARMACOLOGY JI Neuropharmacology PD OCT PY 1990 VL 29 IS 10 BP 965 EP 968 DI 10.1016/0028-3908(90)90149-L PG 4 WC Neurosciences; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA EC685 UT WOS:A1990EC68500015 PM 2255389 ER PT J AU BEGLE, RL SKATRUD, JB AF BEGLE, RL SKATRUD, JB TI HYPERINFLATION AND EXPIRATORY MUSCLE RECRUITMENT DURING NREM SLEEP IN HUMANS SO RESPIRATION PHYSIOLOGY LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. FU NHLBI NIH HHS [1PO1 HL42242-01] NR 25 TC 4 Z9 4 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0034-5687 J9 RESP PHYSIOL JI Respir. Physiol. PD OCT PY 1990 VL 82 IS 1 BP 47 EP 64 DI 10.1016/0034-5687(90)90023-R PG 18 WC Physiology; Respiratory System SC Physiology; Respiratory System GA EJ428 UT WOS:A1990EJ42800005 PM 2270361 ER PT J AU ACHER, CW WYNN, MM ARCHIBALD, J AF ACHER, CW WYNN, MM ARCHIBALD, J TI NALOXONE AND SPINAL-FLUID DRAINAGE AS ADJUNCTS IN THE SURGICAL-TREATMENT OF THORACOABDOMINAL AND THORACIC ANEURYSMS SO SURGERY LA English DT Article; Proceedings Paper CT 47TH ANNUAL MEETING OF THE CENTRAL SURGICAL ASSOC CY MAR 01-03, 1990 CL CHICAGO, IL SP CENT SURG ASSOC C1 UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,SURG SERV,MADISON,WI. RP ACHER, CW (reprint author), UNIV WISCONSIN,DEPT SURG,600 HIGHLAND AVE,MADISON,WI 53719, USA. NR 22 TC 32 Z9 32 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD OCT PY 1990 VL 108 IS 4 BP 755 EP 762 PG 8 WC Surgery SC Surgery GA EB587 UT WOS:A1990EB58700023 PM 2218888 ER PT J AU GRAYBILL, JR STEVENS, DA GALGIANI, JN DISMUKES, WE CLOUD, GA AF GRAYBILL, JR STEVENS, DA GALGIANI, JN DISMUKES, WE CLOUD, GA TI ITRACONAZOLE TREATMENT OF COCCIDIOIDOMYCOSIS SO AMERICAN JOURNAL OF MEDICINE LA English DT Article C1 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. SANTA CLARA VALLEY MED CTR,CALIF INST MED RES,SAN JOSE,CA 95128. STANFORD UNIV,STANFORD,CA 94305. VET ADM MED CTR,MED SERV,TUCSON,AZ 85723. VET ADM MED CTR,RES SERV,TUCSON,AZ 85723. UNIV AUTONOMA NUEVO LAREDO,MONTERREY,MEXICO. WILFORD HALL USAF MED CTR,LACKLAND AFB,TX 78236. UNIV ARIZONA,COLL MED,DEPT MED,TUCSON,AZ 85721. UNIV ALABAMA,SCH MED,DEPT MED,BIRMINGHAM,AL 35233. UNIV ALABAMA,SCH MED,DEPT BIOSTAT,BIRMINGHAM,AL 35233. NIAID,BETHESDA,MD 20205. RP GRAYBILL, JR (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,MED SERV 111,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NCI NIH HHS [CA 13148]; NIAID NIH HHS [N01 AI 82570, N01 AI52562] NR 30 TC 111 Z9 113 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 SEP PY 1990 VL 89 IS 3 BP 282 EP 290 DI 10.1016/0002-9343(90)90339-F PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA DX458 UT WOS:A1990DX45800003 PM 2168126 ER PT J AU PUGH, JA AF PUGH, JA TI FEDERAL INVOLVEMENT IN TECHNOLOGY-ASSESSMENT - A PRIMER SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. 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 7 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9629 J9 AM J MED SCI JI Am. J. Med. Sci. PD SEP PY 1990 VL 300 IS 3 BP 185 EP 188 DI 10.1097/00000441-199009000-00012 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA EG050 UT WOS:A1990EG05000012 PM 2240012 ER PT J AU JACOBS, G CORNELIUS, L KEENE, B RAKICH, P SHUG, A AF JACOBS, G CORNELIUS, L KEENE, B RAKICH, P SHUG, A TI COMPARISON OF PLASMA, LIVER, AND SKELETAL-MUSCLE CARNITINE CONCENTRATIONS IN CATS WITH IDIOPATHIC HEPATIC LIPIDOSIS AND IN HEALTHY CATS SO AMERICAN JOURNAL OF VETERINARY RESEARCH LA English DT Article C1 UNIV GEORGIA,COLL VET MED,DIAGNOST LAB,ATHENS,GA 30602. UNIV WISCONSIN,SCH VET MED,DEPT MED SCI,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP JACOBS, G (reprint author), UNIV GEORGIA,COLL VET MED,DEPT SMALL ANIM MED,ATHENS,GA 30602, USA. NR 19 TC 23 Z9 23 U1 1 U2 4 PU AMER VETERINARY MEDICAL ASSOC PI SCHAUMBURG PA 1931 N MEACHAM RD SUITE 100, SCHAUMBURG, IL 60173-4360 SN 0002-9645 J9 AM J VET RES JI Am. J. Vet. Res. PD SEP PY 1990 VL 51 IS 9 BP 1349 EP 1351 PG 3 WC Veterinary Sciences SC Veterinary Sciences GA DW543 UT WOS:A1990DW54300005 PM 2396782 ER PT J AU DEFAVERI, J SALAZAR, MH RINALDI, MG GRAYBILL, JR AF DEFAVERI, J SALAZAR, MH RINALDI, MG GRAYBILL, JR TI PULMONARY ASPERGILLOSIS IN MICE - TREATMENT WITH A NEW TRIAZOLE SCH39304 SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article C1 CORP INVEST BIOL,MEDELLIN,COLOMBIA. AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,LAB SERV,SAN ANTONIO,TX 78284. RP DEFAVERI, J (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,MED SERV,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 19 TC 9 Z9 9 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 SEP PY 1990 VL 142 IS 3 BP 512 EP 515 PG 4 WC Respiratory System SC Respiratory System GA DX263 UT WOS:A1990DX26300006 PM 2202244 ER PT J AU PFALLER, MA RINALDI, MG GALGIANI, JN BARTLETT, MS BODY, BA ESPINELINGROFF, A FROMTLING, RA HALL, GS HUGHES, CE ODDS, FC SUGAR, AM AF PFALLER, MA RINALDI, MG GALGIANI, JN BARTLETT, MS BODY, BA ESPINELINGROFF, A FROMTLING, RA HALL, GS HUGHES, CE ODDS, FC SUGAR, AM TI COLLABORATIVE INVESTIGATION OF VARIABLES IN SUSCEPTIBILITY TESTING OF YEASTS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article C1 UNIV IOWA,COLL MED,IOWA CITY,IA 52242. VET AFFAIRS MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. VET AFFAIRS MED CTR,TUCSON,AZ 85723. UNIV ARIZONA,COLL MED,TUCSON,AZ 85723. INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46223. UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA 22908. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. MERCK INST THERAPEUT RES,RAHWAY,NJ 07065. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. MAYO CLIN,ROCHESTER,MN 55901. UNIV LEICESTER,LEICESTER LE1 7RH,ENGLAND. BOSTON UNIV,UNIV HOSP,MED CTR,BOSTON,MA 02118. RP PFALLER, MA (reprint author), VET AFFAIRS MED CTR,IOWA CITY,IA 52242, USA. NR 30 TC 164 Z9 164 U1 0 U2 1 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 SEP PY 1990 VL 34 IS 9 BP 1648 EP 1654 PG 7 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA DX529 UT WOS:A1990DX52900006 PM 2285276 ER PT J AU RIESMEYER, JS CRAWFORD, MH AF RIESMEYER, JS CRAWFORD, MH TI SUPERIORITY OF EXERCISE 2-DIMENSIONAL ECHOCARDIOGRAPHY OVER THE ASCENDING AORTA DOPPLER METHOD FOR THE IDENTIFICATION OF JEOPARDIZED MYOCARDIUM AFTER MYOCARDIAL-INFARCTION SO CORONARY ARTERY DISEASE LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 13 TC 2 Z9 2 U1 0 U2 0 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD SEP-OCT PY 1990 VL 1 IS 5 BP 591 EP 595 DI 10.1097/00019501-199009000-00011 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EA895 UT WOS:A1990EA89500011 ER PT J AU BAGCHI, D DAS, DK ENGELMAN, RM PRASAD, MR SUBRAMANIAN, R AF BAGCHI, D DAS, DK ENGELMAN, RM PRASAD, MR SUBRAMANIAN, R TI POLYMORPHONUCLEAR LEUKOCYTES AS POTENTIAL SOURCE OF FREE-RADICALS IN THE ISCHEMIC-REPERFUSED MYOCARDIUM SO EUROPEAN HEART JOURNAL LA English DT Article C1 UNIV CONNECTICUT,SCH MED,SURG RES CTR,DEPT SURG,DIV CARDIOVASC,FARMINGTON,CT 06032. BAYSTATE MED CTR,DEPT CARDIAC SURG,SPRINGFIELD,MA 01107. UNIV WISCONSIN,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. FU NHLBI NIH HHS [HL34360, HL33889, HL22559] NR 32 TC 45 Z9 46 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0195-668X J9 EUR HEART J JI Eur. Heart J. PD SEP PY 1990 VL 11 IS 9 BP 800 EP 813 PG 14 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA DZ498 UT WOS:A1990DZ49800005 PM 2226506 ER PT J AU GARZATREVINO, ES VOLKOW, ND CANCRO, R CONTRERAS, S AF GARZATREVINO, ES VOLKOW, ND CANCRO, R CONTRERAS, S TI NEUROBIOLOGY OF SCHIZOPHRENIC SYNDROMES SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Review C1 AUDIE L MURPHY MEM VET ADM MED CTR,CLIN RES UNIT,SAN ANTONIO,TX 78284. BROOKHAVEN NATL LAB,UPTON,NY 11973. NYU MED CTR,DEPT PSYCHIAT,NEW YORK,NY 10016. TEXAS TECH UNIV,HLTH SCI CTR,LUBBOCK,TX 79430. RP GARZATREVINO, ES (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 100 TC 8 Z9 8 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD SEP PY 1990 VL 41 IS 9 BP 971 EP 980 PG 10 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA DW586 UT WOS:A1990DW58600004 PM 1976589 ER PT J AU GLYNN, SM SUSSMAN, S AF GLYNN, SM SUSSMAN, S TI WHY PATIENTS SMOKE SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Letter C1 UNIV SO CALIF,INST HLTH PROMOT & DIS PREVENT,LOS ANGELES,CA 90089. UNIV SO CALIF,DEPT PREVENT MED,LOS ANGELES,CA 90089. RP GLYNN, SM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA, USA. NR 5 TC 53 Z9 55 U1 1 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD SEP PY 1990 VL 41 IS 9 BP 1027 EP 1028 PG 2 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA DW586 UT WOS:A1990DW58600024 PM 2210702 ER PT J AU BAKER, PJ TAYLOR, CE STASHAK, PW FAUNTLEROY, MB HASLOV, K QURESHI, N TAKAYAMA, K AF BAKER, PJ TAYLOR, CE STASHAK, PW FAUNTLEROY, MB HASLOV, K QURESHI, N TAKAYAMA, K TI INACTIVATION OF SUPPRESSOR T-CELL ACTIVITY BY THE NONTOXIC LIPOPOLYSACCHARIDE OF RHODOPSEUDOMONAS-SPHAEROIDES SO INFECTION AND IMMUNITY LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL LAB,MADISON,WI 53705. STATENS SERUM INST,DEPT VACCINE,DK-2300 COPENHAGEN,DENMARK. RP BAKER, PJ (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK II RES FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 41 TC 20 Z9 21 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 SEP PY 1990 VL 58 IS 9 BP 2862 EP 2868 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA DX607 UT WOS:A1990DX60700021 PM 2143752 ER PT J AU CALHOUN, WJ BUSH, RK AF CALHOUN, WJ BUSH, RK TI ENHANCED REACTIVE OXYGEN SPECIES METABOLISM OF AIRSPACE CELLS AND AIRWAY INFLAMMATION FOLLOW ANTIGEN CHALLENGE IN HUMAN ASTHMA SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article C1 UNIV WISCONSIN,DEPT MED,ALLERGY IMMUNOL SECT,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,ALLERGY SECT,MADISON,WI 53705. RP CALHOUN, WJ (reprint author), UNIV WISCONSIN,DEPT MED,PULM & CRIT CARE MED SECT,H6 384 CSC,MADISON,WI 53792, USA. FU PHS HHS [K08-01828] NR 28 TC 58 Z9 59 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD SEP PY 1990 VL 86 IS 3 BP 306 EP 313 DI 10.1016/S0091-6749(05)80092-2 PN 1 PG 8 WC Allergy; Immunology SC Allergy; Immunology GA EA859 UT WOS:A1990EA85900003 PM 2212406 ER PT J AU GUTIERREZ, GE MUNDY, GR MANNING, DR HEWLETT, EL KATZ, MS AF GUTIERREZ, GE MUNDY, GR MANNING, DR HEWLETT, EL KATZ, MS TI TRANSFORMING GROWTH-FACTOR-BETA ENHANCES PARATHYROID-HORMONE STIMULATION OF ADENYLATE-CYCLASE IN CLONAL OSTEOBLAST-LIKE CELLS SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article 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. UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. UNIV VIRGINIA,DEPT MED,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT PHARMACOL,CHARLOTTESVILLE,VA 22908. FU NIADDK NIH HHS [AM-28149]; NIAID NIH HHS [AI-18000] NR 37 TC 24 Z9 24 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 SEP PY 1990 VL 144 IS 3 BP 438 EP 447 DI 10.1002/jcp.1041440311 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA DX216 UT WOS:A1990DX21600010 PM 2391378 ER PT J AU SHARKEY, PK GRAYBILL, JR RINALDI, MG STEVENS, DA TUCKER, RM PETERIE, JD HOEPRICH, PD GREER, DL FRENKEL, L COUNTS, GW GOODRICH, J ZELLNER, S BRADSHER, RW VANDERHORST, CM ISRAEL, K PANKEY, GA BARRANCO, CP AF SHARKEY, PK GRAYBILL, JR RINALDI, MG STEVENS, DA TUCKER, RM PETERIE, JD HOEPRICH, PD GREER, DL FRENKEL, L COUNTS, GW GOODRICH, J ZELLNER, S BRADSHER, RW VANDERHORST, CM ISRAEL, K PANKEY, GA BARRANCO, CP TI ITRACONAZOLE TREATMENT OF PHEOHYPHOMYCOSIS SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,MED SERV,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. JANSSEN PHARMACEUT,PISCATAWAY,NJ. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121. UNIV N CAROLINA,CHAPEL HILL,NC 27514. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. UNIV ARKANSAS,LITTLE ROCK,AR 72204. STANFORD UNIV,STANFORD,CA 94305. UNIV CALIF DAVIS,SACRAMENTO MED CTR,SACRAMENTO,CA 95817. SANTA CLARA VALLEY MED CTR,INST MED RES,SAN JOSE,CA 95128. LOUISIANA STATE UNIV,MED CTR,NEW ORLEANS,LA 70112. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. NR 15 TC 150 Z9 152 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD SEP PY 1990 VL 23 IS 3 SU S BP 577 EP 586 DI 10.1016/0190-9622(90)70259-K PN 2 PG 10 WC Dermatology SC Dermatology GA DX713 UT WOS:A1990DX71300009 PM 2170477 ER PT J AU TUCKER, RM DENNING, DW ARATHOON, EG RINALDI, MG STEVENS, DA AF TUCKER, RM DENNING, DW ARATHOON, EG RINALDI, MG STEVENS, DA TI ITRACONAZOLE THERAPY FOR NONMENINGEAL COCCIDIOIDOMYCOSIS - CLINICAL AND LABORATORY OBSERVATIONS SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,751 S BASCOM AVE,SAN JOSE,CA 95128. AUDIE L MURPHY MEM VET ADM MED CTR,VET AFFAIRS MYCOL REFERENCE LAB,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. CALIF INST MED RES,SAN JOSE,CA. STANFORD UNIV,MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,STANFORD,CA 94305. OI Denning, David/0000-0001-5626-2251 NR 20 TC 53 Z9 56 U1 0 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD SEP PY 1990 VL 23 IS 3 SU S BP 593 EP 601 DI 10.1016/0190-9622(90)70261-F PN 2 PG 9 WC Dermatology SC Dermatology GA DX713 UT WOS:A1990DX71300011 PM 2170479 ER PT J AU REED, RL GERETY, MB WINOGRAD, CH AF REED, RL GERETY, MB WINOGRAD, CH TI EXPANDED ACCESS TO REHABILITATION SERVICES FOR OLDER-PEOPLE - AN URGENT NEED SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Editorial Material C1 UNIV ARIZONA,DIV RESTORAT MED,TUCSON,AZ 85721. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES & EDUC,SAN ANTONIO,TX 78284. STANFORD UNIV,MED CTR,SCH MED,DEPT MED,DIV GERONTOL,STANFORD,CA 94305. PALO ALTO VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,PALO ALTO,CA. RP REED, RL (reprint author), UNIV ARIZONA,DEPT FAMILY & COMMUNITY MED,GERIATR PROGRAM,TUCSON,AZ 85721, USA. RI Reed, Richard/C-6204-2012 NR 9 TC 5 Z9 5 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 SEP PY 1990 VL 38 IS 9 BP 1055 EP 1056 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA ED207 UT WOS:A1990ED20700020 PM 2212443 ER PT J AU RUBIN, DH MORRISON, AH WITZLEBEN, CL GUICO, CJ PICCOLI, DA AF RUBIN, DH MORRISON, AH WITZLEBEN, CL GUICO, CJ PICCOLI, DA TI SITE OF REOVIRUS REPLICATION IN LIVER IS DETERMINED BY THE TYPE OF HEPATOCELLULAR INSULT SO JOURNAL OF VIROLOGY LA English DT Note C1 UNIV PENN,DEPT MED & MICROBIOL,PHILADELPHIA,PA 19104. UNIV PENN,CHILDRENS HOSP PHILADELPHIA,SCH MED,DEPT PATHOL,PHILADELPHIA,PA 19104. UNIV PENN,CHILDRENS HOSP PHILADELPHIA,SCH MED,DEPT GASTROENTEROL,PHILADELPHIA,PA 19104. RP RUBIN, DH (reprint author), VET AFFAIRS MED CTR,DEPT RES MED,PHILADELPHIA,PA 19104, USA. NR 25 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD SEP PY 1990 VL 64 IS 9 BP 4593 EP 4597 PG 5 WC Virology SC Virology GA DU753 UT WOS:A1990DU75300072 PM 2166834 ER PT J AU FERGUSON, V AF FERGUSON, V TI THE NURSING SHORTAGE - DYNAMICS AND SOLUTIONS - AN OVERVIEW SO NURSING CLINICS OF NORTH AMERICA LA English DT Article RP FERGUSON, V (reprint author), US DEPT VET AFFAIRS,DEPT MED & SURG,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 6 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 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD SEP PY 1990 VL 25 IS 3 BP 503 EP 507 PG 5 WC Nursing SC Nursing GA DU695 UT WOS:A1990DU69500002 PM 2199932 ER PT J AU REGAN, PF AF REGAN, PF TI THE 3 RS - RECRUITMENT, RESTRUCTURING THE ENVIRONMENT, AND REFORMULATING THE CURRICULUM SO NURSING CLINICS OF NORTH AMERICA LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP REGAN, PF (reprint author), US DEPT VET AFFAIRS,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD SEP PY 1990 VL 25 IS 3 BP 517 EP 524 PG 8 WC Nursing SC Nursing GA DU695 UT WOS:A1990DU69500004 PM 2381856 ER PT J AU FREEMAN, BA CORONADO, JR AF FREEMAN, BA CORONADO, JR TI A SUPPORTIVE CLINICAL-PRACTICE MODEL SO NURSING CLINICS OF NORTH AMERICA LA English DT Article RP FREEMAN, BA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,NURSING SERV,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 6 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD SEP PY 1990 VL 25 IS 3 BP 551 EP 560 PG 10 WC Nursing SC Nursing GA DU695 UT WOS:A1990DU69500007 PM 2381858 ER PT J AU COURNOYER, PR AF COURNOYER, PR TI THE ART OF CREATIVE SOLUTIONS SO NURSING CLINICS OF NORTH AMERICA LA English DT Article C1 US DEPT VET AFFAIRS,CENT OFF,WASHINGTON,DC. NR 20 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD SEP PY 1990 VL 25 IS 3 BP 581 EP 586 PG 6 WC Nursing SC Nursing GA DU695 UT WOS:A1990DU69500010 PM 2199935 ER PT J AU GRONVALL, JA AF GRONVALL, JA TI SOLUTIONS IN A PLURALISTIC ENVIRONMENT SO NURSING CLINICS OF NORTH AMERICA LA English DT Article RP GRONVALL, JA (reprint author), US DEPT VET AFFAIRS,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 8 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 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD SEP PY 1990 VL 25 IS 3 BP 587 EP 595 PG 9 WC Nursing SC Nursing GA DU695 UT WOS:A1990DU69500011 PM 2381861 ER PT J AU FERGUSON, V AF FERGUSON, V TI SATISFACTION AND FULFILLMENT SO NURSING CLINICS OF NORTH AMERICA LA English DT Article RP FERGUSON, V (reprint author), US DEPT VET AFFAIRS,DEPT MED & SURG,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD SEP PY 1990 VL 25 IS 3 BP 615 EP 616 PG 2 WC Nursing SC Nursing GA DU695 UT WOS:A1990DU69500014 PM 2381864 ER PT J AU FERGUSON, V AF FERGUSON, V TI THE NURSING SHORTAGE - DYNAMICS AND SOLUTIONS - PREFACE SO NURSING CLINICS OF NORTH AMERICA LA English DT Editorial Material RP FERGUSON, V (reprint author), US DEPT VET AFFAIRS,DEPT MED & SURG,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD SEP PY 1990 VL 25 IS 3 BP R13 EP R13 PG 1 WC Nursing SC Nursing GA DU695 UT WOS:A1990DU69500001 ER PT J AU MELCHIOR, CL AF MELCHIOR, CL TI CONDITIONED TOLERANCE PROVIDES PROTECTION AGAINST ETHANOL LETHALITY SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Note C1 W LOS ANGELES VET ADM,BRENTWOOD DIV RES B151,LOS ANGELES,CA 90073. NR 12 TC 23 Z9 23 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD SEP PY 1990 VL 37 IS 1 BP 205 EP 206 DI 10.1016/0091-3057(90)90063-N PG 2 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA DZ444 UT WOS:A1990DZ44400030 PM 2263663 ER PT J AU DIAN, L CUMMINGS, JL PETRY, S HILL, MA AF DIAN, L CUMMINGS, JL PETRY, S HILL, MA TI PERSONALITY ALTERATIONS IN MULTIINFARCT DEMENTIA SO PSYCHOSOMATICS LA English DT Article C1 W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV 681B111,NEUROBEHAV UNIT,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT GERIATR MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT BEHAV SCI,LOS ANGELES,CA 90024. 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RP TAKAYAMA, K (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCRR NIH HHS [RR-570]; NIGMS NIH HHS [GM-36054] NR 37 TC 64 Z9 65 U1 1 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 15 PY 1990 VL 265 IS 23 BP 14023 EP 14029 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA DU275 UT WOS:A1990DU27500094 PM 2199450 ER PT J AU KOELLER, JM AF KOELLER, JM TI UNDERSTANDING CANCER PAIN SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article; Proceedings Paper CT ROUNDTABLE DISCUSSION ON ANALGESIC THERAPY IN THE TERMINALLY ILL CANCER PATIENT CY DEC 02, 1989 CL ATLANTA, GA SP ELKINS SINN C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED ONCOL 111J,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED & PHARMACOL,SAN ANTONIO,TX 78284. RP KOELLER, JM (reprint author), UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712, USA. NR 6 TC 10 Z9 10 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD AUG PY 1990 VL 47 IS 8 SU 1 BP S3 EP S6 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA DU431 UT WOS:A1990DU43100001 PM 2202210 ER PT J AU FREEMAN, GL AF FREEMAN, GL TI EFFECTS OF INCREASED AFTERLOAD ON LEFT-VENTRICULAR FUNCTION IN CLOSED-CHEST DOGS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP FREEMAN, GL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED CARDIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 30 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 AUG PY 1990 VL 259 IS 2 BP H619 EP H625 PN 2 PG 7 WC Physiology SC Physiology GA DU954 UT WOS:A1990DU95400042 PM 2386232 ER PT J AU MULROW, CD AGUILAR, C ENDICOTT, JE TULEY, MR VELEZ, R CHARLIP, WS RHODES, MC HILL, JA DENINO, LA AF MULROW, CD AGUILAR, C ENDICOTT, JE TULEY, MR VELEZ, R CHARLIP, WS RHODES, MC HILL, JA DENINO, LA TI QUALITY-OF-LIFE CHANGES AND HEARING IMPAIRMENT - A RANDOMIZED TRIAL SO ANNALS OF INTERNAL MEDICINE LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 72 TC 278 Z9 286 U1 1 U2 13 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD AUG 1 PY 1990 VL 113 IS 3 BP 188 EP 194 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA DQ421 UT WOS:A1990DQ42100004 PM 2197909 ER PT J AU VANPUTTEN, T MARDER, SR MINTZ, J AF VANPUTTEN, T MARDER, SR MINTZ, J TI A CONTROLLED DOSE COMPARISON OF HALOPERIDOL IN NEWLY ADMITTED SCHIZOPHRENIC-PATIENTS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article RP VANPUTTEN, T (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,BLDG 210C,LOS ANGELES,CA 90073, USA. NR 29 TC 171 Z9 172 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. 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PD AUG PY 1990 VL 116 IS 8 BP 971 EP 972 PG 2 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA DT075 UT WOS:A1990DT07500017 PM 2378727 ER PT J AU BRUMMER, E SUN, SH HARRISON, JL PERLMAN, AM PHILPOTT, DE STEVENS, DA AF BRUMMER, E SUN, SH HARRISON, JL PERLMAN, AM PHILPOTT, DE STEVENS, DA TI ULTRASTRUCTURE OF PHAGOCYTOSED PARACOCCIDIOIDES-BRASILIENSIS IN NONACTIVATED OR ACTIVATED MACROPHAGES SO INFECTION AND IMMUNITY LA English DT Article C1 CALIF INST MED RES,SAN JOSE,CA 95128. NASA ADMINISTR,AMES RES CTR,MT VIEW,CA 94035. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. STANFORD UNIV,MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,STANFORD,CA 94305. RP BRUMMER, E (reprint author), SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,SAN JOSE,CA 95128, USA. NR 15 TC 13 Z9 14 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 1990 VL 58 IS 8 BP 2628 EP 2636 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA DP893 UT WOS:A1990DP89300032 PM 2370112 ER PT J AU SCHROECKENSTEIN, DC MEIERDAVIS, S BUSH, RK AF SCHROECKENSTEIN, DC MEIERDAVIS, S BUSH, RK TI OCCUPATIONAL SENSITIVITY TO TENEBRIO-MOLITOR LINNAEUS (YELLOW MEALWORM) SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,ALLERGY SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,ALLERGY CLIN IMMUNOL SECT,MADISON,WI 53706. NR 20 TC 21 Z9 24 U1 1 U2 8 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD AUG PY 1990 VL 86 IS 2 BP 182 EP 188 DI 10.1016/S0091-6749(05)80064-8 PG 7 WC Allergy; Immunology SC Allergy; Immunology GA DV316 UT WOS:A1990DV31600007 PM 2384648 ER PT J AU SCHROECKENSTEIN, DC MEIERDAVIS, S YUNGINGER, JW BUSH, RK AF SCHROECKENSTEIN, DC MEIERDAVIS, S YUNGINGER, JW BUSH, RK TI ALLERGENS INVOLVED IN OCCUPATIONAL ASTHMA CAUSED BY BABY BREATH (GYPSOPHILA-PANICULATA) SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,ALLERGY SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,ALLERGY CLIN IMMUNOL SECT,MADISON,WI 53706. MAYO CLIN & MAYO FDN,ALLERGY RES LABS,ROCHESTER,MN 55905. NR 12 TC 12 Z9 12 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD AUG PY 1990 VL 86 IS 2 BP 189 EP 193 DI 10.1016/S0091-6749(05)80065-X PG 5 WC Allergy; Immunology SC Allergy; Immunology GA DV316 UT WOS:A1990DV31600008 PM 2384649 ER PT J AU SCHILLER, JH HORISBERGER, MA BITTNER, G CARLIN, JM STORER, B BYRNE, GI WILLSON, JKV BORDEN, EC AF SCHILLER, JH HORISBERGER, MA BITTNER, G CARLIN, JM STORER, B BYRNE, GI WILLSON, JKV BORDEN, EC TI EFFECTS OF COMBINATIONS OF INTERFERON-BETA-SER AND INTERFERON-GAMMA ON INTERFERON-INDUCIBLE PROTEINS AND ON THE CELL-CYCLE SO JOURNAL OF BIOLOGICAL RESPONSE MODIFIERS LA English DT Article C1 UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,MADISON,WI 53706. UNIV WISCONSIN,CTR CLIN CANC,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,CTR CLIN CANC,DEPT MED MICROBIOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. CIBA GEIGY AG,CH-4002 BASEL,SWITZERLAND. RP SCHILLER, JH (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,ONCOL SECT,ROOM B5055,1900 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 48 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0732-6580 J9 J BIOL RESP MODIF PD AUG PY 1990 VL 9 IS 4 BP 368 EP 377 PG 10 WC Biology; Oncology; Immunology; Medicine, Research & Experimental SC Life Sciences & Biomedicine - Other Topics; Oncology; Immunology; Research & Experimental Medicine GA DT074 UT WOS:A1990DT07400004 PM 2395002 ER PT J AU COLDIRON, BM WILEY, EL RINALDI, MG AF COLDIRON, BM WILEY, EL RINALDI, MG TI CUTANEOUS PHEOHYPHOMYCOSIS CAUSED BY A RARE FUNGAL PATHOGEN, HORMONEMA-DEMATIOIDES - SUCCESSFUL TREATMENT WITH KETOCONAZOLE SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article C1 UNIV TEXAS,SW MED CTR,DALLAS,TX 75230. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP COLDIRON, BM (reprint author), UNIV CINCINNATI,DEPT DERMATOL,234 GOODMAN ST,MAIL LOCAT 523,CINCINNATI,OH 45267, USA. NR 20 TC 13 Z9 13 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD AUG PY 1990 VL 23 IS 2 SU S BP 363 EP 367 DI 10.1016/0190-9622(90)70223-5 PN 2 PG 5 WC Dermatology SC Dermatology GA DU036 UT WOS:A1990DU03600009 PM 2394856 ER PT J AU GERETY, MB CHIODO, LK KANTEN, DN TULEY, MR AF GERETY, MB CHIODO, LK KANTEN, DN TULEY, MR TI IMPROVED SCORES WITH MODIFICATION OF THE FOLSTEIN MINI-MENTAL-STATE-EXAM (MMSE) FOR LONG-TERM CARE - A PILOT-STUDY SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 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 AUG PY 1990 VL 38 IS 8 BP A26 EP A26 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA DW501 UT WOS:A1990DW50100124 ER PT J AU LICHTENSTEIN, MJ DESJARDIN, J ROBERTSON, D TULEY, MR AF LICHTENSTEIN, MJ DESJARDIN, J ROBERTSON, D TULEY, MR TI CLINICAL FACTORS ASSOCIATED WITH POSTURAL BLOOD-PRESSURE (BP) CHANGES IN AGED OUT-PATIENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY 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 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 AUG PY 1990 VL 38 IS 8 BP A26 EP A26 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA DW501 UT WOS:A1990DW50100125 ER PT J AU MILLER, D CASTLE, S NORMAN, D YEH, M AF MILLER, D CASTLE, S NORMAN, D YEH, M TI FEVER RESPONSE IN ELDERLY NURSING-HOME RESIDENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD AUG PY 1990 VL 38 IS 8 BP A31 EP A31 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA DW501 UT WOS:A1990DW50100146 ER PT J AU NGUYEN, L CHANG, MP SMITH, K NORMAN, DC AF NGUYEN, L CHANG, MP SMITH, K NORMAN, DC TI ETHANOL SUPPRESSION OF T-CELL PROLIFERATION IN AGING HUMANS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD AUG PY 1990 VL 38 IS 8 BP A23 EP A23 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA DW501 UT WOS:A1990DW50100111 ER PT J AU TOY, EC RINALDI, MG SAVITCH, CB LEIBOVITCH, ER AF TOY, EC RINALDI, MG SAVITCH, CB LEIBOVITCH, ER TI ENDOCARDITIS AND HIP ARTHRITIS ASSOCIATED WITH SCEDOSPORIUM-INFLATUM SO SOUTHERN MEDICAL JOURNAL LA English DT Article C1 VENTURA CTY MED CTR,OFF MED EDUC,VENTURA,CA. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN MICROBIOL LABS,SAN ANTONIO,TX 78284. NR 17 TC 32 Z9 32 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 AUG PY 1990 VL 83 IS 8 BP 957 EP 960 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA DU997 UT WOS:A1990DU99700025 PM 2200140 ER PT J AU SCHILLER, JH BITTNER, G AF SCHILLER, JH BITTNER, G TI ANTIPROLIFERATIVE EFFECTS OF TUMOR-NECROSIS-FACTOR, GAMMA-INTERFERON AND 5-FLUOROURACIL ON HUMAN COLORECTAL-CARCINOMA CELL-LINES SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article C1 UNIV WISCONSIN,CLIN CANC CTR,MADISON,WI 53792. RP SCHILLER, JH (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DIV ONCOL,MADISON,WI 53705, USA. NR 30 TC 23 Z9 23 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JUL 15 PY 1990 VL 46 IS 1 BP 61 EP 66 DI 10.1002/ijc.2910460113 PG 6 WC Oncology SC Oncology GA DN991 UT WOS:A1990DN99100012 PM 2114374 ER PT J AU OBERLEY, TD OBERLEY, LW SLATTERY, AF LAUCHNER, LJ ELWELL, JH AF OBERLEY, TD OBERLEY, LW SLATTERY, AF LAUCHNER, LJ ELWELL, JH TI IMMUNOHISTOCHEMICAL LOCALIZATION OF ANTIOXIDANT ENZYMES IN ADULT SYRIAN-HAMSTER TISSUES AND DURING KIDNEY DEVELOPMENT SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article C1 UNIV WISCONSIN,DEPT PATHOL,MADISON,WI 53706. UNIV IOWA,RADIAT RES LAB,IOWA CITY,IA 52242. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,PATHOL SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA-41267] NR 44 TC 111 Z9 112 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUL PY 1990 VL 137 IS 1 BP 199 EP 214 PG 16 WC Pathology SC Pathology GA DP474 UT WOS:A1990DP47400020 PM 2372042 ER PT J AU FELDMAN, GM STEPHENSON, RL AF FELDMAN, GM STEPHENSON, RL TI H+ AND HCO3(-) FLUX ACROSS APICAL SURFACE OF RAT DISTAL COLON SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article RP FELDMAN, GM (reprint author), UNIV PENN,SCH MED,VET AFFAIRS MED CTR,DEPT MED,RENAL SECT,ROOM A329R,PHILADELPHIA,PA 19104, USA. NR 31 TC 21 Z9 21 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUL PY 1990 VL 259 IS 1 BP C35 EP C40 PN 1 PG 6 WC Physiology SC Physiology GA DQ456 UT WOS:A1990DQ45600006 PM 2164783 ER PT J AU GREENBERG, DA DURNER, M DELGADOESCUETA, AV JANZ, D AF GREENBERG, DA DURNER, M DELGADOESCUETA, AV JANZ, D TI IS JUVENILE MYOCLONIC EPILEPSY AN AUTOSOMAL RECESSIVE DISEASE SO ANNALS OF NEUROLOGY LA English DT Letter C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. FREE UNIV BERLIN,KLINIKUM CHARLOTTENBURG,NEUROL ABT,W-1000 BERLIN 19,GERMANY. RP GREENBERG, DA (reprint author), MT SINAI MED CTR,DEPT PSYCHIAT,NEW YORK,NY 10029, USA. NR 5 TC 14 Z9 14 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JUL PY 1990 VL 28 IS 1 BP 110 EP 110 DI 10.1002/ana.410280125 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA DP459 UT WOS:A1990DP45900023 PM 2115759 ER PT J AU GROVER, FL HAMMERMEISTER, KE BURCHFIEL, C AF GROVER, FL HAMMERMEISTER, KE BURCHFIEL, C TI INITIAL REPORT OF THE VETERANS-ADMINISTRATION PREOPERATIVE RISK ASSESSMENT STUDY FOR CARDIAC-SURGERY SO ANNALS OF THORACIC SURGERY LA English DT Article C1 DENVER VET HOSP,CARDIOL SECT,DENVER,CO. RP GROVER, FL (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CARDIOTHORAC SURG SECT 112A,7400 MERTON MINTER DR,SAN ANTONIO,TX 78284, USA. NR 25 TC 183 Z9 184 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD JUL PY 1990 VL 50 IS 1 BP 12 EP 28 PG 17 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA DQ420 UT WOS:A1990DQ42000005 PM 2196014 ER PT J AU HURT, MA IGRASERFATY, H STEVENS, CS AF HURT, MA IGRASERFATY, H STEVENS, CS TI ECCRINE SYRINGOFIBROADENOMA (MASCARO) - AN ACROSYRINGEAL HAMARTOMA SO ARCHIVES OF DERMATOLOGY LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DERMATOL,SAN ANTONIO,TX 78284. RP HURT, MA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,DIV SURG PATHOL,CUTANEOUS PATHOL SECT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 27 TC 34 Z9 34 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD JUL PY 1990 VL 126 IS 7 BP 945 EP 949 DI 10.1001/archderm.126.7.945 PG 5 WC Dermatology SC Dermatology GA DM468 UT WOS:A1990DM46800014 PM 2163246 ER PT J AU SIEVER, LJ SILVERMAN, JM HORVATH, TB KLAR, H COCCARO, E KEEFE, RSE PINKHAM, L RINALDI, P MOHS, RC DAVIS, KL AF SIEVER, LJ SILVERMAN, JM HORVATH, TB KLAR, H COCCARO, E KEEFE, RSE PINKHAM, L RINALDI, P MOHS, RC DAVIS, KL TI INCREASED MORBID RISK FOR SCHIZOPHRENIA-RELATED DISORDERS IN RELATIVES OF SCHIZOTYPAL PERSONALITY DISORDERED PATIENTS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP SIEVER, LJ (reprint author), BRONX VET ADM MED CTR,PSYCHIAT SERV 116A,BRONX,NY 10458, USA. NR 49 TC 125 Z9 126 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JUL PY 1990 VL 47 IS 7 BP 634 EP 640 PG 7 WC Psychiatry SC Psychiatry GA DM625 UT WOS:A1990DM62500003 PM 2360857 ER PT J AU BENNETT, CL GERTLER, P GUZE, PA GARFINKLE, JB KANOUSE, DE GREENFIELD, S AF BENNETT, CL GERTLER, P GUZE, PA GARFINKLE, JB KANOUSE, DE GREENFIELD, S TI THE RELATION BETWEEN RESOURCE USE AND IN-HOSPITAL MORTALITY FOR PATIENTS WITH ACQUIRED IMMUNODEFICIENCY SYNDROME-RELATED PNEUMOCYSTIS-CARINII PNEUMONIA SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article C1 RAND CORP,DEPT ECON & STAT,SANTA MONICA,CA 90406. RAND CORP,DEPT BEHAV SCI,SANTA MONICA,CA 90406. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. TUFTS UNIV,DEPT MED,BOSTON,MA 02111. NEW ENGLAND MED CTR,BOSTON,MA 02111. W LOS ANGELES VET ADM HOSP,LOS ANGELES,CA. RP BENNETT, CL (reprint author), RAND CORP,DEPT SOCIAL SCI,1700 MAIN ST,SANTA MONICA,CA 90406, USA. RI Bennett, Charles/C-2050-2008 NR 33 TC 33 Z9 33 U1 2 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 JUL PY 1990 VL 150 IS 7 BP 1447 EP 1452 DI 10.1001/archinte.150.7.1447 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA DN656 UT WOS:A1990DN65600015 PM 2369243 ER PT J AU CHENU, C KURIHARA, N MUNDY, GR ROODMAN, GD AF CHENU, C KURIHARA, N MUNDY, GR ROODMAN, GD TI PROSTAGLANDIN-E2 INHIBITS FORMATION OF OSTEOCLAST-LIKE CELLS IN LONG-TERM HUMAN MARROW CULTURES BUT IS NOT A MEDIATOR OF THE INHIBITORY EFFECTS OF TRANSFORMING GROWTH-FACTOR-BETA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article C1 VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. 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NR 19 TC 232 Z9 238 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JUL PY 1990 VL 28 IS 7 BP 1616 EP 1622 PG 7 WC Microbiology SC Microbiology GA DK194 UT WOS:A1990DK19400025 PM 2380383 ER PT J AU SCHENKER, S JOHNSON, RF HOYUMPA, AM HENDERSON, GI AF SCHENKER, S JOHNSON, RF HOYUMPA, AM HENDERSON, GI TI THIAMINE-TRANSFER BY HUMAN PLACENTA - NORMAL TRANSPORT AND EFFECTS OF ETHANOL SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP SCHENKER, S (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL & NUTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07514] NR 32 TC 31 Z9 31 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 JUL PY 1990 VL 116 IS 1 BP 106 EP 115 PG 10 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA DT024 UT WOS:A1990DT02400016 PM 2376692 ER PT J AU CREGLER, LL SOSA, I DUCEY, S ABBEY, L AF CREGLER, LL SOSA, I DUCEY, S ABBEY, L TI MYOPERICARDITIS IN ACQUIRED-IMMUNODEFICIENCY-SYNDROME DIAGNOSED BY GALLIUM SCINTIGRAPHY SO JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION LA English DT Article RP CREGLER, LL (reprint author), CUNY,MT SINAI SCH MED,BRONX VET ADM MED CTR,DEPT MED,DIV GEN INTERNAL MED,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0027-9684 J9 J NATL MED ASSOC JI J. Natl. Med. Assoc. PD JUL PY 1990 VL 82 IS 7 BP 511 EP 513 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA DN149 UT WOS:A1990DN14900004 PM 2398508 ER PT J AU LAU, PP DUBICK, MA YU, GSM MORRILL, PR GEOKAS, MC AF LAU, PP DUBICK, MA YU, GSM MORRILL, PR GEOKAS, MC TI DYNAMIC CHANGES OF PANCREATIC STRUCTURE AND FUNCTION IN RATS TREATED CHRONICALLY WITH NICOTINE SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article C1 US DEPT VET AFFAIRS,MED CTR,DEPT MED,ENZYMOL RES LAB,MARTINEZ,CA 94455. UNIV CALIF DAVIS,DEPT MED,DAVIS,CA 95616. UNIV CALIF DAVIS,DEPT PATHOL,DAVIS,CA 95616. NR 33 TC 21 Z9 21 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD JUL PY 1990 VL 104 IS 3 BP 457 EP 465 DI 10.1016/0041-008X(90)90167-S PG 9 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA EC993 UT WOS:A1990EC99300009 PM 1696755 ER PT J AU SUCKOW, RF COOPER, TB KAHN, RS AF SUCKOW, RF COOPER, TB KAHN, RS TI HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHIC METHOD FOR THE ANALYSIS OF PLASMA META-CHLOROPHENYLPIPERAZINE SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Note C1 NEW YORK STATE PSYCHIAT INST & HOSP,ANALYT PSYCHOPHARMACOL LAB,NEW YORK,NY 10032. NATHAN S KLINE INST PSYCHIAT RES,ANALYT PSYCHOPHARMACOL LAB,NEW YORK,NY 10032. BRONX VET ADM MED CTR,DEPT PSYCHIAT,BRONX,NY 10468. FU PHS HHS [30906] NR 14 TC 36 Z9 36 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD JUN 8 PY 1990 VL 528 IS 1 BP 228 EP 234 DI 10.1016/S0378-4347(00)82380-4 PG 7 WC Chemistry, Analytical SC Chemistry GA DK673 UT WOS:A1990DK67300025 PM 2384557 ER PT J AU RAEHL, CL BOND, CA PITTERLE, ME AF RAEHL, CL BOND, CA PITTERLE, ME TI HOSPITAL PHARMACY SERVICES IN THE GREAT-LAKES REGION SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,ARRHYTHMIA CLIN,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. RP RAEHL, CL (reprint author), UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706, USA. NR 21 TC 25 Z9 25 U1 0 U2 2 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD JUN PY 1990 VL 47 IS 6 BP 1283 EP 1303 PG 21 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA DF883 UT WOS:A1990DF88300019 PM 2368722 ER PT J AU PITTERLE, ME BOND, CA RAEHL, CL AF PITTERLE, ME BOND, CA RAEHL, CL TI A COMPREHENSIVE MEASURE OF PHARMACEUTICAL SERVICES - THE PHARMACEUTICAL-CARE INDEX SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article C1 UNIV WISCONSIN,SCH MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,ARRHYTHMIA CLIN,MADISON,WI 53705. RP PITTERLE, ME (reprint author), UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706, USA. NR 24 TC 10 Z9 10 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD JUN PY 1990 VL 47 IS 6 BP 1304 EP 1313 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA DF883 UT WOS:A1990DF88300020 PM 2368723 ER PT J AU WEBER, CA DUNCAN, CA LYONS, MJ JENKINSON, SG AF WEBER, CA DUNCAN, CA LYONS, MJ JENKINSON, SG TI DEPLETION OF TISSUE GLUTATHIONE WITH DIETHYL MALEATE ENHANCES HYPERBARIC-OXYGEN TOXICITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR, PULM DIS SECT 111E, 7400 MERTON MINTER BLVD, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, WILFORD HALL MED CTR, LUNG METAB UNIT, SAN ANTONIO, TX 78284 USA. FU NHLBI NIH HHS [HL-30556] NR 20 TC 36 Z9 36 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JUN PY 1990 VL 258 IS 6 BP L308 EP L312 PN 1 PG 5 WC Physiology SC Physiology GA DL731 UT WOS:A1990DL73100082 PM 2360643 ER PT J AU DEFAVERI, J GRAYBILL, JR AF DEFAVERI, J GRAYBILL, JR TI TREATMENT OF CHRONIC MURINE CHROMOBLASTOMYCOSIS WITH THE TRIAZOLE-SCH39304 SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article RP DEFAVERI, J (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,MERTON MINTER,SAN ANTONIO,TX 78284, USA. NR 14 TC 5 Z9 5 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 JUN PY 1990 VL 42 IS 6 BP 601 EP 606 PG 6 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA DP737 UT WOS:A1990DP73700015 PM 2164791 ER PT J AU LIEBERMAN, D AF LIEBERMAN, D TI HEMOCCULT SCREENING AND COLORECTAL NEOPLASMS SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP LIEBERMAN, D (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97207, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JUN 1 PY 1990 VL 112 IS 11 BP 880 EP 880 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA DE903 UT WOS:A1990DE90300015 ER PT J AU WALSH, TJ LESTERMCCULLY, C RINALDI, MG WALLACE, JE BALIS, FM LEE, JW PIZZO, PA POPLACK, DG AF WALSH, TJ LESTERMCCULLY, C RINALDI, MG WALLACE, JE BALIS, FM LEE, JW PIZZO, PA POPLACK, DG TI PENETRATION OF SCH-39304, A NEW ANTIFUNGAL TRIAZOLE, INTO CEREBROSPINAL-FLUID OF PRIMATES SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note C1 NCI,LEUKEMIA BIOL SECT,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. AUDIE L MURPHY MEM VET ADM MED CTR,VET AFFAIRS MYCOL REFERENCE LAB,SAN ANTONIO,TX 78284. RP WALSH, TJ (reprint author), NCI,INFECT DIS SECT,BETHESDA,MD 20892, USA. NR 25 TC 8 Z9 8 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 JUN PY 1990 VL 34 IS 6 BP 1281 EP 1284 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA DH156 UT WOS:A1990DH15600070 PM 2393291 ER PT J AU TALAL, N DAUPHINEE, MJ DANG, H ALEXANDER, SS HART, DJ GARRY, RF AF TALAL, N DAUPHINEE, MJ DANG, H ALEXANDER, SS HART, DJ GARRY, RF TI DETECTION OF SERUM ANTIBODIES TO RETROVIRAL PROTEINS IN PATIENTS WITH PRIMARY SJOGRENS-SYNDROME (AUTOIMMUNE EXOCRINOPATHY) SO ARTHRITIS AND RHEUMATISM LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. TULANE UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,NEW ORLEANS,LA 70112. BIOTECH RES LABS INC,ROCKVILLE,MD. RP TALAL, N (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-28048, AI-22720] NR 33 TC 202 Z9 205 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 JUN PY 1990 VL 33 IS 6 BP 774 EP 781 DI 10.1002/art.1780330603 PG 8 WC Rheumatology SC Rheumatology GA DK308 UT WOS:A1990DK30800003 PM 2363733 ER PT J AU BUSH, RK ZORATTI, E TAYLOR, SL AF BUSH, RK ZORATTI, E TAYLOR, SL TI DIAGNOSIS OF SULFITE AND ASPIRIN SENSITIVITY SO CLINICAL REVIEWS IN ALLERGY LA English DT Review C1 UNIV NEBRASKA,DEPT FOOD SCI & TECHNOL,LINCOLN,NE 68583. UNIV NEBRASKA,CTR FOOD PROC,LINCOLN,NE 68583. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP BUSH, RK (reprint author), UNIV WISCONSIN,DEPT MED,ALLERGY & IMMUNOL SECT,MADISON,WI 53792, USA. NR 46 TC 16 Z9 16 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0731-8235 J9 CLIN REV ALLERG JI Clin. Rev. Allergy PD SUM-FAL PY 1990 VL 8 IS 2-3 BP 159 EP 178 PG 20 WC Allergy SC Allergy GA EN216 UT WOS:A1990EN21600004 PM 2292093 ER PT J AU CLIBON, U BONEWALD, L CARO, J ROODMAN, GD AF CLIBON, U BONEWALD, L CARO, J ROODMAN, GD TI ERYTHROPOIETIN FAILS TO REVERSE THE ANEMIA IN MICE CONTINUOUSLY EXPOSED TO TUMOR NECROSIS FACTOR-ALPHA INVIVO SO EXPERIMENTAL HEMATOLOGY LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. FU NCI NIH HHS [CA-40035] NR 9 TC 33 Z9 34 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JUN PY 1990 VL 18 IS 5 BP 438 EP 441 PG 4 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA DE381 UT WOS:A1990DE38100013 PM 2338132 ER PT J AU WILLIAMS, DM MAGEE, DM BONEWALD, LF SMITH, JG BLEICKER, CA BYRNE, GI SCHACHTER, J AF WILLIAMS, DM MAGEE, DM BONEWALD, LF SMITH, JG BLEICKER, CA BYRNE, GI SCHACHTER, J TI A ROLE INVIVO FOR TUMOR NECROSIS FACTOR-ALPHA IN HOST DEFENSE AGAINST CHLAMYDIA-TRACHOMATIS SO INFECTION AND IMMUNITY LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV WISCONSIN,SCH MED,DEPT MED MICROBIOL,MADISON,WI 53706. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. RP WILLIAMS, DM (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,INFECT DIS SECT,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [AI-19782, AI-21912]; PHS HHS [AL-22380] NR 30 TC 102 Z9 103 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 JUN PY 1990 VL 58 IS 6 BP 1572 EP 1576 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA DF208 UT WOS:A1990DF20800014 PM 2341167 ER PT J AU EBERT, SC CRAIG, WA AF EBERT, SC CRAIG, WA TI PHARMACODYNAMIC PROPERTIES OF ANTIBIOTICS - APPLICATION TO DRUG-MONITORING AND DOSAGE REGIMEN DESIGN SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,MADISON,WI 53706. NR 71 TC 75 Z9 75 U1 3 U2 3 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD JUN PY 1990 VL 11 IS 6 BP 319 EP 326 PG 8 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA DJ763 UT WOS:A1990DJ76300010 PM 2165081 ER PT J AU HERIAN, AM TAYLOR, SL BUSH, RK AF HERIAN, AM TAYLOR, SL BUSH, RK TI IDENTIFICATION OF SOYBEAN ALLERGENS BY IMMUNOBLOTTING WITH SERA FROM SOY-ALLERGIC ADULTS SO INTERNATIONAL ARCHIVES OF ALLERGY AND APPLIED IMMUNOLOGY LA English DT Article C1 UNIV WISCONSIN,INST FOOD RES,DEPT FOOD MICROBIOL & TOXICOL,MADISON,WI 53706. UNIV NEBRASKA,CTR FOOD PROC,LINCOLN,NE 68583. UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,MADISON,WI 53706. UNIV WISCONSIN,CTR CLIN SCI,DEPT MED,MADISON,WI 53706. UNIV NEBRASKA,DEPT FOOD SCI & TECHNOL,LINCOLN,NE 68583. NR 19 TC 96 Z9 102 U1 1 U2 13 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0020-5915 J9 INT ARCH ALLER A IMM PD JUN PY 1990 VL 92 IS 2 BP 193 EP 198 PG 6 WC Allergy; Immunology SC Allergy; Immunology GA EM211 UT WOS:A1990EM21100015 PM 2242931 ER PT J AU TALAL, N GARRY, RF SCHUR, PH ALEXANDER, S DAUPHINEE, MJ LIVAS, IH BALLESTER, A TAKEI, M DANG, H AF TALAL, N GARRY, RF SCHUR, PH ALEXANDER, S DAUPHINEE, MJ LIVAS, IH BALLESTER, A TAKEI, M DANG, H TI A CONSERVED IDIOTYPE AND ANTIBODIES TO RETROVIRAL PROTEINS IN SYSTEMIC LUPUS-ERYTHEMATOSUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. BIOTECH RES LABS INC,ROCKVILLE,MD 20850. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. TULANE UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,NEW ORLEANS,LA 70112. FU NIAID NIH HHS [AI-22720, AI-28048] NR 17 TC 148 Z9 150 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1990 VL 85 IS 6 BP 1866 EP 1871 DI 10.1172/JCI114647 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA DH374 UT WOS:A1990DH37400023 PM 2112156 ER PT J AU KURIHARA, N BERTOLINI, D SUDA, T AKIYAMA, Y ROODMAN, GD AF KURIHARA, N BERTOLINI, D SUDA, T AKIYAMA, Y ROODMAN, GD TI IL-6 STIMULATES OSTEOCLAST-LIKE MULTINUCLEATED CELL-FORMATION IN LONG-TERM HUMAN MARROW CULTURES BY INDUCING IL-1 RELEASE SO JOURNAL OF IMMUNOLOGY LA English DT Article C1 AJINOMOTO INC,TOKYO,JAPAN. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. JICHI MED SCH,DIV HEMATOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. OTSUKA AMER PHARMACEUT,ROCKVILLE,MD 20850. RP ROODMAN, GD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. RI Suda, Toshio/H-6761-2013 OI Suda, Toshio/0000-0001-7540-1771 FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM35188] NR 28 TC 332 Z9 346 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 1 PY 1990 VL 144 IS 11 BP 4226 EP 4230 PG 5 WC Immunology SC Immunology GA DF844 UT WOS:A1990DF84400021 PM 2341718 ER PT J AU STRACK, S LORR, M AF STRACK, S LORR, M TI 3 APPROACHES TO INTERPERSONAL-BEHAVIOR AND THEIR COMMON FACTORS SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article C1 CATHOLIC UNIV AMER,INST LIFE CYCLE,WASHINGTON,DC 20064. RP STRACK, S (reprint author), US DEPT VET AFFAIRS,OUTPATIENT CLIN,425 S HILL ST,LOS ANGELES,CA 90013, USA. NR 39 TC 5 Z9 5 U1 1 U2 1 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0022-3891 J9 J PERS ASSESS JI J. Pers. Assess. PD SUM PY 1990 VL 54 IS 3-4 BP 782 EP 790 DI 10.1207/s15327752jpa5403&4_30 PG 9 WC Psychology, Clinical; Psychology, Social SC Psychology GA DG104 UT WOS:A1990DG10400030 ER PT J AU SHAY, K BERKEY, DB SAXE, SR AF SHAY, K BERKEY, DB SAXE, SR TI NEW PROGRAMS FOR ADVANCED TRAINING IN DENTAL GERIATRICS SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Editorial Material C1 UNIV KENTUCKY,MED CTR,GERIATR DENT FELLOWSHIP PROGRAM,LEXINGTON,KY 40506. UNIV COLORADO,MED SCH FELLOWSHIP GERIATR,BOULDER,CO 80309. UNIV COLORADO,SCH DENT,BOULDER,CO 80309. UNIV KENTUCKY,COLL DENT,LEXINGTON,KY 40506. MED COLL WISCONSIN,CLIN DENT,MILWAUKEE,WI 53226. US DEPT VET AFFAIRS,DENT GERIATR FELLOWSHIP PROGRAM,MILWAUKEE,WI. RP SHAY, K (reprint author), ZABLOCKI DEPT VET AFFAIRS,MED CTR,DENTAL GERIATR SECT 160,MILWAUKEE,WI 53295, USA. FU BHP HRSA HHS [1D31 PE95008, 5D31 PE94006, 5D31 PE98000] NR 8 TC 4 Z9 4 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD JUN PY 1990 VL 120 IS 6 BP 661 EP 663 PG 3 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA DJ196 UT WOS:A1990DJ19600008 PM 2191024 ER PT J AU MINDEL, JS RUBIN, MA KHARLAMB, AB AF MINDEL, JS RUBIN, MA KHARLAMB, AB TI THE PUPIL RESPONSE TO E-10-HYDROXYNORTRIPTYLINE IN RABBITS WITH OCULAR SYMPATHETIC PARESIS SO JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM LA English DT Note C1 CUNY MT SINAI SCH MED,DEPT PHARMACOL,NEW YORK,NY 10029. BRONX VET ADM MED CTR,BRONX,NY. RP MINDEL, JS (reprint author), CUNY MT SINAI SCH MED,DEPT OPHTHALMOL,ANNENBERG BLDG 22-14,NEW YORK,NY 10029, USA. OI Rubin, Mark/0000-0002-8321-9950 FU NEI NIH HHS [EY-0167] NR 7 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-1838 J9 J AUTONOM NERV SYST JI J. Auton. Nerv. Syst. PD JUN PY 1990 VL 30 IS 2 BP 175 EP 177 DI 10.1016/0165-1838(90)90142-6 PG 3 WC Neurosciences SC Neurosciences & Neurology GA DL991 UT WOS:A1990DL99100011 PM 2370421 ER PT J AU HURLEY, RW SUBRAMANIAN, R RAHKO, PS SHELP, WD AF HURLEY, RW SUBRAMANIAN, R RAHKO, PS SHELP, WD TI ISOLATED RIGHT ATRIAL INFARCTION WITH RUPTURE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 MERITER METHODIST HOSP,MADISON,WI 53703. RP HURLEY, RW (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53706, USA. NR 6 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 MAY 31 PY 1990 VL 322 IS 22 BP 1611 EP 1611 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA DF140 UT WOS:A1990DF14000028 PM 2336096 ER PT J AU DENINO, LA MULROW, CD AF DENINO, LA MULROW, CD TI SCREENING FOR HYPERTENSION SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP DENINO, LA (reprint author), UNIV TEXAS,AUDIE L MURPHY MEM VET ADM HOSP,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 4 TC 0 Z9 0 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 MAY 15 PY 1990 VL 112 IS 10 BP 796 EP 797 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA DD179 UT WOS:A1990DD17900017 PM 2109962 ER PT J AU KILCOYNE, RF SHUMAN, WP MATSEN, FA MORRIS, M ROCKWOOD, CA AF KILCOYNE, RF SHUMAN, WP MATSEN, FA MORRIS, M ROCKWOOD, CA TI THE NEER CLASSIFICATION OF DISPLACED PROXIMAL HUMERAL FRACTURES - SPECTRUM OF FINDINGS ON PLAIN RADIOGRAPHS AND CT SCANS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV WASHINGTON,DEPT RADIOL,SEATTLE,WA 98115. UNIV WASHINGTON,DEPT ORTHOPAED SURG,SEATTLE,WA 98115. MASON CLIN,DEPT ORTHOPAED SURG,SEATTLE,WA 98104. UNIV TEXAS,HLTH SCI CTR,DEPT ORTHOPAED SURG,SAN ANTONIO,TX 78284. RP KILCOYNE, RF (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT RADIOL,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 4 TC 20 Z9 20 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 1990 VL 154 IS 5 BP 1029 EP 1033 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA CY905 UT WOS:A1990CY90500018 PM 2108538 ER PT J AU YEAGER, RA MONETA, GL TAYLOR, LM HARRIS, EJ MCCONNELL, DB PORTER, JM AF YEAGER, RA MONETA, GL TAYLOR, LM HARRIS, EJ MCCONNELL, DB PORTER, JM TI IMPROVING SURVIVAL AND LIMB SALVAGE IN PATIENTS WITH AORTIC GRAFT INFECTION SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 76TH ANNUAL MEETING OF THE NORTH PACIFIC SURGICAL ASSOC CY NOV 10-11, 1989 CL VICTORIA, CANADA SP N PACIFIC SURG ASSOC C1 OREGON HLTH SCI UNIV,DEPT SURG,DIV VASC SURG,PORTLAND,OR 97201. RP YEAGER, RA (reprint author), PORTLAND VET AFFAIRS MED CTR,SURG SERV 112P,POB 1034,PORTLAND,OR 97207, USA. NR 21 TC 68 Z9 69 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD MAY PY 1990 VL 159 IS 5 BP 466 EP 469 DI 10.1016/S0002-9610(05)81247-4 PG 4 WC Surgery SC Surgery GA DC976 UT WOS:A1990DC97600006 PM 2334008 ER PT J AU WANG, RY ALTERMAN, AI SEARLES, JS MCLELLAN, T AF WANG, RY ALTERMAN, AI SEARLES, JS MCLELLAN, T TI ALCOHOL-ABUSE IN PATIENTS WITH DILATED CARDIOMYOPATHY - LABORATORY VS CLINICAL DETECTION SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article C1 VET AFFAIRS MED CTR,116,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FU NIDA NIH HHS [DA05186] NR 20 TC 7 Z9 7 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD MAY PY 1990 VL 150 IS 5 BP 1079 EP 1082 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA DC720 UT WOS:A1990DC72000023 PM 1970474 ER PT J AU HO, SP KRAMER, KE ERSHLER, WB AF HO, SP KRAMER, KE ERSHLER, WB TI EFFECT OF HOST AGE UPON INTERLEUKIN-2-MEDIATED ANTITUMOR RESPONSES IN A MURINE FIBROSARCOMA MODEL SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Article C1 UNIV WISCONSIN,DEPT HUMAN ONCOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. NR 25 TC 13 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD MAY PY 1990 VL 31 IS 3 BP 146 EP 150 DI 10.1007/BF01744728 PG 5 WC Oncology; Immunology SC Oncology; Immunology GA DB925 UT WOS:A1990DB92500003 PM 2337904 ER PT J AU REMICK, SC GREM, JL FISCHER, PH TUTSCH, KD ALBERTI, DB NIETING, LM TOMBES, MB BRUGGINK, J WILLSON, JKV TRUMP, DL AF REMICK, SC GREM, JL FISCHER, PH TUTSCH, KD ALBERTI, DB NIETING, LM TOMBES, MB BRUGGINK, J WILLSON, JKV TRUMP, DL TI PHASE-I TRIAL OF 5-FLUOROURACIL AND DIPYRIDAMOLE ADMINISTERED BY 72-HOUR CONCURRENT CONTINUOUS INFUSION SO CANCER RESEARCH LA English DT Article C1 UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53792. UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,MADISON,WI 53792. FU NCI NIH HHS [N01-CM-57735] NR 47 TC 49 Z9 49 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAY 1 PY 1990 VL 50 IS 9 BP 2667 EP 2672 PG 6 WC Oncology SC Oncology GA DA592 UT WOS:A1990DA59200022 PM 2328492 ER PT J AU KURIHARA, N CHENU, C MILLER, M CIVIN, C ROODMAN, GD AF KURIHARA, N CHENU, C MILLER, M CIVIN, C ROODMAN, GD TI IDENTIFICATION OF COMMITTED MONONUCLEAR PRECURSORS FOR OSTEOCLAST-LIKE CELLS FORMED IN LONG-TERM HUMAN MARROW CULTURES SO ENDOCRINOLOGY LA English DT Article C1 VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. JOHNS HOPKINS UNIV,CTR ONCOL,BALTIMORE,MD 21209. FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM-35188] NR 29 TC 186 Z9 187 U1 0 U2 2 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAY PY 1990 VL 126 IS 5 BP 2733 EP 2741 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA DB394 UT WOS:A1990DB39400068 PM 2184023 ER PT J AU HARMS, BA ROSENFELD, DJ PAHL, AC CONHAIM, RL STARLING, JR AF HARMS, BA ROSENFELD, DJ PAHL, AC CONHAIM, RL STARLING, JR TI PULMONARY TRANSVASCULAR FLUID FILTRATION RESPONSE TO HYPOPROTEINEMIA AND HESPAN INFUSION SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 1989 ANNUAL MEETING OF THE ASSOC FOR ACADEMIC SURGERY CY NOV 15-18, 1989 CL LOUISVILLE, KY SP ASSOC ACAD SURG C1 UNIV WISCONSIN,DEPT PREVENT MED,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP HARMS, BA (reprint author), UNIV WISCONSIN,DEPT SURG,MADISON,WI 53792, USA. NR 19 TC 9 Z9 9 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 0022-4804 J9 J SURG RES JI J. Surg. Res. PD MAY PY 1990 VL 48 IS 5 BP 408 EP 414 DI 10.1016/0022-4804(90)90004-L PG 7 WC Surgery SC Surgery GA DG557 UT WOS:A1990DG55700004 PM 1693707 ER PT J AU DUMITRU, D KALANTRI, A AF DUMITRU, D KALANTRI, A TI ELECTROPHYSIOLOGIC INVESTIGATION OF THALLIUM POISONING SO MUSCLE & NERVE LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DUMITRU, D (reprint author), UNIV TEXAS,HLTH SCI CTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 15 TC 17 Z9 18 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD MAY PY 1990 VL 13 IS 5 BP 433 EP 437 DI 10.1002/mus.880130510 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA DC310 UT WOS:A1990DC31000009 PM 2161080 ER PT J AU HART, RG FOSTER, JW LUTHER, MF KANTER, MC AF HART, RG FOSTER, JW LUTHER, MF KANTER, MC TI STROKE IN INFECTIVE ENDOCARDITIS SO STROKE LA English DT Article C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP HART, RG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED NEUROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 39 TC 158 Z9 159 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD MAY PY 1990 VL 21 IS 5 BP 695 EP 700 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA DD829 UT WOS:A1990DD82900001 PM 2187287 ER PT J AU WITTE, JT HASSON, JE HARMS, BA CORRIGAN, TE LOVE, RB AF WITTE, JT HASSON, JE HARMS, BA CORRIGAN, TE LOVE, RB TI FATAL GASTRIC ARTERY DISSECTION AND RUPTURE OCCURRING AS A PARAESOPHAGEAL MASS - A CASE-REPORT AND LITERATURE-REVIEW SO SURGERY LA English DT Review C1 UNIV WISCONSIN HOSP & CLIN,DEPT SURG,H4-328 CSC,600 HIGHLAND AVE,MADISON,WI 53792. UNIV WISCONSIN HOSP & CLIN,DEPT GASTROENTEROL,MADISON,WI 53792. UNIV WISCONSIN HOSP & CLIN,DEPT PATHOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,SURG SERV,MADISON,WI 53705. FU Wellcome Trust [089701] NR 23 TC 11 Z9 12 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD MAY PY 1990 VL 107 IS 5 BP 590 EP 594 PG 5 WC Surgery SC Surgery GA DC243 UT WOS:A1990DC24300019 PM 2185570 ER PT J AU KARGAS, G RUDY, T SPENNETTA, T TAKAYAMA, K QUERISHI, N SHRAGO, E AF KARGAS, G RUDY, T SPENNETTA, T TAKAYAMA, K QUERISHI, N SHRAGO, E TI SEPARATION AND QUANTITATION OF LONG-CHAIN FREE FATTY-ACIDS IN HUMAN SERUM BY HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Article C1 UNIV WISCONSIN,DEPT MED,1415 LINDEN DR,MADISON,WI 53706. UNIV WISCONSIN,DEPT NUCL SCI,MADISON,WI 53706. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. UNIV WISCONSIN,DEPT BACTERIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NIDDK NIH HHS [5P30-DK-26659]; NIGMS NIH HHS [GM 14033] NR 22 TC 29 Z9 30 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD APR 6 PY 1990 VL 526 IS 2 BP 331 EP 340 DI 10.1016/S0378-4347(00)82517-7 PG 10 WC Chemistry, Analytical SC Chemistry GA DA202 UT WOS:A1990DA20200003 PM 2361977 ER PT J AU MILLER, WE RICHARDS, KL CRAWFORD, MH AF MILLER, WE RICHARDS, KL CRAWFORD, MH TI ACCURACY OF MITRAL DOPPLER ECHOCARDIOGRAPHIC CARDIAC-OUTPUT DETERMINATIONS IN ADULTS SO AMERICAN HEART JOURNAL LA English DT Article C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 12 TC 9 Z9 9 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD APR PY 1990 VL 119 IS 4 BP 905 EP 910 DI 10.1016/S0002-8703(05)80330-8 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA CX205 UT WOS:A1990CX20500020 PM 2321509 ER PT J AU FEIFEL, H AF FEIFEL, H TI PSYCHOLOGY AND DEATH - MEANINGFUL REDISCOVERY SO AMERICAN PSYCHOLOGIST LA English DT Article; Proceedings Paper CT 1989 MEETING OF THE AMERICAN PSYCHOLOGICAL ASSOC CY AUG, 1989 CL NEW ORLEANS, LA SP AMER PSYCHOL ASSOC RP FEIFEL, H (reprint author), US DEPT VET AFFAIRS,OUTPATIENT CLIN,PSYCHOL SERV 116B,425 S HILL ST,LOS ANGELES,CA 90013, USA. NR 41 TC 61 Z9 62 U1 0 U2 5 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0003-066X J9 AM PSYCHOL JI Am. Psychol. PD APR PY 1990 VL 45 IS 4 BP 537 EP 543 DI 10.1037/0003-066X.45.4.537 PG 7 WC Psychology, Multidisciplinary SC Psychology GA CY599 UT WOS:A1990CY59900007 PM 2186680 ER PT J AU DEFAVERI, J SUN, SH GRAYBILL, JR AF DEFAVERI, J SUN, SH GRAYBILL, JR TI TREATMENT OF MURINE COCCIDIOIDAL MENINGITIS WITH SCH39304 SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note RP DEFAVERI, J (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 13 TC 12 Z9 12 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 APR PY 1990 VL 34 IS 4 BP 663 EP 664 PG 2 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA CY163 UT WOS:A1990CY16300032 PM 2160794 ER PT J AU LEVINE, BA CURTSINGER, LJ SIRINEK, KR AF LEVINE, BA CURTSINGER, LJ SIRINEK, KR TI VAGOTOMY EFFECT ON GASTRIC PROSTAGLANDINS - PRIMARILY NEURAL OR SECONDARY TO HYPOACIDITY SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 13TH ANNUAL MEETING OF THE ASSOC OF VETERANS ADMINISTRATION SURGEONS CY MAY 04, 1989 CL SAN ANTONIO, TX SP ASSOC VET ADM SURGEONS C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP LEVINE, BA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT SURG,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 14 TC 2 Z9 2 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD APR PY 1990 VL 125 IS 4 BP 457 EP 459 PG 3 WC Surgery SC Surgery GA CX521 UT WOS:A1990CX52100008 PM 2108654 ER PT J AU TAKAHASHI, LK KALIN, NH BAKER, EW AF TAKAHASHI, LK KALIN, NH BAKER, EW TI CORTICOTROPIN-RELEASING FACTOR ANTAGONIST ATTENUATES DEFENSIVE-WITHDRAWAL BEHAVIOR ELICITED BY ODORS OF STRESSED CONSPECIFICS SO BEHAVIORAL NEUROSCIENCE LA English DT Note C1 UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,MADISON,WI 53706. RP TAKAHASHI, LK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PSYCHIAT SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NHLBI NIH HHS [HL-35143]; NIMH NIH HHS [MH-40855] NR 11 TC 30 Z9 30 U1 0 U2 0 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 APR PY 1990 VL 104 IS 2 BP 386 EP 389 DI 10.1037/0735-7044.104.2.386 PG 4 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA DC200 UT WOS:A1990DC20000015 PM 2346630 ER PT J AU CHOI, JI KORNMAN, KS FRIEDMAN, DJ AF CHOI, JI KORNMAN, KS FRIEDMAN, DJ TI A POSSIBLE MOLECULAR MECHANISM OF CANDIDAL ADHERENCE TO MADNI-DARBY CANINE KIDNEY (MDCK) EPITHELIAL-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV HEMATOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PERIODONT,SAN ANTONIO,TX 78284. NR 0 TC 4 Z9 4 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 1990 VL 38 IS 2 BP A554 EP A554 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA CZ244 UT WOS:A1990CZ24401874 ER PT J AU FRIEDMAN, DJ TAMI, JA TEGELER, DR BOLDT, DH AF FRIEDMAN, DJ TAMI, JA TEGELER, DR BOLDT, DH TI IDENTIFICATION OF CELLULAR ADHESION BY LAK CELLS TO TUMOR-CELL GLYCOPROTEINS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV HEMATOL,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 1990 VL 38 IS 2 BP A547 EP A547 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA CZ244 UT WOS:A1990CZ24401830 ER PT J AU HERBERT, V SHAW, S JAYATILLEKE, E LAM, P GULLE, V AF HERBERT, V SHAW, S JAYATILLEKE, E LAM, P GULLE, V TI EVIDENCE IN SERUM FOR FOOD VITAMIN-B12 (COBALAMIN) MALABSORPTION IN AIDS - HIGH GASTRIN, LOW COBALAMIN ON TRANSCOBALAMIN-II, AND CIRCULATING ANTIBODY TO INTRINSIC-FACTOR DESPITE NORMAL SERUM TOTAL COBALAMIN LEVELS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,BRONX,NY. NR 1 TC 5 Z9 5 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 1990 VL 38 IS 2 BP A361 EP A361 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA CZ244 UT WOS:A1990CZ24400771 ER PT J AU KURIHARA, N GLUCK, S ROODMAN, GD AF KURIHARA, N GLUCK, S ROODMAN, GD TI EXPRESSION OF THE OSTEOCLASTIC VACUOLAR PROTON PUMP DURING OSTEOCLAST (OCL) DEVELOPMENT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,SAN ANTONIO,TX. WASHINGTON UNIV,ST LOUIS,MO 63130. 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 APR PY 1990 VL 38 IS 2 BP A462 EP A462 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA CZ244 UT WOS:A1990CZ24401346 ER PT J AU MCBRIDE, WS AGUILAR, C MULROW, CD TULEY, MR AF MCBRIDE, WS AGUILAR, C MULROW, CD TULEY, MR TI SCREENING-TESTS FOR HEARING-LOSS IN THE ELDERLY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 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 1990 VL 38 IS 2 BP A707 EP A707 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA CZ244 UT WOS:A1990CZ24402777 ER PT J AU SCHENKER, S JOHNSON, RF HOYUMPA, AM HENDERSON, GH AF SCHENKER, S JOHNSON, RF HOYUMPA, AM HENDERSON, GH TI THIAMINE TRANSFER BY HUMAN PLACENTA - NORMAL TRANSPORT AND EFFECTS OF ETHANOL 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 1990 VL 38 IS 2 BP A294 EP A294 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA CZ244 UT WOS:A1990CZ24400388 ER PT J AU CARNES, M LENT, SJ GOODMAN, B MUELLER, C SAYDOFF, J ERISMAN, S AF CARNES, M LENT, SJ GOODMAN, B MUELLER, C SAYDOFF, J ERISMAN, S TI EFFECTS OF IMMUNONEUTRALIZATION OF CORTICOTROPIN-RELEASING HORMONE ON ULTRADIAN RHYTHMS OF PLASMA ADRENOCORTICOTROPIN SO ENDOCRINOLOGY LA English DT Article C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,DEPT COMPARAT BIOSCI,MADISON,WI 53705. UNIV WISCONSIN,CTR SPACE SCI & ENGN,MADISON,WI 53705. RP CARNES, M (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIATR SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NIDDK NIH HHS [DK-40759]; NIGMS NIH HHS [R01 GM088477] NR 43 TC 51 Z9 51 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 APR PY 1990 VL 126 IS 4 BP 1904 EP 1913 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA CW900 UT WOS:A1990CW90000018 PM 2156671 ER PT J AU HURLEY, J LINZ, D SWINT, E AF HURLEY, J LINZ, D SWINT, E TI ASSESSING THE EFFECTS OF THE MEDICARE PROSPECTIVE PAYMENT SYSTEM ON THE DEMAND FOR VA INPATIENT SERVICES - AN EXAMINATION OF TRANSFERS AND DISCHARGES OF PROBLEM PATIENTS SO HEALTH SERVICES RESEARCH LA English DT Article C1 VET AFFAIRS MED CTR,DEPT VET AFFAIRS,MED DIST 9,DECATUR,GA. UNIV CALIF SANTA BARBARA,DEPT COMMUN,SANTA BARBARA,CA 93106. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DIV HLTH SERV RES,MADISON,WI 53705. RP HURLEY, J (reprint author), MCMASTER UNIV,HLTH SCI CTR,CTR HLTH ECON & POLICY ANAL,DEPT CLIN EPIDEMIOL & BIOSTAT,RM 3H2,HAMILTON L8N 3Z5,ONTARIO,CANADA. NR 17 TC 11 Z9 11 U1 0 U2 0 PU HEALTH ADMINISTRATION PRESS PI MELROSE PARK PA C/O FOUNDATION AMER COLL HEALTHCARE EXECUTIVES 1951 CORNELL AVE, MELROSE PARK, IL 60160 SN 0017-9124 J9 HEALTH SERV RES JI Health Serv. Res. PD APR PY 1990 VL 25 IS 1 BP 239 EP 255 PN 2 PG 17 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA DB371 UT WOS:A1990DB37100008 PM 2109742 ER EF