FN Thomson Reuters Web of Science™ VR 1.0 PT J AU GOODFRIEND, TL LEE, WMP BALL, DL ELLIOTT, ME AF GOODFRIEND, TL LEE, WMP BALL, DL ELLIOTT, ME TI SPECIFICITY AND MECHANISM OF FATTY-ACID INHIBITION OF ALDOSTERONE SECRETION SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article; Proceedings Paper CT 2nd International Round Table on Fatty Acids in Cell Signalling CY JUN 12-13, 1994 CL UNIV WISCONSIN MADISON, MADISON, WI HO UNIV WISCONSIN MADISON ID ANGIOTENSIN-II; EICOSAPENTAENOIC ACID; BLOOD-PRESSURE; ADRENAL-CORTEX; RECEPTORS; IDENTIFICATION; EXPRESSION; CELLS AB We have shown that unesterified, unsaturated long-chain fatty acids inhibit angiotensin II (AII) binding to receptors in adrenal glomerulosa cells, In this report, we show that oleic and arachidonic acids are specific inhibitors of the AT(1) subtype of angiotensin receptor, and exert no effect on receptors of the AT(2) subtype. By contrast, decanoic acid is a weak inhibitor of the AT(2) subtype only, Our previous work on a post-receptor locus of inhibition by fatty acids of aldosterone biosynthesis showed that the 18-oxidase step is uniquely sensitive, In brief, the first and last steps involved in angiotensin-stimulated aldosterone secretion are particularly sensitive to inhibition by fatty acids. These results suggest a specific role for unesterified fatty acids in regulation of salt and water metabolism. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,DEPT PHARMACOL,MADISON,WI 53705. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 20 TC 9 Z9 10 U1 0 U2 1 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD FEB-MAR PY 1995 VL 52 IS 2-3 BP 145 EP 149 DI 10.1016/0952-3278(95)90013-6 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA QJ382 UT WOS:A1995QJ38200014 PM 7784450 ER PT J AU SLATER, EJ GLAZER, W AF SLATER, EJ GLAZER, W TI USE OF OBRA-87 GUIDELINES FOR PRESCRIBING NEUROLEPTICS IN A VA NURSING-HOME SO PSYCHIATRIC SERVICES LA English DT Note ID FACILITIES; INDICATORS C1 YALE UNIV,SCH MED,NEW HAVEN,CT 06520. RP SLATER, EJ (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 17 TC 10 Z9 10 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1075-2730 J9 PSYCHIATR SERV JI Psychiatr. Serv. PD FEB PY 1995 VL 46 IS 2 BP 119 EP 121 PG 3 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA QP099 UT WOS:A1995QP09900003 PM 7712245 ER PT J AU CATES, JA ABEDIN, MZ SAUNDERSKIRKWOOD, KD MOSER, AJ GIURGIU, DIN ROSLYN, JJ AF CATES, JA ABEDIN, MZ SAUNDERSKIRKWOOD, KD MOSER, AJ GIURGIU, DIN ROSLYN, JJ TI PROTEIN-KINASE-C REGULATES PRAIRIE DOG GALLBLADDER ION-TRANSPORT SO SURGERY LA English DT Article ID CHOLESTEROL GALLSTONE FORMATION; ELECTROLYTE TRANSPORT; PHOSPHATIDYLINOSITOL TURNOVER; CA-2+ CALMODULIN; NA+/H+ EXCHANGER; PHORBOL ESTERS; CALCIUM-ION; ABSORPTION; ACTIVATION; SECRETION AB Background. Gallstone formation is characterized by increased biliary calcium (Ca2+) level and altered gallbladder absorption. Recent studies suggest that luminal Ca2+ regulates gallbladder ion transport via intracellular calcium ([Ca2+](ic)). Ca2+-calmodulin and protein kinase C (PKC) are two major systems through which [Ca2+](ic) carries out second-messenger functions in many cell types. We have previously shown that Ca2+-calmodulin regulates basal gallbladder ion transport in prairie dog. The present study tests the hypothesis that PKC is also essential in regulation of gallbladder ion transport in this model. Methods. The role of PKC in regulation of gallbladder ion transport was determined by studying the effects of phorbol esters, synthetic analogues of diacylglycerol, which directly activates PKC. Gallbladders were mounted in Ussing chambers, and standard electrophysiologic parameters were recorded after exposing tissues to either 10(-5) mol/L of 4-alpha-phorbol 12, 13-didecanoate (PDD), 4-beta-phorbol 12-myristate 13-acetate, 4-beta-phorbol 12, 13-dibutyrate (PDB), or 10(-4) mol/L serotonin. Unidirectional Na+, Cl-, and H2O fluxes were measured before and after treatment with only inactive PDD and most active PDB. Results. Mucosal and serosal exposure of tissues to either 4-beta-phorbol 12-myristate 13-acetate or PDB resulted in a decrease in short-circuit current and transepithelial potential difference without any change in tissue resistance. Serotonin induced similar changes in gallbladder electrical properties. PDB caused an inhibition of mucosal to serosal fluxes of Na+, Cl-, and H2O, with a decrease in net Na+ absorption, an increase in net Cl- secretion, and a conversion of net H2O absorption to net H2O secretion. Serosal-to-mucosal fluxes of Na+, Cl-, and H2O did not change. Inactive PDD had no effect on either electrophysiologic parameters or ion and water fluxes. Pretreatment of tissues with PKC antagonist 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine blocked the phorbol ester-induced inhibition of ion transport. Conclusion. PKC regulates gallbladder ion transport in the prairie dog by inhibiting Na+ absorption and stimulating Cl- secretion. C1 MED COLL PENN,DEPT SURG,PHILADELPHIA,PA 19129. UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,LOS ANGELES,CA 90024. SEPULVEDA VET AFFAIRS MED CTR,DEPT SURG,RES SERV,SEPULVEDA,CA. PHILADELPHIA VET AFFAIRS MED CTR,DEPT SURG,PHILADELPHIA,PA. NR 42 TC 10 Z9 10 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD FEB PY 1995 VL 117 IS 2 BP 206 EP 212 DI 10.1016/S0039-6060(05)80087-X PG 7 WC Surgery SC Surgery GA QF384 UT WOS:A1995QF38400013 PM 7846627 ER PT J AU WALKER, RP LAWRENCE, AM PALOYAN, E AF WALKER, RP LAWRENCE, AM PALOYAN, E TI NODULAR DISEASE DURING PREGNANCY SO SURGICAL CLINICS OF NORTH AMERICA LA English DT Article AB Thyroid disease during pregnancy is a significant issue, especially because the incidence of autoimmune disease of the thyroid approaches 10% in women. Exposure to head and neck irradiation in childhood is one of the most significant factors in the development of thyroid neoplasia. However, genetic, environmental, and racial factors have prevailed throughout recorded history and will continue to prevail long after the radiation effect has waned. Well-differentiated thyroid carcinoma occurs predominantly in young women.(5) Pregnancy may be regarded as an enhancing factor in individuals genetically or environmentally predisposed to the development of thyroid neoplasia. The renal loss of iodine in certain developing countries and in mountainous areas of the world, due to the increase in the glomerular filtration rate that occurs in pregnancy, can lead to a relative iodine deficiency and the development of thyroid-stimulating hormone (TSH)induced goiters, especially if dietary supplements are not provided. Furthermore, elevated estrogen levels in pregnancy lead to the hyperproduction of thyroid-binding globulin by the liver, which results in a rise in the number of T-4 binding sites, which is responsible for a decrease in T-3 uptake and an elevated total serum T-4. However, free thyroid hormone levels (free T-3 or free T-4) corrected for the elevated thyroid-binding globulin are in the normal range in pregnancy. The role of TSH in the development of thyroid neoplasia in pregnancy is not well characterized. However, other stimulators of thyroid neoplasia occur in pregnancy in the form of chorionic TSH, and human chorionic gonadotropin (hCG) has a mild TSH effect. Other growth factors may also have a role in thyroid neoplasia, such as somatomedins, growth-stimulating immunoglobulins, placental lactogen, epidermal growth factor, and growth hormone itself. The survival of a placental allograft (the fetus) requires a state of altered immunologic tolerance that is regarded as a condition conducive to the growth of neoplasms and includes the presence of embryogenic antigens both in the placental allograft and in the neoplasms.(2) These immunologic changes which occur in pregnancy are reflected in a reduction in killer cells and helper T cells, the presence of serologic blocking factors, the presence of suppressor T cells and leukocyte migration and enhancement factors in amniotic fluid, alteration of surface antigenicity, and the natural immunosuppressive effect of estrogen, progesterone, and hCG.(1,2,6) C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,RES SERV,HINES,IL 60141. LOYOLA UNIV,MED CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,MAYWOOD,IL 60153. LOYOLA UNIV,MED CTR,DEPT MED,MAYWOOD,IL 60153. UNIV ILLINOIS,DEPT SURG,CHICAGO,IL 60680. NR 6 TC 2 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 0039-6109 J9 SURG CLIN N AM JI Surg. Clin.-North Am. PD FEB PY 1995 VL 75 IS 1 BP 53 EP 58 PG 6 WC Surgery SC Surgery GA QG317 UT WOS:A1995QG31700006 PM 7855718 ER PT J AU KOWLURU, A SEAVEY, SE RABAGLIA, ME METZ, SA AF KOWLURU, A SEAVEY, SE RABAGLIA, ME METZ, SA TI NONSPECIFIC STIMULATORY EFFECTS OF MASTOPARAN ON PANCREATIC-ISLET NUCLEOSIDE DIPHOSPHOKINASE ACTIVITY - DISSOCIATION FROM INSULIN-SECRETION SO BIOCHEMICAL PHARMACOLOGY LA English DT Note DE PANCREATIC BETA CELLS; INSULIN SECRETION; MASTOPARAN; NUCLEOSIDE DIPHOSPHOKINASE; GTP-BINDING PROTEINS; AMPHIPHILIC CATIONIC DRUGS ID DIPHOSPHATE KINASE; SUBSTANCE-P; WASP VENOM; CELLS; ACTIVATION; EXOCYTOSIS; PROTEINS AB We examined whether mastoparan (MAS)-induced insulin secretion might involve the activation of nucleoside diphosphokinase (NDP kinase), which catalyzes the conversion of GDP to GTP, a known permissive factor for insulin secretion. MAS and MAS 7 (which activate GTP-binding proteins), but not MAS 17 (an inactive analog), stimulated insulin secretion from normal rat islets. In contrast to their specific effects on insulin secretion, MAS, MAS 7 and MAS 17 each stimulated formation of the phosphoenzyme-intermediate of NDP kinase, as well as its catalytic activity. These effects were mimicked by several cationic drugs. Thus, caution is indicated in using MAS to study cellular regulation, since some of its effects appear to be non-specific, and may be due, in part, to its amphiphilic, cationic nature. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,ENDOCRINOL SECT,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NIDDK NIH HHS [DK37312] NR 16 TC 23 Z9 23 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 JAN 18 PY 1995 VL 49 IS 2 BP 263 EP 266 DI 10.1016/S0006-2952(94)00489-7 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QE673 UT WOS:A1995QE67300017 PM 7840804 ER PT J AU RAHMAN, MU HUDSON, AP AF RAHMAN, MU HUDSON, AP TI NATURE AND TRANSCRIPTIONAL ROLE OF CATALYTIC SUBUNITS OF YEAST MITOCHONDRIAL CAMP-DEPENDENT PROTEIN-KINASE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID SACCHAROMYCES-CEREVISIAE; CYCLIC-AMP; STRINGENT RESPONSE; CATABOLITE REPRESSION; REGULATORY SUBUNIT; GLUCOSE REPRESSION; STRAINS; BINDING; GENES; RNA AB We have shown that mitochondrial (mt) transcription in yeast (S. cerevisiae) is governed in part by cAMP via a mt cAMP-dependent protein kinase (cAPK), and that the BCY1 gene product acts as regulatory subunit for that organellar enzyme, as it does for cytoplasmic cAPK. Here we assess mt cAPK activity and mt transcription in mutants for the TPK1, TPK2, and TPK3 genes, which encode catalytic subunits of cytoplasmic cAPK. Protein extracts from purified mitochondria from each of the three possible double TPK mutants show mt cAMP-dependent protein phosphorylation. Relative mt transcript levels in these mutants, however, suggest that TPK2 functions less well than does TPK1 or TPK3 in organellar transcriptional control. Thus, both mt and cytoplasmic cAPKs employ the same species of regulatory and catalytic proteins, and versions of the enzyme having various combinations of catalytic species function differentially in cAMP-dependent mt transcriptional control. (C) 1995 Academic Press, Inc. C1 DEPT VET AFFAIRS MED CTR,MED RES SERV,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. NR 22 TC 11 Z9 11 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JAN 17 PY 1995 VL 206 IS 2 BP 756 EP 763 DI 10.1006/bbrc.1995.1107 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QC115 UT WOS:A1995QC11500046 PM 7826397 ER PT J AU KLEYMAN, TR ROBERTS, C LING, BN AF KLEYMAN, TR ROBERTS, C LING, BN TI A MECHANISM FOR PENTAMIDINE-INDUCED HYPERKALEMIA - INHIBITION OF DISTAL NEPHRON SODIUM-TRANSPORT SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE HYPERKALEMIA; PENTAMIDINE; ACQUIRED IMMUNODEFICIENCY SYNDROME; ION TRANSPORT; POTASSIUM ID PNEUMOCYSTIS-CARINII PNEUMONIA; CORTICAL COLLECTING TUBULE; POTASSIUM CHANNELS; PRIMARY CULTURES; THERAPY; AIDS AB Objectives: To determine whether pentamidine directly affects the transport of renal ions and thus provides a mechanism for hyperkalemia, which develops in as many as 100% of patients with the acquired immunodeficiency syndrome (AIDS) who receive pentamidine for more than 6 days. Design: Transepithelial and single-channel electrical measurements were made on two models of distal-nephron ion transport: an amphibian distal-nephron cell line (A6) and primary cultures of rabbit cortical collecting tubules. Results: Luminal bath application of pentamidine to A6 monolayers inhibited the amiloride-sensitive, short-circuit current with a 50% inhibitory concentration of 700 mu M (five experiments). In the principal cell apical membranes of cortical collecting tubule primary cultures, amiloride-sensitive, 4-picosiemen Na+ channels in cell-attached patches were also identified. When the luminal membrane was directly exposed to 1.0 mu M of pentamidine in the patch pipette solution, channel activity decreased by 40% (11 experiments). Channel inhibition rapidly reversed with washout of intrapipette pentamidine (four experiments). In contrast, replacement of either the luminal bath outside the patch pipette (four experiments) or the serosal bath (five experiments) with pentamidine did not significantly affect Na+ channel activity in the patches. Conclusions: Luminal or ''urinary'' pentamidine inhibits distal nephron reabsorption of Na+ by blocking apical Na+ channels in a manner similar to ''potassium-sparing'' diuretics (for example, amiloride and triamterene). This results in a decrease in the electrochemical gradients that drive secretion of distal nephron K+. Because pentamidine is eliminated through urinary excretion, this renal tubular effect provides a mechanism for pentamidine-induced hyperkalemia. C1 EMORY UNIV,SCH MED,DIV RENAL,ATLANTA,GA 30322. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,ATLANTA,GA 30033. FU NIDDK NIH HHS [K08-DK02111] NR 22 TC 46 Z9 47 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 JAN 15 PY 1995 VL 122 IS 2 BP 103 EP 106 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA QC059 UT WOS:A1995QC05900004 PM 7992983 ER PT J AU SHEKELLE, PG MARKOVICH, M LOUIE, R AF SHEKELLE, PG MARKOVICH, M LOUIE, R TI COMPARING THE COSTS BETWEEN PROVIDER TYPES OF EPISODES OF BACK PAIN CARE SO SPINE LA English DT Article AB Study Design. This study was a prospective, community-based, observational design. Objectives. The authors compared the costs of episodes of back pain care between different provider types in a population representative of the U.S. Summary of Background Data. Previous comparisons between provider types of the costs for back pain care have been restricted to the worker's compensation population or have used something other than the episode as the unit of analysis. Methods. Data from the RAND Health Insurance Experiment (HIE) were analyzed. Insurance claims forms were examined for all visits specified by the patient as occurring for back pain. Visits were grouped into episodes using decision rules and clinical judgement. The primary provider was defined as the provider who delivered most of the care. Comparisons of costs between provider types were made. Results. There were 1020 episodes of back pain care made by 686 different persons and encompassing 8825 visits. Chiropractors and general practitioners were the primary providers for 40% and 26% of episodes, respectively. Chiropractors had a significantly greater mean number of visits per episode (10.4) than did other practitioners. Orthopedic physicians and ''other'' basis. Orthopedists had the highest mean total cost per episode, and general practitioners the lowest. Chiropractors had the highest, and general practitioners the lowest mean outpatient cost per episode. Conclusions. These are economically significant differences in the costs of back pain care of persons seeing chiropractors, general practitioners, internists, and orthopedists. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. FU AHRQ HHS [1RO3HS06920-01] NR 0 TC 70 Z9 71 U1 2 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0362-2436 J9 SPINE JI SPINE PD JAN 15 PY 1995 VL 20 IS 2 BP 221 EP 226 DI 10.1097/00007632-199501150-00018 PG 6 WC Clinical Neurology; Orthopedics SC Neurosciences & Neurology; Orthopedics GA QD345 UT WOS:A1995QD34500018 PM 7716629 ER PT J AU KANOFSKY, JR SIMA, PD AF KANOFSKY, JR SIMA, PD TI REACTIVE ABSORPTION OF OZONE BY AQUEOUS BIOMOLECULE SOLUTIONS - IMPLICATIONS FOR THE ROLE OF SULFHYDRYL COMPOUNDS AS TARGETS FOR OZONE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE ASCORBIC ACID; CYSTEINE; GLUTATHIONE; METHIONINE; OZONE; REACTIVE ABSORPTION; THIOSULFATE ID REVERSE MICELLES; WATER; OZONATION; LYSOZYME; OLEATE; MODEL; RATES; ACID AB The rates of reactive absorption of ozone by various biomolecule solutions were measured. At pH 7, the ability of various biomolecules to reactively absorb ozone was in the following sequence: thiosulfate > ascorbate > cysteine approximate to methionine > glutathione. The rates of reactive absorption under a variety of conditions were then analyzed using a mathematical model in order to estimate the reaction rate constants for the various ozone-biomolecule reactions. Compared to the ozone-methionine rate constant, the relative rate constants for thiosulfate, ascorbate, cysteine, and glutathione reactions were 18 +/- 2, 12 +/- 1, 1.1 +/- 0.1, and 0.62 +/- 0.03, respectively. Using an ozone-methionine reaction rate constant of 4 x 10(6) M(-1) s(-1), the rate constants for thiosulfate, ascorbate, cysteine, and glutathione were 7:2 X 10(7), 4.8 X 10(7), 4.4 X 10(6), and 2.5 X 10(6) M(-1) s(-1), respectively. Competitive studies using tryptophan as a standard ozone target were consistent with these rate constants. Compared to tryptophan, the relative ozone reaction rate constants for methionine, cysteine, and glutathione were 0.77 +/- 0.08, 0.88 +/- 0.19, and 0.42 +/- 0.01, respectively. These relative rate constants refer to ozone consumption rather than biomolecule consumption, so they may be compared with the relative rate constants obtained from reactive absorption. In addition, various inconsistencies in the literature regarding the rates of the ozone-cysteine and the ozone-glutathione reactions were reviewed. (C) 1995 Academic Press, Inc. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,RES SERV,HINES,IL 60141. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT MOLEC & CELLULAR BIOCHEM,MAYWOOD,IL 60153. RP KANOFSKY, JR (reprint author), US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MED SERV,POB 278,HINES,IL 60141, USA. NR 26 TC 50 Z9 52 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN 10 PY 1995 VL 316 IS 1 BP 52 EP 62 DI 10.1006/abbi.1995.1009 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QJ933 UT WOS:A1995QJ93300009 PM 7840660 ER PT J AU THIELEN, RJ FRAZER, A AF THIELEN, RJ FRAZER, A TI EFFECTS OF NOVEL 5-HT1A RECEPTOR ANTAGONISTS ON MEASURES OF POSTSYNAPTIC 5-HT1A RECEPTOR ACTIVATION IN-VIVO SO LIFE SCIENCES LA English DT Letter DE 5-HT1A RECEPTOR; ANTAGONIST; HYPOTHERMIA; SEROTONIN SYNDROME ID AGONISTS; HYPOTHERMIA; 8-OH-DPAT; SEROTONIN; RESERVE AB The effects of two putative 5-HT1A antagonists, 4-(2'-methoxyphenyl)-1-[2'-[N-(2''-pyridinyl)-p-iodobenzamido]ethyl]piperazine (p-MPPI) and 4-(2'-methoxyphenyl)-1-[2'-[N-(2''-pyridinyl)-p-flourobenzamido]ethyl]piperazine (p-MPPF), were examined in vivo in two tests of postsynaptic 5-HT1A receptor activation, hypothermia and reciprocal forepaw treading, in the rat. Both p-MPPI (10 mg/kg, i.p.) and p-MPPF (10 mg/kg, i.p.) antagonized the hypothermia induced by the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (0.5 mg/kg, s.c.). Neither p-MPPI nor p-MPPF administered alone at a dose of 10 mg/kg (i.p.) induced hypothermia. Similarly, both p-MPPI (10 mg/kg, i.p.) and p-MPPF (2.5 mg/kg, i.p.) completely antagonized 8-OH-DPAT (2 mg/kg, s.c.)-induced forepaw treading in rats pretreated with reserpine (1 mg/kg, s.c., 18-24 hours prior to the experiment). p-MPPI and p-MPPF, at doses of 10 mg/kg (i.p.) did not induce forepaw treading in reserpine pretreated animals. The results of the present study demonstrate that p-MPPI and p-MPPF act as 5-HT1A receptor antagonists in these measures of postsynaptic 5-HT1A receptor activation. C1 DEPT VET AFFAIRS MED CTR,SAN ANTONIO,TX. RP THIELEN, RJ (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 17 TC 16 Z9 17 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. PD JAN 6 PY 1995 VL 56 IS 7 BP PL163 EP PL168 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA QA168 UT WOS:A1995QA16800011 ER PT J AU DAVIS, RF METZGER, DS MEYERS, K MCLELLAN, AT MULVANEY, FD NAVALINE, HA WOODY, GE AF DAVIS, RF METZGER, DS MEYERS, K MCLELLAN, AT MULVANEY, FD NAVALINE, HA WOODY, GE TI LONG-TERM CHANGES IN PSYCHOLOGICAL SYMPTOMATOLOGY ASSOCIATED WITH HIV SEROSTATUS AMONG MALE INJECTING DRUG-USERS SO AIDS LA English DT Article DE INJECTING DRUG USERS; METHADONE; PSYCHOLOGICAL SYMPTOMATOLOGY; HIV; AIDS ID DEPENDENCE TREATMENT PROGRAMS; HUMAN-IMMUNODEFICIENCY-VIRUS; METHADONE-MAINTENANCE; ABUSE PATIENTS; RISK; SEVERITY; AIDS AB Objective: To examine long-term changes in psychological symptomatology from 6 to 24 months after notification of HIV serostatus among male injecting drug users (IDU). Design: Self-report and interview data were collected at 6-month intervals as part of a longitudinal study monitoring HIV infection and risk-associated behaviors among IDU. Setting: A community-based methadone-maintenance clinic. Participants: Ninety-seven male IDU (81 HIV-seronegative, 16 HIV-seropositive), including both methadone-maintained and out-of-treatment IDU. Main outcome measures: Analyses of long-term changes in psychological symptomatology associated with HIV serostatus among male IDU. Results: Analyses of long-term changes in psychological symptomatology between groups revealed no significantly greater levels of overall psychological distress or significant elevations on subscales of the Symptom Checklist-90 for HIV-seropositive compared with HIV-seronegative male IDU. Also, no significantly higher scores on the Beck Depression Inventory or the psychiatric composite score of the Addiction Severity Index were observed between groups. Conclusions: Our results suggest that HIV-seropositive male IDU do not express greater levels of psychological symptomatology from 6 to 24 months following notification of seropositivity compared with HIV-seronegative male IDU. Several explanations for these findings are considered. Future work should examine why male IDU do not report significant and long-term elevations in symptoms post-notification of HIV seropositivity. Also, studies of changes in psychological symptomatology as a function of HIV serostatus among female IDU need to be conducted to assess implications for treatment interventions among this underserved population. C1 UNIV PENN,CTR STUDIES ADDICT,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. RI Metzger, David/D-9499-2012 FU NIAID NIH HHS [Y01-AI-20025-01]; NIDA NIH HHS [R01-DA05593] NR 23 TC 19 Z9 19 U1 1 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD JAN PY 1995 VL 9 IS 1 BP 73 EP 79 DI 10.1097/00002030-199501000-00010 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QB059 UT WOS:A1995QB05900010 PM 7893444 ER PT J AU CUMMINGS, JL ROSS, W ABSHER, J GORNBEIN, J HADJIAGHAI, L AF CUMMINGS, JL ROSS, W ABSHER, J GORNBEIN, J HADJIAGHAI, L TI DEPRESSIVE SYMPTOMS IN ALZHEIMER-DISEASE - ASSESSMENT AND DETERMINANTS SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article DE DEPRESSION; DELUSIONS; ACETYLCHOLINE ID COGNITIVE STATUS EXAMINATION; MINI-MENTAL STATE; RATING-SCALE; BIOCHEMICAL MANIFESTATIONS; PSYCHIATRIC-SYMPTOMS; PARKINSONS-DISEASE; DEMENTIA; MOOD; NEUROBIOLOGY; INDUCTION AB Depression is difficult to assess in Alzheimer disease (AD) and controversy surrounds the prevalence, etiology, and characteristics of mood alterations in patients with this disorder. We used a variety of standardized instruments to assess mood changes in 33 patients with AD. The frequency of depression ranged from 6 to 30%, depending on the diagnostic criteria employed. No relationship was found between patient depression and dementia severity, self-awareness of cognitive deficits (as measured by a memory self-rating scale), or mood of the caregiver. Delusional patients had higher scores on mood rating scales than nondelusional patients. The results suggest that depression in AD is not severe and is unrelated to patient self-awareness of illness. We hypothesize that the cholinergic deficit of AD may ameliorate depressive symptoms. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOMATH,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,BEHAV NEUROSCI SECT,LOS ANGELES,CA 90073. RP CUMMINGS, JL (reprint author), UNIV CALIF LOS ANGELES,SCH MED,REED NEUROL RES CTR,DEPT NEUROL,710 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. FU NIA NIH HHS [AG 10123] NR 57 TC 82 Z9 84 U1 1 U2 3 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. PY 1995 VL 9 IS 2 BP 87 EP 93 DI 10.1097/00002093-199509020-00005 PG 7 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA RB473 UT WOS:A1995RB47300005 PM 7662328 ER PT J AU SINGH, BN KEHOE, R WOOSLEY, RL SCHEINMAN, M QUART, B BAUERNFEIND, R GREENSPON, A HEGER, JJ ZIPES, DP KERIN, NZ KEHOE, RF MARTINS, JB PETER, T RUFFY, R RUSKIN, JN SCHEINMAN, MM NADEMANEE, K ECHT, D AF SINGH, BN KEHOE, R WOOSLEY, RL SCHEINMAN, M QUART, B BAUERNFEIND, R GREENSPON, A HEGER, JJ ZIPES, DP KERIN, NZ KEHOE, RF MARTINS, JB PETER, T RUFFY, R RUSKIN, JN SCHEINMAN, MM NADEMANEE, K ECHT, D TI MULTICENTER TRIAL OF SOTALOL COMPARED WITH PROCAINAMIDE IN THE SUPPRESSION OF INDUCIBLE VENTRICULAR-TACHYCARDIA - A DOUBLE-BLIND, RANDOMIZED PARALLEL EVALUATION SO AMERICAN HEART JOURNAL LA English DT Article ID CORONARY-ARTERY DISEASE; ISOLATED CARDIAC-MUSCLE; ANTI-ARRHYTHMIC ACTION; ANTIARRHYTHMIC DRUGS; ANTIFIBRILLATORY ACTIONS; DEXTROROTATORY ISOMERS; ORAL SOTALOL; EFFICACY; TACHYARRHYTHMIAS; PROLONGATION AB Sotalol is the prototype class III agent that combines beta-blocking properties with the propensity to prolong the effective refractory period by lengthening the action potential duration. Its precise effect on the prevention of ventricular tachycardia-ventricular fibrillation (VTVF) compared to class I agents has not been evaluated in a blinded study. In a double-blind parallel-design multicenter study, the electrophysiologic and antiarrhythmic effects of intravenous and oral sotalol (n = 55) and procainamide (n = 55) were therefore compared in patients with VTVF inducible by programmed electric stimulation. Sotalol produced a greater effect on lengthening the ventricular effective refractory period (VERP), It prevented the inducibility of VTVF in 30% versus 20% for procainamide, but this was not significantly different. In an alternate therapy group (n = 41) of similar patients previously refractory to or intolerant of procainamide, intravenous sotalol prevented inducibility in 32%. The pooled overall sotalol efficacy rate was 31%. There was a significant relation between the increase in the VERP and the prevention of inducibility of VTVF (n = 56; p < 0.02). VERP of greater than or equal to 300 msec was critical for the prevention of VTVF inducibility. Thirteen sotalol and 6 procainamide responders from the randomized group and 30 from the nonrandomized groups completed 1 year of oral sotalol therapy follow-up. Life-table analysis of these patient in each group showed a trend in favor of sotalol; however, statistical analysis was not possible because of the small numbers of patients. Both sotalol and procainamide were well tolerated. In the randomized group there was one case of sudden death during treatment with sotalol and two cases of nonfatal torsades de pointes in the procainamide group and two in the sotalol group; in the nonrandomized alternate therapy group, there were 6 cases of nonfatal torsades de pointes. The data support the emerging role of sotalol in the control of symptomatic ventricular tachycardia and fibrillation. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC. UNIV CALIF SAN FRANCISCO,SCH MED,SAN FRANCISCO,CA. BRISTOL MYERS SQUIBB CO,PRINCETON,NJ. RP SINGH, BN (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DEPT CARDIOL,CARDIOL SECT,691-W111E,WILSHIRE SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. NR 49 TC 36 Z9 37 U1 0 U2 3 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 JAN PY 1995 VL 129 IS 1 BP 87 EP 97 DI 10.1016/0002-8703(95)90048-9 PG 11 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QB188 UT WOS:A1995QB18800015 PM 7817931 ER PT J AU Scurfield, RM AF Scurfield, RM TI Healing the warrior: Admission of two American Indian war-veteran cohort groups to a specialized inpatient PTSD unit SO AMERICAN INDIAN AND ALASKA NATIVE MENTAL HEALTH RESEARCH LA English DT Article ID THERAPY AB The American Lake VA Post-Traumatic Stress Disorder (PTSD) Treatment Program provides intensive inpatient treatment for war-related PTSD and associated conditions. As part of a substantial outreach effort to American Indians (Al) in the Northwest U.S., the program significantly modified its admission criteria and treatment to be more clinically and culturally relevant. An all-Al cohort, and then a group that was 50% Al, were admitted. Highlighted are lessons learned regarding: treating ''traditional'' versus more ''assimilated'' Al veterans; culture-specific additions of building and utilizing a sweatlodge on the hospital grounds, hiring an Al spiritual leader as a clinical advisor, and promoting attendance at weekend Pow-Wows; the relevance of the ''regular'' treatment components; and the need for regular debriefings about counter-transference dynamics among staff. RP Scurfield, RM (reprint author), US DEPT VET AFFAIRS,PTSD,CTR PACIFIC,1132 BISHOP ST,SUITE 307,HONOLULU,HI 96813, USA. NR 17 TC 4 Z9 4 U1 0 U2 2 PU UNIVERSITY PRESS COLORADO PI NIWOT PA PO BOX 849, NIWOT, CO 80544 SN 0893-5394 J9 AM INDIAN ALASKA NAT JI Am. Indian Alsk. Nativ. Ment. Health Res. PY 1995 VL 6 IS 3 BP 1 EP 22 PG 22 WC Psychology, Clinical SC Psychology GA TL534 UT WOS:A1995TL53400001 PM 8555350 ER PT J AU SINGARAM, C TORBEY, CF JACOBY, RF AF SINGARAM, C TORBEY, CF JACOBY, RF TI DELAYED POSTPOLYPECTOMY BLEEDING SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Note ID COMPLICATIONS; POLYPECTOMY; COLONOSCOPY; HEMORRHAGE AB Complications of colonoscopic polypectomy include perforation, infection, and bleeding. The incidence of bleeding after polypectomy is reported to range from one to seven per 1000 polypectomies. This complication usually occurs within a few days after the standard procedure using bipolar electrocautery. The longest time interval between polypectomy and significant bleeding thus far reported is 14 days. Most cases of postpolypectomy bleeding are easily recognizable and can be effectively treated by colonoscopic electrocauterization. We report here a patient who underwent colonoscopic removal of a flat adenomatous polyp at the cecum and presented 29 days postprocedure with acute onset of severe bleeding from the polypectomy site. A repeat colonoscopy identified this lesion, and cauterization successfully stopped this bleeding. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP SINGARAM, C (reprint author), UNIV WISCONSIN HOSP & CLIN,CTR CLIN SCI,DEPT MED,DIV GASTROENTEROL,H6-510,MADISON,WI 53792, USA. FU NCI NIH HHS [1U01-CA 59352] NR 8 TC 31 Z9 32 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD JAN PY 1995 VL 90 IS 1 BP 146 EP 147 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QA696 UT WOS:A1995QA69600034 PM 7801918 ER PT J AU KOVACS, TOG LLOYD, KCK WONG, H WALSH, JH AF KOVACS, TOG LLOYD, KCK WONG, H WALSH, JH TI INHIBITION OF BOMBESIN-STIMULATED ACID-SECRETION BY IMMUNONEUTRALIZATION OF GASTRIN IN DOGS SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE GASTRIN-RELEASING PEPTIDE; MONOCLONAL ANTIBODY; NEURAL REGULATION ID SOMATOSTATIN SECRETION; PEPTIDES; RAT; CHOLECYSTOKININ; RELEASE; REGULATORS; STOMACH; POTENCY AB Bombesin-like peptides stimulate gastrin release and gastric acid secretion. The increase in gastric acid output is thought to be secondary to gastrin release. A monoclonal antibody (MAb) directed specifically to gastrin (MAb 28.2) was used to study the role of circulating gastrin in the regulation of bombesin-stimulated acid secretion in dogs. Seven conscious, fasted dogs with gastric fistulas received intravenous bombesin infusions in fourfold increasing doses from 200 to 3,200 pmol.kg(-1).h(-1). Each dose was given for 45 min. On separate days, dogs were pretreated with an intravenous infusion of 7 mg of MAb 28.2 or vehicle (0.1% canine serum albumin). Samples of gastric effluent were collected by gravity drainage through the gastric fistula, and acid output was measured by titration of gastric effluent to pH 7.0, using 0.2 N NaOH. Plasma gastrin concentrations were determined by radioimmunoassay. Bombesin infusion produced dose-dependent increases in plasma gastrin concentrations and gastric acid output. Administration of gastrin MAb 28.2 abolished bombesin-stimulated gastric acid output. Immunoneutralization of circulating gastrin in vivo using a gastrin monoclonal antibody in dogs indicates that the acid stimulatory response to bombesin is mediated by gastrin. C1 W LOS ANGELES VET AFFAIRS MED CTR, RES SERV, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, MED SERV, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PHYSIOL, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, GASTROENTER BIOL CTR, CTR ULCER RES & EDUC, LOS ANGELES, CA 90073 USA. FU NIDDK NIH HHS [DK-41301] NR 34 TC 6 Z9 6 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD JAN PY 1995 VL 268 IS 1 BP G54 EP G58 PG 5 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA QB678 UT WOS:A1995QB67800008 PM 7840208 ER PT J AU LLOYD, KCK WANG, J AURANG, K GRONHED, P COY, DH WALSH, JH AF LLOYD, KCK WANG, J AURANG, K GRONHED, P COY, DH WALSH, JH TI ACTIVATION OF SOMATOSTATIN RECEPTOR SUBTYPE-2 INHIBITS ACID-SECRETION IN RATS SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE STOMACH; RECEPTOR AGONIST; ACID INHIBITION ID ENTEROCHROMAFFIN-LIKE CELLS; HISTAMINE-RELEASE; GASTRIN RECEPTORS; PARIETAL-CELLS; CLONING; IMMUNOREACTIVITY; IDENTIFICATION; EXPRESSION; ATROPINE; STOMACH AB Somatostatin is a potent inhibitor of gastric acid secretion. Recently, at least five distinct somatostatin receptor subtypes (SSTR) have been characterized and evaluated using relatively selective peptide analogues of somatostatin. We sought to determine which somatostatin receptor subtypes are involved in peripheral regulation of gastric acid secretion. Fasted, male Sprague-Dawley rats were anesthetized and were implanted with a double-lumen cannula in the stomach. Acid secretion was measured in gastric samples collected every 10 min by backtitration to pH 7. After a 30-min basal period, a 2-h intravenous infusion of pentagastrin (24 mu g.kg(-1).h(-1) iv) was started. During the second pentagastrin hour, a l-h intravenous infusion of either vehicle (0.1% canine serum albumin in 0.9% saline) or somatostatin receptor agonists was begun. The somatostatin receptor agonists included peptides with relative specificity for SSTR(1-5) (somatostatin-14; 10 nmol.kg(-1).h(-1)); SSTR(2), SSTR(3), and SSTR(5) [SMS-(201--995); 10 nmol kg(-1).h(-1)]; SSTR(2) (1-1,000 nmol kg(-1).h(-1)); SSTR(3) (10-1,000 nmol.kg(-1).h(-1)); and SSTR(5) (10-1,000 nmol.kg(-1).h(-1)). The SSTR(2) agonist decreased pentagastrin-stimulated acid secretion dose dependently, from 82 +/- 7% of maximum acid output at 1 nmol.kg(-1).h(-1) to 4 +/- 7% of maximum at 100 nmol.kg(-1).h(-1). At 10 nmol.kg(-1).h(-1), the SSTR(2) agonist inhibited acid secretion (40 +/- 7% of maximum) similarly to somatostatin (37 +/- 4% of maximum) and SMS-(201--995) (31 +/- 4% of maximum). The SSTR(2) agonist inhibited acid secretion approximately 10- to 100-fold more potently than either the SSTR(3) or the SSTR(5) agonist. These results indicate that somatostatin regulates gastric acid secretion by activation of SSTR(2) receptors. C1 W LOS ANGELES VET AFFAIRS MED CTR, RES SERV, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, MED SERV, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, CTR GASTROENTER BIOL, CTR ULCER RES & EDUC, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PHYSIOL, LOS ANGELES, CA 90073 USA. TULANE UNIV, MED CTR, SCH MED, DEPT MED, NEW ORLEANS, LA 70112 USA. FU NIDDK NIH HHS [DK-41301, DK-45752] NR 34 TC 41 Z9 42 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD JAN PY 1995 VL 268 IS 1 BP G102 EP G106 PG 5 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA QB678 UT WOS:A1995QB67800014 PM 7840190 ER PT J AU BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG AF BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG TI A NONINDUCIBLE CYSTINE TRANSPORT-SYSTEM IN RAT ALVEOLAR TYPE-II CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY LA English DT Article DE GLUTATHIONE; EPITHELIAL CELLS; CYSTEINE; ENDOTHELIAL CELLS ID MOUSE PERITONEAL-MACROPHAGES; HUMAN-DIPLOID FIBROBLASTS; ENDOTHELIAL-CELLS; MEMBRANE-TRANSPORT; GLUTATHIONE LEVELS; SODIUM ARSENITE; DIETHYL MALEATE; ACID UPTAKE; HYPEROXIA; INDUCTION AB Type II lung epithelial cells are different from other lung cell types in their means of processing and regulating intracellular glutathione (GSH) levels. In lung cell types, including endothelial cells, fibroblasts, smooth muscle cells, and macrophages, oxidants, sulfhydryl reagents, and electrophilic agents have been shown to induce cystine uptake and concomitantly increase GSH levels, suggesting that cysteine, formed by intracellular reduction of cystine, is a rate-limiting substrate for GSH synthesis. The cystine transport increase was reportedly due to increase in activity of a sodium-independent transport system designated x(c)(-). We have now examined cultures of rat lung type II cells exposed to diethylmaleic acid and arsenite. Although a rise in cellular GSH occurred, cystine transport was not induced. Cystine transport in type II cells was found to differ from the x(c)(-) system previously described. Type II cell cystine transport is primarily sodium dependent and is inhibitable by aspartate as well as glutamate and homocysteate. We conclude that the type II cell. differs from other lung cell types in both its cystine transport mechanism and method of GSH regulation. C1 AUDIE L MURPHY MEM VET ADM MED CTR, PULM DIS SECT 111E, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV PULM DIS CRIT CARE MED, SAN ANTONIO, TX 78284 USA. FU NHLBI NIH HHS [HL-32824] NR 36 TC 31 Z9 31 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1040-0605 J9 AM J PHYSIOL-LUNG C JI Am. J. Physiol.-Lung Cell. Mol. Physiol. PD JAN PY 1995 VL 268 IS 1 BP L21 EP L26 PG 6 WC Physiology; Respiratory System SC Physiology; Respiratory System GA QB292 UT WOS:A1995QB29200005 PM 7840224 ER PT J AU WEINDRUCH, R MARRIOTT, BM CONWAY, J KNAPKA, JJ LANE, MA CUTLER, RG ROTH, GS INGRAM, DK AF WEINDRUCH, R MARRIOTT, BM CONWAY, J KNAPKA, JJ LANE, MA CUTLER, RG ROTH, GS INGRAM, DK TI MEASURES OF BODY-SIZE AND GROWTH IN RHESUS AND SQUIRREL-MONKEYS SUBJECTED TO LONG-TERM DIETARY RESTRICTION SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE NUTRITION; OBESITY; ADIPOSITY; DEVELOPMENT; AGING; MORPHOMETRY; SKIN-FOLD THICKNESS; MACACA MULATTA; SAIMIRI SP ID FOOD RESTRICTION; PHYSICAL GROWTH; ENERGY-INTAKE; BABOONS; MALNUTRITION; WEIGHT; MICE; NUTRITION; PRIMATES; BIRTH AB Although many studies have reported the robust effects of dietary restriction (DR) in retarding numerous aging processes in rodents, little is known about the outcomes of reducing caloric intake of a nutritious diet on aging in primates. Most primate studies have concerned the effects of malnutrition. We hypothesized that DR influences aging processes in primate species as it does in rodents. In the present study, 24 male rhesus (Macaca mulatta) monkeys (ages 0.6-5 years) and 25 male squirrel (Saimiri sp.) monkeys (ages 0.3-10 years) were provided diets formulated differently for each species but both fortified with vitamins and minerals (40% above recommended levels) as controls (approximating ad libitum levels) or experimentals (about 30% below the level of diet provided controls of comparable age and body weight). The results reported here concern the hypothesis that DR imposed during various developmental stages in these two primate species would affect morphometric parameters obtained at different occasions during the first 5 years of the study. Groups of older monkeys (rhesus: 18-25 years, n = 3; squirrel: 10-15 years, n = 4) were also included as controls for comparative purposes. Among groups of rhesus monkeys begun on DR prior to 6 years of age, growth in body weight and crown-rump length was reduced about 10-20% beginning after 1 year on the diet, with estimated food intake being reduced about 30-35% over this period. Measures of skin-fold thickness and various body circumference measures were also reduced in experimental groups of rhesus monkeys. In contrast, the DR regimen involving a different diet produced little impact on comparable measures in squirrel monkeys, with the estimated food intake being reduced only about 20-25% over this period. However, evidence of divergence in some morphometric parameters in squirrel monkeys was beginning to emerge in young groups (<5 years) after 3 years on the diet. (C) 1995 Wiley-Liss, Inc.* C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI. NATL ACAD SCI,FOOD & NUTR BOARD,WASHINGTON,DC 20418. USDA,BELTSVILLE HUMAN NUTR RES CTR,ENERGY & PROT NUTR LAB,BELTSVILLE,MD 20705. NIH,NATL CTR RES RESOURCES,BETHESDA,MD 20892. NIA,HOPKINS BAYVIEW MED CTR,CTR GERONTOL RES,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224. NR 47 TC 25 Z9 25 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1995 VL 35 IS 3 BP 207 EP 228 DI 10.1002/ajp.1350350304 PG 22 WC Zoology SC Zoology GA QJ092 UT WOS:A1995QJ09200003 ER PT J AU WHALEN, C HORSBURGH, CR HOM, D LAHART, C SIMBERKOFF, M ELLNER, J AF WHALEN, C HORSBURGH, CR HOM, D LAHART, C SIMBERKOFF, M ELLNER, J TI ACCELERATED COURSE OF HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION AFTER TUBERCULOSIS SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID TUMOR-NECROSIS-FACTOR; NEW-YORK-CITY; HIV-INFECTION; COHORT; RISK; AIDS; PROGRESSION; EXPRESSION; SURVIVAL; CELLS AB To determine the effect of active tuberculosis on survival and the incidence of opportunistic infections in HIV-infected patients, we performed a retrospective cohort study at four U.S. medical centers to compare the survival and incidence rate of opportunistic infections in 106 HIV-infected patients with active tuberculosis (cases) with that of 106 HIV-infected patients without tuberculosis (control subjects) but with a similar level of immunosuppression (measured by the absolute CD4+ lymphocyte count) as the cases. Cases and control subjects were similar with regard to age, sex, race, previous opportunistic infection, and use of antiretroviral therapy, but they were more likely than control subjects to have a history of intravenous drug use (49 versus 19%). The mean CD4+ counts were similar for cases and control subjects (154 versus 153 cells/mu l, respectively). The incidence rate of new AIDS-defining opportunistic infections in cases was 4.0 infections per 100 person-months compared with 2.8 infections per 100 person-months in control subjects for an incidence rate ratio (RR) of 1.42 (95% confidence interval: 0.94-2.11). Cases also had a shorter overall survival than did controls subjects (p = 0.001). Active tuberculosis was associated with an increased risk for death (odds ratio = 2.17), even when controlling for age, intravenous drug use, previous opportunistic infection, baseline CD4+ count, and antiretroviral therapy. Although active tuberculosis may be an independent marker of advanced immunosuppression in HIV-infected patients, it may also act as a cofactor to accelerate the clinical course of HIV infection. C1 CLEVELAND VET AFFAIRS MED CTR,DEPT MED,DIV GEN INTERNAL MED & INFECT DIS,CLEVELAND,OH. UNIV CLEVELAND HOSP,DEPT MED,CLEVELAND,OH 44106. NYU,MANHATTAN VET AFFAIRS MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,NEW YORK,NY. BAYLOR COLL MED,HOUSTON VET AFFAIRS MED CTR,DEPT MED,MED SERV,AIDS UNIT,HOUSTON,TX 77030. CTR DIS CONTROL,NATL CTR INFECT DIS,DIV HIV AIDS,ATLANTA,GA 30333. EMORY UNIV,DEPT MED,ATLANTA,GA 30322. GRADY MEM HOSP,ATLANTA,GA. RP WHALEN, C (reprint author), CASE WESTERN RESERVE UNIV,SCH MED,DEPT EPIDEMIOL & BIOSTAT,WG-49,2109 ADELBERT RD,CLEVELAND,OH 44106, USA. NR 35 TC 385 Z9 393 U1 0 U2 4 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD JAN PY 1995 VL 151 IS 1 BP 129 EP 135 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA QA903 UT WOS:A1995QA90300021 PM 7812542 ER PT J AU BROTHERS, TE ELLIOTT, BM ROBISON, JG RAJAGOPALAN, PR AF BROTHERS, TE ELLIOTT, BM ROBISON, JG RAJAGOPALAN, PR TI STRATIFICATION OF MORTALITY RISK FOR RENAL-ARTERY SURGERY SO AMERICAN SURGEON LA English DT Article; Proceedings Paper CT 62nd Annual Scientific Meeting of the Southeastern Surgical Conference CY FEB 06-10, 1994 CL LAKE BUENA VISTA, FL ID ABDOMINAL AORTIC-ANEURYSM; RENOVASCULAR HYPERTENSION; INTESTINAL ISCHEMIA; SURGICAL-TREATMENT; NATURAL-HISTORY; LUNG INJURY; DISEASE; RECONSTRUCTION; REVASCULARIZATION; RADICALS AB Seventy consecutive operations involving the renal arteries were reviewed to identify factors linked to perioperative mortality. Aortorenal bypass (n=29), endarterectomy (n=12), extraanatomic bypass (n=12), thrombectomy (n=4), and reimplantation (n=13) were associated with a 16% perioperative mortality that was often secondary to multisystem organ failure. Patients who died exhibited a higher serum creatinine (3.4 vs 2.1 mg/dL; P<0.05). Stratification of patients by risk revealed higher American Society of Anesthesiologists (ASA) (P<0.005) and modified Acute Physiology Score, and Chronic Health Evaluation (APACHE II) (P<0.02) score among patients who died. Higher mortality was also observed after bilateral renal artery operations (31% vs 5%; P<0.005) or concomitant mesenteric revascularization (37% vs 12%; P<0.05), but not simultaneous aortic procedures (18% vs 11%; P=NS). Bilateral operation (P<0.0001), age (P<0.001), and ASA class (P<0.01) were independent predictors of mortality according to multivariate analysis. Because of higher mortality in these specific situations, modification or limitation of operative scope may be appropriate. C1 MED UNIV S CAROLINA,CHARLESTON,SC. RALPH HENRY JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. NR 41 TC 6 Z9 7 U1 0 U2 0 PU SOUTHEASTERN SURGICAL CONGRESS PI ATLANTA PA 1776 PEACHTREE RD, NW., SUITE 410N, ATLANTA, GA 30309-2352 SN 0003-1348 J9 AM SURGEON JI Am. Surg. PD JAN PY 1995 VL 61 IS 1 BP 45 EP 51 PG 7 WC Surgery SC Surgery GA QC078 UT WOS:A1995QC07800010 PM 7832381 ER PT J AU MANDELKERN, MA AF MANDELKERN, MA TI NUCLEAR TECHNIQUES FOR MEDICAL IMAGING - POSITRON EMISSION TOMOGRAPHY SO ANNUAL REVIEW OF NUCLEAR AND PARTICLE SCIENCE LA English DT Review DE NUCLEAR MEDICINE; DIAGNOSTIC IMAGING; TRACER; TOMOGRAPHY; PET; PHYSIOLOGICAL IMAGING ID ATTENUATION CORRECTION; PET SCANNER; CAMERA; PERFORMANCE; DETECTOR; PROJECTIONS; RESOLUTION; ALGORITHM; CHAMBER; IMAGES AB Positron emission tomography (PET) is a new technique increasingly used in clinical medicine and research to create images that show physicians and scientists how effectively certain tissues are performing their physiological functions. It does this by determining the spatial distribution of radioactive nuclei that emit a positron. These nuclei are introduced to the body as ''labels'' on tracer molecules designed to probe physiological processes such as tissue perfusion or sugar metabolism. The PET scanner, based on detection techniques from nuclear and particle physics, produces three-dimensional (3-D) images using the methods of computed tomography (CT). PET isotopes are produced on-site by small cyclotrons or linear accelerators and are synthesized into highly specific chemical agents by automated systems. Physiological modeling is used to relate the PET measurements to metabolic parameters. PET plays an increasingly important role in the diagnosis of cancer, heart disease, and illnesses of the brain such as epilepsy, stroke, and the dementias. It is used as a basic research tool in studying the functional anatomy of the brain. C1 W LOS ANGELES VET AFFAIRS MED CTR,NUCL MED SERV,LOS ANGELES,CA 90073. RP MANDELKERN, MA (reprint author), UNIV CALIF IRVINE,DEPT PHYS,IRVINE,CA 92717, USA. NR 69 TC 7 Z9 7 U1 1 U2 5 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0163-8998 J9 ANNU REV NUCL PART S JI Annu. Rev. Nucl. Part. Sci. PY 1995 VL 45 BP 205 EP 254 PG 50 WC Physics, Nuclear; Physics, Particles & Fields SC Physics GA TJ992 UT WOS:A1995TJ99200007 ER PT J AU ABBOUD, HE AF ABBOUD, HE TI ROLE OF PLATELET-DERIVED GROWTH-FACTOR IN RENAL INJURY SO ANNUAL REVIEW OF PHYSIOLOGY LA English DT Review DE KIDNEY; GLOMERULONEPHRITIS; DIABETES; SIGNALING ID MESANGIAL PROLIFERATIVE NEPHRITIS; FACTOR-B-CHAIN; PDGF-RECEPTOR; FACTOR-BETA; EXTRACELLULAR-MATRIX; CELL-PROLIFERATION; MESSENGER-RNA; DNA-SYNTHESIS; EXPRESSION; RAT C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP ABBOUD, HE (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. NR 49 TC 100 Z9 106 U1 0 U2 0 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4278 J9 ANNU REV PHYSIOL JI Annu. Rev. Physiol. PY 1995 VL 57 BP 297 EP 309 PG 13 WC Physiology SC Physiology GA QN292 UT WOS:A1995QN29200016 PM 7778870 ER PT S AU Graybill, JR AF Graybill, JR BE Jungkind, DL Mortensen, JE Fraimow, HS Calandra, GB TI Antifungal drugs and resistance SO ANTIMICROBIAL RESISTANCE: A CRISIS IN HEALTH CARE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT Symposium on Antimicrobial Resistance: A Crisis in Healthcare - Clinical Laboratory and Epidemiologic Considerations CY NOV 11-12, 1993 CL PHILADELPHIA, PA SP Amer Soc Microbiol, E Penn Branch, Lederle Labs, Merck Inc, Miles Pharm, Pfizer Roerig Div, MetPath, Becton Dickinson, Pfizer Labs, Ortho Pharm, Remel Microbiol Prod, Baxter Microscan, Penn Dept Hlth, Gwynedd Mercy Coll, Hahnemann Univ, Natl Lab Training Network, Penn Coll Podiatr Med, Philadelphia Coll Osteopath Med, St Christophers Hosp, Temple Univ Sch Med, Thomas Jefferson Univ, Univ Penn ID CANDIDA-KRUSEI INFECTION; AMPHOTERICIN-B; CRYPTOCOCCAL MENINGITIS; INVASIVE ASPERGILLOSIS; FLUCONAZOLE RESISTANCE; IMMUNOCOMPROMISED PATIENTS; ITRACONAZOLE TREATMENT; TRANSPLANT RECIPIENTS; FUNGAL-INFECTIONS; INVIVO EFFICACIES RP Graybill, JR (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,DIV INFECT DIS,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 96 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45207-3 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 390 BP 217 EP 234 PG 18 WC Medicine, Research & Experimental; Microbiology SC Research & Experimental Medicine; Microbiology GA BF46X UT WOS:A1995BF46X00019 PM 8718616 ER PT J AU LYON, JG AF LYON, JG TI DRAWING - ITS VALUE AS A COMMUNICATION AID FOR ADULTS WITH APHASIA SO APHASIOLOGY LA English DT Article ID REHABILITATION; DEFICITS; LESIONS RP LYON, JG (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT VET AFFAIRS,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. RI Page, Andrew/G-5438-2012 OI Page, Andrew/0000-0003-3133-2844 NR 50 TC 35 Z9 35 U1 1 U2 9 PU TAYLOR & FRANCIS LTD LONDON PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0268-7038 J9 APHASIOLOGY JI Aphasiology PD JAN-FEB PY 1995 VL 9 IS 1 BP 33 EP 94 DI 10.1080/02687039508248687 PG 62 WC Clinical Neurology SC Neurosciences & Neurology GA QB072 UT WOS:A1995QB07200003 ER PT J AU LYON, JG AF LYON, JG TI COMMUNICATIVE DRAWING - AN AUGMENTATIVE MODE OF INTERACTION SO APHASIOLOGY LA English DT Article RP LYON, JG (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT VET AFFAIRS,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 7 TC 7 Z9 7 U1 0 U2 1 PU TAYLOR & FRANCIS LTD LONDON PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0268-7038 J9 APHASIOLOGY JI Aphasiology PD JAN-FEB PY 1995 VL 9 IS 1 BP 84 EP 94 DI 10.1080/02687039508248694 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA QB072 UT WOS:A1995QB07200010 ER PT J AU KIENZLE, TE HENKEL, JS LING, JY BANKS, MC BEERS, DR JONES, B STROOP, WG AF KIENZLE, TE HENKEL, JS LING, JY BANKS, MC BEERS, DR JONES, B STROOP, WG TI CLONING AND RESTRICTION-ENDONUCLEASE MAPPING OF HERPES-SIMPLEX VIRUS TYPE-1 STRAINS H129 AND +GC SO ARCHIVES OF VIROLOGY LA English DT Note ID CENTRAL-NERVOUS-SYSTEM; COMPLETE DNA-SEQUENCE; LONG UNIQUE REGION; SEIZURE MODEL; REPEAT REGION; VIRAL-DNA; GENOME; NEUROVIRULENCE; ENCEPHALITIS; VIRULENCE AB EcoRI fragments of herpes simplex virus I (HSV-1) strains H129 and +GC were cloned and the EcoRI and BglII restriction enzyme sites were mapped. Comparison of these enzyme sites with the sequence of HSV-1 strain 17syn+ demonstrated that all EcoRI sites were identical. For H129, the BglII sites were also found to match strain 17syn+ BglII sites. With one exception, the BglII sites in strain +GC also aligned with the strain 17syn+ sequence. The one exception was a missing BglII site from strain +GC located between bases 25 149 and 25154 in the EcoRI D fragment within the viral deoxyribonuclease gene (UL(12)). The BglII site represents the first difference to be mapped within HSV-1 strains 11129 and +GC which have unique pathobiological properties in animal models of acute and reactivated infections. C1 UNIV ARKANSAS MED SCI HOSP,DEPT MICROBIOL & IMMUNOL,LITTLE ROCK,AR 72205. JOHN MCCLELLAN VET AFFAIRS MED CTR,LITTLE ROCK,AR. BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT OPHTHALMOL,HOUSTON,TX 77030. HOUSTON VET AFFAIRS MED CTR,HOUSTON,TX. VET AFFAIRS MED CTR,SALT LAKE CITY,UT 84148. UNIV ARKANSAS MED SCI HOSP,DEPT PATHOL,LITTLE ROCK,AR 72205. UNIV ARKANSAS MED SCI HOSP,DEPT OPHTHALMOL,LITTLE ROCK,AR 72205. FU NIDCD NIH HHS [5R01 DC1706]; NIMH NIH HHS [F31 MH10094] NR 39 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1995 VL 140 IS 9 BP 1663 EP 1675 DI 10.1007/BF01322540 PG 13 WC Virology SC Virology GA RU149 UT WOS:A1995RU14900014 PM 7487498 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R KLEIN, RL AF SILVA, JA LEONG, GB WEINSTOCK, R KLEIN, RL TI PSYCHIATRIC FACTORS ASSOCIATED WITH DANGEROUS MISIDENTIFICATION DELUSIONS SO BULLETIN OF THE AMERICAN ACADEMY OF PSYCHIATRY AND THE LAW LA English DT Article; Proceedings Paper CT 24th Annual Meeting of the American-Academy-of-Psychiatry-and-the-Law CY OCT 21-24, 1993 CL SAN ANTONIO, TX SP Amer Acad Psychiat & Law ID CAPGRAS SYNDROME; VIOLENCE AB The delusional misidentification syndromes are characterized by misidentification delusions of others or of the self. Aggressive ideas or behaviors often accompany these delusions. The relationship between delusional misidentification and dangerousness remains for the most part poorly understood. In the present article, we compare a group of dangerous individuals suffering from dangerous misidentification delusions with a group of dangerous individuals suffering from other types of delusions. individuals with dangerous misidentification delusions were more likely to experience grandiose ideation, thought disorder, generalized hostility, excitement, general psychopathology, and a previous history of violence than dangerous delusional individuals with no delusional misidentification. The group with dangerous delusional misidentification syndromes was less likely to attack others with weapons than were the dangerous delusional group with no delusional misidentification. C1 UNIV TEXAS,CTR HLTH SCI,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF IRVINE,GRAD SCH MANAGEMENT,IRVINE,CA 92717. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 35 TC 20 Z9 20 U1 0 U2 3 PU AMER ACAD PSYCHIATRY LAW PI BLOOMFIELD PA ONE REGENCY DR, PO BOX 30, BLOOMFIELD, CT 06002 SN 0091-634X J9 B AM ACAD PSYCH LAW JI Bull. Amer. Acad. Psychiat. Law PY 1995 VL 23 IS 1 BP 53 EP 61 PG 9 WC Law; Psychiatry SC Government & Law; Psychiatry GA QU923 UT WOS:A1995QU92300005 PM 7599372 ER PT J AU WEINSTOCK, R GARRICK, T AF WEINSTOCK, R GARRICK, T TI IS LIABILITY POSSIBLE FOR FORENSIC PSYCHIATRISTS SO BULLETIN OF THE AMERICAN ACADEMY OF PSYCHIATRY AND THE LAW LA English DT Article; Proceedings Paper CT 24th Annual Meeting of the American-Academy-of-Psychiatry-and-the-Law CY OCT 21-24, 1993 CL SAN ANTONIO, TX SP Amer Acad Psychiat & Law AB Forensic psychiatrists are not as vulnerable to liability as general psychiatrists. The absence of a traditional physician-patient relationship and judicial and quasijudicial immunity are all protective against malpractice actions. Although the absence of a doctor-patient relationship removes an essential element of malpractice, other types of liability such as defamation and ordinary negligence are possible and may not be covered by malpractice insurance. A model is proposed for forensic psychiatry of a partial secondary doctor-patient relationship out-weighed in most circumstances by duties to truth and/or the hiring attorney. Such a model seems most consistent with conflicting duties currently forced on all psychiatrists. This model has advantages of a duty, a violation of which is likely to be covered by malpractice insurance. Rather than deemphasizing partial secondary physician-patient responsibilities, it is advised to stress the protection provided by judicial and quasijudicial immunity. C1 UNIV CALIF LOS ANGELES,FORENS PSYCHIAT TRAINING PROGRAM,LOS ANGELES,CA 90024. RP WEINSTOCK, R (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV 116AC,WILSHIRE & SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. NR 12 TC 8 Z9 8 U1 0 U2 0 PU AMER ACAD PSYCHIATRY LAW PI BLOOMFIELD PA ONE REGENCY DR, PO BOX 30, BLOOMFIELD, CT 06002 SN 0091-634X J9 B AM ACAD PSYCH LAW JI Bull. Amer. Acad. Psychiat. Law PY 1995 VL 23 IS 2 BP 183 EP 193 PG 11 WC Law; Psychiatry SC Government & Law; Psychiatry GA RG949 UT WOS:A1995RG94900002 PM 8605402 ER PT J AU ROODMAN, GD AF ROODMAN, GD TI APPLICATION OF BONE-MARROW CULTURES TO THE STUDY OF OSTEOCLAST FORMATION AND OSTEOCLAST PRECURSORS IN MAN SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article; Proceedings Paper CT NIA/NIDR Workshop on Human Models of Skeletal Aging CY MAR 01-02, 1994 CL WASHINGTON, DC SP NIA, NIDR ID TRANSFORMING GROWTH-FACTOR; MULTINUCLEATED CELLS; INHIBITS FORMATION; PAGETS-DISEASE; TRANSPLANTATION; OSTEOPETROSIS; PHENOTYPE; INVITRO RP ROODMAN, GD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 15 TC 10 Z9 10 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 1995 VL 56 SU 1 BP S22 EP S23 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QE653 UT WOS:A1995QE65300010 PM 7719977 ER PT J AU PRABHU, SD FREEMAN, GL AF PRABHU, SD FREEMAN, GL TI EFFECT OF TACHYCARDIA HEART-FAILURE ON THE RESTITUTION OF LEFT-VENTRICULAR FUNCTION IN CLOSED-CHEST DOGS SO CIRCULATION LA English DT Article DE MECHANICS; CALCIUM; MYOCARDIAL CONTRACTION; HEART FAILURE ID END-SYSTOLIC PRESSURE; FORCE-INTERVAL RELATIONSHIP; SARCOPLASMIC-RETICULUM; MECHANICAL RESTITUTION; GENE-EXPRESSION; MAJOR CAUSE; CALCIUM; MYOCARDIUM; DYSFUNCTION; RELAXATION AB Background Cardiac mechanical restitution and relaxation restitution are thought to be physiological correlates of the recovery kinetics of Ca2+ release mechanisms and sequestration capacity of the sarcoplasmic reticulum (SR). Since congestive heart failure is characterized by abnormal intracellular Ca2+ handling, we sought to delineate changes in mechanical and relaxation restitution produced by heart failure. Methods and Results Six dogs instrumented with left ventricular (LV) micromanometers and piezoelectric dimension crystals were studied under control conditions and after tachycardia heart failure (THF) produced by rapid LV pacing for 3 to 4 weeks. After priming at a basic cycle length of 375 ms, test pulses were delivered at graded extrasystolic intervals (ESIs). Mechanical response was assessed from single-beat elastance. Relaxation was assessed from the time constant of isovolumic relaxation (tau), the average rate of pressure fall during isovolumic relaxation (R(avg)) and peak negative dP/dt, the first derivative of LV pressure. Normalized mechanical and relaxation responses plotted against ESI produced monoexponential curves of mechanical and relaxation restitution. THF depressed baseline contractile and relaxation parameters compared with control (end-systolic elastance, 4.7+/-0.4 versus 7.1+/-0.5 mm Hg/mL, P<.005; tau, 34.8+/-2.2 versus 26.7+/-1.2 ms, P<.05; all values mean+/-SEM). THF slowed mechanical restitution and delayed development of peak contractile response, with the time constant of mechanical restitution increasing from 61.8+/-6.9 to 100.2+/-9.6 ms, P<.01. THF abolished the biphasic behavior of relaxation restitution, and this relation was approximated by a single monoexponential function. There was no difference in the time constants of the first phase of relaxation restitution at control and after THF (TCR1, normalized 1/R(avg), 44.3+/-5.6 versus 42.0+/-8.5 ms, P=NS; TCR1, normalized (dP/dt(min))(-1), 42.2+/-6.3 versus 36.7+/-4.3 ms, P=NS). Conclusions These results indicate that THF alters the recovery kinetics of SR Ca2+ release to a significantly greater extent than those of SR Ca2+ sequestration and that the abnormal time course of Ca2+ availability to the myofilaments is the rate-limiting step in the recovery of cardiac function after a depolarization. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP PRABHU, SD (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED CARDIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78229, USA. RI Prabhu, Sumanth/D-5223-2009 NR 40 TC 40 Z9 41 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 JAN 1 PY 1995 VL 91 IS 1 BP 176 EP 185 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA PZ555 UT WOS:A1995PZ55500026 PM 7805200 ER PT J AU DUNKIN, JJ OSATO, S LEUCHTER, AF AF DUNKIN, JJ OSATO, S LEUCHTER, AF TI RELATIONSHIPS BETWEEN EEG COHERENCE AND NEUROPSYCHOLOGICAL TESTS IN DEMENTIA SO CLINICAL ELECTROENCEPHALOGRAPHY LA English DT Article DE DEMENTIA; EEG COHERENCE; NEUROPSYCHOLOGICAL TESTS; QUANTITATIVE EEG ID MULTI-INFARCT DEMENTIA; ALZHEIMERS-DISEASE; HUMAN-BRAIN; DIAGNOSIS; POTENTIALS; PATTERNS; TASK C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP DUNKIN, JJ (reprint author), UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,QUANTITAT EEG LAB,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. FU NIA NIH HHS [P30 AG10123]; NIMH NIH HHS [MH00665, MH 40705] NR 31 TC 34 Z9 35 U1 0 U2 1 PU CLINICAL EEG PI ELM GROVE PA 850 ELM GROVE RD,SUITE 11, ELM GROVE, WI 53122 SN 0009-9155 J9 CLIN ELECTROENCEPHAL JI Clin. Electroencephalogr. PD JAN PY 1995 VL 26 IS 1 BP 47 EP 59 PG 13 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA PY166 UT WOS:A1995PY16600005 PM 7882542 ER PT J AU Minassian, BA Sainz, J DelgadoEscueta, AV AF Minassian, BA Sainz, J DelgadoEscueta, AV TI Genetics of myoclonic and myoclonus epilepsies SO CLINICAL NEUROSCIENCE LA English DT Article DE myoclonic and myoclonus epilepsies; chromosomal locus; genetic linkage mapping ID DENTATORUBRAL-PALLIDOLUYSIAN ATROPHY; RAGGED-RED FIBERS; IDIOPATHIC GENERALIZED EPILEPSY; BATTEN-DISEASE; UNVERRICHT-LUNDBORG; LINKAGE ANALYSIS; CHROMOSOME 6P; LOCUS; LOCALIZATION; REGION AB Mendelian forms of benign myoclonic epilepsies where a chromosomal locus has been defined include (1) the autosomal dominant (AD) juvenile myoclonic epilepsy (JME) in chr. 6p11, (2) the autosomal dominant childhood absence epilepsy which evolves to JME in chr. 1p, (3) familial adult myoclonic epilepsy of Yasuda and Inazuki, and (4) possibly JME within the idiopathic generalized epilepsy susceptibility gene in chr. 8 reported by Zara et al (1995). Other myoclonic epilepsy syndromes with onset in the first year of life (Aicardi's Neonatal (Early) Myoclonic Encephalopathy, West's Syndrome, Dravet's Severe Myoclonic Epilepsy, and Dravet's Benign Myoclonic Epilepsy of Infancy), in early childhood (Lennox-Gastaut-Dravet Syndrome, Myoclonic Variant of Lennox Gastaut Dravet Syndrome, Myoclonic-Astatic Epilepsy of Doose, Benign Myoclonic Epilepsies (BME), or even in late childhood (Childhood Absence Epilepsy with myoclonias, vs. Myoclonic Absence Epilepsy) are probably genetically complex diseases. Amongst the progressive myoclonus epilepsy syndromes, specific mutations have already been defined in Unverricht Lundborg disease, ceroid lipofuscinoses 3 or Spielmayer Voight syndrome within Battens disease, sialidosis, dentadorubropallidoluysian atrophy and the mitochondrial syndrome MERRF. Most recently our laboratories established the locus for Lafora's disease in chr. 6q and results are speadily moving towards the definition of its mutation. (C) 1996 Wiley-Liss, Inc. C1 W LOS ANGELES VET AFFAIRS MED CTR,CTR EPILEPSY,LOS ANGELES,CA 90073. UNIV TORONTO,HOSP SICK CHILDREN,DEPT NEUROL,TORONTO,ON M5G 1X8,CANADA. CALIF COMPREHENS EPILEPSY PROGRAM,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. NR 87 TC 13 Z9 14 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 1065-6766 J9 CLIN NEUROSCI JI Clin. Neurosci. PY 1995 VL 3 IS 4 BP 223 EP 235 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA VK158 UT WOS:A1995VK15800008 PM 8891396 ER PT J AU Frueh, BC Turner, SM Beidel, DC AF Frueh, BC Turner, SM Beidel, DC TI Exposure therapy for combat-related PTSD: A critical review SO CLINICAL PSYCHOLOGY REVIEW LA English DT Review ID POSTTRAUMATIC-STRESS-DISORDER; OBSESSIVE-COMPULSIVE DISORDER; VIETNAM VETERANS; PSYCHOPHYSIOLOGICAL ASSESSMENT; PERSONALITY-DISORDERS; EMOTIONAL IMAGERY; CARDIAC RESPONSE; RELEVANT STIMULI; FLOODING THERAPY; ANXIETY AB This review critically examines the treatment outcome literature using exposure treatment for combat-related Posttraumatic Stress Disorder (PTSD). Although the current literature is quite underdeveloped, available data suggest that exposure is superior to wait-list controls and ''standard treatment.'' In particular; exposure treatment results in decreased symptoms of intrusive images, cognitions, and physiological arousal. Treatment gains are maintained for as long as 6 months. Limitations of current studies, important procedural variables, patient characteristics, and issues of measurement are highlighted. Finally, efficacy of exposure alone as a treatment for PTSD and the need for addition of other behavioral treatment strategies to exposure is discussed. C1 MED UNIV S CAROLINA, DEPT PSYCHIAT & BEHAV SCI, ANXIETY PREVENT & TREATMENT RES CTR, CHARLESTON, SC USA. MED UNIV S CAROLINA, DEPT PSYCHIAT & BEHAV SCI, RALPH H JOHNSON VET AFFAIRS MED CTR, CHARLESTON, SC USA. NR 115 TC 41 Z9 41 U1 0 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0272-7358 J9 CLIN PSYCHOL REV JI Clin. Psychol. Rev. PY 1995 VL 15 IS 8 BP 799 EP 817 DI 10.1016/0272-7358(95)00049-6 PG 19 WC Psychology, Clinical SC Psychology GA TK788 UT WOS:A1995TK78800005 ER PT J AU ALTSTIEL, LD LAWLOR, B MOHS, R SCHMEIDLER, J DALTON, A MEHTA, P DAVIS, K AF ALTSTIEL, LD LAWLOR, B MOHS, R SCHMEIDLER, J DALTON, A MEHTA, P DAVIS, K TI ELEVATED ALPHA(1)-ANTICHYMOTRYPSIN SERUM LEVELS IN A SUBSET OF NONDEMENTED FIRST-DEGREE RELATIVES OF ALZHEIMERS-DISEASE PATIENTS SO DEMENTIA LA English DT Article DE ALZHEIMERS-DISEASE; FIRST-DEGREE RELATIVE; ACUTE PHASE REACTANT; ALPHA(1)-ANTICHYMOTRYPSIN ID DOWNS-SYNDROME; ALPHA-1-ANTICHYMOTRYPSIN; PLAQUES; STATE AB A portion of Alzheimer's disease (AD) patients have elevated serum levels of the acute phase reactant a(1)-antichymotrypsin (A1ACT) compared to age-matched controls. We measured serum levels of A1ACT in AD patients, age-matched controls, Down's syndrome patients, and nondemented first-degree relatives of AD patients. Significantly elevated levels of A1ACT were found in both AD patients and first-degree-relatives. In AD patients, serum A1ACT concentrations decreased with increasing severity of cognitive impairment. These results may suggest that inflammatory phenomena may be an early component of AD pathophysiology. C1 BRONX VET ADM MED CTR,PSYCHIAT SERV,NEW YORK,NY. ST JAMES HOSP,DEPT PSYCHIAT TCD,DUBLIN 8,IRELAND. NEW YORK STATE INST BASIC RES DEV DISABIL,STATEN ISL,NY 10314. RP ALTSTIEL, LD (reprint author), CUNY MT SINAI SCH MED,DEPT PSYCHIAT,1 GUSTAVE LEVY PL,NEW YORK,NY 10029, USA. FU NIA NIH HHS [AG-05138, AG-02219]; NIDDK NIH HHS [DK-31775] NR 23 TC 28 Z9 28 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1013-7424 J9 DEMENTIA JI Dementia PD JAN-FEB PY 1995 VL 6 IS 1 BP 17 EP 20 DI 10.1159/000106917 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QF036 UT WOS:A1995QF03600003 PM 7728215 ER PT S AU LopesVirella, MF Virella, G AF LopesVirella, MF Virella, G BE Baba, S Kaneko, T TI Immune-mediated mechanisms of atherogenesis in diabetes SO DIABETES 1994 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 15th International-Diabetes-Federation Congress CY NOV 06-11, 1994 CL KOBE, JAPAN SP Int Diabet Federat DE adhesion molecules; cytokines; endothelial damage; foam cells; glycation; LDL-immune complexes; macrophages; modified lipoproteins; oxidation C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,DIV METAB ENDOCRINOL & NUTR,DEPT MED,CHARLESTON,SC 29403. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81725-5 J9 INT CONGR SER PY 1995 VL 1100 BP 399 EP 405 PG 3 WC Endocrinology & Metabolism; Medicine, General & Internal SC Endocrinology & Metabolism; General & Internal Medicine GA BE46T UT WOS:A1995BE46T00069 ER PT J AU DAVIS, KL YANG, RK DAVIDSON, M MOHS, RC RYAN, TM SCHMEIDLER, J KNOTT, PJ THAL, LJ GAMZU, ER AF DAVIS, KL YANG, RK DAVIDSON, M MOHS, RC RYAN, TM SCHMEIDLER, J KNOTT, PJ THAL, LJ GAMZU, ER TI ALZHEIMERS-DISEASE - TACRINE AND TACRINE METABOLITE CONCENTRATIONS IN PLASMA AND COGNITIVE CHANGE SO DRUG DEVELOPMENT RESEARCH LA English DT Article DE ALZHEIMERS DISEASE; TACRINE; TACRINE METABOLITES; COGNITIVE IMPROVEMENT ID PERFORMANCE LIQUID-CHROMATOGRAPHY; DOUBLE-BLIND; HUMAN-SERUM; PHARMACOKINETICS; HYDROCHLORIDE; MEMORY; TETRAHYDROAMINOACRIDINE; LECITHIN; DEMENTIA; 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE AB In a clinical trial of tacrine in patients with Alzheimer's disease, improvement, measured by changes on both total (ADAST) and the cognitive sub-component (ADASC) of the Alzheimer's Disease Assessment Scale (ADAS) over a 6-week period, correlated significantly with plasma levels of tacrine. Change on the ADAS (both total and the cognitive subcomponent) also correlated significantly with three monohydroxylated metabolites of tacrine 1,hydroxy-tacrine (1-OH-THA), 2,hydroxy-tacrine (2-OH-THA), and 4,hydroxy-tacrine (4-OH-THA). However, changes of the relatively small non-cognitive component of the ADAS were not significantly correlated with plasma levels of tacrine. Multiple correlational analysis revealed that the combined influences of these metabolites were no greater than the effects of tacrine alone in ameliorating the symptoms of Alzheimer's disease. An alternative measure of cognitive performance, the Mini Mental State Exam (MMSE) did not correlate significantly with plasma concentrations of tacrine or its metabolites. Tacrine and these metabolites are bound to plasma proteins. In 10 patients with Alzheimer's disease receiving tacrine, the percentage of tacrine, 1-OH-THA, 2-OH-THA, and 4-OH-THA, that was free in plasma was found to be 19.7 +/- 3.3, 51.3 +/- 7.7, 40.7 +/- 6.9, and 42.4 +/- 6.3 (mean +/- SD), respectively. (C) 1995 Wiley-Liss, Inc. C1 CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT PHARMACOL,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT NEUROBIOL,NEW YORK,NY 10029. BRONX VET ADM MED CTR,DIV PSYCHIAT,BRONX,NY. UNIV CALIF SAN DIEGO,DEPT NEUROSCI,SAN DIEGO,CA 92103. CAMBRIDGE NEUROSCI INC,CAMBRIDGE,MA. NR 35 TC 3 Z9 3 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0272-4391 J9 DRUG DEVELOP RES JI Drug Dev. Res. PD JAN PY 1995 VL 34 IS 1 BP 55 EP 65 DI 10.1002/ddr.430340109 PG 11 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QH392 UT WOS:A1995QH39200008 ER PT B AU FREEDMAN, R LEONARD, S ADLER, L BICKFORD, P BYERLEY, W COON, H MILLER, C LUNTZLEYBMAN, V MYLESWORSLEY, M NAGAMOTO, H ROSE, G STEVENS, K WALDO, M AF FREEDMAN, R LEONARD, S ADLER, L BICKFORD, P BYERLEY, W COON, H MILLER, C LUNTZLEYBMAN, V MYLESWORSLEY, M NAGAMOTO, H ROSE, G STEVENS, K WALDO, M BE Clarke, PBS Quik, M Adlkofer, F Thurau, K TI Nicotinic receptors and the pathophysiology of schizophrenia SO EFFECTS OF NICOTINE ON BIOLOGICAL SYSTEMS II SE ADVANCES IN PHARMACOLOGICAL SCIENCES LA English DT Proceedings Paper CT Satellite Symposium on The Effects of Nicotine on Biological Systems II, at the Congress of the International-Union-of-Pharmacology CY JUL 21-24, 1994 CL SAINTE ADELE, CANADA SP INT UNION PHARM, VERUM FDN RP DENVER VAMC,DEPT PSYCHIAT,DENVER,CO 80262, USA. RI Bickford, Paula/J-5970-2012 OI Bickford, Paula/0000-0001-9657-7725 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIRKHAUSER VERLAG PI BASEL PA PO BOX 133, CH-4010 BASEL, SWITZERLAND BN 3-7643-5083-0 J9 ADV PHAR SC PY 1995 BP 307 EP 312 PG 6 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA BC71W UT WOS:A1995BC71W00040 ER PT J AU UDDIN, S KIRSTEINS, L LAPAGLIA, N EMANUELE, NV LAWRENCE, AM KELLEY, MR EMANUELE, MA AF UDDIN, S KIRSTEINS, L LAPAGLIA, N EMANUELE, NV LAWRENCE, AM KELLEY, MR EMANUELE, MA TI FAILURE OF ETHANOL METABOLITES TO ALTER GONADOTROPIN-SECRETION OR LUTEINIZING-HORMONE SYNTHESIS IN-VITRO SO ENDOCRINE RESEARCH LA English DT Article ID PITUITARY-GONADAL AXIS; TESTOSTERONE SYNTHESIS; FEMALE RATS; CELLS; RELEASE; TRANSCRIPTION; ACETALDEHYDE; INHIBITION; ALCOHOL; LEVEL AB The impact of ethanol on the male reproductive axis are multiple and varied, with both gonadal and control hypothalamic-pituitary pertubations being reported. There appears to be a discrepancy, however, between the in vivo and in vitro effects of ethanol on hypothalamic luteinizing hormones releasing hormone (LHRH) and the pituitary gonadotropins luteinizing hormone (LH) and follicle stimulating hormone(FSH). While in vivo data suggests a decrease in LHRH release after EtOH, in vitro studies find no effect on secretion. Similarity, in vivo acute EtOH profoundly diminishes LH synthesis and secretion, while in vitro impaired release with no alteration in the transcription of beta LH has been found. A potential exploration for these discrept results could be the in vivo metabolism of EtOH into acetaldehyde and acetate, or the subsequent formation of salsolinol, a product of acetate combining with dopamine. To test this possibility, a series of in vitro experiments were conducted exposing dispensed anterior pituitary cells from male rats to different doses of acetaldehyde, acetate or salsolinol for varying amounts of time for which gonadotropin secretion and beta LH mRNA levels were assessed. The results demonstrated no effect of either acetaldehyde or acetate on basal or LHRH stimulated LH release, FSH release or steady-state beta LH mRNA levels. These data suggest that the metabolites of EtOH, which occur in vivo but not in vitro, are not responsible for the discrepant gonadotropin changes reported between the in vivo and in vitro setting. Other potential mechanisms to explain this phenomenon include differences in the molarity of EtOH, hyperprolactinemia and suprapituitary influences including hypothalamic LHRH, catecholamines, excitatory amino acids, substance P and beta endorphin. C1 LOYOLA UNIV,STRITCH SCH MED,PROGRAM MOLEC BIOL,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,RES SERV,HINES,IL 60141. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MED SERV,HINES,IL 60141. INDIANA UNIV,SCH MED,DEPT PEDIAT,PEDIAT ENDOCRINOL SECT,INDIANAPOLIS,IN 46202. INDIANA UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOL,INDIANAPOLIS,IN 46202. RP UDDIN, S (reprint author), LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153, USA. FU NIAAA NIH HHS [5 R01 AA08661-05]; PHS HHS [2 R01 A067555-08] NR 36 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1995 VL 21 IS 3 BP 653 EP 670 PG 18 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RT309 UT WOS:A1995RT30900012 PM 7588434 ER PT J AU Klitzman, D Almenoff, PL Cardozo, C Lesser, M AF Klitzman, D Almenoff, PL Cardozo, C Lesser, M TI Bradykinin-induced airway microvascular leakage is potentiated by enalaprilat but not by phosphoramidon SO ENZYME & PROTEIN LA English DT Article DE endopeptidase 24.11; neutral endopeptidase; angiotensin-converting enzyme; bradykinin; phosphoramidon; enalaprilat; microvascular permeability ID PLATELET-ACTIVATING-FACTOR; GUINEA-PIG AIRWAYS; PLASMA EXUDATION; INDUCED BRONCHOCONSTRICTION; NEUTRAL ENDOPEPTIDASE; PULMONARY CIRCULATION; SUBSTANCE-P; HUMAN-LUNG; HISTAMINE; ASTHMA AB The objective of the study was to determine if bradykinin-induced airway microvascular leakage in rats was altered by pretreatment of animals with enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), or phosphoramidon, an inhibitor of endopeptidase 24.11 (EP 24.11). We found that the intravascular infusion of bradykinin induced microvascular leakage of Evans blue dye in tracheal tissue (0.088+/-0.035 mu g/mg tissue) that was significantly amplified by pretreatment with 3.27 mM enalaprilat (0.458+/-0.226 mu g/mg tissue), but not by pretreatment with 10 mM phosphoramidon (0.082+/-0.0453 mu g/mg tissue). Leakage in carinal tissue was also amplified by pretreatment with 3.27 mM enalaprilat (0.205+/-0.050 vs. 0.036+/-0.006 mu g/mg tissue for bradykinin alone), whereas no amplification was observed in parenchymal tissue by pretreatment with either inhibitor. These findings indicate that in the rat, ACE, but not EP 24.11, modulates bradykinin-induced airway microvascular leakage following intravascular infusion of these agents. C1 BRONX VET AFFAIRS MED CTR,PULM SECT,BRONX,NY 10468. MT SINAI SCH MED,DEPT MED,NEW YORK,NY. MT SINAI SCH MED,DEPT PHARMACOL,NEW YORK,NY. NR 37 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1019-6773 J9 ENZYME PROTEIN JI Enzyme Protein PY 1995 VL 48 IS 4 BP 191 EP 196 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU473 UT WOS:A1995TU47300001 ER PT J AU SWARTZ, BE HALGREN, E KRISTAKUMDORN, T DAIMES, R AF SWARTZ, BE HALGREN, E KRISTAKUMDORN, T DAIMES, R TI LATERALIZATION OF FUNCTION DURING THE INTRACAROTID AMYTAL TEST (IAP) - TEMPORAL-LOBE EPILEPSY (TLE) SO EPILEPSIA LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,LOS ANGELES,CA 90024. SANTA MONICA HOSP MED CTR,CAL CEP & NEUROEPILEPSY PROGRAM,SANTA MONICA,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 4 BP 127 EP 127 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA TD347 UT WOS:A1995TD34700038 ER PT J AU LICHT, EA SANKAR, R GEE, M MASON, BA AF LICHT, EA SANKAR, R GEE, M MASON, BA TI PREGNANCIES OF WOMEN WITH EPILEPSY - A SURVEY OF PHYSICIAN PRACTICE PATTERNS SO EPILEPSIA LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PEDIAT,DIV PEDIAT NEUROL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DEPT NEUROL,EPILEPSY UNIT,LOS ANGELES,CA 90073. WAYNE STATE UNIV,DEPT OBSTET & GYNECOL,DETROIT,MI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 4 BP 616 EP 616 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA TD347 UT WOS:A1995TD34700611 ER PT J AU OHARA, K CHIN, M COOKE, C HYNEMAN, A AF OHARA, K CHIN, M COOKE, C HYNEMAN, A TI SEIZURE PRECAUTIONS - A NEW LOOK SO EPILEPSIA LA English DT Meeting Abstract C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA. COLL PHARM & SCI,PHILADELPHIA,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1995 VL 36 SU 4 BP H6 EP H6 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA TD347 UT WOS:A1995TD34700367 ER PT J AU MARDER MELTZER AF MARDER MELTZER TI INTOLERANCE TO NEUROLEPTIC DRUGS - THE ART OF AVOIDING EXTRAPYRAMIDAL SYNDROMES - DISCUSSION SO EUROPEAN PSYCHIATRY LA English DT Article RP MARDER (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0767-399X J9 EUR PSYCHIAT JI Eur. Psychiat. PY 1995 VL 10 SU 1 BP S32 EP S32 PG 1 WC Psychiatry SC Psychiatry GA QW115 UT WOS:A1995QW11500008 ER PT J AU MARDER, S AF MARDER, S TI DEFINING AND CHARACTERIZING TREATMENT-RESISTANT SCHIZOPHRENIA SO EUROPEAN PSYCHIATRY LA English DT Article DE SCHIZOPHRENIA; TREATMENT; CLOZAPINE AB This paper argues for a brooder definition of treatment refractoriness that would include patients with partial drug responses, a relatively recent onset, less dramatic symptoms and intolerance to conventional drugs. The drug trials that define their responsiveness should be carefully conducted over a prolonged period of time, but need not include high doses or supplemental medications. If the consensus conference can agree on a definition of responsiveness, it will provide important guidance to clinicians as well as researchers. RP MARDER, S (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0767-399X J9 EUR PSYCHIAT JI Eur. Psychiat. PY 1995 VL 10 SU 1 BP S7 EP S10 DI 10.1016/0767-399X(96)80078-2 PG 4 WC Psychiatry SC Psychiatry GA QW115 UT WOS:A1995QW11500002 PM 19698382 ER PT J AU GOODFRIEND, TL EGAN, B STEPNIAKOWSKI, K BALL, DL AF GOODFRIEND, TL EGAN, B STEPNIAKOWSKI, K BALL, DL TI RELATIONSHIPS AMONG PLASMA-ALDOSTERONE, HIGH-DENSITY-LIPOPROTEIN CHOLESTEROL, AND INSULIN IN HUMANS SO HYPERTENSION LA English DT Article DE INSULIN RESISTANCE; ADRENAL GLOMERULOSA; HYPERTENSION, CORONARY DISEASE RISK ID ZONA GLOMERULOSA CELLS; BLOOD-PRESSURE; ESSENTIAL-HYPERTENSION; WEIGHT-REDUCTION; OBESE PATIENTS; FATTY-ACIDS; GLUCOSE; RENIN; SECRETION; MEN AB To investigate the pathogenesis of hypertension in patients with obesity and insulin resistance and to explore the role of plasma lipids, we studied 30 subjects at the end of 7 days of low (20 mEq/d) then high (200 mEq/d) sodium diets. Glucose and insulin tolerance tests were performed at the end of each week and blood and urine collected for measurements of plasma aldosterone, renin activity, electrolytes, insulin, and lipoproteins. There was a strong negative correlation between plasma aldosterone and high-density lipoprotein cholesterol during both diets. There were weaker positive correlations between plasma aldosterone and insulin or triglycerides. When the aldosterone-renin ratio was the dependent variable and the correlation controlled for serum potassium, the inverse relationship with high-density lipoprotein cholesterol and the positive correlation with insulin remained, but only during the high salt diet. Subjects were divided into three groups based on high-density lipoprotein cholesterol. Subjects with the lowest high-density lipoprotein cholesterol levels showed the highest aldosterone, plasma triglycerides, body mass index, and waist-to-hip ratio. Those subjects also demonstrated the greatest resistance to insulin action on glucose and plasma unesterified fatty acids. There was a weak direct correlation between plasma aldosterone and systolic blood pressure during the high salt diet. These data suggest that high aldosterone levels may be a link between dyslipidemia, insulin resistance, and hypertension, a relationship made more evident by high salt intake. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI. UNIV WISCONSIN,DEPT PHARMACOL,MADISON,WI 53706. MED UNIV S CAROLINA,DEPT PHARMACOL,DIV CLIN PHARMACOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCRR NIH HHS [M01-RR00058, M01-RR01070]; PHS HHS [R01-43164] NR 26 TC 53 Z9 56 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1995 VL 25 IS 1 BP 30 EP 36 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QA740 UT WOS:A1995QA74000004 PM 7843750 ER PT S AU Kunkel, LA Vescio, R Cao, J Hong, CH Kim, A Schiller, GJ Lichtenstein, AK Berenson, JR AF Kunkel, LA Vescio, R Cao, J Hong, CH Kim, A Schiller, GJ Lichtenstein, AK Berenson, JR BE Casali, P Silberstein, LE TI Analysis of multiple myeloma third complementarity-determining regions reveals characteristics of prenatal B cells SO IMMUNOGLOBULIN GENE EXPRESSION IN DEVELOPMENT AND DISEASE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Immunoglobulin Gene Expression in Development and Disease CY JUL 13-17, 1994 CL MONTREAL, CANADA SP New York Acad Sci ID DIVERSITY C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. RP Kunkel, LA (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DIV HEMATOL ONCOL,LOS ANGELES,CA 90024, USA. NR 3 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-933-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 764 BP 519 EP 522 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Immunology GA BE39E UT WOS:A1995BE39E00079 PM 7486579 ER PT J AU CHIAPPELLI, F KUNG, MA VILLANUEVA, P LEE, P FROST, P PRIETO, N AF CHIAPPELLI, F KUNG, MA VILLANUEVA, P LEE, P FROST, P PRIETO, N TI IMMUNOTOXICITY OF COCAETHYLENE SO IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY LA English DT Article ID COCAINE; ETHANOL; ALCOHOL; METABOLITE; CONCURRENT AB This report describes the response of normal human T cells to stimulation in vitro in the presence of nano-micromolar concentrations of cocaethylene. Thymidine incorporation by concanavalin A-stimulated peripheral blood mononuclear cells was generally blunted by cocaethylene, albeit to different degrees depending upon the donor tested. The formation of concanavalin A-induced blast cells was decreased by increasing concentrations of cocaethylene. The production of interleukin-2 was also blunted in a dose-dependent fashion by cocaethylene, and this outcome was more consistently observed in stimulated peripheral blood mononuclear cells, compared to unseparated whole blood preparations. An inverse dose dependence was obtained in relation to the response of blast cells to recombinant human interleukin-2 in the presence of cocaethylene. These lines of evidence, taken together with our preliminary studies aimed at testing the effect of cocaethylene on the expression of certain membrane markers of activation (i.e., interleukin-2 receptor, transferrin receptor, serine aminopeptidase IV) and the expression of the proliferating cell nuclear antigen (cyclin PCNA), suggest that cocaethylene modulates relatively early events following T cell stimulation probably related to the interleukin-2 system. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROBIOL,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,HUMAN IMMUNOL & PSYCHONEUROIMMUNOL LAB,LOS ANGELES,CA 90073. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES,SCH DENT,DIV DIAGNOST SCI,HUMAN ORAL & MOLEC IMMUNOL LAB,LOS ANGELES,CA 90024, USA. OI Frost, Patrick/0000-0003-3348-5983 FU NIDA NIH HHS [DA07683] NR 31 TC 4 Z9 4 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0892-3973 J9 IMMUNOPHARM IMMUNOT JI Immunopharmacol. Immunotoxicol. PY 1995 VL 17 IS 2 BP 399 EP 417 DI 10.3109/08923979509019759 PG 19 WC Immunology; Pharmacology & Pharmacy; Toxicology SC Immunology; Pharmacology & Pharmacy; Toxicology GA RB111 UT WOS:A1995RB11100012 PM 7650298 ER PT J AU DENCKER, SJ GOLDBERG, D LADER, M LIBERMAN, RP AF DENCKER, SJ GOLDBERG, D LADER, M LIBERMAN, RP TI IMPROVEMENT OF THE QUALITY-OF-LIFE IN SCHIZOPHRENIA - IMPROVEMENT OF COMPLIANCE - QUALITY ASSURANCE - INCREASED QUALITY-OF-LIFE IN COMMUNITY CARE OF SCHIZOPHRENIA - PAPERS PRESENTED DURING THE XIITH AEP CONGRESS, COPENHAGEN, SEPTEMBER 1994 SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY LA English DT Editorial Material C1 GOTHENBURG UNIV,DEPT CLIN NEUROSCI,GOTHENBURG,SWEDEN. INST PSYCHIAT,LONDON SE5 8AF,ENGLAND. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,CAMARILLO STATE HOSP,CAMARILLO RES CTR,LOS ANGELES,CA. RP DENCKER, SJ (reprint author), SAHLGRENS UNIV HOSP,PSYCHIAT SECT,S-41345 GOTHENBURG,SWEDEN. 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 0268-1315 J9 INT CLIN PSYCHOPHARM JI Int. Clin. Psychopharmacol. PD JAN PY 1995 VL 9 SU 5 BP 3 EP 3 PG 1 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA QT372 UT WOS:A1995QT37200001 ER PT J AU LIBERMAN, RP KOPELOWICZ, A AF LIBERMAN, RP KOPELOWICZ, A TI BASIC ELEMENTS IN BIOBEHAVIORAL TREATMENT AND REHABILITATION OF SCHIZOPHRENIA SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT XIIth AEP (Average Evoked Potential) Congress CY SEP, 1994 CL COPENHAGEN, DENMARK DE SCHIZOPHRENIA; BIOBEHAVIORAL THERAPY ID SOCIAL SKILLS; EXPRESSED EMOTION; CONTROLLED TRIAL; MENTALLY-ILL; MANAGEMENT; INTERVENTION; HALOPERIDOL; FAMILIES; RELAPSE AB The psychopathology and associated disabilities experienced by persons with schizophrenia have only partially responded to conventional pharmacological and psychosocial treatment approaches. Biobehavioral therapy employs behavioral and symptomatic assessment, social learning principles, and skills training, to amplify the effects of pharmacotherapy. Comprehensive, continuous, and integrated biobehavioral therapy-aiming at early detection and treatment of schizophrenic symptoms, family and social skills training, and teaching coping and illness self-management skills-has been documented to improve the course and outcome of schizophrenia as measured by symptom recurrence, social functioning, and quality of life, Biobehavioral therapies must be delivered in the context of a collaborative relationship among patients, families and clinicians that together can optimize outcomes. Services need to be provided by assertive, outreach, community-based teams that tailor the type, frequency and scope of services to the phase of the individual's illness. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,CAMARILLO STATE HOSP,CAMARILLO RES CTR,LOS ANGELES,CA. LOS ANGELES CTY DEPT MENTAL HLTH,SAN FERNANDO MENTAL HLTH CLIN,LOS ANGELES,CA. RP LIBERMAN, RP (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. OI kopelowicz, alex/0000-0002-1728-4105 NR 52 TC 17 Z9 17 U1 2 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0268-1315 J9 INT CLIN PSYCHOPHARM JI Int. Clin. Psychopharmacol. PD JAN PY 1995 VL 9 SU 5 BP 51 EP 58 DI 10.1097/00004850-199501005-00009 PG 8 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA QT372 UT WOS:A1995QT37200009 PM 7622835 ER PT J AU DENCKER, SJ LIBERMAN, RP AF DENCKER, SJ LIBERMAN, RP TI FROM COMPLIANCE TO COLLABORATION IN THE TREATMENT OF SCHIZOPHRENIA SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT XIIth AEP (Average Evoked Potential) Congress CY SEP, 1994 CL COPENHAGEN, DENMARK ID MANAGEMENT C1 GOTHENBURG UNIV,DEPT CLIN NEUROSCI,GOTHENBURG,SWEDEN. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,CAMARILLO STATE HOSP,CAMARILLO RES CTR,LOS ANGELES,CA. RP DENCKER, SJ (reprint author), SAHLGRENS UNIV HOSP,PSYCHIAT SECT,S-41345 GOTHENBURG,SWEDEN. NR 12 TC 16 Z9 17 U1 2 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0268-1315 J9 INT CLIN PSYCHOPHARM JI Int. Clin. Psychopharmacol. PD JAN PY 1995 VL 9 SU 5 BP 75 EP 78 DI 10.1097/00004850-199501005-00012 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA QT372 UT WOS:A1995QT37200012 PM 7622838 ER PT J AU CRAIG, WA AF CRAIG, WA TI KINETICS OF ANTIBIOTICS IN RELATION TO EFFECTIVE AND CONVENIENT OUTPATIENT PARENTERAL THERAPY SO INTERNATIONAL JOURNAL OF ANTIMICROBIAL AGENTS LA English DT Article DE OUTPATIENT PARENTERAL ANTIBIOTIC THERAPY (OPAT); KINETICS OF DRUGS ID PENICILLIN-G; PHARMACOKINETICS; SUSCEPTIBILITY; EFFICACY; INVITRO AB An important goal of outpatient parenteral antibiotic therapy (OPAT) is to provide a drug and dosing regimen that allows for convenient administration of the antibiotic in the outpatient setting. While once-daily administration or handling of the drug would be ideal, dosing frequencies up to three times a day for intravenous administration and twice daily for intramuscular injection can be tolerated by most patients. The frequency and method of antimicrobial administration is dependent not only on the kinetics of drug concentrations in serum and tissues (i.e pharmacokinetics), but also on the kinetics or time course of the drug's antimicrobial activity (i.e. pharmacodynamics). This short review will focus on the interaction between pharmacokinetics and pharmacodynamics for the major classes of antibacterial agents used for outpatient parenteral therapy. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 19 TC 9 Z9 9 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-8579 J9 INT J ANTIMICROB AG JI Int. J. Antimicrob. Agents PD JAN PY 1995 VL 5 IS 1 BP 19 EP 22 DI 10.1016/0924-8579(94)00048-Y PG 4 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA QE147 UT WOS:A1995QE14700005 PM 18611640 ER PT J AU MENDEZ, MF AF MENDEZ, MF TI THE NEUROPSYCHIATRY OF MULTIPLE-SCLEROSIS SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE MULTIPLE SCLEROSIS; DEMENTIA; DEPRESSION; APRAXIA; CORPUS CALLOSUM; DISCONNECTION; DEMYELINATION ID COGNITIVE FUNCTION; CORPUS-CALLOSUM; DEMENTIA; IMPAIRMENT; DISORDER; DISEASE; ANTEROGRADE; DISABILITY; DEPRESSION; ATROPHY AB Objective: This article examines the cognitive and psychiatric features of multiple sclerosis. MS can manifest as a neuropsychiatric disturbance even in the absence of physical disabilities. Method: Two MS patients with predominant behavioral symptoms are described, and the literature is reviewed. Results: The first patient had an interhemispheric disconnection syndrome, and the second patient had cognitive fatigue and depression. Other patients have slowed information processing speed, memory retrieval difficulty, frontal-executive dysfunction, and visuospatial difficulty. Conclusions: MS results in specific cognitive deficits and mood disorders. These two patients had organic mental disorders from cerebral demyelination particularly affecting the corpus callosum. Other patients have neuropsychiatric symptoms from extensive demyelination of prefrontal-subcortical circuits. Evaluation and management strategies are discussed. C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA. RP MENDEZ, MF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROBEHAV UNIT,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 53 TC 12 Z9 13 U1 2 U2 4 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1995 VL 25 IS 2 BP 123 EP 135 DI 10.2190/NK8F-MTUW-QHH1-0531 PG 13 WC Psychiatry SC Psychiatry GA RN036 UT WOS:A1995RN03600001 PM 7591490 ER PT J AU MENDEZ, MF AF MENDEZ, MF TI THE NEUROPSYCHIATRIC ASPECTS OF BOXING SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE BOXING; PUGILISM; DEMENTIA PUGILISTICA; PUNCH DRUNK; HEAD TRAUMA; CHRONIC TRAUMATIC ENCEPHALOPATHY; CLOSED HEAD INJURY; CONCUSSION; POST-CONCUSSION SYNDROME ID CHRONIC BRAIN-DAMAGE; ACTIVE AMATEUR BOXERS; DEMENTIA-PUGILISTICA; HEAD-INJURY; NEUROFIBRILLARY TANGLES; ALZHEIMERS-DISEASE; PROFESSIONAL BOXERS; COMPUTED-TOMOGRAPHY; LEAD; CT AB Objective: To review the neuropsychiatry of boxing. Method: This update considers the clinical, neuropsychological, diagnostic, neurobiological, and management aspects of boxing-related brain injury. Results: Professional boxers with multiple bouts and repeated head blows are prone to chronic traumatic encephalopathy (CTE). Repeated head blows produce rotational acceleration of the brain, diffuse axonal injury, and other neuropathological features. CTE includes motor changes such as tremor, dysarthria, and parkinsonism; cognitive changes such as mental slowing and memory deficits; and psychiatric changes such as explosive behavior, morbid jealousy, pathological intoxication, and paranoia. Screening with neuropsychological tests and neuroimaging may help predict those boxers at risk for CTE. Conclusions: Boxing results in a spectrum of CTE ranging from mild, nonprogressive motor changes to dementia pugilistica. Recent emphasis on safety in the ring, rehabilitation techniques, and other interventions do not eliminate the risk for CTE. For this reason, there is an active movement to ban boxing. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. RP MENDEZ, MF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROBEHAV UNIT 691116AF,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 75 TC 74 Z9 75 U1 0 U2 12 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1995 VL 25 IS 3 BP 249 EP 262 DI 10.2190/CUMK-THT1-X98M-WB4C PG 14 WC Psychiatry SC Psychiatry GA TF010 UT WOS:A1995TF01000003 PM 8567192 ER PT J AU Silva, JA Leong, GB Tekell, JL Bowden, CL AF Silva, JA Leong, GB Tekell, JL Bowden, CL TI Visual perceptual disturbances in delusional misidentification SO ISRAEL JOURNAL OF PSYCHIATRY AND RELATED SCIENCES LA English DT Article ID CAPGRAS SYNDROME; DISORDER; SELF AB The delusional misidentification syndromes can involve physical misidentification. Delusional misidentification of the physical make-up of the self shares delusional dysmorphic symptoms with delusional disorder of the somatic type. In this article, we discuss how the study of delusional and perceptual symptoms in delusional misidentification syndromes may lead to a better understanding of the delusional dysmorphic process. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA 90073. RP Silva, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 20 TC 0 Z9 0 U1 0 U2 0 PU GEFEN PUBL HOUSE LTD PI JERUSALEM PA PO BOX 6056, JERUSALEM 91060, ISRAEL SN 0333-7308 J9 ISRAEL J PSYCHIAT JI Isr. J. Psychiatr. Relat. Sci. PY 1995 VL 32 IS 4 BP 286 EP 290 PG 5 WC Psychiatry SC Psychiatry GA TQ656 UT WOS:A1995TQ65600014 PM 8641858 ER PT J AU COMPTON, PA LING, W CHARUVASTRA, VC WESSON, DR AF COMPTON, PA LING, W CHARUVASTRA, VC WESSON, DR TI BUPRENORPHINE AS A PHARMACOTHERAPY FOR COCAINE ABUSE - A REVIEW OF THE EVIDENCE SO JOURNAL OF ADDICTIVE DISEASES LA English DT Review ID RHESUS-MONKEYS; OPIOID DEPENDENCE; METHADONE-MAINTENANCE; WITHDRAWAL; DETOXIFICATION; ANTAGONISTS; ADDICTS; TRIAL AB The partial mu-opiate agonist, buprenorphine, is the subject of recent evaluation as a potential pharmacotherapy for cocaine dependence. This paper reviews the extant preclinical and clinical evidence of buprenorphine effectiveness in treating cocaine abuse, including data from our large methadone comparison trial and a smaller buprenorphine dose ranging study. Although buprenorphine appears to reduce cocaine self-administration in studies of non-opiate dependent animals, clinical evidence for the same response in opiate addicts abusing cocaine has not been demonstrated. Further efficacy trials should await preclinical demonstrations of effectiveness in samples with opiate and cocaine exposure. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA. SUMMIT MED CTR,OAKLAND,CA. RP COMPTON, PA (reprint author), LOS ANGELES ADDICT TREATMENT RES CTR,10350 SANTA MONICA BLVD,SUITE 340,LOS ANGELES,CA 90025, USA. FU NIDA NIH HHS [DA 06082] NR 56 TC 18 Z9 18 U1 2 U2 3 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1995 VL 14 IS 3 BP 97 EP 114 DI 10.1300/J069v14n03_07 PG 18 WC Substance Abuse SC Substance Abuse GA TC347 UT WOS:A1995TC34700007 PM 8555282 ER PT J AU LEAF, DA MACRAE, H AF LEAF, DA MACRAE, H TI VALIDITY OF 2 INDIRECT MEASURES OF ENERGY-EXPENDITURE DURING WALKING IN THE ELDERLY SO JOURNAL OF AGING AND PHYSICAL ACTIVITY LA English DT Article DE PHYSICAL ACTIVITY; KILOCALORIE EXPENDITURE; EXERCISE ID PHYSICAL-ACTIVITY; RUNNING ECONOMY; EXERCISE; OLD AB The purpose of this study was to examine the criterion-related validity of two indirect measures of energy expenditure (EE): American College of Sports Medicine (ACSM) predictive equations, and estimated EE based on the Caltrac accelerometer. These measures were compared in 20 community-dwelling older men and women (mean age 71 years). The strength of the relationships among major determinants of EE during self-selected speeds of treadmill and outdoor walking was also examined. EE measured by respiratory gas analysis during an exercise stress test was highly correlated with ACSM predictive equations and poorly correlated with Caltrac. Multivariate regression equations were established to evaluate the ability of independent variables-body weight and height, age, and preferred treadmill walking speed-to predict EE (dependent variable). It was concluded that the ACSM predictive equations are suitable for use in elderly individuals, and that the apparent differences in the relationships between treadmill and outdoor walking speeds on EE deserve further investigation. C1 PEPPERDINE UNIV,DEPT SPORTS MED,MALIBU,CA 90263. RP LEAF, DA (reprint author), UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073, USA. NR 25 TC 2 Z9 2 U1 1 U2 5 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST BOX 5076, CHAMPAIGN, IL 61820-5076 SN 1063-8652 J9 J AGING PHYS ACTIV JI J. Aging Phys. Act. PD JAN PY 1995 VL 3 IS 1 BP 97 EP 106 PG 10 WC Geriatrics & Gerontology; Gerontology; Sport Sciences SC Geriatrics & Gerontology; Sport Sciences GA QA358 UT WOS:A1995QA35800007 ER PT J AU BRIDGES, AJ AF BRIDGES, AJ TI RHEUMATIC DISORDERS IN PATIENTS WITH SILICONE IMPLANTS - A CRITICAL-REVIEW SO JOURNAL OF BIOMATERIALS SCIENCE-POLYMER EDITION LA English DT Review DE RHEUMATIC DISEASE; SCLERODERMA; MYOSITIS; CONNECTIVE TISSUE DISEASE; SILICONE ID CONNECTIVE-TISSUE DISEASE; GEL BREAST IMPLANTS; SYSTEMIC-SCLEROSIS; AUGMENTATION MAMMOPLASTY; REVISED CRITERIA; SCLERODERMA; WOMEN; CLASSIFICATION; DERMATOMYOSITIS; AUTOANTIBODIES AB More than 1000 patients with rheumatic disorders and silicone implants have been reported. In this review, the clinical features of patients with scleroderma, inflammatory myositis, systemic lupus erythematosus and silicone implants are discussed. The clinical features of the most common rheumatic disorder associated with silicone implants, the ''Silicone Implant Associated Syndrome'', are introduced. In addition, other local regional, and neurologic disorders associated with silicone implants are discussed. This comprehensive clinical review provides the clinician with information regarding the common symptoms, signs and laboratory features of rheumatic disorders of patients with silicone implants. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,CLIN IMMUNOL LAB,MADISON,WI 53706. RP BRIDGES, AJ (reprint author), UNIV WISCONSIN,SCH MED,RHEUMATOL SECT,MADISON,WI 53706, USA. NR 50 TC 19 Z9 20 U1 0 U2 0 PU VSP BV PI ZEIST PA PO BOX 346, 3700 AH ZEIST, NETHERLANDS SN 0920-5063 J9 J BIOMAT SCI-POLYM E JI J. Biomater. Sci.-Polym. Ed. PY 1995 VL 7 IS 2 BP 147 EP 157 PG 11 WC Engineering, Biomedical; Materials Science, Biomaterials; Polymer Science SC Engineering; Materials Science; Polymer Science GA QZ524 UT WOS:A1995QZ52400006 PM 7654629 ER PT J AU SANCHEZ, CP GOODMAN, WG BRANDLI, D GOLDENHERSH, M MURRAY, C CARLTON, E HAHN, T SALUSKY, IB AF SANCHEZ, CP GOODMAN, WG BRANDLI, D GOLDENHERSH, M MURRAY, C CARLTON, E HAHN, T SALUSKY, IB TI SKELETAL RESPONSE TO RECOMBINANT HUMAN GROWTH-HORMONE (RHGH) IN CHILDREN TREATED WITH LONG-TERM CORTICOSTEROIDS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID JUVENILE CHRONIC ARTHRITIS; FACTOR-I; LINEAR GROWTH; BONE TURNOVER; GH DEFICIENCY; SERUM; SOMATOMEDIN; 1,25-DIHYDROXYVITAMIN-D; PROLIFERATION; RETARDATION AB Corticosteroid therapy causes osteopenia and growth retardation in children; such changes are associated with diminished rates of bone formation and turnover. Since growth hormone activates bone remodeling, the biochemical and skeletal responses to rhGH were evaluated in four pediatric patients, aged 12.8 +/- 3 years, with long-term corticosteroid use (5 +/- 2 years). Recombinant human growth hormone (rhGH), 0.125 mg/kg, was given 3 times/week by subcutaneous injection for 12 months. Iliac crest bone biopsies were obtained after double tetracycline labeling before and at the end of rhGH therapy; serum levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone (intact), 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D-3, osteocalcin (BGP), and insulin-like growth factor-1 (IGF-1) were measured every 3 months during the treatment period. The average dose of prednisone was 0.24 +/- 0.05 mg/kg/day initially, and this did not change during the study. Serum calcium, phosphorus, alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D-3, and BGP were unchanged during the rhGH therapy, but the serum IGF-1 level increased by 71%, p < 0.01. Eroded bone perimeter and cancellous bone area did not change significantly during rhGH therapy. Bone formation rates rose from 423 +/- 475 to 781 +/- 407 mu m(2)/mm(2)/day, p < 0.05, and the length of double tetracycline-labeled bone perimeter increased by 85%, p < 0.05. The bone formation rate in the growth hormone group exceeded the values of an age-matched reference group (14.3 +/- 3 years), 780 +/- 407 mu m(2)/mm(2)/day versus 411 +/- 479 mu m(2)/mm(2)/day,p < 0.05. Thus, rhGH therapy increases osteoblastic activity, bone formation, and possibly bone turnover despite continued and prolonged corticosteroid administration in children. C1 NICHOLS INST,SAN JUAN CAPISTRANO,CA. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. FU NCRR NIH HHS [RR-00865]; NIDDK NIH HHS [DK-35423] NR 39 TC 28 Z9 29 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JAN PY 1995 VL 10 IS 1 BP 2 EP 6 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PZ869 UT WOS:A1995PZ86900002 PM 7747627 ER PT J AU WRIGHT, NM RENAULT, J HOLLIS, B BELL, NH KEY, LL AF WRIGHT, NM RENAULT, J HOLLIS, B BELL, NH KEY, LL TI EFFECT OF GROWTH-HORMONE ON BONE - BONE-MINERAL DENSITY, TRABECULAR BONE VOLUME, AND ALKALINE-PHOSPHATASE IMPROVE OR ARE RESTORED IN THE DWARF RAT TREATED WITH GROWTH-HORMONE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID OSTEOBLAST-LIKE CELLS; FACTOR-I; MEN; ABSORPTIOMETRY; DEFICIENCY; THERAPY; PUBERTY AB Studies were performed to determine whether serum total alkaline phosphatase (SAP), an index of bone formation; body weight; total body bone mineral density (BMD), measured by dual-energy X-ray absorptiometry; and tibial trabecular bone volume (TBV), measured by histomorphometry, are reduced in a-week-old female sexually immature Lewis dwarf (dw/dw) rats (DW-CT, n = 9) with isolated growth hormone (GH) deficiency and, if so, whether recombinant human GH (rhGH), 200 mu g/day subcutaneously for 4 weeks (DW-GH, n = 7), restores them. Studies were also performed to determine if 30% dietary restriction in 2-week-old female Lewis rats (LW-DR, n = 11) alters SAP, body weight, total BMD), or TBV compared with pair-fed controls (LW-CT, n = 7) given an ad libitum diet. Mean SAP (91 +/- 5 versus 109 +/- 5 U/l), body weight (102 +/- 11 versus 140 +/- 10 g), total BMD (88.5 +/- 0.3 versus 101.4 +/- 2.0 mg/cm(2)), and TBV (19.0 +/- 1.0 versus 27.0 +/- 1.4%) were significantly lower in DW-CT than in LW-CT animals,p < 0.05. In DW-GH, rhGH significantly increased mean SAP (130 +/- 7 U/l), bodyweight (133 +/- 10 g), total BMD (92.7 +/- 1.3), and TBV (24.0 +/- 1.9) compared with DW-CT animals. Compared with LW-CT rats, mean body weight and TBV were not different, but mean SAP was significantly higher (p < 0.01) and mean total BMD was significantly lower (p < 0.003) in DW-GH rats. In LW-DR compared with LW-CT animals, dietary restriction significantly reduced mean body weight (p < 0.05) but did not alter mean SAP, total BMD, or TBV. Thus, body weight, SAP, total BMD, and TBV were lower in DW-CT than in LW-CT rats. In the dose administered, SAP is markedly increased and reductions in body weight, total BMD, and TBV are completely or partially restored by treatment with rhGH in young female rats caused by isolated GH deficiency. Dietary restriction in young female rats with intact secretion of GH prevents weight gain but does not alter SAP, total BMD, or TBV compared with animals fed ad libitum. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC. RP WRIGHT, NM (reprint author), MED UNIV S CAROLINA,DEPT PEDIAT,DIV ENDOCRINOL,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 27 TC 17 Z9 17 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JAN PY 1995 VL 10 IS 1 BP 127 EP 131 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PZ869 UT WOS:A1995PZ86900016 PM 7747619 ER PT J AU VADAKEKALAM, J STAMOS, T SHENKER, Y AF VADAKEKALAM, J STAMOS, T SHENKER, Y TI SOMETIMES THE HOOVES DO BELONG TO ZEBRAS - AN UNUSUAL CASE OF HYPOPITUITARISM SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR, MED SERV, ENDOCRINOL SECT, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT MED, ENDOCRINOL SECT, MADISON, WI 53792 USA. NR 9 TC 5 Z9 5 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 17 EP 20 DI 10.1210/jc.80.1.17 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000004 PM 7829607 ER PT J AU KANNER, AM RAMIREZ, L JONES, JC AF KANNER, AM RAMIREZ, L JONES, JC TI THE UTILITY OF PLACING SPHENOIDAL ELECTRODES UNDER THE FORAMEN OVALE WITH FLUOROSCOPIC GUIDANCE SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Article DE SPHENOIDAL ELECTRODES; FLUOROSCOPY; ANTEROTEMPORAL SPIKES; FORAMEN OVALE; TEMPORAL LOBECTOMY ID TEMPORAL SPIKES; LOCALIZATION; EEG; EPILEPSY; SEIZURES AB Although sphenoidal electrodes are widely used to detect epileptiform activity, there is no agreement on an optimal target to which electrodes should be aimed. The purpose of this study was to determine whether fluoroscopic guidance is a reliable method for placing electrodes directly below the foramen ovale and whether such positioning enhances their capacity to detect epileptiform activity when compared to similar electrodes placed blindly into the infratemporal fossa. We examined the surface/sphenoidal EEG recordings of 17 patients with intractable partial seizures of anterotemporal origin, after fluoroscopically placed sphenoidal electrodes (FPSE) had been inserted to lie just below the foramen ovale. A criterion for eligibility was a previous prolonged video/EEG monitoring with blindly placed sphenoidal electrodes (BPSE) that failed to detect seizures with a focal onset, No blindly placed electrode, for which there was radiographic documentation, reached the foramen ovale. Fluoroscopic guidance assured accurate targeting. FPSE detected a unilateral anterotemporal interictal focus in four patients in whom BPSE had failed to record any interictal spikes and detected bitemporal independent interictal foci in one patient in whom BPSE had identified only unilateral spikes. In nine other patients, the spike count obtained with FPSE recordings increased by >100% when compared to that obtained with BPSE recordings. FPSE recorded seizures with an anterotemporal focal onset pattern in 10 patients in whom BPSE had recorded seizures with a regional, lateralized, or nonlocalized onset pattern. In nine of these 10 patients, this was adequate to recommend surgery and avoid invasive monitoring. Fluoroscopic guidance assures accurate targeting of the foramen ovale. When compared to BPSE, FPSE resulted in better detection of interictal and ictal epileptiform activity of mesial-basal-temporal origin. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT NEUROL,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT NEUROSURG,MADISON,WI. UNIV WISCONSIN,HOSP & CLIN,SCH MED,MADISON,WI 53792. NR 16 TC 32 Z9 32 U1 0 U2 0 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 JAN PY 1995 VL 12 IS 1 BP 72 EP 81 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA PY513 UT WOS:A1995PY51300008 PM 7896912 ER PT J AU MCCALL, WV MANN, SC SHELP, FE CAROFF, SN AF MCCALL, WV MANN, SC SHELP, FE CAROFF, SN TI FATAL PULMONARY-EMBOLISM IN THE CATATONIC SYNDROME - 2 CASE-REPORTS AND A LITERATURE-REVIEW SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID NEUROLEPTIC MALIGNANT SYNDROME; AMOBARBITAL INTERVIEW; LETHAL CATATONIA; BENZODIAZEPINES; STATES; STUPOR; MUTISM; DEATH; ECT AB Background: Catatonia is associated with excess early mortality when it is unrecognized or inadequately treated. The characteristics of the lethal catatonia subtype are now well described, but the excess mortality of the remaining patients with catatonic syndrome, particularly from pulmonary embolism, appears to be inadequately recognized. The fatal risk of the catatonic Syndrome is reviewed. Method: Two new case reports of sudden death from pulmonary embolism in catatonic syndrome are presented. The world literature on morbidity, mortality, and pulmonary embolism in catatonia was reviewed by a search of MEDLINE and PsychInfo from 1966 to the present. Additional older references were discovered by screening bibliographies from articles produced by the searches. Results: Twenty cases of autopsy-confirmed pulmonary embolism were found in patients with catatonic syndrome. Catatonic patients were more likely to die of pulmonary embolism and die earlier than patients with other types of schizophrenia. Death from pulmonary embolism did not occur until after the second week of catatonic symptoms and often occurred without warning. Conclusion: Risk of a fatal pulmonary embolism is inherent in persistent catatonic symptoms and may explain the observed excess early mortality. Prompt resolution of the catatonic syndrome with benzodiazepines, barbiturates, or electroconvulsive therapy is the best way to reduce risk of pulmonary embolism. The prophylactic value of physical therapy or anticoagulation merits further investigation. Despite the absence of controlled trials of treatment effectiveness, the catastrophic outcome of acute pulmonary embolism warrants early and vigorous intervention in catatonic patients. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNITED BEHAV SERV,RICHMOND,VA. RP MCCALL, WV (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PSYCHIAT & BEHAV MED,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. NR 50 TC 52 Z9 53 U1 0 U2 1 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JAN PY 1995 VL 56 IS 1 BP 21 EP 25 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA QE919 UT WOS:A1995QE91900004 PM 7836335 ER PT J AU HOUSER, BE ALDER, ME MCANEAR, JT AF HOUSER, BE ALDER, ME MCANEAR, JT TI DENSITY VARIATIONS OF AUTOLOGOUS BONE-GRAFTS ADJACENT TO DENTAL IMPLANTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HSC,SAN ANTONIO,TX 78285. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 111 EP 111 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800794 ER PT J AU SAUNDERS, MJ PAUNOVICH, ED CORNELL, JE AF SAUNDERS, MJ PAUNOVICH, ED CORNELL, JE TI ORAL HEALTH QUALITY-OF-LIFE INVENTORY - DEVELOPMENT AND VALIDATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,RCOHA,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 168 EP 168 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801246 ER PT J AU MCANEAR, JT SAUNDERS, MJ VENUS, CA CHAMBERLAIN, CK SMITH, C AF MCANEAR, JT SAUNDERS, MJ VENUS, CA CHAMBERLAIN, CK SMITH, C TI BITE FORCE FOLLOWING OSSEOINTEGRATED MAXILLARY BONE-GRAFTS AND IMPLANTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 170 EP 170 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801264 ER PT J AU VENUS, CA CHAMBERLAIN, CK SAUNDERS, MJ MCANEAR, JT AF VENUS, CA CHAMBERLAIN, CK SAUNDERS, MJ MCANEAR, JT TI CHANGES IN SPEECH ARTICULATION FOLLOWING REMOVAL OF DENTURES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 226 EP 226 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801710 ER PT J AU OLSEN, J SALIH, M HARRISON, JL HERRERA, I LUTHER, MF LIFSCHITZ, MD KATZ, MS YEH, CK AF OLSEN, J SALIH, M HARRISON, JL HERRERA, I LUTHER, MF LIFSCHITZ, MD KATZ, MS YEH, CK TI EFFECTS OF FOOD RESTRICTION ON INTRACELLULAR CALCIUM SIGNALING IN PAROTID ACINAR-CELLS OF AGING RATS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UTHSCSA,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 229 EP 229 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801735 ER PT J AU JONES, JD WILLMANN, DE ARNOLD, R SAUNDERS, MJ AF JONES, JD WILLMANN, DE ARNOLD, R SAUNDERS, MJ TI ASSESSING RELIABILITY OF RETENTION AND STABILITY MEASUREMENTS IN EVALUATING COMPLETE DENTURES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,RCOHA,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 240 EP 240 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801824 ER PT J AU ROYALL, DR MAHURIN, RK CORNELL, J AF ROYALL, DR MAHURIN, RK CORNELL, J TI EFFECT OF DEPRESSION ON DEMENTIA PRESENTATION - QUALITATIVE ASSESSMENT WITH THE QUALITATIVE EVALUATION OF DEMENTIA (QED) SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID MINI-MENTAL STATE; COGNITIVE IMPAIRMENT; ALZHEIMER TYPE; SUBCORTICAL DEMENTIA; BEDSIDE ASSESSMENT; SENILE DEMENTIA; DISEASE; PSEUDODEMENTIA; CRITERIA; FEATURES AB Two novel, bedsides, dementia assessment instruments, the Executive Interview (EXIT) and the Qualitative Evaluation of Dementia (QED) were used to examine the effects of DSM-III-R major depressive episodes on the clinical presentation of patients diagnosed with NINCDS ''possible'' AD. Intergroup comparisons were made of the various bedside cognitive measures given to 102 to 118 consecutive patients presenting to a university geriatric assessment clinic and consultation service. The assessment instruments used were: (1) the EXIT: a 15-minute, 25-item bedside interview for the assessment of executive control function (ECF); (2) the QED: a brief, clinically based checklist that operationalizes the approach of a geriatric psychiatrist to the qualitative assessment of dementing illnesses (when QED scores are mapped against EXIT scores, a qualitative picture of dementia typology emerges); and (3) the Mini-Mental State Exam (MMSE): a familiar bedside measure of cognitive function. Depressed and nondepressed patients differed significantly on the QED. There was no overlap in the QED scores of patients with probable AD versus those with depression. The QED discriminated between depressed and nondepressed patients with possible AD. Possible AD patients with depression could not be qualitatively distinguished from those with depression alone, although they could be discriminated by the EXIT. Only 44% of possible AD cases fall within the EXIT x QED 90% confidence limits for probable AD. No differences were found on either the QED or the MMSE between depressed non-AD patients and nondepressed patients exhibiting ''dementia with no cortical features.'' The MMSE was insensitive to cognitive impairment in non-AD cases. NINCDS ''possible'' AD is a qualitatively heterogeneous group. Depression alters the presentation of AD, with depressed Alzheimer's patients appearing qualitatively similar to other depressed patients, but with far more executive impairment. Patients with the ''dementia of depression'' cannot be qualitatively distinguished from those with subcortical dementias. The MMSE underestimates the level of executive cognitive impairment in qualitatively subcortical dementia. These distinctions can be made at the bedside through the combined use of the EXIT and the QED. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 55 TC 13 Z9 13 U1 4 U2 4 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON ST, PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD JAN PY 1995 VL 8 IS 1 BP 4 EP 11 PG 8 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA QE715 UT WOS:A1995QE71500002 PM 7710646 ER PT J AU DORFMAN, R WALTERS, K BURKE, P HARDIN, L KARANIK, T RAPHAEL, J SILVERSTEIN, E AF DORFMAN, R WALTERS, K BURKE, P HARDIN, L KARANIK, T RAPHAEL, J SILVERSTEIN, E TI OLD, SAD AND ALONE - THE MYTH OF THE AGING HOMOSEXUAL SO JOURNAL OF GERONTOLOGICAL SOCIAL WORK LA English DT Article ID DEPRESSIVE SYMPTOMS; SOCIAL SUPPORT; GAY AB This paper reports the findings of a survey of 108 elderly heterosexual and homosexual men and women in urban Central and Southern California. The purpose of the study was to test the assumption that elderly gay men and lesbians are more depressed and socially-isolated than their heterosexual cohort. The findings indicate that there are no significant differences between older heterosexuals and homosexuals in regard to depression and social support. However, the sources of social support vary with gay men and lesbians deriving significantly more support from friends, while heterosexual elderly derive more support from family. The findings suggest a need to redefine the concept of family to include ''friendship families.'' Future research which investigates the way in which these friendship families are created and maintained has the potential to benefit all elderly, especially those who have no biological families or whose biological families are unavailable for support. C1 W LOS ANGELES VET ADM,LOS ANGELES,CA. LOS ANGELES CTY DEPT CHILDRENS PROTECT SERV,LOS ANGELES,CA. MAPLE CTR,BEVERLY HILLS,CA. RP DORFMAN, R (reprint author), UNIV CALIF LOS ANGELES,DEPT SOCIAL WELFARE,LOS ANGELES,CA 90024, USA. NR 39 TC 34 Z9 34 U1 0 U2 1 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0163-4372 J9 J GERONTOL SOC WORK JI J. Gerontol. Soc. Work PY 1995 VL 24 IS 1-2 BP 29 EP 44 PG 16 WC Geriatrics & Gerontology; Social Work SC Geriatrics & Gerontology; Social Work GA TA219 UT WOS:A1995TA21900004 ER PT J AU Shenkar, R Cohen, AJ Vestweber, D Miller, YE Tuder, R Abraham, E AF Shenkar, R Cohen, AJ Vestweber, D Miller, YE Tuder, R Abraham, E TI Hemorrhage and resuscitation alter the expression of ICAM-1 and P-selectin in mice SO JOURNAL OF INFLAMMATION LA English DT Article DE inflammatory lung injury; blood loss; trauma; neutrophil infiltration; cell trafficking ID INTERCELLULAR-ADHESION MOLECULE-1; RESPIRATORY-DISTRESS SYNDROME; TUMOR-NECROSIS-FACTOR; HUMAN-ENDOTHELIAL-CELLS; GROWTH-FACTOR-BETA; WEIBEL-PALADE BODIES; OXYGEN-TOXICITY; FACTOR-ALPHA; LUNG INJURY; GMP-140 AB Acute inflammatory lung injury is a common clinical occurrence following blood loss and trauma, and is characterized by massive neutrophil infiltration into the lung. In order to better examine cell trafficking that may contribute to lung injury in this setting, we investigated in vivo mRNA levels and immunohistochemically determined expression of the adhesion molecules P-selectin and the intercellular adhesion molecule (ICAM)-1 in murine lungs over the 3-day period following hemorrhage and resuscitation. Significant increases in P-selectin mRNA levels were present in lungs obtained 3 days after hemorrhage. ICAM-1 mRNA levels were significantly increased 6 and 72 hr after hemorrhage. Immunohistochemical staining for P-selectin was enhanced on pulmonary vascular endothelium in all visible vessels at 6, 24, and 72 hr after hemorrhage. ICAM-1 immunoreactivity was significantly increased on the alveolar epithelium at 6 and 72 hr post-hemorrhage. These results suggest that increased expression of adhesion molecules in the lung at early post-hemorrhage timepoints may contribute to neutrophil infiltration into the lungs and the frequent development of acute lung injury following blood loss and trauma. (C) 1995 Wiley-Liss, Inc. C1 UNIV COLORADO,HLTH SCI CTR,DIV PULM SCI & CRIT CARE MED,DENVER,CO 80262. MAX PLANCK INST IMMUNBIOL,SPEMAN LABS,FREIBURG ZAHRINGER,GERMANY. DENVER VET AFFAIRS MED CTR,DENVER,CO. OI Vestweber, Dietmar/0000-0002-3517-732X FU NCI NIH HHS [P50 CA 58187]; NHLBI NIH HHS [HL 50284, R01 HL 45745] NR 53 TC 15 Z9 15 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 1078-7852 J9 J INFLAMM JI J. Inflamm. PY 1995 VL 45 IS 4 BP 248 EP 259 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Hematology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Hematology; Immunology GA TT108 UT WOS:A1995TT10800003 PM 8867669 ER PT J AU NETSCHER, DT WALKER, LE WEIZER, G THORNBY, J WIGODA, P BOWEN, D AF NETSCHER, DT WALKER, LE WEIZER, G THORNBY, J WIGODA, P BOWEN, D TI A REVIEW OF 198 PATIENTS (389 IMPLANTS) WHO HAD BREAST IMPLANTS REMOVED SO JOURNAL OF LONG-TERM EFFECTS OF MEDICAL IMPLANTS LA English DT Article DE BREAST IMPLANTS; RUPTURE RATE; FACTORS ASSOCIATED WITH RUPTURE ID CAPSULAR CONTRACTURE; AUGMENTATION MAMMAPLASTY; SILICONE GEL; PROSTHESES; DISEASE; RUPTURE; SAFETY AB Because of the large number of women now returning to their plastic surgeons with concerns about their breast implants many years after surgery, we are afforded an ideal opportunity to evaluate these patients over the long-term. This study reviewed 198 patients (389 implants) who underwent explantation by two surgeons over a 2-year period, correlating prosthesis type, location, and length of time since implantation with two adverse endpoints, implant rupture and symptomatic capsular contracture. Significant findings included a relatively high rate of implant rupture in patients whose implants had been in place over 20 years, an increased incidence of both symptomatic capsular contracture and implant rupture in single lumen gel implants and a positive correlation between severity of capsular contracture and implant rupture. C1 BAYLOR COLL MED,HOUSTON,TX 77030. DEPT VET AFFAIRS MED CTR,HOUSTON,TX 77030. UNIV TEXAS,SOUTHWESTERN MED CTR,DALLAS,TX 75235. RP NETSCHER, DT (reprint author), BAYLOR COLL MED,DIV PLAST SURG,6560 FANNIN,SUITE 800,HOUSTON,TX 77030, USA. NR 21 TC 12 Z9 12 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, STE 1202, NEW YORK, NY 10016-7892 SN 1050-6934 J9 J LONG-TERM EFF MED JI J. Long-Term Eff. Med. Implants PY 1995 VL 5 IS 1 BP 11 EP 18 PG 8 WC Engineering, Biomedical; Medicine, Research & Experimental; Orthopedics; Pathology SC Engineering; Research & Experimental Medicine; Orthopedics; Pathology GA TF738 UT WOS:A1995TF73800002 PM 10163505 ER PT J AU MONTOYA, ID HAERTZEN, C HESS, JM COVI, L FUDALA, PJ JOHNSON, RE GORELICK, DA AF MONTOYA, ID HAERTZEN, C HESS, JM COVI, L FUDALA, PJ JOHNSON, RE GORELICK, DA TI COMPARISON OF PSYCHOLOGICAL SYMPTOMS BETWEEN DRUG-ABUSERS SEEKING AND NOT SEEKING TREATMENT SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Note ID COCAINE ABUSERS; PSYCHOPATHOLOGY; ADDICTS C1 UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. RP MONTOYA, ID (reprint author), NIDA,INTRAMURAL RES PROGRAM,POB 5180,BALTIMORE,MD 21224, USA. FU Intramural NIH HHS [Z99 DA999999] NR 16 TC 5 Z9 6 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD JAN PY 1995 VL 183 IS 1 BP 50 EP 53 DI 10.1097/00005053-199501000-00011 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QB802 UT WOS:A1995QB80200010 PM 7807072 ER PT J AU Syndulko, K Woldanski, A Baumhefner, RW Tourtellotte, WW AF Syndulko, K Woldanski, A Baumhefner, RW Tourtellotte, WW TI Preliminary evaluation of lowering tympanic temperature for the symptomatic treatment of multiple sclerosis SO JOURNAL OF NEUROLOGIC REHABILITATION LA English DT Article DE multiple sclerosis; cooling; symptomatic treatment; cooling garment ID SEVERITY; SCALE; HEAD AB Objective: Two pilot studies were designed to assess the effects of acute cooling in the laboratory (experiment one) and daily home cooling (experiment two) on objective indices of MS impairment and disability. Methods: Experiment one was a single group, repeated measures design in which nine MS outpatients with a history of heat lability were tested for immediate effects of lowering tympanic temperature in the laboratory. Subjects were tested under three experimental conditions separated by about one week: cooling with each of two cooling garments (the Life Support Systems, Inc., Mark VII MicroClimate System(TM) and the SteeleVest(TM) Body Cooling System) and no cooling. Experiment two was a prospective, unblinded, parallel group study in which twelve chronic progressive MS outpatients with a history of heat lability entered a six-week cooling protocol. Subjects used a cooling suit at home to lower body temperature two times per day. Five additional MS patients were in a non-cooling control group. In both experiments subjects were evaluated by clinical, neuroperformance, and quality of life indices, and were tested with a reduced battery of indices immediately before and after cooling on their weekly visit to the laboratory. Results: In experiment one, significant temperature decreases (mean 0.6 degrees C) were achieved with both cooling garments, but no statistically significant change in performance post-cooling was found on any test measure. In experiment: two, eight out of twelve subjects reported reduced fatigue and improved ability to ambulate immediately after and up to two to three hours after cooling. There was a significant immediate post-cooling (non-cumulative) improvement on tandem gait and standing balance. Additionally, seven subjects reported long-term improvements in quality of life over the cooling weeks. No statistically significant cumulative effect of cooling was found on objective indices of motor and cognitive function. Conclusions: The results provided weak subjective support for both acute and cumulative effects of cooling. A placebo effect cannot be ruled out. The study raised important questions regarding development of an appropriate sham cooling procedure, measurement of core temperature changes, and other design issues in evaluating cooling in MS patients. C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. NR 27 TC 11 Z9 11 U1 1 U2 1 PU DEMOS PUBLICATIONS PI NEW YORK PA 386 PARK AVE S STE 201, NEW YORK, NY 10016-8804 SN 0888-4390 J9 J NEUROL REHABIL JI J. Neurol. Rehabil. PY 1995 VL 9 IS 4 BP 205 EP 215 PG 11 WC Clinical Neurology; Rehabilitation SC Neurosciences & Neurology; Rehabilitation GA VP017 UT WOS:A1995VP01700004 ER PT J AU BROTHERS, TE ROBISON, JG ELLIOTT, BM BOGGS, JM FRANKEL, AE WILLINGHAM, MC AF BROTHERS, TE ROBISON, JG ELLIOTT, BM BOGGS, JM FRANKEL, AE WILLINGHAM, MC TI UP-REGULATION OF B-FGF RECEPTOR EXPRESSION AFTER CAROTID BYPASS SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT Annual Symposium of the Association-of-Veterans-Administration-Surgeons CY MAY 05-07, 1994 CL RENO, NV SP ASSOC VET ADM SURGEONS ID FIBROBLAST GROWTH-FACTOR; SMOOTH-MUSCLE CELLS; INTIMAL HYPERPLASIA; ARTERIES; ATHEROSCLEROSIS; PREVENTION; RESTENOSIS; INJURY; GRAFT; TOXIN AB Basic fibroblast growth factor (b-FGF) appears to be an important positive modulator of the neointimal hyperplasia that occurs after prosthetic vascular graft implantation through its effects on vascular myointimal/smooth muscle cell migration and proliferation. The distribution and extent of b-FGF receptor (b-FGFR1) expression was compared using immunohistochemical techniques in normal porcine carotid arteries and at various times up to 6 weeks following implantation of small caliber prosthetic vascular grafts. At the time of graft harvest, specimens were infused with OCT medium at 100 mm Hg and rapidly frozen in liquid nitrogen. Transverse sections of the perianastomotic arterial tissues were labeled with primary mouse monoclonal antibody directed toward the extracellular domain of the receptor, followed by goat-anti mouse IgG and rabbit anti-goat IgG conjugated to horseradish peroxidase. The b-FGFR1-positive cells were identified by peroxidase activity within the Golgi complex of smooth muscle cells. Normal porcine carotid arteries showed no evidence of staining for b-FGFR1. However, at 6 weeks cells in the perianastomotic area clearly showed significant b-FGFR1 localization. Anti-muscle actin labeling confirmed these to be smooth muscle cells. The observed upregulation of b-FGFR1 expression supports the concept of positive feedback by cytokines as a contributing factor to the hyperplastic response of smooth muscle cells after prosthetic vascular graft implantation. This finding further supports a potential strategy to specifically target activated smooth muscle cells through use of mitotoxin therapy. (C) 1995 Academic Press, Inc. C1 MED UNIV S CAROLINA,MED CTR,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,MED CTR,DEPT PATHOL,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. RP BROTHERS, TE (reprint author), MED UNIV S CAROLINA,MED CTR,DEPT SURG,CHARLESTON,SC 29425, USA. NR 26 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JAN PY 1995 VL 58 IS 1 BP 28 EP 32 DI 10.1006/jsre.1995.1005 PG 5 WC Surgery SC Surgery GA QD067 UT WOS:A1995QD06700005 PM 7830402 ER PT J AU GLATT, CR AF GLATT, CR TI ANCIENT ZIONISM - THE BIBLICAL ORIGINS OF THE NATIONAL IDEA - ERLICH,A SO LIBRARY JOURNAL LA English DT Book Review RP GLATT, CR (reprint author), PHILADELPHIA VA MED CTR,PHILADELPHIA,PA, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 SN 0363-0277 J9 LIBR J JI Libr. J. PD JAN PY 1995 VL 120 IS 1 BP 107 EP 107 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA QC391 UT WOS:A1995QC39100139 ER PT J AU MCHORNEY, CA WARE, JE AF MCHORNEY, CA WARE, JE TI CONSTRUCTION AND VALIDATION OF AN ALTERNATE FORM GENERAL MENTAL-HEALTH SCALE FOR THE MEDICAL OUTCOMES STUDY SHORT-FORM 36-ITEM HEALTH SURVEY SO MEDICAL CARE LA English DT Article DE HEALTH STATUS ASSESSMENT; MENTAL HEALTH; ALTERNATE FORMS; RELIABILITY; INSTRUMENT DEVELOPMENT ID QUALITY-OF-LIFE; FUNCTIONAL STATUS; RANDOMIZED TRIAL; SURVEY SF-36; PRIMARY CARE; VALIDITY; INSTRUMENT; RELIABILITY; PROFILE; IMPACT AB Alternate-form health measures are useful for clinical trials or health services research requiring repeated administrations over a short interval of time. Further, by using alternate-form methodology, they can be utilized to estimate score reliability. Data from the Medical Outcomes Study were used to evaluate five alternate forms of the Short-Form 36-Item Health Survey (SF-36) general mental health scale (MHI-5). Well-established psychometric criteria were used to select the best alternate form and to estimate the reliability of the MHI-5 using the alternate-form methodology. Although a considerable degree of comparability across the five alternate forms was observed for criteria pertaining to estimates of item-internal consistency and reliability, distributional characteristics of scales, tests of empirical validity, and score equivalence at the individual level, we recommend one alternate form that satisfied all evaluation criteria and did so better than any other alternate form. Using the alternate-form methodology of estimating reliability, results suggest that the internal-consistency method underestimates the reliability of the MHI-5 by 3%. The methodology presented here should prove useful to others interested in constructing and evaluating alternate forms, and the alternate form recommended here (MHI-5AF) should prove useful across many health status assessment applications. C1 UNIV WISCONSIN, SCH MED, DEPT PREVENT MED, MADISON, WI USA. TUFTS UNIV NEW ENGLAND MED CTR, INST HLTH, BOSTON, MA 02111 USA. RP MCHORNEY, CA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR, HLTH SERV RES & DEV FIELD PROGRAM, 2500 OVERLOOK TERRACE, MADISON, WI 53705 USA. NR 49 TC 124 Z9 126 U1 0 U2 7 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD JAN PY 1995 VL 33 IS 1 BP 15 EP 28 DI 10.1097/00005650-199501000-00002 PG 14 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA QB423 UT WOS:A1995QB42300002 PM 7823644 ER PT B AU OGAWA, M HIRAYAMA, F AF OGAWA, M HIRAYAMA, F BE Mihich, E Metcalf, D TI Cytokine regulation of lymphohemopoietic progenitors SO NORMAL AND MALIGNANT HEMATOPOIESIS: NEW ADVANCES SE PEZCOLLER FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT 6th Pezcoller Symposium on Normal and Malignant Hematopoiesis - New Advances CY JUN 29-JUL 01, 1994 CL ROVERETO, ITALY SP Pezcoller Fdn C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. NR 0 TC 6 Z9 6 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45136-0 J9 PEZ FDN SYM PY 1995 VL 6 BP 11 EP 14 PG 4 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Research & Experimental Medicine; Microbiology GA BE24B UT WOS:A1995BE24B00002 ER PT J AU KATO, K MARTINEZ, V STPIERRE, S TACHE, Y AF KATO, K MARTINEZ, V STPIERRE, S TACHE, Y TI CGRP ANTAGONISTS ENHANCE GASTRIC-ACID SECRETION IN 2-H PYLORUS-LIGATED RATS SO PEPTIDES LA English DT Article DE CGRP; CGRP(8-37); CGRP ANTIBODY; GASTRIC ACID SECRETION; PYLORUS LIGATION; PENTAGASTRIN ID GENE-RELATED PEPTIDE; THYROTROPIN-RELEASING-HORMONE; SENSORY NEURONS; MONOCLONAL-ANTIBODY; CALCITONIN; CAPSAICIN; INHIBITION; STOMACH; IMMUNONEUTRALIZATION; AFFERENT AB The influence of calcitonin gene-related peptide (CGRP) antagonists on gastric acid secretion was investigated in rats. Intravenous injection of the CGRP receptor antagonist, CGRP(8-37)(128 nmol/kg) or the CGRP antibody #4901 (4.8 mg/kg, IV) completely prevented alpha-CGRP (3.9 nmol/kg/h)-induced inhibition of acid response to pentagastrin in urethane-anesthetized rats with gastric fistula. CGRP antibody (4.8 mg/kg, IV) increased by 93% gastric acid secretion in conscious rats with pylorus ligation for 2 h. CGRP(8-37) (128 nmol/kg, IV) also enhanced the acid response measured 2 h after pylorus ligation in conscious rats and in urethane-anesthetized rats infused with pentagastrin by 91% and 56%, respectively. These results suggest that endogenous CGRP attenuates the gastric acid response measured 2 h after pylorus ligation. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR ULCER RES & EDUC,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90073. UNIV QUEBEC,INST NATL RECH SCI SANTE,POINTE CLAIRE,PQ H9R 1G6,CANADA. RI Martinez, Vicente/N-1189-2014 FU NIDDK NIH HHS [DK-41301, DK-30110]; NIMH NIH HHS [MH-00663] NR 38 TC 23 Z9 23 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 PY 1995 VL 16 IS 7 BP 1257 EP 1262 DI 10.1016/0196-9781(95)02004-G PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA TA633 UT WOS:A1995TA63300014 PM 8545247 ER PT J AU MILLER, M HAROUTUNIAN, V WILTSHIRECLEMENT, M AF MILLER, M HAROUTUNIAN, V WILTSHIRECLEMENT, M TI ALTERED ALERTNESS OF VASOPRESSIN-SECRETING TRANSGENIC MICE SO PEPTIDES LA English DT Article DE ADH; AVP; BEHAVIOR; EMOTIONALITY; LEARNING; MEMORY; TRANSGENIC MICE; VASOPRESSIN ID DEFICIENT BRATTLEBORO RAT; BRIGHTNESS-DISCRIMINATION; BEHAVIOR; OXYTOCIN; MEMORY; REVERSAL; PEPTIDES; GENE AB We evaluated behavior and cognitive performance in a line of transgenic mice that overexpress the rat gene for vasopressin. Open field testing revealed greatest habituation in homozygous mice. Passive avoidance performance indicated equal learning and memory ability of transgenic compared to normal mice. Drinking behavior following exposure to 10% sucrose solution suggested diminished neophobia in homozygous mice. These observations are consistent with enhanced attention and alertness in the transgenic animals and support prior observations on the effects of vasopressin on behavior and cognitive function. C1 CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,NEW YORK,NY 10029. RP MILLER, M (reprint author), CUNY MT SINAI SCH MED,DEPT GERIATR & ADULT DEV,BOX 1070,1 GUSTAVE L LEVY PL,NEW YORK,NY 10029, USA. NR 29 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 PY 1995 VL 16 IS 8 BP 1329 EP 1333 DI 10.1016/0196-9781(95)02047-0 PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA TK330 UT WOS:A1995TK33000002 PM 8745040 ER PT J AU EJAZ, AA MCSHANE, AP GANDHI, VC LEEHEY, DJ ING, TS AF EJAZ, AA MCSHANE, AP GANDHI, VC LEEHEY, DJ ING, TS TI HYPOMAGNESEMIA IN CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS PATIENTS DIALYZED WITH A LOW-MAGNESIUM PERITONEAL-DIALYSIS SOLUTION SO PERITONEAL DIALYSIS INTERNATIONAL LA English DT Article DE HYPOMAGNESEMIA; MAGNESIUM AB Objective: Previous studies have shown a decrease in serum magnesium (Mg) concentration when continuous ambulatory peritoneal dialysis (CAPD) patients previously maintained on a 1.0 - 1.2 mEq/L Mg peritoneal dialysis solution (PDS) were dialyzed with a 0.5 mEq/L Mg PDS. However, the prevalence of hypomagnesemia in CAPD patients dialyzed with low-Mg PDS is unknown. Design: A retrospective study to determine the prevalence of hypomagnesemia and the factors associated with its occurrence in CAPD patients dialyzed using a 0.5 mEq/L Mg PDS. Setting: A CAPD unit in a large Veterans Affairs Hospital. Patients: All our CAPD patients (33) enrolled over a 52-month period. Results: All patients had serum magnesium levels higher than 1.25 mEq/L prior to use of low-Mg PDS, Hypomagnesemia (serum Mg <1.25 mEq/L) developed in 21/33 patients (64%) when a 0.5 mEq/L Mg PDS was employed. Hypomagnesemia developed a mean of 8.2 months after beginning treatments. The duration of dialysis and the number of episodes of peritonitis did not differ between patients with and those without hypomagnesemia. Serum albumin levels were significantly lower in patients with hypomagnesemia (2.5+/-0.12 g/dL vs 3.2+/-0.12, p <0.01). Magnesium supplements were given to 13 patients; following this therapy, serum magnesium values became normal. Conclusions: CAPD patients dialyzed with a 0.5 mEq/L Mg PDS may develop a considerable fall in serum magnesium level and may require magnesium supplements in order to restore normal serum values. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,DEPT MED,HINES,IL 60141. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. NR 28 TC 31 Z9 31 U1 0 U2 0 PU MULTIMED INC PI TORONTO PA 1120 FINCH AVE WEST SUITE 601, TORONTO ON M3J 3H7, CANADA SN 0896-8608 J9 PERITON DIALYSIS INT JI Perit. Dial. Int. PY 1995 VL 15 IS 1 BP 61 EP 64 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA QH586 UT WOS:A1995QH58600011 PM 7734563 ER PT J AU SCHUMACHER, HR AF SCHUMACHER, HR TI MICROVASCULAR PERMEABILITY AND THE EFFECTS OF JOINT MOTION SO SCANDINAVIAN JOURNAL OF RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 6th Bertine Koperberg Conference - Chronic Arthritis: Why the Joints CY APR 28-30, 1994 CL NIJMEGEN, NETHERLANDS ID RHEUMATOID-ARTHRITIS; PRESSURE CHANGES; EXERCISE; SYNOVIUM; KNEE C1 UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. RP SCHUMACHER, HR (reprint author), VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 27 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 0300-9742 J9 SCAND J RHEUMATOL JI Scand. J. Rheumatol. PY 1995 SU 101 BP 17 EP 20 PG 4 WC Rheumatology SC Rheumatology GA QW129 UT WOS:A1995QW12900003 ER PT J AU SCHUMACHER, HR AF SCHUMACHER, HR TI HOW MICROORGANISMS ARE HANDLED TO LOCALIZE TO JOINTS AND WITHIN JOINTS SO SCANDINAVIAN JOURNAL OF RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 6th Bertine Koperberg Conference - Chronic Arthritis: Why the Joints CY APR 28-30, 1994 CL NIJMEGEN, NETHERLANDS ID RHEUMATOID-ARTHRITIS; SYNOVIAL-MEMBRANE; BORRELIA-BURGDORFERI; COLLAGENOUS TISSUES; KNEE JOINTS; IDENTIFICATION; DESTRUCTION; MECHANISM; DISEASE; BIOPSY C1 UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. RP SCHUMACHER, HR (reprint author), VET AFFAIRS MED CTR,CTR ARTHRIT IMMUNOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 36 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 0300-9742 J9 SCAND J RHEUMATOL JI Scand. J. Rheumatol. PY 1995 SU 101 BP 199 EP 202 PG 4 WC Rheumatology SC Rheumatology GA QW129 UT WOS:A1995QW12900033 ER PT J AU IVERSEN, P MADSEN, PO CORLE, DK AF IVERSEN, P MADSEN, PO CORLE, DK TI RADICAL PROSTATECTOMY VERSUS EXPECTANT TREATMENT FOR EARLY CARCINOMA OF THE PROSTATE - 23-YEAR FOLLOW-UP OF A PROSPECTIVE RANDOMIZED STUDY SO SCANDINAVIAN JOURNAL OF UROLOGY AND NEPHROLOGY LA English DT Article DE RADICAL PROSTATECTOMY; EXPECTANT TREATMENT; EARLY CARCINOMA OF THE PROSTATE ID STAGE-I; CANCER; MANAGEMENT; SURVIVAL; IMPACT; RISK AB In a study by the Veterans Administration Cooperative Urological Research Group (VACURG),142 patients with localized prostate cancer, VACURG stage I and II, were randomized between radical prostatectomy plus placebo versus placebo alone as initial treatment. 111 patients were evaluable for treatment comparison. Median follow-up for survival is 23 years. The prognostic value of Gleason histologic grading was confirmed. A difference in overall survival in favor of radical prostatectomy was observed in stage I patients. However, after adjustment for imbalance in age distribution, no statistically significant differences in survival could be demonstrated in either stage or in both stages combined. The results are discussed considering the small sample size and the limited statistical power of the study. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,MADISON,WI 53705. UNIV COPENHAGEN,RIGSHOSP,DEPT UROL,DK-2100 COPENHAGEN,DENMARK. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI. NCI,DIV CANC CONTROL,BETHESDA,MD 20892. NR 34 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 0036-5599 J9 SCAND J UROL NEPHROL JI Scand. J. Urol. Nephrol. PY 1995 SU 172 BP 65 EP 72 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA RX700 UT WOS:A1995RX70000013 ER PT J AU DRESCHER, P RAUCH, D KNES, JM MADSEN, PO AF DRESCHER, P RAUCH, D KNES, JM MADSEN, PO TI CONTRAST-MEDIUM INDUCED RENAL VASOCONSTRICTION, ROLE OF ALPHA-RECEPTORS SO SCANDINAVIAN JOURNAL OF UROLOGY AND NEPHROLOGY LA English DT Article DE RENAL ARTERY; RADIOCONTRAST MEDIUM; ALPHA(1) RECEPTORS ID SUBTYPES; ARTERIES; RABBIT; NEPHROTOXICITY; INSUFFICIENCY; ADRENOCEPTORS; DIATRIZOATE; AGONISTS; SAFETY; DOGS AB Standard imaging techniques for evaluation of renal and renovascular disease require the application of radiocontrast medium. The use of high osmolar, ionic radio contrast medium is however associated with adverse effects including acute renal insufficiency. Renal vasoconstriction seems to play an important role in the pathomechanism of this side effect. The cellular mechanisms however remain unsolved. Alpha1 - adrenoceptors and their subtypes are the crucial link between sympathetic stimulation and renal vasoconstriction. We investigated the role of alpha(1)-receptors and the alpha(1A) and alpha(1B) subtypes in the renal artery and in sodium/meglumine diatrizoate induced renal artery smooth muscle contraction. Alpha1-receptor induced rabbit renal artery contraction was produced by stimulation with the specific agonist phenylephrine which was antagonized dose-dependently and reversibly by the alpha(1A)-blockers prazosin, terazosin and YM 617. The alpha(1A)-receptor was the prevalent receptor subtype in rabbit renal artery. This was identified by applying the specific alpha(1A)-receptor antagonist 5-methylurapidil and the irreversible alpha(1B)-receptor antagonist chloroethylclonidine. These two inhibited the PE induced contraction by 96% and 66%,respectively. Sodium/meglumine diatrizoate elicited renal artery contraction at 25% of the phenylephrine control. This contraction was not influenced by alpha(1)-blockers indicating the absence of an alpha(1)-receptor mediated process. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI. RP DRESCHER, P (reprint author), MED COLL WISCONSIN,DEPT RADIOL,MILWAUKEE,WI 53226, USA. NR 40 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 0036-5599 J9 SCAND J UROL NEPHROL JI Scand. J. Urol. Nephrol. PY 1995 SU 172 BP 103 EP 108 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA RX700 UT WOS:A1995RX70000018 ER PT J AU AMIN, F DAVIDSON, M KAHN, RS SCHMEIDLER, J STERN, R KNOTT, PJ APTER, S AF AMIN, F DAVIDSON, M KAHN, RS SCHMEIDLER, J STERN, R KNOTT, PJ APTER, S TI ASSESSMENT OF THE CENTRAL DOPAMINERGIC INDEX OF PLASMA HVA IN SCHIZOPHRENIA SO SCHIZOPHRENIA BULLETIN LA English DT Article ID HOMOVANILLIC-ACID CONCENTRATION; NORADRENERGIC NEURONAL-ACTIVITY; CATECHOLAMINE METABOLITES; DEAMINATED METABOLITES; NEUROLEPTIC TREATMENT; CEREBROSPINAL-FLUID; URINARY-EXCRETION; HUMAN-BRAIN; DEBRISOQUIN; RAT AB Under fasting conditions, the dopamine (DA) metabolite homovanillic acid (HVA) in plasma originates mainly from central DA neurons or from central and peripheral noradrenergic (NA) neurons. The latter source contributes, in addition to HVA, the norepinephrine metabolites, for example, 3-methoxy-4-hydroxyphenylglycol (MHPG). It has been shown in primates that the association between HVA and MHPG in plasma or urine under varying rates elf NA metabolism can be used to obtain an estimate of the central DA neuronal contribution of HVA to plasma or urine. This estimate is called the central dopaminergic index (CDI). Two studies presented here examine the applicability of this model in schizophrenia patients. The results were consistent with the proposed model and suggested that only about 30 percent of the total plasma HVA concentrations in our patients were derived from central DA neurons. A convenient modification of this model is proposed for future studies. Since the CDI of plasma HVA is not likely to be confounded by NA activity, this tool may prove useful in disentangling the roles played by the DA and NA systems in schizophrenia. C1 BAYLOR COLL MED,HOUSTON,TX. CUNY MT SINAI SCH MED,DEPT PSYCHIAT,DIV CLIN RES,NEW YORK,NY. UNIV UTRECHT HOSP,DEPT PSYCHIAT,UTRECHT,NETHERLANDS. CUNY MT SINAI SCH MED,DEPT BIOMATH SCI,NEW YORK,NY. RP AMIN, F (reprint author), HOUSTON VET AFFAIRS MED CTR,PSYCHIAT SERV,RM 6C-316,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 60 TC 37 Z9 38 U1 1 U2 1 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 1995 VL 21 IS 1 BP 53 EP 66 PG 14 WC Psychiatry SC Psychiatry GA QK967 UT WOS:A1995QK96700006 PM 7770741 ER PT J AU DASSORI, AM MILLER, AL SALDANA, D AF DASSORI, AM MILLER, AL SALDANA, D TI SCHIZOPHRENIA AMONG HISPANICS - EPIDEMIOLOGY, PHENOMENOLOGY, COURSE, AND OUTCOME SO SCHIZOPHRENIA BULLETIN LA English DT Article ID MENTAL-HEALTH-SERVICES; ETHNIC-MINORITY GROUPS; PSYCHIATRIC-DISORDERS; LIFETIME PREVALENCE; EXPRESSED EMOTION; SYMPTOMS; INSTRUMENT; LANGUAGE; FAMILIES; ILLNESS AB A number of studies point to the influence of culture and ethnicity on the presentation and course of schizophrenia. In general, a relatively powerful influence of environmental factors is identified. This article reviews the literature on schizophrenia among Hispanics in the United States and uses the results of this review as a basis for identifying directions for future study. Research is divided into three major areas: epidemiology, phenomenology, and illness course and outcome. Ethnic comparisons suggest similar prevalence rates of schizophrenia. However, differences in illness phenomenology between certain subgroups of Hispanics are also observed. Moreover, culture can affect various aspects of the illness process, including illness definition, help-seeking behavior, response to treatment, and posttreatment adjustment. Proposed guidelines to direct future research ventures include (1) better delineation of the sociocultural attributes of the group under study, (2) validation of assessment instruments across ethnic groups, (3) use of innovative approaches to assess incidence and prevalence, (4) incorporation of qualitative methodology, (5) use of illness behavior models to provide a conceptual framework to guide investigations, and (6) integration of cross-cultural and biological studies. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. SAN ANTONIO STATE HOSP,SAN ANTONIO,TX. RP DASSORI, AM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 53 TC 15 Z9 16 U1 4 U2 5 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 1995 VL 21 IS 2 BP 303 EP 312 PG 10 WC Psychiatry SC Psychiatry GA QX822 UT WOS:A1995QX82200015 PM 7631176 ER PT J AU DAVIDSON, M POWCHIK, P AF DAVIDSON, M POWCHIK, P TI COMMENTARY TO LATE-ONSET SCHIZOPHRENIA AND LATE PARAPHRENIA SO SCHIZOPHRENIA BULLETIN LA English DT Editorial Material AB The biological bases for late-life psychotic disorders are unknown. Thus, diverse clinical phenomenology that is often described by a single nominative may actually represent multiple biological abnormalities. Conversely, several differently named disorders may actually have similar biological substrates. Until there is a greater understanding of the biological underpinnings of such disorders, diagnostic nomenclature should not only be rigorously applied, but consistent across the scientific community. The review of the use of the term ''late paraphrenia'' by Riecher-Rossler et al. (1995, this issue) underscores the potential confusion of multiple nominatives, and their suggestion to abandon the term ''late paraphrenia'' in ICD-10 merits serious consideration. C1 MT SINAI SCH MED,NEW YORK,NY 10029. RP DAVIDSON, M (reprint author), BRONX VET AFFAIRS MED CTR,DIV CLIN RES,PSYCHIAT 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1995 VL 21 IS 3 BP 355 EP 356 PG 2 WC Psychiatry SC Psychiatry GA RN381 UT WOS:A1995RN38100002 ER PT J AU BARNES, JL MILANI, S AF BARNES, JL MILANI, S TI IN-SITU HYBRIDIZATION IN THE STUDY OF THE KIDNEY AND RENAL DISEASES SO SEMINARS IN NEPHROLOGY LA English DT Review ID RECEPTOR GENE-EXPRESSION; LOCALLY RESTRICTED EXPRESSION; MOUSE EMBRYONIC-DEVELOPMENT; DEVELOPING EXCRETORY SYSTEM; MESSENGER-RIBONUCLEIC-ACID; HEPATOCYTE GROWTH-FACTOR; HUMAN-FETAL KIDNEY; PAIRED BOX GENE; INSITU HYBRIDIZATION; RAT-KIDNEY C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV FLORENCE,DEPT CLIN PATHOPHYSIOL,GASTROENTEROL UNIT,FLORENCE,ITALY. RP BARNES, JL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL FR,SAN ANTONIO,TX 78284, USA. OI milani, stefano/0000-0002-1337-9107 NR 175 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9295 J9 SEMIN NEPHROL JI Semin. Nephrol. PD JAN PY 1995 VL 15 IS 1 BP 9 EP 28 PG 20 WC Urology & Nephrology SC Urology & Nephrology GA QF380 UT WOS:A1995QF38000003 PM 7754257 ER PT J AU NEUSTADTER, LM WEISS, M AF NEUSTADTER, LM WEISS, M TI MEDICATION-INDUCED CHANGES OF BONE SO SEMINARS IN ROENTGENOLOGY LA English DT Article ID 13-CIS-RETINOIC ACID; EPIPHYSEAL; IFOSFAMIDE; FRACTURES; CHILDREN; THERAPY; RICKETS C1 ST CHRISTOPHERS MED CTR,PHILADELPHIA,PA. RP NEUSTADTER, LM (reprint author), HOSP UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 33 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 0037-198X J9 SEMIN ROENTGENOL JI Semin. Roentgenology PD JAN PY 1995 VL 30 IS 1 BP 88 EP 95 DI 10.1016/S0037-198X(05)80009-4 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QB954 UT WOS:A1995QB95400009 PM 7899887 ER PT J AU Myklebust, JB Cusick, JF Boerboom, LE Prieto, TE Khan, TA AF Myklebust, JB Cusick, JF Boerboom, LE Prieto, TE Khan, TA TI Vascular effects of spinal cord stimulation in the monkey SO STEREOTACTIC AND FUNCTIONAL NEUROSURGERY LA English DT Article DE spinal cord stimulation; microspheres; evoked potentials; sympathetic nervous system; monkey; peripheral vascular disease; regional blood flow ID DORSAL COLUMN STIMULATION; BLOOD-FLOW; ELECTRICAL-STIMULATION; DISEASE; EXTREMITIES; IMPROVEMENT AB Because of clinical reports suggesting beneficial effects of electrical stimulation in peripheral vascular disease, studies have been conducted in the monkey. Regional blood flow was measured prior to, during and following the application of electrical currents to the spinal cord. The flow measurements were made using radioactive microspheres. In addition, tissue temperatures and venous and arterial concentrations of epinephrine and norepinephrine were measured. The results show that electrical stimulation increases blood flow to the skin and muscle. It is hypothesized that the effect is due to sympathetic inactivation secondary to the application of electrical currents. C1 ZABLOCKI VET ADM MED CTR,MILWAUKEE,WI 53295. MARQUETTE UNIV,DEPT BIOMED ENGN,MILWAUKEE,WI 53233. MED COLL WISCONSIN,MILWAUKEE,WI 53226. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,CTR REHABIL R&D,HINES,IL 60141. OI Myklebust, Joel/0000-0002-8709-9706 NR 28 TC 11 Z9 12 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1011-6125 J9 STEREOT FUNCT NEUROS JI Stereotact. Funct. Neurosurg. PY 1995 VL 64 IS 1 BP 32 EP 39 PG 8 WC Neurosciences; Neuroimaging; Surgery SC Neurosciences & Neurology; Surgery GA TK820 UT WOS:A1995TK82000004 PM 8751312 ER PT S AU Cummings, JL AF Cummings, JL BE Grafman, J Holyoak, KJ Boller, F TI Anatomic and behavioral aspects of frontal-subcortical circuits SO STRUCTURE AND FUNCTIONS OF THE HUMAN PREFRONTAL CORTEX SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Workshop on Structure and Functions of the Human Prefrontal Cortex CY MAR 02-04, 1995 CL NEW YORK, NY SP New York Acad Sci ID OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; PARKINSONS-DISEASE; RHESUS-MONKEY; STRIATOPALLIDAL SYSTEM; PARALLEL ORGANIZATION; THALAMIC INFARCTION; HUNTINGTONS-DISEASE; PREFRONTAL CORTEX; SECONDARY MANIA AB Five parallel circuits connect discrete regions of the frontal lobes with specific subregions of the striatum, globus pallidus, and thalamus. One circuit mediates motor function, another eye movements, and three of the circuits mediate cognitive, emotional, and motivational processes. The circuits serve as organizational axes integrating related information from widespread areas of the brain and mediating diverse behaviors. This review describes the anatomy of the circuits and the major transmitters present within the circuits. Circuit-specific behaviors (those that appear to be mediated exclusively by circuit structures) and circuit-related behaviors (those that involve both circuit and noncircuit structures) are discussed. Drugs that alter behavior through effects on the circuits are presented. The three circuits that are most relevant to understanding behavior are emphasized. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,BEHAV NEUROSCI SECT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,REED NEUROL RES CTR,DEPT NEUROL,LOS ANGELES,CA 90024. FU NIA NIH HHS [AG 10123] NR 69 TC 225 Z9 228 U1 3 U2 8 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-991-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 769 BP 1 EP 13 DI 10.1111/j.1749-6632.1995.tb38127.x PG 13 WC Multidisciplinary Sciences; Neurosciences; Psychology SC Science & Technology - Other Topics; Neurosciences & Neurology; Psychology GA BE92F UT WOS:A1995BE92F00001 PM 8595019 ER PT B AU SCHMID, P CONRAD, A SYNDULKO, K SINGER, EJ LI, XM TAO, GM HANDLEY, D FAHYCHANDON, B TOURTELLOTTE, WW AF SCHMID, P CONRAD, A SYNDULKO, K SINGER, EJ LI, XM TAO, GM HANDLEY, D FAHYCHANDON, B TOURTELLOTTE, WW BE Major, EO Levy, JA Schoenberg, D TI Techniques in PCR and PCR evaluation technology and its application to the study of cerebrospinal fluid in HIV disease SO TECHNICAL ADVANCES IN AIDS RESEARCH IN THE HUMAN NERVOUS SYSTEM LA English DT Proceedings Paper CT NIH Symposium on Technical Advances in AIDS Research in the Human Nervous System CY OCT 04-05, 1993 CL WASHINGTON, DC SP NIH C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45000-3 PY 1995 BP 301 EP 316 PG 16 WC Infectious Diseases; Medicine, Research & Experimental; Neurosciences SC Infectious Diseases; Research & Experimental Medicine; Neurosciences & Neurology GA BD83E UT WOS:A1995BD83E00022 ER PT J AU ALEXANDER, JK AF ALEXANDER, JK TI AGE, ALTITUDE, AND ARRHYTHMIA SO TEXAS HEART INSTITUTE JOURNAL LA English DT Review DE AGE FACTORS; AGED; ALTITUDE; ANOXIA; ARRHYTHMIA; HYPOXIA; MOUNTAINEERING AB Continuous electrocardiographic recording by Holter monitor was carried out during a climb to 5,895 m by an unacclimatized 65-year-old man confirmed to be without cardiac disease on rigorous examination. During ascent, marked ventricular ectopy and multiple runs of left ventricular bigeminy developed in association with an increase in P-wave amplitude of lead V-2,V- and unchanged QT interval. With the diminished aerobic stress of descent, bigeminy disappeared, although premature ventricular complexes, apparently of right ventricular origin, remained increased throughout the climb. Arrhythmogenic mechanisms activated by prolonged exercise under hypoxic conditions are reviewed in relation to age. RP ALEXANDER, JK (reprint author), DEPT VET AFFAIRS MED CTR,CARDIOL SECT 111B,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU TEXAS HEART INST PI HOUSTON PA PO BOX 20345, HOUSTON, TX 77225-0345 SN 0730-2347 J9 TEX HEART I J JI Tex. Heart Inst. J. PY 1995 VL 22 IS 4 BP 308 EP 316 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TH902 UT WOS:A1995TH90200006 PM 8605431 ER PT J AU WEISS, TW AF WEISS, TW TI IMPROVEMENTS IN VA HEALTH-SERVICES FOR WOMEN VETERANS SO WOMEN & HEALTH LA English DT Article; Proceedings Paper CT 12th Annual VA HSR&D Service Meeting CY APR, 1994 CL WASHINGTON, DC SP VA HSR&D ID FEMALE VETERANS AB Since the early 1980s, health care for women veterans in the Department of Veterans Affairs (VA) has improved considerably, although problems still remain. The lack of privacy for women at many VA facilities and the provision of incomplete physical examinations for women continue to be problematic issues. A 1992 congressional appropriation of $7.5 million has substantially increased the awareness of women veterans health care in the VA. This appropriation, from Public Law 102-585, Veterans Health Care Act of 1992, Title I-Women Veterans Health Programs, has allowed VA to expand services for women veterans. Using these funds, VA has established eight comprehensive women veterans health centers, 23 full-time women veterans coordinators, and four regional stress disorder teams. This paper describes these and other important new initiatives and discusses how they will serve as the foundation on which VA expands care for women within the context of a changing health care system. C1 BAYLOR COLL MED,HOUSTON,TX 77030. RP WEISS, TW (reprint author), HOUSTON VAMC,HOUSTON CTR QUAL CARE & UTILIZAT STUDIES,VA HSR&D FIELD PROGRAM,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 24 TC 14 Z9 14 U1 1 U2 1 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0363-0242 J9 WOMEN HEALTH JI Women Health PY 1995 VL 23 IS 2 BP 1 EP 12 DI 10.1300/J013v23n02_01 PG 12 WC Public, Environmental & Occupational Health; Women's Studies SC Public, Environmental & Occupational Health; Women's Studies GA TE921 UT WOS:A1995TE92100001 PM 8585222 ER PT J AU MULROW, CD CORNELL, JA HERRERA, CR KADRI, A FARNETT, L AGUILAR, C AF MULROW, CD CORNELL, JA HERRERA, CR KADRI, A FARNETT, L AGUILAR, C TI HYPERTENSION IN THE ELDERLY - IMPLICATIONS AND GENERALIZABILITY OF RANDOMIZED TRIALS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID CORONARY HEART-DISEASE; BLOOD-PRESSURE; CARDIOVASCULAR HEALTH; SYSTOLIC HYPERTENSION; RISK-FACTORS; MANAGEMENT; MORTALITY; MORBIDITY; PREVALENCE; THERAPY AB Objective.-To estimate morbidity and mortality benefits of drug therapy for hypertensive elderly subjects, compare these benefits with effects in younger subjects, and provide a framework for generalizing results derived from trials to actual patients. Data Sources.-A literature search using MEDLINE from 1966 to 1993, references from reviews and trial articles, and experts. Study Selection.-Randomized trials lasting at least 1 year that evaluated effects of drug treatment on morbidity and mortality outcomes in hypertensive persons. Data Extraction.-Four independent reviewers appraised protocol characteristics and quality of selected trials. Data Synthesis.-There were 13 trials involving 16 564 elderly persons (age 60 years and older). The prevalence of cardiovascular risk factors, cardiovascular disease, and competing comorbid diseases was lower among trial participants than the general population of hypertensive elderly persons. When the six large high-quality trials were combined, trial results showed 43 subjects (95% confidence interval [CI], 31 to 69) and 61 subjects (95% CI, 39 to 141) needed to be treated for 5 years to prevent one cerebrovascular event and one coronary heart disease event, respectively. Including the other seven trials did not change the results significantly. Only 18 subjects (95% CI, 14 to 25) needed to be treated to prevent one cardiovascular event (cerebrovascular or cardiac). Twelve trials in primarily younger and middle-aged adults involved approximately 33 000 persons. For all outcomes except cardiac mortality, two to four times as many of the younger subjects as the older subjects needed to be treated for 5 years to prevent morbid and mortal events. No significant effect on cardiac mortality was seen among younger subjects, while 78 older subjects (95% CI, 50 to 180) needed to be treated to prevent a fatal cardiac event. Conclusions.-Randomized trials demonstrate that treating healthy older persons with hypertension is highly efficacious. Five-year morbidity and mortality benefits derived from trials are greater for older than younger subjects. Extrapolating benefits from trials to individual patients is difficult, but should take into account multiple issues including the patient's risk factors, preexisting cardiovascular disease, and competing comorbid illnesses. C1 UNIV TEXAS, HLTH SCI CTR, HOUSTON, TX USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX USA. RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR, CTR GERIATR RES EDUC & CLIN, 7400 MERTON MINTER BLVD, SAN ANTONIO, TX 78284 USA. NR 51 TC 188 Z9 189 U1 0 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 EI 1538-3598 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD DEC 28 PY 1994 VL 272 IS 24 BP 1932 EP 1938 DI 10.1001/jama.272.24.1932 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA PX927 UT WOS:A1994PX92700039 PM 7990246 ER PT J AU SRIKANTH, S RADO, TA AF SRIKANTH, S RADO, TA TI A 30-BASE PAIR ELEMENT IS RESPONSIBLE FOR THE MYELOID-SPECIFIC ACTIVITY OF THE HUMAN NEUTROPHIL ELASTASE PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN MYELOPEROXIDASE GENE; CD11B PROMOTER; NF-M; EXPRESSION; PROTEIN; DIFFERENTIATION; CELLS; IDENTIFICATION; PROTOONCOGENE; REGION AB Human neutrophil elastase (HNE), a serine protease, is expressed only in the promyelocytic stages of granulocyte maturation. We examined several regions of the promoter for transcriptional activity and report that a 30-base pair (bp) element located between -76 and -106 in the 5'-flanking region of HNE is sufficient for myeloid-specific expression of HNE. Gel shift assays using nuclear extracts from myeloid and non-myeloid cells reveal several myeloid-specific complexes binding to the 30-bp element. Examination of DNA-protein interactions shows that at least two myeloid-specific proteins of 38 and 55 kDa bind to this element. DNase I protection analysis reveals two distinct footprints between -80 to -91 and -94 to -104 within this element. Transient expression studies using deletion constructs of the HNE 5'-flanking region show that the 30-bp element is active in myeloid cells It 562 and U 937 but not in HeLa cells. Internal deletion of this element results in a 60-85% loss of promoter activity in myeloid cells. Additional functional studies also show that a 19-bp region between -112 and -131 contributes to transcriptional activity of the elastase promoter as well. C1 UNIV ALABAMA,DEPT MED,DIV HEMATOL,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MICROBIOL,DIV HEMATOL,BIRMINGHAM,AL 35294. BIRMINGHAM VET AFFAIRS MED CTR,BIRMINGHAM,AL 35294. FU NIDA NIH HHS [R01 DA07237] NR 43 TC 17 Z9 17 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 DEC 23 PY 1994 VL 269 IS 51 BP 32626 EP 32633 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PX304 UT WOS:A1994PX30400090 PM 7798268 ER PT J AU BESRA, GS SIEVERT, T LEE, RE SLAYDEN, RA BRENNAN, PJ TAKAYAMA, K AF BESRA, GS SIEVERT, T LEE, RE SLAYDEN, RA BRENNAN, PJ TAKAYAMA, K TI IDENTIFICATION OF THE APPARENT CARRIER IN MYCOLIC ACID SYNTHESIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MYCOBACTERIA; 6-O-MYCOLYL-MANNOSYL-1-PHOSPHOPOLYPRENOL; ANTITUBERCULOSIS DRUGS ID CELL-FREE SYSTEM; MYCOBACTERIUM-TUBERCULOSIS; CORYNEBACTERIUM-DIPHTHERIAE; HOMOLOGOUS SERIES; SMEGMATIS; BIOSYNTHESIS; EXTRACT; ESTER; H37RA AB The mycolic acids are large (C-70-90) alpha-alkyl, beta-hydroxy fatty acids and are the major determinants of the mycobacterial cell wall's impermeable barrier. The biosynthesis of mycolic acids is barely understood (they are probably the products of specialized elongation and Claisen-type condensation), and yet their synthesis is the site of action of several mainline antituberculosis drugs. We describe the isolation from Mycobacterium smegmatis and the full characterization of a 6-O-mycolyl-beta-D-mannopyranosyl-1-monophosphoryl-3,7,11, 15,19,23,27-heptamethyl-(2Z,6E,10E)-octacosatrien-1-ol. The identification of a mycolyl-mannosylphosphopolyprenol supported by cell-free labeling experiments and earlier literature suggests unusual biochemical pathways in which mature mycolic acids are formed from beta-oxo precursors while attached to a mannosyl-P-polyprenol, in which form they are transported through the membrane prior to final deposition as arabinan-bound mycolates. C1 UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,MYCOBACTERIOL RES LAB,MADISON,WI 53706. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. RP BESRA, GS (reprint author), COLORADO STATE UNIV,DEPT MICROBIOL,FT COLLINS,CO 80523, USA. RI Lee, Richard/J-4997-2013; Slayden, Richard/O-8626-2016 OI Lee, Richard/0000-0002-2397-0443; Slayden, Richard/0000-0001-6857-7277; Besra, Gurdyal/0000-0002-5605-0395 FU NIAID NIH HHS [AI 30189]; PHS HHS [AZ-18357] NR 36 TC 70 Z9 73 U1 1 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 20 PY 1994 VL 91 IS 26 BP 12735 EP 12739 DI 10.1073/pnas.91.26.12735 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA PY294 UT WOS:A1994PY29400079 PM 7809112 ER PT J AU THOMPSON, NM GULLEY, ML ROGENESS, GA CLAYTON, RJ JOHNSON, C HAZELTON, B CHO, CG ZELLMER, VT AF THOMPSON, NM GULLEY, ML ROGENESS, GA CLAYTON, RJ JOHNSON, C HAZELTON, B CHO, CG ZELLMER, VT TI NEUROBEHAVIORAL CHARACTERISTICS OF CGG AMPLIFICATION STATUS IN FRAGILE-X FEMALES SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE TRINUCLEOTIDE REPEAT; NEUROPSYCHOLOGICAL; PSYCHIATRIC; INTELLIGENCE ID DISORDERS; CARRIERS; REGION; WOMEN; GENE; DNA AB Neurobehavioral correlates of CGG amplification were studied in 17 nonretarded adult female carriers of fragile X syndrome. The results revealed a significant relationship between IQ and the number of CGG repeats in the 5' untranslated region of the FMR1 gene. Women with a full mutation (>200 CGG repeats) scored below average in IQ, visual-spatial perception, visual-spatial organization, and executive function. There were no differences in hue motor dexterity or memory as a function of CGG amplification status. A history of major depressive disorder was identified in 71% of the sample, but incidence of depression was not associated with the degree of CGG amplification. Schizotypal features were noted in 18%. No intellectual or neuropsychological deficit was found in women with a premutation (<200 CGG repeats). Decrements in IQ, visual-spatial perception, and executive function appear to arise as a consequence of the CGG amplification. (C) 1994 Wiley-Liss, Inc, C1 UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. ST MARYS UNIV,DEPT PSYCHOL,SAN ANTONIO,TX. NR 28 TC 45 Z9 45 U1 1 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD DEC 15 PY 1994 VL 54 IS 4 BP 378 EP 383 DI 10.1002/ajmg.1320540418 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA QF860 UT WOS:A1994QF86000017 PM 7726212 ER PT J AU SINGER, EJ STONER, GL SINGER, P TOMIYASU, U LICHT, E FAHYCHANDON, B TOURTELLOTTE, WW AF SINGER, EJ STONER, GL SINGER, P TOMIYASU, U LICHT, E FAHYCHANDON, B TOURTELLOTTE, WW TI AIDS PRESENTING AS PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY WITH CLINICAL-RESPONSE TO ZIDOVUDINE SO ACTA NEUROLOGICA SCANDINAVICA LA English DT Note DE PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; JC VIRUS; AIDS; HIV-1; ZIDOVUDINE; CYTARABINE; VIRUS-SPECIFIC PCR ID HUMAN-IMMUNODEFICIENCY-VIRUS; POLYMERASE CHAIN-REACTION; JC-VIRUS; NERVOUS-SYSTEM; INFECTION; DNA; BRAIN; PATHOGENESIS; CYTARABINE; AUTOPSY AB Progressive multifocal leukoencephalopathy (PML) due to JC virus can be the initial manifestation of AIDS. A 40-year-old man seropositive for HIV-1 presented with aphasia, hemiparesis, and hemianopsia, and with magnetic resonance imaging of the brain typical of PML. He quickly became bed bound, incontinent, and mute. The diagnosis of PML was established by histopathology in a brain biopsy with positive immunocytochemistry for polyomavirus capsid proteins, and detection of JCV DNA by polymerase chain reaction using JCV-specific primers. High dose zidovudine therapy was initiated (1200 mg/day). Within two weeks the patient began to respond, and after three months he was able to walk and care for himself and was discharged. He lived for two years from the onset of PML. While cytarabine has been the drug most widely used for PML treatment, this is the second confirmed case with apparent response to zidovudine. High dose zidovudine may benefit some previously untreated AIDS patients with onset as PML. C1 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PATHOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. NINCDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. RP SINGER, EJ (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV W127,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. FU NIMH NIH HHS [MH47281 RO1] NR 27 TC 19 Z9 19 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-6314 J9 ACTA NEUROL SCAND JI Acta Neurol. Scand. PD DEC PY 1994 VL 90 IS 6 BP 443 EP 447 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA PW675 UT WOS:A1994PW67500012 PM 7892765 ER PT J AU SMALL, GW AF SMALL, GW TI HANNAHS HEIRS - THE QUEST FOR THE GENETIC ORIGINS OF ALZHEIMERS-DISEASE - POLLEN,DA SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Book Review C1 UNIV CALIF LOS ANGELES, INST NEUROPSYCHIAT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES HOSP, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA USA. RP SMALL, GW (reprint author), UNIV CALIF LOS ANGELES, SCH MED, GERIATR CONSULTAT PSYCHIAT SERV, LOS ANGELES, CA USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD WIN PY 1994 VL 2 IS 1 BP 86 EP 87 PG 2 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA MY119 UT WOS:A1994MY11900011 ER PT J AU PIERCE, GF TARPLEY, JE ALLMAN, RM GOODE, PS SERDAR, CM MORRIS, B MUSTOE, TA BERG, JV AF PIERCE, GF TARPLEY, JE ALLMAN, RM GOODE, PS SERDAR, CM MORRIS, B MUSTOE, TA BERG, JV TI TISSUE-REPAIR PROCESSES IN HEALING CHRONIC PRESSURE ULCERS TREATED WITH RECOMBINANT PLATELET-DERIVED GROWTH-FACTOR BB SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID EXTRACELLULAR-MATRIX; HUMAN-FIBROBLASTS; MESSENGER-RNA; WOUND REPAIR; FACTOR-BETA; COLLAGEN; FIBRONECTIN; STIMULATION; PDGF; DEPOSITION AB Cellular and molecular mechanisms responsible for the observed vulnerary effects of recombinant human platelet-derived growth factor BB (rPDGF-BB) in man have not been elucidated In a double-blinded trial, patients having chronic pressure ulcers were treated topically with either rPDGF-BB or placebo for 28 days. To explore how rPDGF-BB may induce chronic wounds to heal, biopsies were taken from the ulcers of a cohort of 20 patients from the trial and evaluated in a blinded fashion by light microscopy for 1), fibroblast content, 2), neovessel formation, and 3), collagen deposition. Electron microscopy also was used to assess fibroblast activation and collagen deposition. Before initiation of therapy most wounds had few fibroblasts and most of those present were not activated. When mean scores for the total active treatment phase (days 8, 15, and 29) for rPDGF-BB-treated ulcers were compared with the scores for placebo-treated ulcers, fibroblast content was significantly higher for the rPDGF-BB-treated ulcers (P = 0.03, Kruskal-Wallis test). More significant differences in fibroblast and neovessel content were observed when six nonhealing wounds were eliminated from the analysis (three placebo, three treatment). Thus, in all healing wounds, rPDGF-BB therapy significantly increased fibroblast (P = 0.0007) and neovessel (P = 0.02) content. These results were correlated with increased collagen fibrillogenesis by fibroblasts from healing rPDGF-BB-treated wounds, as assessed by intracellular procollagen type I immunostaining, and by electron microscopy, and were concordant with clinical measurements (eg, area of ulcer opening and ulcer volume) which showed greater healing in rPDGF-BB-treated wounds. These results suggest induction of fibroblast proliferation and differentiation is one mechanism by which rPDGF-BB can accelerate wound healing and that rPDGF-BB can augment healing responses within a majority of, but not all, nonhealing chronic pressure ulcers in man. C1 AMGEN INC,DEPT EXPTL PATHOL,THOUSAND OAKS,CA 91320. UNIV ALABAMA,CTR AGING,DEPT MED,BIRMINGHAM,AL. BIRMINGHAM VET AFFAIRS MED CTR,BIRMINGHAM,AL. AMGEN INC,DEPT CLIN AFFAIRS,THOUSAND OAKS,CA 91320. NORTHWESTERN UNIV,DIV PLAST & RECONSTRUCT SURG,CHICAGO,IL 60611. UNIV CALIF SAN DIEGO,VET AFFAIRS MED CTR,CORE ELECTRON MICROSCOPY LAB,SAN DIEGO,CA 92161. RI Allman, Richard/D-5964-2011 NR 45 TC 60 Z9 61 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 1994 VL 145 IS 6 BP 1399 EP 1410 PG 12 WC Pathology SC Pathology GA PW173 UT WOS:A1994PW17300019 PM 7992843 ER PT J AU KIRALY, A SUTO, G LIVINGSTON, EH GUTH, PH STPIERRE, S TACHE, Y AF KIRALY, A SUTO, G LIVINGSTON, EH GUTH, PH STPIERRE, S TACHE, Y TI CENTRAL VAGAL ACTIVATION BY TRH INDUCES GASTRIC HYPEREMIA - ROLE OF CGRP IN CAPSAICIN-SENSITIVE AFFERENTS IN RATS SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE CALCITONIN GENE RELATED PEPTIDE ANTAGONIST; VAGAL EFFERENT; CAPSAICIN-SENSITIVE SPLANCHNIC AFFERENT FIBERS; NITRIC OXIDE; GASTRIC MUCOSAL BLOOD FLOW; THYROTROPIN-RELEASING HORMONE ANALOG; RX-77368; BETHANECHOL; SUBSTANCE P ANTAGONIST ID GENE-RELATED PEPTIDE; MUCOSAL BLOOD-FLOW; THYROTROPIN-RELEASING-HORMONE; HYDROGEN GAS CLEARANCE; NITRIC-OXIDE; SENSORY NEURONS; SUBSTANCE-P; CALCITONIN; ANALOG; ACID AB The role of calcitonin gene-related peptide (CGRP) in the vagal cholinergic-mediated increase in gastric mucosal blood flow (GMBF) induced by the stable thyrotropin-releasing hormone (TRH) analogue RX-77368 injected intracisternally (ic, 30 ng) was investigated in urethan-anesthetized rats using the hydrogen gas clearance technique. alpha-CGRP (14 mu g.kg(-1).h(-1)) or bethanechol (150 mu g.kg(-1).h(-1)) infused close intra-arterially to the stomach or RX-77368 injected intracisternally increased GMBF by 76, 102, and 131%, respectively, 30 min after administration. The CGRP antagonist, human CGRP-(8-37) [hCGRP-(8-37)], injected intravenously (15 mu g/kg bolus and 3 mu g.kg(-1).h(-1)) inhibited by 100, 97, and 73% the gastric hyperemic response to alpha-CGRP, TRH analogue, and bethanechol, respectively, whereas the substance P antagonist CP-96,345 (3 mg/kg iv) had no effect. In capsaicin-pretreated rats, hCGRP-(8-37) no longer blocked the increase in GMBF induced by intracisternal RX-77368. These results suggest that the gastric hyperemic response to central vagal activation induced by intracisternal TRH analogue at 30 ng is mediated by local effector function of capsaicin-sensitive afferent fibers releasing CGRP. C1 UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, CTR ULCER RES & EDUC, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, DEPT MED & SURG, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, INST BRAIN RES, LOS ANGELES, CA 90073 USA. UNIV QUEBEC, INST NATL RECH SCI SANTE, POINTE CLAIRE, PQ H9R 1G6, CANADA. NR 39 TC 30 Z9 30 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD DEC PY 1994 VL 267 IS 6 BP G1041 EP G1049 PG 9 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA PY111 UT WOS:A1994PY11100013 ER PT J AU ZITTEL, TT ROTHENHOFER, I MEYER, JH RAYBOULD, HE AF ZITTEL, TT ROTHENHOFER, I MEYER, JH RAYBOULD, HE TI SMALL-INTESTINAL CAPSAICIN-SENSITIVE AFFERENTS MEDIATE FEEDBACK INHIBITION OF GASTRIC-EMPTYING IN RATS SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Note DE SENSORY; DUODENUM; SMALL INTESTINE; LIPID; HYDROCHLORIC ACID; GLUCOSE; NUTRIENTS ID SENSORY NEURONS; NERVE-FIBERS; GLUCOSE AB Functional studies have implied the existence of small intestinal receptive mechanisms for components of chyme to mediate feedback inhibition of gastric function. However, it is not known if the sensors are in the wall of the small intestine or located at another site. The present studies evaluated the localization of receptive mechanisms mediating intestinal feedback inhibition of gastric emptying by functional ablation of intestinal capsaicin-sensitive afferents. Perfusion of the small intestine of conscious rats with hydrochloric acid (0.1 N; total amount 50 meg), glucose (1 M; total amount 90 mg), or a lipid emulsion (Intralipid 10%; total amount 50 mg) inhibited gastric emptying. One to 7 days after perfusion of the intestine with capsaicin (3.6 mu mol), feedback inhibition of gastric emptying produced by acid, glucose, or lipid was inhibited 100, 59, and 42%, respectively. We conclude that acid-induced inhibition of gastric emptying is mediated entirely by small intestinal capsaicin-sensitive afferent neurons and that a major portion of the glucose-induced inhibition of gastric emptying is mediated by small intestinal afferents. However, only a minor part of the response to lipid is mediated by this pathway. C1 UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, CTR ULCER RES & EDUC, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, DEPT PHYSIOL, LOS ANGELES, CA 90073 USA. NR 22 TC 43 Z9 43 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD DEC PY 1994 VL 267 IS 6 BP G1142 EP G1145 PG 4 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA PY111 UT WOS:A1994PY11100025 ER PT J AU HAMMOND, TG MAJEWSKI, RR MUSE, KE OBERLEY, TD MORRISSEY, LW AMENDTRADUEGE, AM AF HAMMOND, TG MAJEWSKI, RR MUSE, KE OBERLEY, TD MORRISSEY, LW AMENDTRADUEGE, AM TI ENERGY-TRANSFER ASSAYS OF RAT RENAL CORTICAL ENDOSOMAL FUSION - EVIDENCE FOR SUPERFUSION SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article; Proceedings Paper CT 25th Annual Meeting of the American-Society-of-Nephrology CY NOV 15-18, 1992 CL BALTIMORE, MD SP AMER SOC NEPHROL DE KIDNEY; FLOW CYTOMETRY; ENERGY TRANSFER; ENDOCYTOSIS; CYTOSOL ID CELL-FREE SYSTEM; MEMBRANE-VESICLES; PROTEINS; ENDOCYTOSIS; SECRETION; RECEPTORS; WATER AB The complex of components necessary to allow endosomal fusion includes both membrane-bound receptors and several soluble proteins. Although these factors have been isolated from cultured cell lines, and endosomal fusion has been reconstituted in vitro for vesicular systems from yeast to synaptosomes, there is a paucity of data from mammalian systems. To investigate fusion in rat renal cortical endosomes, we began by developing a fusion assay. As the immunoglobulin and avidin-based probes almost universally employed in fusion assays are excluded by the glomerular ultrafiltration barrier, it was necessary to begin by finding ultrafilterable probes which could serve as a fusion assay. We labeled the apical endosomal pathway of the renal proximal tubule by intravenous infusion of ultrafilterable fluorescent dextrans. Energy transfer from entrapped fluorescein-dextran to rhodamine-dextran had a narrow concentration dependence but allowed fluorometric assay of endosomal fusion. The ''spectroscopic ruler'' property of energy transfer, whereby it will only occur at < 60 Angstrom, makes fusion measurements unequivocal. The energy transfer efficiency of fluorometric (48 +/- 1%) and flow cytometry (57 +/- 1%) assays were close to the theoretical optimum (57%). Energy transfer is detected as a decrease in fluorescence of the fluorescein donor and an increase in fluorescence of the rhodamine acceptor. Our endosomal fusion assay was utilized to determine the optimal conditions for fusion of rat renal cortical light endosomes and heavy endosomes. Independent measurements of fluorescein-dextran and rhodamine-dextran on an endosome-by-endosome basis using dual-beam two-color flow cytometry demonstrated that each fusion event involves multiple endosomes rather than a single pair of endosomes. Electron microscopy analysis demonstrated that the average vesicle diameter was five times larger in the fused heavy endosomal fractions compared with control fractions without fusion. Hence, fusion of mammalian renal cortical endosomes reconstituted in vitro is consistent with multiple fusion events dubbed superfusion. C1 UNIV WISCONSIN, HOSP & CLIN, DEPT MED, MADISON, WI 53706 USA. UNIV WISCONSIN, HOSP & CLIN, DEPT PATHOL, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53706 USA. UNIV WISCONSIN, CTR COMPREHENS CANC, FLOW CYTOMETRY LAB, MADISON, WI 53792 USA. NR 32 TC 10 Z9 10 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrol. Physiol. PD DEC PY 1994 VL 267 IS 6 BP F1021 EP F1033 PG 13 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA PX951 UT WOS:A1994PX95100016 ER PT J AU BENNETT, CL WEINSTEIN, RA SHAPIRO, MF KESSLER, HA DICKINSON, GM PETERSON, B COHN, SE GEORGE, WL GILMAN, SC AF BENNETT, CL WEINSTEIN, RA SHAPIRO, MF KESSLER, HA DICKINSON, GM PETERSON, B COHN, SE GEORGE, WL GILMAN, SC TI A RAPID PREADMISSION METHOD FOR PREDICTING INPATIENT COURSE OF DISEASE FOR PATIENTS WITH HIV-RELATED PNEUMOCYSTIS-CARINII PNEUMONIA SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; IN-HOSPITAL MORTALITY; SERUM LACTATE-DEHYDROGENASE; SYSTEM; EXPERIENCE; ERROR AB Pneumocystis carinii pneumonia (FCP) has been the most common reason for hospitalization and the most common cause of death for persons with HIV infection. Hospital mortality rates for PCP range from 10 to 60%. Studies that evaluate differences in hospital mortality rates must control for differences in patient severity of illness. We developed a simple staging system for categorizing severity of illness in patients with PCP. We analyzed the relation between clinical factors and in-hospital mortality for 576 hospitalized patients with HIV-related PCP treated at 56 hospitals for the years 1987 to 1990. Four stages of PCP could be identified based on three routinely measured clinical variables: alveolar-arterial oxygen difference, total lymphocyte count, and body mass index. The mortality rate increased by stage: 1% for Stage 1, 8% for Stage 2, 23% for Stage 3, and 48% for Stage 4. The four-stage severity system compared well with previous models developed for AIDS and for PCP, and is easier to use in clinical practice. Our staging system identifies patients with a high and low risk of in-hospital death upon admission. Physicians may benefit from consideration of PCP stage in deciding on management strategies. In addition, researchers involved in clinical trials of new agents for FCP might consider stratification by PCP stage in order to define homogenous groups. C1 DURHAM VET ADM HOSP,DIV HLTH SERV RES,DURHAM,NC. DUKE UNIV,DIV HEMATOL ONCOL,DURHAM,NC. DUKE UNIV,CTR HLTH POLICY RES & EDUC,DURHAM,NC. DUKE UNIV,DIV BIOSTAT,DURHAM,NC. DUKE UNIV,DEPT MED,DURHAM,NC. RUSH PRESBYTERIAN ST LUKES MED SCH,CHICAGO,IL. UNIV ILLINOIS,URBANA,IL 61801. UNIV ROCHESTER,ROCHESTER,NY. UNIV MIAMI,MIAMI,FL 33152. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. RAND CORP,SANTA MONICA,CA. VET ADM MED CTR,WESTERN REG SPECIAL STUDIES GRP,LONG BEACH,CA 90822. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP BENNETT, CL (reprint author), LAKESIDE VET ADM MED CTR,111,333 E HURON ST,CHICAGO,IL 60611, USA. RI Bennett, Charles/C-2050-2008 FU AHRQ HHS [1-RO1-HS-06494-01]; PHS HHS [1 R03 H 507846-1] NR 18 TC 38 Z9 39 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD DEC PY 1994 VL 150 IS 6 BP 1503 EP 1507 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA PV967 UT WOS:A1994PV96700004 PM 7952607 ER PT J AU BARKLEY, B LICHTENSTEIN, MJ GARZA, C HAZUDA, HP AF BARKLEY, B LICHTENSTEIN, MJ GARZA, C HAZUDA, HP TI CLINICAL VALIDATION OF THE WELCH-ALLYN PNEUMOCHECK(TM) HAND-HELD SPIROMETER SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Article DE AGED; PULMONARY FUNCTION TESTING; VALIDATION STUDY ID MORTALITY; OBSTRUCTION; POPULATION; DISEASE; ADULTS; SAMPLE AB Pulmonary function is predictive of morbidity and mortality. Therefore, in epidemiologic studies, researchers seek to measure pulmonary function with portable spirometers feasible for use in clinics or participants' homes. The purpose of this study was to validate a hand held spirometer, the Welch-Allyn Pneumocheck(TM), against standard pulmonary function tests. The authors used a convenience sample of 66 subjects. All subjects were asked to perform three vital capacity maneuvers with the Welch-Allyn Pneumocheck(TM) and then either a water seal spirometer or heated pneumotach in a hospital pulmonary function laboratory. The mean forced vital capacity (FVC) obtained with the Pneumocheck(TM) was 3.50 liters (standard deviation (SD) = 1.28) compared with 3.31 liters (SD = 1.24) for the pulmonary function laboratory. The correlation between the two measures was 0.98; the mean difference was 0.19 L (95% confidence interval = 0.12 to 0.26). The mean forced expiratory volume at one second (FEV(1)) was 2.31 L (SD = 1.07) for the Pneumocheck(TM) compared with 2.32 L (SD = 1.06) for the pulmonary function laboratory values. The correlation between the two measures was 0.99; the mean difference was 0.01 L (95% confidence interval = -0.03 to 0.04). Of the 46 subjects originally classified by the Pneumocheck(TM) as having FEV(1)/FVC ratios of less than 0.75, 10 (22%) had ratios greater than or equal to 0.75 after correcting for the FVC difference between methods. Therefore, there was an excellent correlation between the Welch-Allyn Pneumocheck(TM) and pulmonary function laboratory values for FVC and FEV(1). Small systematic differences in FVC measures can lead to substantial misclassification rates when evaluating FEV(1)/FVC ratios. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 181,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,PULM FUNCT LAB,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV CLIN EPIDEMIOL,SAN ANTONIO,TX. FU NCRR NIH HHS [M01-RR-01346]; NIA NIH HHS [1-R01-AG10939-01, T-35-AG00230-01] NR 7 TC 4 Z9 4 U1 0 U2 1 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 1994 VL 308 IS 6 BP 357 EP 359 DI 10.1097/00000441-199412000-00009 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA PV995 UT WOS:A1994PV99500009 PM 7985725 ER PT J AU MONTOYA, ID HESS, JM COVI, L FUDALA, PJ JOHNSON, RE AF MONTOYA, ID HESS, JM COVI, L FUDALA, PJ JOHNSON, RE TI A COMPARATIVE-STUDY OF PSYCHOPATHOLOGY AND COGNITIVE FUNCTIONS BETWEEN COCAINE-DEPENDENT AND OPIATE-DEPENDENT PATIENTS SO AMERICAN JOURNAL ON ADDICTIONS LA English DT Article; Proceedings Paper CT International Narcotics Research Conference CY JUN 23-27, 1992 CL KEYSTONE, CO ID OPIOID ADDICTS; ABUSERS; DISORDERS; IMPAIRMENT; DIAGNOSIS; ALCOHOL; MMPI AB The authors examined cognitive and psychological differences between cocaine- and opiate-dependent individuals, using the Symptom Check List-90-Revised (SCL-90-R) and the Shipley Institute of Living Scale (SILS). They studied a sample of 135 cocaine-dependent and 162 opiate-dependent patients entering drug abuse treatment studies at the National Institute on Drug Abuse-Addiction Research Center (NIDA-ARC) outpatient clinic. Cocaine-dependent patients had significantly higher estimated Wechsler Adult Intelligence Scale (WAIS-R) IQ, vocabulary, abstraction, and total T scores, as measured by the SILS. On the SCL-90-R, cocaine-dependent patients had significantly higher scores for interpersonal sensitivity, anxiety, phobic anxiety, paranoid ideation, and psychoticism; opiate-dependent patients had higher scores for somatization, The results suggest that cocaine-dependent patients have better cognitive function and more psychopathology than opiate-dependent patients entering drug abuse outpatient treatment studies. C1 DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. RP MONTOYA, ID (reprint author), NIDA,ARC,TREATMENT BRANCH,POB 5180,BALTIMORE,MD 21224, USA. NR 31 TC 3 Z9 3 U1 1 U2 6 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1055-0496 J9 AM J ADDICTION JI Am. J. Addict. PD WIN PY 1994 VL 3 IS 1 BP 36 EP 42 PG 7 WC Substance Abuse SC Substance Abuse GA MY146 UT WOS:A1994MY14600004 ER PT J AU ABRUTYN, E KAYE, D AF ABRUTYN, E KAYE, D TI ASYMPTOMATIC BACTERIURIA AND SURVIVAL - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 MED COLL PENN,PHILADELPHIA,PA 19129. HAHNEMANN UNIV,PHILADELPHIA,PA 19129. RP ABRUTYN, E (reprint author), VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 3 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 DEC 1 PY 1994 VL 121 IS 11 BP 896 EP 896 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA PT628 UT WOS:A1994PT62800017 ER PT J AU DALEY, J GROVER, FL HAMMERMEISTER, KE AF DALEY, J GROVER, FL HAMMERMEISTER, KE TI USING OUTCOMES DATA TO IMPROVE CLINICAL-PRACTICE - BUILDING ON MODELS FROM CARDIAC-SURGERY - JUNE 6-7, 1994 KEYSTONE, COLORADO SO ANNALS OF THORACIC SURGERY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA. DENVER VA MED CTR,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,BOULDER,CO 80309. RP DALEY, J (reprint author), BROCKTON W ROXBURY VET AFFAIRS MED CTR,BROCKTON,MA, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD DEC PY 1994 VL 58 IS 6 BP 1807 EP 1808 PG 2 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA PU986 UT WOS:A1994PU98600078 ER PT J AU HAMMERMEISTER, KE DALEY, J GROVER, FL AF HAMMERMEISTER, KE DALEY, J GROVER, FL TI USING OUTCOMES DATA TO IMPROVE CLINICAL-PRACTICE - WHAT WE HAVE LEARNED SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT National Symposium on Using Outcomes Data to Improve Clinical Practice - Building on Models from Cardiac Surgery CY JUN 06-07, 1994 CL KEYSTONE, CO C1 DENVER VA MED CTR,SURG SERV,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DIV CARDIOTHORAC SURG,DENVER,CO 80262. BROCKTON W ROXBURY VET AFFAIRS MED CTR,HLTH SERV RES & DEV,BOSTON,MA. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,BOSTON,MA. RP HAMMERMEISTER, KE (reprint author), DENVER VA MED CTR,SERV CARDIOL,1055 CLERMONT,DENVER,CO 80220, USA. NR 18 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD DEC PY 1994 VL 58 IS 6 BP 1809 EP 1811 PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA PU986 UT WOS:A1994PU98600079 PM 7979773 ER PT J AU SINGH, AK DHAUNSI, GS GUPTA, MP ORAK, JK ASAYAMA, K SINGH, I AF SINGH, AK DHAUNSI, GS GUPTA, MP ORAK, JK ASAYAMA, K SINGH, I TI DEMONSTRATION OF GLUTATHIONE-PEROXIDASE IN RAT-LIVER PEROXISOMES AND ITS INTRAORGANELLAR DISTRIBUTION SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID SUPEROXIDE-DISMUTASE; HUMAN-PLASMA; HUMAN-DISEASES; FREE-RADICALS; PROTEINS; PURIFICATION; ENZYME; IDENTIFICATION; METABOLISM; SEQUENCE AB Earlier, we reported that rat liver peroxisomes contain Cu-Zn superoxide dismutase (J. Biol. Chem. 267, 6870), thereby suggesting a new antioxidant role for this organelle in free radical metabolism. In this study, we report for the first time that mammalian peroxisomes also contain glutathione peroxidase. Using highly purified rat Liver peroxisomes isolated by Nycodenz gradient, we found that peroxisomes contain glutathione peroxidase which shows enzymatic activity with different substrates such as hydrogen peroxide, cumene hydroperoxide, and t-butyl hydroperoxide. This activity could be inhibited in vitro by mercaptosuccinate. Western blot analysis revealed that peroxisomes from control and ciprofibrate-treated Livers show immunoreactive bands with antibodies raised against glutathione peroxidase. The intraperoxisomal distribution of glutathione peroxidase was investigated by using peroxisomal membrane and matrix proteins. The results revealed that glutathione peroxidase is a matrix enzyme. The presence of glutathione peroxidase in peroxisomes provides an alternate enzyme system responsible for the degradation of organic peroxides and the degradation of H2O2 under conditions in which catalase is inactivated (e.g., ischemia-reperfusion and endotoxemia). These findings suggest that glutathione peroxidase in peroxisomes may play a novel role in the cellular antioxidant responses to various oxidative stress conditions. (C) 1994 Academic Press, Inc. C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. YAMANASHI MED COLL,DEPT PEDIAT,YAMANASHI 40938,JAPAN. RP SINGH, AK (reprint author), RALPH H JOHNSON VET ADM MED CTR,DEPT PATHOL & LAB MED,109 BEE ST,CHARLESTON,SC 29401, USA. FU NINDS NIH HHS [NS-22576] NR 52 TC 36 Z9 38 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD DEC PY 1994 VL 315 IS 2 BP 331 EP 338 DI 10.1006/abbi.1994.1508 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA PV829 UT WOS:A1994PV82900017 PM 7986075 ER PT J AU GREEN, MF NUECHTERLEIN, KH MINTZ, J AF GREEN, MF NUECHTERLEIN, KH MINTZ, J TI BACKWARD-MASKING IN SCHIZOPHRENIA AND MANIA .1. SPECIFYING A MECHANISM SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID COLLEGE-STUDENTS; PATTERN MASKING; DISORDERS; DEFICIT AB Background: Backward masking is a neuropsychological procedure that involves the earliest phases of visual processing. Compared with normal controls, the performance of schizophrenic patients is more disrupted by a visual mask. Masking procedures used previously with schizophrenic patients have combined two separate masking mechanisms (interruption and integration), which prevent interpretation pf the nature of the abnormality. The current study systematically limited the masking mechanism to interruption to specify the underlying mechanisms. Manic patients were included to examine diagnostic specificity. Methods: Sixty-three schizophrenic inpatients, 31 manic inpatients, and 48 normal controls received three versions of the backward masking procedure. One version used a high-energy mask that combines both integration and interruption mechanisms. Another procedure used a low-energy mask that works mainly through interruption. A final condition altered the features of the mask so that masking was almost entirely through interruption. Results: Schizophrenic patients showed performance deficits across masking conditions, even in procedures that were largely limited to masking by interruption. The masking performance of the patients did not appear to fit a simple generalized deficit. Manic patients performed significantly worse than normal controls and comparably with the schizophrenic patients. Conclusions: Schizophrenic patients have abnormalities at least with interruptive mechanisms. The results suggest that deficits on masking procedures are not entirely specific to schizophrenia because comparable masking deficits were found in manic inpatients with chronic disease. The current study addresses the neuropsychological mechanisms of the masking deficit. The next step will be to investigate the contributions of two distinct neuroanatomical visual pathways to the masking abnormality in schizophrenia. C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. RP UNIV CALIF LOS ANGELES, CLIN RES CTR, DEPT PSYCHIAT & BIOBEHAV SCI, BOX 6022, CAMARILLO, CA 93011 USA. RI Mintz, Jim/N-7385-2014 OI Mintz, Jim/0000-0002-8299-5851 FU NIMH NIH HHS [MH-43292] NR 27 TC 149 Z9 149 U1 1 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0003-990X EI 1538-3636 J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD DEC PY 1994 VL 51 IS 12 BP 939 EP 944 PG 6 WC Psychiatry SC Psychiatry GA PW005 UT WOS:A1994PW00500001 PM 7979881 ER PT J AU GREEN, MF NUECHTERLEIN, KH MINTZ, J AF GREEN, MF NUECHTERLEIN, KH MINTZ, J TI BACKWARD-MASKING IN SCHIZOPHRENIA AND MANIA .2. SPECIFYING THE VISUAL CHANNELS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CEREBRAL LATERALITY; LOCALIZATION; INTEGRATION; DEPRESSION AB Background: The backward masking procedures that have been used in psychopathology research have confounded two types of masking mechanisms (integration and interruption) and two types of visual channels (transient and sustained). In an earlier study, we attempted to limit the masking mechanism to interruption The current study limited the role of sustained (parvocellular) visual channels to masking performance. Methods: Masking procedures were altered in the following two ways to reduce reliance on sustained visual channels: (1) the spatial frequency was lowered by blurring the target and (2) a location task was used instead of an identification task. Manic patients were included to examine the specificity of deficits on these tasks to schizophrenia and to test the hypothesis that mania is associated with abnormalities on visuospatial tasks. Results: Schizophrenic patients differed significantly from normal controls on both masking conditions. Manic patients also showed deficits relative to normal controls. Manic patients showed a significantly different masking function from that of schizophrenic patients on the location condition. Conclusions: Schizophrenic deficits within masking paradigms may involve abnormalities in transient, as opposed to sustained, visual channels. Masking performance deficits were also found in manic patients, but the underlying processes are probably different. A reformulation is offered concerning the nature of early visual processing deficits in schizophrenia. C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. RP UNIV CALIF LOS ANGELES, CLIN RES CTR, DEPT PSYCHIAT & BIOBEHAV SCI, BOX 6022, CAMARILLO, CA 93011 USA. FU NIMH NIH HHS [MH-43292] NR 24 TC 145 Z9 147 U1 1 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0003-990X EI 1538-3636 J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD DEC PY 1994 VL 51 IS 12 BP 945 EP 951 PG 7 WC Psychiatry SC Psychiatry GA PW005 UT WOS:A1994PW00500002 PM 7979882 ER PT J AU HOGAN, K POWERS, PA GREGG, RG AF HOGAN, K POWERS, PA GREGG, RG TI CLONING OF THE HUMAN SKELETAL-MUSCLE ALPHA(1) SUBUNIT OF THE DIHYDROPYRIDINE-SENSITIVE L-TYPE CALCIUM-CHANNEL (CACNL1A3) SO GENOMICS LA English DT Note ID CHAIN C1 UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53705. UNIV WISCONSIN,DEPT PEDIAT,MADISON,WI 53705. UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV,MADISON,WI 53705. RP HOGAN, K (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT ANESTHESIOL,B6-319 CLIN SCI CTR,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 8 TC 19 Z9 20 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD DEC PY 1994 VL 24 IS 3 BP 608 EP 609 DI 10.1006/geno.1994.1677 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA PZ985 UT WOS:A1994PZ98500031 PM 7713519 ER PT J AU SINGARAM, C SENGUPTA, A SWEET, MA SUGARBAKER, DJ GOYAL, RK AF SINGARAM, C SENGUPTA, A SWEET, MA SUGARBAKER, DJ GOYAL, RK TI NITRINERGIC AND PEPTIDERGIC INNERVATION OF THE HUMAN ESOPHAGUS SO GUT LA English DT Article ID LOWER ESOPHAGEAL SPHINCTER; NITRIC-OXIDE SYNTHASE; GENE-RELATED PEPTIDE; NEURONAL NADPH DIAPHORASE; SMOOTH-MUSCLE; SUBSTANCE-P; OPOSSUM; CALCITONIN; MEDIATOR; PIG AB The distribution, colocalisation, and interconnections of nitrinergic and peptidergic neurons and nerves in the human oesophagus were examined. Cryosections of surgically resected tissues from eight subjects were studied with indirect immunofluorescence for the presence of 11 neuropeptides and neuron specific enolase. After immunohistochemistry, nitric oxide synthase was shown on the same sections with the beta nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemical reaction. The histochemical findings were verified immunohistochemically on other sections with an antiserum against nitric oxide synthase. Most myenteric neurons (55%) were nitrinergic. Most (96%) received terminations positive for vasoactive intestinal polypeptide (VIP), calcitonin gene related peptide (CGRP) (80%), and galanin (59%). The neuronal somata of 14% also contained VIP, while 10% had galanin. Of the NADPH-diaphorase containing fibres seen in the muscle layers, many had closely associated VIP and galanin, but only rarely CGRP and substance P. Thus, despite abundant representation of both peptidergic and nitrinergic systems in oesophageal smooth muscle, only VIP and galanin colocalised to any significant extent with the nitrinergic elements. These findings provide morphological support for the role of nitric oxide as the non-adrenergic non-cholinergic inhibitory mediator in the human oesophagus and for its possible interactive role with the peptidergic system. fluorescence were nitrinergic. Most (96%) terminations Dositive for C1 UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,DIV GASTROENTEROL,MADISON,WI. BOSTON UNIV,SCH MED,DIV PEDIAT GASTROENTEROL & NUTR,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV GASTROENTEROL,BOSTON,MA 02215. FU NIDDK NIH HHS [DK 31092] NR 33 TC 55 Z9 59 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0017-5749 J9 GUT JI Gut PD DEC PY 1994 VL 35 IS 12 BP 1690 EP 1696 DI 10.1136/gut.35.12.1690 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PW402 UT WOS:A1994PW40200003 PM 7530228 ER PT J AU FRIEDBERG, RC AF FRIEDBERG, RC TI TRANSFUSION THERAPY IN THE PATIENT UNDERGOING HEMATOPOIETIC STEM-CELL TRANSPLANTATION SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID BONE-MARROW TRANSPLANTATION; HUMAN FETAL BLOOD; PLATELET TRANSFUSIONS; PROGENITOR CELLS; HLA; ALLOIMMUNIZATION; RECONSTITUTION; RECIPIENTS; BANK AB Optimal transfusion therapy for the patient undergoing stem cell transplantation will vary, depending on a variety of independent factors. These factors include the source of hematopoietic progenitor cells, The relationship between donor and recipient, and the timing of the transfusion relative to the transplant. Stem cell transplantation also changes the traditional views of blood groups: a patient may have more than one of the traditional blood groups at different stages of transplantation. C1 BIRMINGHAM VET AFFAIRS MED CTR,PATHOL & LAB MED SERV,BIRMINGHAM,AL. RP FRIEDBERG, RC (reprint author), UNIV ALABAMA,DEPT PATHOL,DIV LAB MED,WP-230,619 S 19TH ST,BIRMINGHAM,AL 35233, USA. NR 34 TC 4 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD DEC PY 1994 VL 8 IS 6 BP 1105 EP 1116 PG 12 WC Oncology; Hematology SC Oncology; Hematology GA PT766 UT WOS:A1994PT76600005 PM 7860439 ER PT J AU FRIEDBERG, RC AF FRIEDBERG, RC TI ISSUES IN TRANSFUSION THERAPY IN THE PATIENT WITH MALIGNANCY SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID VERSUS-HOST DISEASE; BONE-MARROW TRANSPLANTATION; CYTOMEGALO-VIRUS INFECTION; WHITE CELL-REDUCTION; PROPHYLACTIC PLATELET TRANSFUSION; RED-BLOOD-CELL; RECOMBINANT-HUMAN-ERYTHROPOIETIN; OPEN-HEART SURGERY; ACUTE LUNG INJURY; LEUKOCYTE-DEPLETION AB The role of transfusion therapy has become increasingly more critical as improved therapeutic regimens augment the survival of the patient with malignancy. Curiously, these improvements have led to the realization that transfusion therapy has significant but previously unexpected sequelae. Fortunately, many of these complications are controllable with modified or specifically selected components. C1 BIRMINGHAM VET AFFAIRS MED CTR,PATHOL & LAB MED SERV,BIRMINGHAM,AL. RP FRIEDBERG, RC (reprint author), UNIV ALABAMA,DEPT PATHOL,DIV LAB MED,WP-230,619 S 19TH ST,BIRMINGHAM,AL 35233, USA. NR 212 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD DEC PY 1994 VL 8 IS 6 BP 1223 EP 1253 PG 31 WC Oncology; Hematology SC Oncology; Hematology GA PT766 UT WOS:A1994PT76600012 PM 7860446 ER PT J AU TSUANG, JW LOHR, JB AF TSUANG, JW LOHR, JB TI EFFECTS OF ALCOHOL ON SYMPTOMS IN ALCOHOLIC AND NONALCOHOLIC PATIENTS WITH SCHIZOPHRENIA SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Note ID ABUSE C1 VET AFFAIRS MED CTR,PSYCHIAT SERV,SAN DIEGO,CA 92161. UNIV CALIF SAN DIEGO,SCH MED,SAN DIEGO,CA 92103. RP TSUANG, JW (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. FU NIMH NIH HHS [R29-MH45142-01] NR 10 TC 4 Z9 4 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 DEC PY 1994 VL 45 IS 12 BP 1229 EP 1230 PG 2 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA PV435 UT WOS:A1994PV43500013 PM 7868108 ER PT J AU GUDMUNDSSON, S VOGELMAN, B CRAIG, WA AF GUDMUNDSSON, S VOGELMAN, B CRAIG, WA TI DECREASED BACTERICIDAL ACTIVITY DURING THE PERIOD OF THE POSTANTIBIOTIC EFFECT SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID BENZYLPENICILLIN; THERAPY; INVITRO; INVIVO AB Standard and clinical strains of Staphylococcus aureus, Escherichia coli and Klebsiella pneumoniae were subjected to continuous exposure to beta-lactams and aminoglycosides during the postantibiotic effect phase induced by rifampicin or erythromycin (for S. aureus). A significant inhibition of bactericidal activity by these agents during the PAE period was observed. The degree of inhibition was dependent both on the class of antimicrobial agent (beta-lactams > aminoglycosides) and the microorganism (Gram-negative bacilli > S. aureus). C1 UNIV ICELAND, SCH MED, REYKJAVIK, ICELAND. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MED SERV, MADISON, WI USA. UNIV WISCONSIN, DEPT MED, MADISON, WI USA. RP GUDMUNDSSON, S (reprint author), LANDSPITALINN, DEPT MED, REYKJAVIK, ICELAND. NR 19 TC 16 Z9 16 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD DEC PY 1994 VL 34 IS 6 BP 921 EP 930 DI 10.1093/jac/34.6.921 PG 10 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA QE597 UT WOS:A1994QE59700007 PM 7730235 ER PT J AU HAMM, J SCHILLER, JH CUFFIE, C OKEN, M FISHER, RI SHEPHERD, F KAISER, G AF HAMM, J SCHILLER, JH CUFFIE, C OKEN, M FISHER, RI SHEPHERD, F KAISER, G TI DOSE-RANGING STUDY OF RECOMBINANT HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR IN SMALL-CELL LUNG-CARCINOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID AUTOLOGOUS BONE-MARROW; GM-CSF; ADVANCED MALIGNANCY; CANCER; CHEMOTHERAPY; THERAPY; NEUTROPHILS; SURVIVAL; TOXICITY; TUMORS AB Purpose: This randomized, multicenter, dose-finding study was undertaken to determine the dose of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) that can safely reduce neutropenia after cyclophosphamide, doxorubicin, and etoposide (CAVP-16) chemotherapy in patients with small-cell lung cancer (SCLC). Secondary clinical end points included incidence of infection, intravenous (IV) antimicrobial use, and chemotherapy delivered. Patients and Methods: A total of 290 newly diagnosed SCLC patients were to receive six cycles of standard CAVP-16 chemotherapy on days 1 to 3 of every 21 days alone or with rhGM-CSF at 5, 10, or 20 mu g/kg, administered subcutaneously (SC) on days 4 to 13 of each cycle. Results: In cycle 1, median absolute neutrophil count (ANC) nadirs were twofold to threefold higher in patients who received rhGM-CSF, although all values were less than 500/mu L, and recovery from neutropenia was faster at all rhGM-CSF dosages versus observation (P less than or equal to .01). In cycle 2, 56% of all patients given rhGM-CSF received full chemotherapy dosages (87.5% to 112.% of projected dose) versus 36% of observation patients. During days 5 to 21 of cycle 1, fewer patients who received 10 mu g/kg of rhGM-CSF required antibiotics compared with observation patients (11% v 29%, P less than or equal to .01). Adverse events that occurred more frequently in rhGM-CSF-treated patients included injection-site reaction, edema, asthenia, paesthesia, diarrhea, myalgia, musculoskeletal pain, pruritus, and rash (P less than or equal to .10). Fewer occurred more frequently in the 10- and 20-mu g/kg rhGM-CSF groups than in the observation groups. The incidence in the 5-mu g/kg group was comparable to that in observation patients. Patients who received rhGM-CSF had a higher incidence of thrombocytopenia. Conclusion: rhGM-CSF at 5 to 10 mu g/kg reduces chemotherapy-associated neutropenia and should be the dose range used in future studies. C1 UNIV LOUISVILLE,JAMES GRAHAM BROWN CANC CTR,LOUISVILLE,KY 40292. UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. SCHERING PLOUGH CORP,RES INST,KENILWORTH,NJ 07033. ABBOTT NW HOSP,PIPER CANC INST,MINNEAPOLIS,MN. LOYOLA UNIV,MED CTR,MAYWOOD,IL 60153. TORONTO GEN HOSP,TORONTO,ON,CANADA. MUNICIPAL MED CTR,MED DEPT HEMATOL ONCOL 5,NURNBERG,GERMANY. NR 32 TC 39 Z9 39 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD DEC PY 1994 VL 12 IS 12 BP 2667 EP 2676 PG 10 WC Oncology SC Oncology GA PV811 UT WOS:A1994PV81100022 PM 7989942 ER PT J AU LEWIN, L GONZALES, LR AF LEWIN, L GONZALES, LR TI TREATMENT OF URETHRAL CATHETER DEPENDENCE - A CASE-STUDY OF INTERVENTION IN THE INTERDISCIPLINARY GERIATRIC SETTING SO JOURNAL OF CLINICAL PSYCHOLOGY IN MEDICAL SETTINGS LA English DT Article DE URETHRAL CATHETER DEPENDENCE; PHOBIA; DECONDITIONING; INTERDISCIPLINARY AB This case report describes the assessment and treatment of a 69-year-old male medical patient with urethral catheter dependence. Assessment revealed an anxiety/phobic component to the dependence and hypothesized detrusor muscle deconditioning. Retraining of the bladder and desensitization to the anxiety-provoking situation were achieved by exposure to decatheterization in the context of a supportive adult day health care setting. Interdisciplinary collaboration between nursing and psychology were associated with successful functional social, and psychological outcomes. C1 OREGON HLTH SCI UNIV,DEPT MED PSYCHOL,PORTLAND,OR 97201. PORTLAND VA MED CTR,PORTLAND,OR. RP LEWIN, L (reprint author), CLARK COLL,FOSTER HALL,1800 E MCLOUGHLIN BLVD,VANCOUVER,WA 98663, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 1068-9583 J9 J CLIN PSYCHOL MED S JI J. Clin. Psychol. Med. Settings PD DEC PY 1994 VL 1 IS 4 BP 363 EP 373 DI 10.1007/BF01991079 PG 11 WC Psychology, Clinical SC Psychology GA RK317 UT WOS:A1994RK31700008 PM 24225862 ER PT J AU MCLELLAN, AT ALTERMAN, AI METZGER, DS GRISSOM, GR WOODY, GE LUBORSKY, L OBRIEN, CP AF MCLELLAN, AT ALTERMAN, AI METZGER, DS GRISSOM, GR WOODY, GE LUBORSKY, L OBRIEN, CP TI SIMILARITY OF OUTCOME PREDICTORS ACROSS OPIATE, COCAINE, AND ALCOHOL TREATMENTS - ROLE OF TREATMENT SERVICES SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY LA English DT Article ID ADDICTION SEVERITY INDEX; SUBSTANCE-ABUSE TREATMENT; PSYCHOPATHOLOGY AB This study examined the patient and treatment factors associated with 6-month outcome in 649 opiate-, alcohol-, and cocaine-dependent (male and female) adults, treated in inpatient and outpatient settings, in 22 publicly and privately funded programs. Outcomes were predicted by similar factors, regardless of the drug problem of the patient or the type of treatment setting or funding. Greater substance use at follow-up was predicted only by greater severity of alcohol and drug use at treatment admission, not by the number of services received during treatment. Better social adjustment at follow-up was negatively predicted by more severe psychiatric, employment, and family problems at admission and positively predicted C1 INTEGRA INC,RADNOR,PA. RP MCLELLAN, AT (reprint author), UNIV PENN,SCH MED,VET AFFAIRS MED CTR,CTR STUDIES ADDICT,DEPT PSYCHIAT,BLDG 7,UNIV AVE,PHILADELPHIA,PA 19104, USA. RI Metzger, David/D-9499-2012 NR 48 TC 262 Z9 266 U1 0 U2 3 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0022-006X J9 J CONSULT CLIN PSYCH JI J. Consult. Clin. Psychol. PD DEC PY 1994 VL 62 IS 6 BP 1141 EP 1158 DI 10.1037//0022-006X.62.6.1141 PG 18 WC Psychology, Clinical SC Psychology GA PX232 UT WOS:A1994PX23200006 PM 7860812 ER PT J AU FLESCHER, E LEDBETTER, JA SCHIEVEN, GL VELAROCH, N FOSSUM, D DANG, H OGAWA, N TALAL, N AF FLESCHER, E LEDBETTER, JA SCHIEVEN, GL VELAROCH, N FOSSUM, D DANG, H OGAWA, N TALAL, N TI LONGITUDINAL EXPOSURE OF HUMAN T-LYMPHOCYTES TO WEAK OXIDATIVE STRESS SUPPRESSES TRANSMEMBRANE AND NUCLEAR SIGNAL-TRANSDUCTION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PROTEIN-TYROSINE PHOSPHORYLATION; CELL ANTIGEN RECEPTOR; DNA-BINDING PROTEINS; TRANSCRIPTION FACTOR; HYDROGEN-PEROXIDE; N-ACETYLCYSTEINE; PHOSPHOLIPASE-C; HEAT-SHOCK; POLYAMINE OXIDATION; GENE-EXPRESSION AB Products of polyamine oxidase activity, at micromolar levels and during a period of 2 to 3 days, down-regulate IL-2 mRNA levels and activity in human lymphocytes. We studied whether this suppression was associated with signal transduction abnormalities. We found that polyamine oxidase activity suppresses both anti-CD3-induced IL-2 production and protein tyrosine phosphorylation. Polyamine oxidase activity also caused a reduction in intracellular calcium mobilization after mitogenic stimulation. The most distal step of CD3-mediated signal transduction is dependent upon transcription factors that regulate a set of genes, including IL-2. We found that polyamine oxidase-treated cells exhibited very low DNA binding activity of two such factors: NFAT and NF-kappa B. On the other hand, AP-1 DNA binding activity was enhanced in polyamine oxidase-treated cells, suggesting a possible role for AP-1 in the human lymphocyte stress response. In accordance with the oxidation dependence of this suppressive mechanism, N-acetylcysteine (NAC; an antioxidant) significantly reversed the polyamine oxidase effects on lymphokine production and signal transduction. These results suggest that NAC contributes, under oxidizing conditions, to the preservation of immune function. In summary, our data suggest that chronic low-level oxidative stress; via suppression of mitogen-induced transmembrane signaling (protein-tyrosine phosphorylation and calcium mobilization), causes a decrease in the DNA binding activity of transcription factors that regulate the IL-2 gene. This results in decreased IL-2 production. C1 UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. FU NIDCR NIH HHS [DE09311, DE10863] NR 56 TC 89 Z9 90 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD DEC 1 PY 1994 VL 153 IS 11 BP 4880 EP 4889 PG 10 WC Immunology SC Immunology GA PT301 UT WOS:A1994PT30100004 PM 7963551 ER PT J AU ALBERT, MM ADAMS, K LUTHER, MJ SUN, SH GRAYBILL, JR AF ALBERT, MM ADAMS, K LUTHER, MJ SUN, SH GRAYBILL, JR TI EFFICACY OF AMBISOME IN MURINE COCCIDIOIDOMYCOSIS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Note ID AMPHOTERICIN-B AMBISOME; FORMULATION AMBISOME; MENINGITIS AB ICR mice were infected intranasally with arthroconidia of Coccicioides immitis. Mice were treated intravenously with amphotericin B deoxycholate (Fungizone) or an amphotericin B-lipid vehicle (AmBisome). Doses ranged from 0.05 to 1.0 mg kg(-1). Lung weight, which parallels disease severity and fungal burden in this infection, was used as the index of protection. Both Fungizone and AmBisome were significantly and equally protective at 0.3 and 1.0 mg kg(-1) body weight. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT RES,SAN ANTONIO,TX 78284. NR 23 TC 12 Z9 12 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. PD DEC PY 1994 VL 32 IS 6 BP 467 EP 471 PG 5 WC Mycology SC Mycology GA QJ945 UT WOS:A1994QJ94500007 PM 7738729 ER PT J AU ROYALL, DR MAHURIN, R AF ROYALL, DR MAHURIN, R TI EXIT, QED, AND DSM-IV - REGIONAL SYNDROMES SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Letter C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX, USA. NR 8 TC 2 Z9 2 U1 1 U2 1 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 WIN PY 1994 VL 6 IS 1 BP 60 EP 62 PG 3 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MV318 UT WOS:A1994MV31800014 PM 8148641 ER PT J AU ROYALL, DR MAHURIN, R AF ROYALL, DR MAHURIN, R TI EXIT, QED, AND DSM-IV - VERY EARLY ALZHEIMERS-DISEASE SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Letter C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX, USA. NR 12 TC 14 Z9 14 U1 1 U2 1 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 WIN PY 1994 VL 6 IS 1 BP 62 EP 64 PG 3 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MV318 UT WOS:A1994MV31800015 PM 8148642 ER PT J AU MATSUYAMA, SS BONDAREFF, W AF MATSUYAMA, SS BONDAREFF, W TI TAN-LIKE IMMUNOREACTIVITY IN ALZHEIMER AND CONTROL SKIN FIBROBLASTS SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE TAU; MICROTUBULES; INTERMEDIATE FILAMENTS ID PAIRED HELICAL FILAMENTS; PROTEIN-TAU; AMYLOID PRECURSOR; DISEASE; PHOSPHORYLATION; ANTIBODY; ISOFORMS; BRAIN; CORE AB The presence of the microtubule-associated protein tan in skin fibroblasts derived from Alzheimer patients and normal controls was investigated using a panel of well-characterized anti-tau antibodies against epitopes spanning the tau protein from the amino to the carboxyl end. The antibodies immunolabeled a fine, fibrillar cytoplasmic network in all skin fibroblasts. Disruption of the microtubule network with colchicine did not affect the immunolabeling of the fibrillar network nor did treatment with cytochalasin B known to disrupt the microfilament network. Immunoelectron microscopy with the antitau antibodies revealed colocalization of the label with the 10 nm intermediate filaments, Furthermore, immunoblots found no reactivity against purified vimentin, suggesting that the antibodies recognize an intermediate filament-associated protein. The findings indicate the presence of tau or a protein with considerable homology to tau in fibroblasts associated with intermediate filaments and not microtubules. (C) 1994 Wiley-Liss, Inc. C1 W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHOGERIATR UNIT & LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV SO CALIF,DEPT PSYCHIAT,DIV GERIATR PSYCHIAT,LOS ANGELES,CA. FU NIA NIH HHS [P30 AG10123] NR 31 TC 8 Z9 8 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD DEC 1 PY 1994 VL 39 IS 5 BP 519 EP 524 DI 10.1002/jnr.490390503 PG 6 WC Neurosciences SC Neurosciences & Neurology GA QF969 UT WOS:A1994QF96900002 PM 7534356 ER PT J AU RITTENHOUSE, PA BAKKUM, EA LEVY, AD LI, Q CARNES, M VANDEKAR, LD AF RITTENHOUSE, PA BAKKUM, EA LEVY, AD LI, Q CARNES, M VANDEKAR, LD TI EVIDENCE THAT ACTH-SECRETION IS REGULATED BY SEROTONIN(2A/2C) (5-HT2A/2C) RECEPTORS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; HYPOTHALAMIC PARAVENTRICULAR NUCLEUS; SERUM CORTICOSTERONE CONCENTRATION; PITUITARY-ADRENOCORTICAL AXIS; RENIN SECRETION; 5-HT RECEPTORS; RAT-BRAIN; SYMPATHOADRENOMEDULLARY SYSTEM; PARA-CHLOROAMPHETAMINE; MESSENGER-RNA AB The present study characterized the serotonin (5-HT) receptor subtypes mediating adrenal corticotropic hormone (ACTH) and corticosterone responses to 5-HT agonists in conscious rats. The 5-HT2A/5-HT2C agonist (+/--1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HC1 (DOl) increased plasma ACTH and corticosterone in a dose-dependent manner. The 5-HT2A/5HT(2C) antagonist ritanserin (0.01 and 0.1 mg/kg sc) inhibited the DOl-induced increase in plasma ACTH, but not corticosterone. Low doses of spiperone (0.01 and 0.1 mg/kg sc) significantly reduced the ACTH response to DOl. Because spiperone has a higher affinity for 5-HT2A than 5-HT2C receptors, these data suggest that DOl stimulates ACTH secretion through 5-HT2A receptors. 5-methoxy-3-[1,2,3,4-tetrahydro-4-pyridinyl]-1 H-indole (RU 24969) is a potent 5-HT1A/1B and moderate S-HT2C agonist that also has been suggested to release 5-HT. However, p-chlorophenylalanine (PCPA) did not reduce the effect of RU 24969 on plasma ACTH, suggesting that RU 24969 only acts as a direct agonist. and 6-methyl-1-[1-methylethyl]ergoline-8-carboxylic acid (LY53857) injected into the lateral cerebral ventricles (i.c.v.) inhibited the ACTH, but not corticosterone response to peripheral injection of RU 24969, suggesting that central 5-HT2A/2C receptors mediate the ACTH response. LY53857 injection (i.c.v.) also inhibited the effect of p-chloroamphetamine (i.c.v.) on plasma ACTH. However, the corticosterone response was not inhibited by LY53857, suggesting a distinct location of 5-HT receptors regulating corticosterone secretion. Lesions using the cell-selective neurotoxin ibotenic acid in the hypothalamic paraventricular nucleus significantly lowered the ACTH response to both RU 24969 (43% decrease) and p-chloroamphetamine (26% decrease). In contrast, lesions in the dorsomedial or ventromedial nuclei did not alter the ACTH response to p-chloroamphetamine. The corticosterone response followed the ACTH response in each of these experiments. The results from these experiments suggest the following: (1) a greater role exists for 5-HT2A than 5-HT2C receptors in the hypothalamus in mediating DOl's effect on ACTH secretion; (2) a peripheral 5-HT receptor is important in stimulating corticosterone secretion, independent or separate from control by ACTH and (3) relatively modest increases in plasma ACTH produce maximal increases in plasma corticosterone. C1 LOYOLA UNIV,STRITCH SCH MED,DEPT PHARMACOL,MAYWOOD,IL 60153. BOSTON UNIV,MED CTR,DEPT PHARMACOL,BOSTON,MA 02118. WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIATR SECT,MADISON,WI 53705. FU NIMH NIH HHS [MH-45812] NR 55 TC 42 Z9 44 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 DEC PY 1994 VL 271 IS 3 BP 1647 EP 1655 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA PX343 UT WOS:A1994PX34300071 PM 7996480 ER PT J AU SZACHNOWSKI, P BRIDGES, AJ AF SZACHNOWSKI, P BRIDGES, AJ TI SUBCUTANEOUS CHOLESTEROL NODULES SO JOURNAL OF RHEUMATOLOGY LA English DT Letter ID DIAGNOSIS; DISEASE RP SZACHNOWSKI, P (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD DEC PY 1994 VL 21 IS 12 BP 2391 EP 2392 PG 2 WC Rheumatology SC Rheumatology GA PX446 UT WOS:A1994PX44600047 PM 7699652 ER PT J AU YOSHIKAWA, TT AF YOSHIKAWA, TT TI RISKS OF LONG-TERM URETHRAL CATHETERIZATION SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Editorial Material ID URINARY RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,WASHINGTON,DC, USA. NR 9 TC 1 Z9 1 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 DEC PY 1994 VL 42 IS 12 BP 1304 EP 1304 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA PV279 UT WOS:A1994PV27900017 PM 7983299 ER PT J AU OBARA, K MEYER, JS MORTEL, KF MURAMATSU, K AF OBARA, K MEYER, JS MORTEL, KF MURAMATSU, K TI COGNITIVE DECLINES CORRELATE WITH DECREASED CORTICAL VOLUME AND PERFUSION IN DEMENTIA OF ALZHEIMER-TYPE SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE ALZHEIMERS DISEASE; CEREBRAL ATROPHY; CEREBRAL BLOOD FLOW; COMPUTED TOMOGRAPHY; CT DENSITY; LONGITUDINAL STUDIES ID CEREBRAL BLOOD-FLOW; COMPUTED-TOMOGRAPHY; SENILE DEMENTIA; PRESENILE-DEMENTIA; VENTRICULAR SIZE; LONGITUDINAL CT; DISEASE; PROGRESSION; PERFORMANCE; DIAGNOSIS AB Cerebral CT changes are correlated with cognitive declines among 18 patients with probable dementia of Alzheimer type (DAT) (7 men, 11 women, mean age 75.4 years) and are compared for control purposes with similar measures among 18 age-matched normal volunteers (8 men, 10 women, mean age 73.7 years). Mean follow-up intervals are 28.6 months for DAT and 27.0 months for controls. For DAT, annual rates for ventricular volume enlargement are + 9.2% and for cortical atrophy are -2.1%. Annual reductions in regional cerebral perfusions per 100 g brain/min, are: total cortex -1.1 ml, frontal -1.2 ml, temporal and parietal -0.9 ml, basal ganglia -1.6 ml, thalamus - 2.5 ml, total white matter - 0.6 ml, frontal white matter - 0.7 ml. At entry evaluation, compared to normals, DAT patients had reduced CT densities in white matter, but not in cortex. Nevertheless, cortical CT densities declined progressively at annual rates of -0.72 Hounsfield units (HU), but remained constant in white matter. Annual point score declines for Cognitive Capacity Screening Examinations were -2.0 and for Mini Mental State: -2.8. Controls showed no cognitive change. Multiple regression analyses correlate cognitive declines with: (1) reductions in perfusion within parietal cortex (p = 0.015), (2) decreases in cortical volume (p = 0.019), and (3) decreases in HU within subcortical gray matter (p = 0.007). C1 BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBROVASC RES LABS,HOUSTON,TX. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX. NR 42 TC 35 Z9 35 U1 2 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD DEC 1 PY 1994 VL 127 IS 1 BP 96 EP 102 DI 10.1016/0022-510X(94)90141-4 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA PX672 UT WOS:A1994PX67200013 PM 7699398 ER PT J AU SPARWASSER, C DRESCHER, P WILL, JA MADSEN, PO AF SPARWASSER, C DRESCHER, P WILL, JA MADSEN, PO TI SMOOTH-MUSCLE TONE REGULATION IN RABBIT CAVERNOSAL AND SPONGIOSAL TISSUE BY CYCLIC-AMP-DEPENDENT AND CYCLIC-GMP-DEPENDENT MECHANISMS SO JOURNAL OF UROLOGY LA English DT Article DE CYCLIC AMP; CYCLIC GMP; NITRIC OXIDE; PHOSPHODIESTERASE INHIBITORS; PENIS ID NITRIC-OXIDE; CORPUS CAVERNOSUM; PENILE ERECTION; NONCHOLINERGIC NEUROTRANSMISSION; RELAXATION; CGMP; ENDOTHELIUM; MEDIATOR; PEPTIDE; SIN-1 AB The relaxing effects of several specific and nonspecific inhibitors of phosphodiesterases (PDE) on rabbit isolated corpus cavernosum (CC) and spongiosum (CS) were investigated. Preparations were mounted in organ baths, and isometric tension was recorded. The results were compared with the effects of direct administration of analogs of the second messenger cyclic nucleotides and the effects of forskolin, a direct stimulator of adenylate cyclase, and the nitric oxide donor 3-morpholinosydnonimine (SIN 1). All drugs relaxed the phenylephrine-induced contractions in CC and CS in a dose-dependent fashion. In CC: and CS, type III (SK&F 95654) and type V (zaprinast and dipyramidole) PDE inhibitors, as well as the nonspecific inhibitors papaverine and trequinsin, showed no differences in IC50. The type IV inhibitor rolipram relaxed CC and CS at significantly lower concentrations (p<0.005) than any other PDE inhibitor, and in CC the type III and IV inhibitor zardaverine was more potent (p<0.05) than SK&F 95654. SIN 1 stimulates guanylate cyclase and effectively inhibits contractions in CC and CS. Activation of adenylate cyclase by forskolin also was highly effective (p<0.005). It is concluded that PDE inhibition constitutes an effective relaxing mechanism in rabbit CC and CS. The marked effects of the different types of PDE inhibitors support the importance of cyclic guanosine 3',5'-monophosphate and cyclic adenosine 3',5'-monophosphate in smooth muscle relaxation in erectile tissue. C1 UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT ANESTHESIOL,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT ANIM HLTH & BIOMED SCI,MADISON,WI. NR 27 TC 34 Z9 34 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD DEC PY 1994 VL 152 IS 6 BP 2159 EP 2163 PN 1 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA PR245 UT WOS:A1994PR24500081 PM 7966707 ER PT J AU BOLDT, DH KOPECKY, KJ HEAD, D GEHLY, G RADICH, JP APPELBAUM, FR AF BOLDT, DH KOPECKY, KJ HEAD, D GEHLY, G RADICH, JP APPELBAUM, FR TI EXPRESSION OF MYELOID ANTIGENS BY BLAST CELLS IN ACUTE LYMPHOBLASTIC-LEUKEMIA OF ADULTS - THE SOUTHWEST-ONCOLOGY-GROUP EXPERIENCE SO LEUKEMIA LA English DT Article ID ACUTE LYMPHOCYTIC-LEUKEMIA; IMMUNOLOGICAL MARKERS; CLASSIFICATION; DIAGNOSIS AB A subset of adult acute lymphoblastic leukemia (ALL) patients have blast cells which ce-express myeloid-associated antigens (MY+ ALL). We have analyzed 113 adult ALL cases for expression of MY-associated antigens (MAA). ALL was diagnosed by standard morphology, cytochemistry, and immunophenotype in central review. MY+ ALL was diagnosed when greater than or equal to 20% of lymphoblasts co-expressed CD13 and/or CD33. Overall incidence of MY+ was 31/113 (27%). MAA expression was not significantly correlated with WBC, blast count, hemoglobin, or hematocrit. MY+ cases were more likely to express B-associated antigens, especially CALLA, and to be FAB L2, Ph+, or to have the BCR-ABL translocation by PCR, but these differences were not statistically significant. All patients were induced with a L10M regimen, and 67 (59%) achieved CR: 43/66 (65%) of B MY neg; 14/29 (48%) of B MY+; 10/16 (63%) T MY neg; and 0/2 T MY+. In age-adjusted analyses CR rate did not differ significantly between MY+ and MY neg patients or between B- and T-cell patients. Of the 113 patients, 84 have died and the remaining 29 patients have been followed for a median of 49 months. In proportional hazards regression analyses adjusting for age and WBC, heterogeneity of survival among the four groups was statistically significant (p = 0.021), largely due to MY status. The mortality rate was 85% greater for MY+ patients compared to MY neg patients (two-tailed p = 0.013). By contrast, survival did not vary significantly between B- and T cell patients. The data indicate that MAA expression is useful for predicting overall survival of adult patients with ALL treated in a L10M protocol. As a predictive factor MAA expression is comparable to the WBC and superior to the more standard stratification by B- or T-cell markers for this group of patients. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. SW ONCOL GRP, CTR STAT, SEATTLE, WA USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38105 USA. FRED HUTCHINSON CANC RES CTR, DIV CLIN RES, SEATTLE, WA 98104 USA. FRED HUTCHINSON CANC RES CTR, DIV EXPTL PATHOL, SEATTLE, WA 98104 USA. UNIV WASHINGTON, DEPT MED, SEATTLE, WA USA. SW ONCOL GRP, LEUKEMIA BIOL PROGRAM, SAN ANTONIO, TX USA. RP BOLDT, DH (reprint author), UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV HEMATOL, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. FU NCI NIH HHS [CA 32102] NR 31 TC 45 Z9 45 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD DEC PY 1994 VL 8 IS 12 BP 2118 EP 2126 PG 9 WC Oncology; Hematology SC Oncology; Hematology GA QB451 UT WOS:A1994QB45100013 PM 7807999 ER PT J AU GLATT, CR AF GLATT, CR TI LETTERS AND DISPATCHES, 1924-1944 - WALLENDERG,R SO LIBRARY JOURNAL LA English DT Book Review RP GLATT, CR (reprint author), PHILADELPHIA VA MED CTR,PHILADELPHIA,PA, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 SN 0363-0277 J9 LIBR J JI Libr. J. PD DEC PY 1994 VL 119 IS 21 BP 104 EP 104 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA PX313 UT WOS:A1994PX31300134 ER PT J AU CUMMINGS, JL MEGA, M GRAY, K ROSENBERGTHOMPSON, S CARUSI, DA GORNBEIN, J AF CUMMINGS, JL MEGA, M GRAY, K ROSENBERGTHOMPSON, S CARUSI, DA GORNBEIN, J TI THE NEUROPSYCHIATRIC INVENTORY - COMPREHENSIVE ASSESSMENT OF PSYCHOPATHOLOGY IN DEMENTIA SO NEUROLOGY LA English DT Article ID PROBABLE ALZHEIMERS-DISEASE; PSYCHIATRIC PHENOMENA; RATING-SCALE; PERSONALITY ALTERATIONS; DISORDERS; PSYCHOSIS; DELUSIONS; SYMPTOMS; PREDICTORS; DEPRESSION AB We developed a new instrument, the Neuropsychiatric Inventory (NPI), to assess 10 behavioral disturbances occurring in dementia patients: delusions, hallucinations, dysphoria, anxiety, agitation/aggression, euphoria, disinhibition, irritability/lability, apathy, and aberrant motor activity. The NPI uses a screening strategy to minimize administration time, examining and scoring only those behavioral domains with positive responses to screening questions. Both the frequency and the severity of each behavior are determined. Information for the NPI is obtained from a caregiver familiar with the patient's behavior. Studies reported here demonstrate the content and concurrent validity as well as between-rater, test-retest, and internal consistency reliability; the instrument is both valid and reliable. The NPI has the advantages of evaluating a wider range of psychopathology than existing instruments, soliciting information that may distinguish among different etiologies of dementia, differentiating between severity and frequency of behavioral changes, and minimizing administration time. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOMATH,BIOMATH CONSULTING UNIT,LOS ANGELES,CA 90024. RP CUMMINGS, JL (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,DEPT NEUROL,PSYCHIAT SERV,LOS ANGELES,CA 90073, USA. FU NIA NIH HHS [AG10123] NR 37 TC 3525 Z9 3617 U1 16 U2 120 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD DEC PY 1994 VL 44 IS 12 BP 2308 EP 2314 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA PW548 UT WOS:A1994PW54800016 PM 7991117 ER PT J AU SPIELMAN, AI HUQUE, T NAGAI, H WHITNEY, G BRAND, JG AF SPIELMAN, AI HUQUE, T NAGAI, H WHITNEY, G BRAND, JG TI GENERATION OF INOSITOL PHOSPHATES IN BITTER TASTE TRANSDUCTION SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE TASTE; BITTER; INOSITOL PHOSPHATES; G-PROTEINS; PHOSPHOLIPASE C; SIGNAL TRANSDUCTION; INOSITOL 1,4,5-TRISPHOSPHATE ID GTP-BINDING PROTEINS; PHOSPHOLIPASE-C; CELLS; CAFFEINE; CALCIUM; RELEASE; MICE; IDENTIFICATION; MECHANISMS; MEMBRANES AB It is probable that there is a diversity of mechanisms involved in the transduction of bitter taste. One of these mechanisms uses the second messengers, inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). Partial membrane preparations from circumvallate and foliate taste regions of mice tongues responded to the addition of known bitter taste stimuli by increasing the amount of inositol phosphates produced after 30 s incubation. Addition of both the bitter stimulus, sucrose octaacetate and the G-protein stimulant, GTP gamma S, led to an enhanced production of inositol phosphates compared with either alone. Pretreatment of the tissue samples with pertussis toxin eliminated all response to sucrose octaacetate plus GTP gamma S, whereas pretreatment with cholera toxin was without effect. Western blots of solubilized tissue from circumvallate and foliate regions probed with antibodies to the alpha-subunit of several types of G-proteins revealed bands reactive to antibodies against G alpha(i1-2), and G alpha(0),, with no apparent activity to antibodies against G alpha(i3). Given the results from the immunoblots and those of the toxin experiments, it is proposed that the transduction of the bitter taste of sucrose octaacetate in mice involves a receptor-mediated activation of a G(i)-type protein which activates a phospholipase C to produce the two second messengers, IP3 and DAG. C1 MONELL CHEM SENSES CTR, PHILADELPHIA, PA 19104 USA. NYU, COLL DENT, DIV BASIC SCI, NEW YORK, NY USA. SUNTORY LTD, INST FUNDAMENTAL RES, OSAKA, JAPAN. FLORIDA STATE UNIV, DEPT PSYCHOL, TALLAHASSEE, FL 32306 USA. DEPT VET AFFAIRS MED CTR, PHILADELPHIA, PA 19104 USA. UNIV PENN, SCH DENT MED, PHILADELPHIA, PA 19104 USA. NR 35 TC 55 Z9 55 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD DEC PY 1994 VL 56 IS 6 BP 1149 EP 1155 DI 10.1016/0031-9384(94)90359-X PG 7 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA PU103 UT WOS:A1994PU10300006 PM 7878084 ER PT J AU GENTILI, A SEEGER, LL YAO, L DO, HM AF GENTILI, A SEEGER, LL YAO, L DO, HM TI ANTERIOR CRUCIATE LIGAMENT TEAR - INDIRECT SIGNS AT MR-IMAGING SO RADIOLOGY LA English DT Article DE KNEE, LIGAMENTS, MENISCI, AND CARTILAGE; KNEE, MR; LIGAMENTS, INJURIES; LIGAMENTS, MR ID KNEE; PATTERNS; INJURY; TIBIA AB PURPOSE: To establish the sensitivity and specificity of indirect signs at magnetic resonance (MR) imaging of anterior cruciate ligament (ACL) tear. MATERIALS AND METHODS: MR images of the knees of 89 consecutive patients (54 with torn and 35 with normal ACLs) were reviewed. RESULTS: The indirect signs were as follows (first percentage is sensitivity; the second, specificity): angle between lateral tibial plateau and ACL less than 45 degrees (90%, 97%); angle between Blumenstaat line and ACL more than 15 degrees (89%, 100%); bone contusions in lateral compartment (54%, 100%); position of posterior cruciate ligament (PCL) line (52%, 91%); PCL angle less than 107 degrees (52%, 94%); PCL bowing ratio more than 0.39 (34%, 100%); posterior displacement of lateral meniscus more than 3.5 mm (44%, 94%); anterior displacement of tibia more than 7 mm (41%, 91%); and lateral femoral sulcus deeper than 1.5 mm (19%, 100%). CONCLUSION: Because the specificity is high, the presence of indirect signs corroborates the diagnosis of ACL tear. Because the sensitivity is low, the absence of these signs does not exclude the diagnosis of ACL tear. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT RADIOL,LOS ANGELES,CA 90073. RP GENTILI, A (reprint author), UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT RADIOL SCI,LOS ANGELES,CA 90073, USA. RI Gentili, Amilcare/G-1238-2013 OI Gentili, Amilcare/0000-0002-5623-7512 NR 20 TC 84 Z9 94 U1 0 U2 2 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD DEC PY 1994 VL 193 IS 3 BP 835 EP 840 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA PT553 UT WOS:A1994PT55300049 PM 7972834 ER PT J AU BRIDGES, AJ HSU, KC SINGH, A CHURCHILL, R MILES, J AF BRIDGES, AJ HSU, KC SINGH, A CHURCHILL, R MILES, J TI FIBRODYSPLASIA (MYOSITIS) OSSIFICANS PROGRESSIVA SO SEMINARS IN ARTHRITIS AND RHEUMATISM LA English DT Article ID SOFT-TISSUE; DIPHOSPHONATE; ISOTRETINOIN; THERAPY; CT AB Fibrodysplasia ossificans progressiva (FOP) is a rare hereditary connective tissue disorder. Patients with FOP develop progressive ossification of muscle and connective tissue associated with pain and disability. Onset is typically in childhood, and congenital anomalies of the feet are an early sign of this condition. Pain and stiffness of the spine or an inflammatory mass are common presenting features of FOP. Involvement of the spine often leads to complete fusion mimicking ankylosing spondylitis. Studies of twins and families suggest that FOP is a genetically inherited autosomal dominant trait with complete penetrance but variable expressivity. While radionuclide imaging and computed tomography are very sensitive for new bone formation and greatly assist the diagnosis of FOP, unfortunately, effective therapy is unavailable. We present twins with FOP and review the clinical, radiographic, and genetic manifestations of this disorder. Copyright (C) 1994 by W.B. Saunders Company C1 UNIV MISSOURI HOSP & CLIN,DEPT INTERNAL MED,COLUMBIA,MO. UNIV MISSOURI HOSP & CLIN,DEPT RADIOL,COLUMBIA,MO. UNIV MISSOURI HOSP & CLIN,DEPT NUCL MED,COLUMBIA,MO. UNIV MISSOURI HOSP & CLIN,DEPT PEDIAT,COLUMBIA,MO. RP BRIDGES, AJ (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT INTERNAL MED,MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53792, USA. NR 70 TC 29 Z9 30 U1 1 U2 1 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 DEC PY 1994 VL 24 IS 3 BP 155 EP 164 DI 10.1016/0049-0172(94)90071-X PG 10 WC Rheumatology SC Rheumatology GA PX513 UT WOS:A1994PX51300001 PM 7899873 ER PT J AU ROSS, RJ BALL, WA DINGES, DF KRIBBS, NB MORRISON, AR SILVER, SM MULVANEY, FD AF ROSS, RJ BALL, WA DINGES, DF KRIBBS, NB MORRISON, AR SILVER, SM MULVANEY, FD TI MOTOR DYSFUNCTION DURING SLEEP IN POSTTRAUMATIC-STRESS-DISORDER SO SLEEP LA English DT Article DE POSTTRAUMATIC STRESS DISORDER; REM BEHAVIOR DISORDER; MUSCLE TWITCH BURSTS; PERIODIC LIMB MOVEMENTS; NIGHTMARES ID PERIODIC LEG MOVEMENTS; CORTISOL EXCRETION; REM-SLEEP; STARTLE; WAKEFULNESS; VETERANS; COMBAT AB A subjective disturbance of sleep, including the occurrence of repetitive, stereotypical anxiety dreams, is characteristic of posttraumatic stress disorder (PTSD). The phenomenology of the PTSD anxiety dream has seemed most consistent with an underlying rapid eye movement (REM.) sleep dysfunction. However, motor behavior reportedly can accompany PTSD dreams, and normal REM sleep typically involves a nearly total paralysis of the body musculature. As a means of understanding this discrepancy, anterior tibialis muscle activity during sleep was studied in a group of Vietnam combat veterans with current PTSD and in an age-matched normal control group. The PTSD subjects had a higher percentage of REM sleep epochs with at least one prolonged twitch burst; they also were more likely to have periodic limb movements in sleep, during nonrapid eye movement sleep. Both these forms of muscle activation also have been observed in REM behavior disorder (RED), a parasomnia characterized by the actual enactment of dream sequences during REM sleep. The identification of RED-like signs in PTSD adds to the evidence for a fundamental disturbance of REM sleep phasic mechanisms in PTSD. C1 PHILADELPHIA VET AFFAIRS MED CTR,RES SERV,PHILADELPHIA,PA. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH VET MED,DEPT ANIM BIOL,PHILADELPHIA,PA 19104. COATESVILLE VET AFFAIRS MED CTR,COATESVILLE,PA. FU NIMH NIH HHS [F32-MH-09584-01, MH-42903] NR 46 TC 79 Z9 79 U1 0 U2 3 PU AMER SLEEP DISORDERS ASSOC PI ROCHESTER PA 1610 14TH STREET NW SUITE 300, ROCHESTER, MN 55806 SN 0161-8105 J9 SLEEP JI Sleep PD DEC PY 1994 VL 17 IS 8 BP 723 EP 732 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QB731 UT WOS:A1994QB73100009 PM 7701184 ER PT J AU ABBOTT, RD BEHRENS, GR SHARP, DS RODRIGUEZ, BL BURCHFIELD, CM ROSS, W YANO, K CURB, JD AF ABBOTT, RD BEHRENS, GR SHARP, DS RODRIGUEZ, BL BURCHFIELD, CM ROSS, W YANO, K CURB, JD TI BODY MASS INDEX AND THROMBOEMBOLIC STROKE IN NONSMOKING MEN IN OLDER MIDDLE-AGE - THE HONOLULU-HEART-PROGRAM SO STROKE LA English DT Article DE BODY MASS INDEX; CEREBROVASCULAR DISORDERS RISK FACTORS; THROMBOEMBOLISM ID RISK-FACTORS; PHYSICAL-ACTIVITY; JAPANESE MEN; FOLLOW-UP; CARDIOVASCULAR-DISEASE; CIGARETTE-SMOKING; BLOOD-PRESSURE; MORTALITY; OBESITY; TRENDS AB Background and Purpose While evidence suggests that obesity has an independent relation to coronary artery disease, similar findings for stroke have not been established. The purpose of this study was to examine the relation between body mass index and the risk of thromboembolic stroke independently of other risk factors. Methods Since 1965, the Honolulu Heart Program has followed a cohort of men in a prospective study of cardiovascular disease. This article examines the relationship between the baseline measurement of body mass index and the risk of thromboembolic stroke in 1163 nonsmoking men in older middle age (55 to 68 years). Men who had an elevated risk of stroke due to hypertension, diabetes, and other risk factors were excluded from the analysis. Results After 22 years of follow-up, the rate of stroke increased significantly with increasing levels of body mass (P<.01). In the bottom tertile of the body mass index, the rate of thromboembolic stroke was 28.7 per 1000 (11/383). In the middle tertile, the rate was increased by 40% to 40.7 per 1000 (16/393), and in the top tertile, the rate of thromboembolic stroke was 55.4 per 1000 (21/387), a twofold excess compared with the bottom tertile. After adjustment for age and the residual effects of confounding risk factors, including systolic blood pressure and serum glucose, the estimated relative risk of stroke for the average body mass index in the top tertile (26.6 kg/m(2) compared with that in the bottom tertile (20.3 kg/m(2)) was 2.1 (95% confidence interval, 1.1 to 4.1). These findings were not affected by coronary events that occurred in the course of follow-up, nor did they appear to be influenced by deaths from other causes. Conclusions We conclude that elevated body mass is associated with an increased risk of thromboembolic stroke in nonsmoking men in older middle age who are free of commonly observed conditions related to cardiovascular disease. C1 HONOLULU HEART PROGRAM,HONOLULU,HI. NATL HEART LUNG & BLOOD INST,EPIDEMIOL & BIOMETRY PROGRAM,HONOLULU EPIDEMIOL RES SECT,HONOLULU,HI. UNIV HAWAII,JOHN A BURNS SCH MED,DEPT MED,HONOLULU,HI 96822. US DEPT VET AFFAIRS,KUAKINI MED CTR,HONOLULU ASIA AGING STUDY,HONOLULU,HI. RP ABBOTT, RD (reprint author), UNIV VIRGINIA,SCH MED,DEPT MED,DIV BIOSTAT,BOX 432,CHARLOTTESVILLE,VA 22908, USA. FU NCRR NIH HHS [RR-00847]; NHLBI NIH HHS [N01-HC-05102] NR 45 TC 64 Z9 67 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 DEC PY 1994 VL 25 IS 12 BP 2370 EP 2376 PG 7 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA PV675 UT WOS:A1994PV67500007 PM 7974575 ER PT J AU HERSHMAN, JM AF HERSHMAN, JM TI HIGHLIGHTS OF THIS ISSUE SO THYROID LA English DT Editorial Material RP HERSHMAN, JM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BLDG 114,ROOM 200,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD WIN PY 1994 VL 4 IS 4 BP 397 EP 397 DI 10.1089/thy.1994.4.397 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QB897 UT WOS:A1994QB89700001 ER PT J AU BRUNICARDI, FC KLEINMAN, RM OHNING, G LLOYD, K GINGERICH, R WONG, H WALSH, J AF BRUNICARDI, FC KLEINMAN, RM OHNING, G LLOYD, K GINGERICH, R WONG, H WALSH, J TI THE INHIBITORY ROLE OF INTRAISLET SOMATOSTATIN ON GLUCAGON-SECRETION IN THE ISOLATED-PERFUSED HUMAN PANCREAS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 2nd International Congress of the Cell-Transplant-Society CY MAY 01-04, 1994 CL MINNEAPOLIS, MN SP Cell Transplant Soc ID MONOCLONAL-ANTIBODY; PARACRINE; INSULIN; INVITRO; INVIVO; CELL C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT SURG,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,CURE,LOS ANGELES,CA. WASHINGTON UNIV,SCH MED,DEPT PEDIAT,ST LOUIS,MO. RP BRUNICARDI, FC (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,CTR HLTH SCI,ROOM 72-244,10833 LE CONTE AVE,LOS ANGELES,CA 90024, USA. NR 14 TC 4 Z9 4 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD DEC PY 1994 VL 26 IS 6 BP 3451 EP 3452 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA PW987 UT WOS:A1994PW98700171 PM 7998217 ER PT J AU HEYDARI, AR TAKAHASHI, R GUTSMANN, A YOU, S RICHARDSON, A AF HEYDARI, AR TAKAHASHI, R GUTSMANN, A YOU, S RICHARDSON, A TI HSP70 AND AGING SO EXPERIENTIA LA English DT Review DE AGING; LIVER; TRANSCRIPTION; HEAT SHOCK TRANSCRIPTION FACTOR; RAT; SENESCENCE ID HEAT-SHOCK PROTEINS; AGE-DEPENDENT RESPONSE; GENE-EXPRESSION; TRANSCRIPTIONAL ACTIVATION; DIPLOID FIBROBLASTS; STRESS; CELLS; THERMOSENSITIVITY; OLIGOMERIZATION; STIMULATION AB An alteration in the ability of cells to express heat shock proteins could be physiologically important in aging because all living organisms show a reduced ability to respond to stress with increasing age. Using hepatocytes freshly isolated from young adult and old rats, we have shown that the induction of hsp70 expression by heat shock is reduced approximately 50% with age. The decrease in hsp70 expression occurs at the level of transcription and appears to arise from a defect in the heat shock transcription factor. Other investigators have also shown that the induction of hsp70 expression by heat shock as well as other stresses declines significantly with age in a variety of tissues from rats as well as mononuclear cells from human subjects, In addition, a decrease in the inducibility of hsp70 is observed with cell senescence in cultured cells. Therefore, it appears that a reduced ability to express hsp70 in response to stress may be a common phenomenon underlying the aging process. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG01548] NR 43 TC 86 Z9 90 U1 1 U2 5 PU BIRKHAUSER VERLAG AG PI BASEL PA PO BOX 133 KLOSTERBERG 23, CH-4010 BASEL, SWITZERLAND SN 0014-4754 J9 EXPERIENTIA JI Experientia PD NOV 30 PY 1994 VL 50 IS 11-12 BP 1092 EP 1098 DI 10.1007/BF01923466 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA PV784 UT WOS:A1994PV78400016 PM 7988669 ER PT J AU SHEA, JA BERLIN, JA ESCARCE, JJ CLARKE, JR KINOSIAN, BP CABANA, MD TSAI, WW HORANGIC, N MALET, PF SCHWARTZ, JS WILLIAMS, SV AF SHEA, JA BERLIN, JA ESCARCE, JJ CLARKE, JR KINOSIAN, BP CABANA, MD TSAI, WW HORANGIC, N MALET, PF SCHWARTZ, JS WILLIAMS, SV TI REVISED ESTIMATES OF DIAGNOSTIC-TEST SENSITIVITY AND SPECIFICITY IN SUSPECTED BILIARY-TRACT DISEASE SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID ACUTE CHOLECYSTITIS; NATURAL-HISTORY; HEPATOBILIARY SCINTIGRAPHY; GALLBLADDER-DISEASE; CHOLESCINTIGRAPHY; ULTRASONOGRAPHY; GALLSTONE; CHOLECYSTOGRAPHY; CHOLELITHIASIS; TC-99M-PIPIDA AB Background: The purpose of this study was to estimate the sensitivity and specificity of diagnostic tests for gallstones and acute cholecystitis. Methods: All English-language articles published from 1966 through 1992 about tests used in the diagnosis of biliary tract disease were identified through MEDLINE. From 1614 titles, 666 abstracts were examined and 322 articles were read to identify 61 articles with information about sensitivity and specificity. Application of exclusion criteria based on clinical and methodologic criteria left 30 articles for analysis. Cluster-sampling methods were adapted to obtain combined estimates of sensitivities and specificities. Adjustments were made to estimates that were biased because the gold standard was applied preferentially to patients with positive test results. Results: Ultrasound has the best unadjusted sensitivity (0.97; 95% confidence interval, 0.95 to 0.99) and specificity (0.95; 95% confidence interval, 0.88 to 1.00) for evaluating patients with suspected gallstones. Adjusted values are 0.84 (0.76 to 0.92) and 0.99 (0.97 to 1.00), respectively. Adjusted and unadjusted results for oral cholecystogram were lower. Radionuclide scanning has the best sensitivity (0.97; 95% confidence interval, 0.96 to 0.98) and specificity (0.90; 95% confidence interval, 0.86 to 0.95) for evaluating patients with suspected acute cholecystitis; test performance is unaffected by delayed imaging. Unadjusted sensitivity and specificity of ultrasound in evaluating patients with suspected acute cholecystitis are 0.94 (0.92 to 0.96) and 0.78 (0.61 to 0.96); adjusted values are 0.88 (0.74 to 1.00) and 0.80 (0.62 to 0.98). Conclusions: Ultrasound is superior to oral cholecystogram for diagnosing cholelithiasis, and radionuclide scanning is the test of choice for acute cholecystitis. However, sensitivities and specificities are somewhat lower than commonly reported. We recommend estimates that are midway between the adjusted and unadjusted values. C1 UNIV PENN,CTR CLIN EPIDEMIOL & BIOSTAT,PHILADELPHIA,PA 19104. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. UNIV PENN,DEPT MED,DIV GASTROENTEROL,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT SURG,PHILADELPHIA,PA 19129. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. RP SHEA, JA (reprint author), UNIV PENN,DEPT MED,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104, USA. FU AHRQ HHS [HS06481] NR 58 TC 104 Z9 105 U1 0 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 NOV 28 PY 1994 VL 154 IS 22 BP 2573 EP 2581 DI 10.1001/archinte.154.22.2573 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA PU597 UT WOS:A1994PU59700006 PM 7979854 ER PT J AU TAKAHASHI, S REDDY, SV CHIRGWIN, JM DEVLIN, R HAIPEK, C ANDERSON, J ROODMAN, GD AF TAKAHASHI, S REDDY, SV CHIRGWIN, JM DEVLIN, R HAIPEK, C ANDERSON, J ROODMAN, GD TI CLONING AND IDENTIFICATION OF ANNEXIN-II AS AN AUTOCRINE/PARACRINE FACTOR THAT INCREASES OSTEOCLAST FORMATION AND BONE-RESORPTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN MARROW CULTURES; MULTINUCLEATED CELLS; OSTEOTROPIC HORMONES; GROWTH-FACTOR; EXPRESSION; DEXAMETHASONE; STIMULATION; PRECURSORS; PHENOTYPE; ACID AB Autocrine products of osteoclasts such as interleukin-6 may play an important role in normal osteoclast formation and activity, To identify novel stimulatory factors for osteoclasts, we have prepared a mammalian cDNA expression library generated from highly purified human osteoclast-like multinucleated cells (MNC) formed in long term bone marrow cultures and screened this library for autocrine factors that enhance MNC formation. A candidate clone which stimulated MNC formation was isolated. Sequence analysis showed that this cDNA encoded annexin II (AXII). Purified recombinant AXII significantly increased MNC formation in human bone marrow cultures in the absence of 1,25-(OH)(2) vitamin D-3 and enhanced MNC formation in mouse bone marrow cultures treated with 10(-9) M 1,25-(OH)(2) vitamin D-3. The enhanced MNC formation in murine marrow cultures resulted in increased bone resorption. Treatment of fetal rat long bones with AXII and 1,25 (OH)(2) vitamin D-3 significantly increased bone resorption compared to 1,25-(OH)(2) vitamin D-3 alone. Reverse transcriptase polymerase chain reaction analysis demonstrated that AXII mRNA was expressed at high levels in RNA isolated from highly purified giant cells from osteoclastomas, human osteoclast-like MNC, and pagetic bone. Western blot analysis of conditioned media collected from human marrow cultures showed that AXII was present in the media. Furthermore, approximately 50% of total AXII produced by cells transfected with AXII cDNA was present in the conditioned media. These data suggest that the AXII is an autocrine factor that enhances osteoclast formation and bone resorption and demonstrate a previous unknown function for AXII. C1 VET ADM MED CTR,DEPT MED HEMATOL & ENDOCRINOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM 35188]; NIAMS NIH HHS [AR 41336, AR 39539] NR 24 TC 71 Z9 74 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 18 PY 1994 VL 269 IS 46 BP 28696 EP 28701 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PU168 UT WOS:A1994PU16800030 PM 7961821 ER PT J AU ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH AF ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH TI FUNCTIONAL-CHARACTERIZATION OF THE HEMIN RESPONSIVE ELEMENT OF THE MESSENGER TRAP GENE SO BLOOD LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A39 EP A39 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75400145 ER PT J AU ALSINA, M BOYCE, B MUNDY, GR ROODMAN, GD AF ALSINA, M BOYCE, B MUNDY, GR ROODMAN, GD TI AN IN-VIVO MODEL OF HUMAN MULTIPLE-MYELOMA (MM) BONE-DISEASE (BD) SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. VET ADM MED CTR, SAN ANTONIO, TX USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A170 EP A170 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75400664 ER PT J AU BACHIER, C CRAIG, F ROODMAN, GD AF BACHIER, C CRAIG, F ROODMAN, GD TI CD34+ STEM-CELL SELECTION AND IMMUNOMAGNETIC PURGING (IMP) TO REMOVE CHRONIC LYMPHOCYTIC-LEUKEMIA (CLL) CELLS FROM BONE-MARROW (BM) SO BLOOD LA English DT Meeting Abstract C1 VET ADM MED CTR, SAN ANTONIO, TX USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A726 EP A726 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75402884 ER PT J AU BACHIER, C FREYTES, CO SALZMAN, D CASTRO, J BOLDT, D ROODMAN, GD HARRIS, K CRAIG, F WIESNER, A LEMAISTRE, CF AF BACHIER, C FREYTES, CO SALZMAN, D CASTRO, J BOLDT, D ROODMAN, GD HARRIS, K CRAIG, F WIESNER, A LEMAISTRE, CF TI BONE-MARROW TRANSPLANTATION (BMT) FOR ADULT POOR-RISK HIGH-GRADE NON-HODGKINS-LYMPHOMA (HGNHL) SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY VET ADM HOSP,SAN ANTONIO,TX 78284. S TEXAS CANC INST,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A703 EP A703 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75402794 ER PT J AU BALL, TC HIRAYAMA, F OGAWA, M AF BALL, TC HIRAYAMA, F OGAWA, M TI LYMPHOHEMATOPOIETIC PROGENITORS OF NORMAL MICE SO BLOOD LA English DT Meeting Abstract C1 RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A434 EP A434 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75401716 ER PT J AU BROUNS, MC DELOUGHERY, TG NICHOLS, MJ AF BROUNS, MC DELOUGHERY, TG NICHOLS, MJ TI FATAL THROMBOSIS COMPLICATING ALL-TRANS-RETINOIC ACID (ATRA) THERAPY FOR ACUTE PROMYELOCYTIC LEUKEMIA (APL) SO BLOOD LA English DT Meeting Abstract C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A616 EP A616 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75402446 ER PT J AU CASTRO, J BACHIER, C BOLDT, DH FREYTES, C HARRIS, K ROODMAN, D SALZMAN, D TAMI, J MENEGHETTI, C SHERIDANLEOS, N LEMAISTRE, CF AF CASTRO, J BACHIER, C BOLDT, DH FREYTES, C HARRIS, K ROODMAN, D SALZMAN, D TAMI, J MENEGHETTI, C SHERIDANLEOS, N LEMAISTRE, CF TI CRYOPRESERVED MATCHED RELATED DONOR MARROW ENGRAFTS PROMPTLY FOLLOWING ALLOGENEIC BONE-MARROW TRANSPLANTATION SO BLOOD LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,S TEXAS CANC INST,SAN ANTONIO,TX 78284. NR 1 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A93 EP A93 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75400360 ER PT J AU FREYTES, CO BACHIER, C SALZMAN, D VUKELIA, S CASTRO, J BOLDT, D ROODMAN, GD CRAIG, F HARRIS, K TSAI, T SHERIDANLEOS, N HILSENBECK, S TAMI, J BURRELL, L LEMAISTRE, CF AF FREYTES, CO BACHIER, C SALZMAN, D VUKELIA, S CASTRO, J BOLDT, D ROODMAN, GD CRAIG, F HARRIS, K TSAI, T SHERIDANLEOS, N HILSENBECK, S TAMI, J BURRELL, L LEMAISTRE, CF TI HIGH-DOSE CHEMOTHERAPY WITH AUTOLOGOUS STEM-CELL RESCUE IN RESISTANT OR RECURRENT LOW-GRADE LYMPHOMA SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY VET ADM HOSP,S TEXAS CANC INST,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A709 EP A709 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75402816 ER PT J AU GRELLIER, PC ABBOUD, SL AF GRELLIER, PC ABBOUD, SL TI EXPRESSION AND REGULATION OF INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEINS (IGFBPS) IN MURINE PROGENITORS SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A125 EP A125 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75400484 ER PT J AU KAWASHIMA, I LAVER, JH LEARY, AG OGAWA, M AF KAWASHIMA, I LAVER, JH LEARY, AG OGAWA, M TI LOW C-KIT EXPRESSION BY PRIMITIVE HEMATOPOIETIC PROGENITORS IN UMBILICAL-CORD BLOOD SO BLOOD LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON DVA MED CTR,CHARLESTON,SC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A271 EP A271 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75401069 ER PT J AU LIU, K SANROMAN, J KAMALI, V NAUGHTON, BA KELLER, J RUSCETTI, FW ROODMAN, D BONEWALD, L MEAGHER, RM PURCHIO, AF TWARDZIK, DR AF LIU, K SANROMAN, J KAMALI, V NAUGHTON, BA KELLER, J RUSCETTI, FW ROODMAN, D BONEWALD, L MEAGHER, RM PURCHIO, AF TWARDZIK, DR TI PURIFICATION OF STEM-CELL PROLIFERATION FACTOR (SCPF), A CYTOKINE THAT STIMULATES THE EXPANSION OF HUMAN CD34+ CELLS IN-VITRO SO BLOOD LA English DT Meeting Abstract C1 ADV TISSUE SCI INC,LA JOLLA,CA. NCI,LEUKOCYTE BIOL LAB,FREDERICK,MD 21701. UNIV CINCINNATI,MED CTR,HOXWORTH BLOOD CTR,CINCINNATI,OH 45267. VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A275 EP A275 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75401082 ER PT J AU ROGERS, WO FRIEDBERG, RC TILDEN, AB VAUGHAN, WP AF ROGERS, WO FRIEDBERG, RC TILDEN, AB VAUGHAN, WP TI TRANSFUSION-RELATED ACUTE LUNG INJURY (TRALI) DURING ALLOGENEIC HLA-IDENTICAL BONE-MARROW INFUSION SO BLOOD LA English DT Meeting Abstract C1 UNIV ALABAMA,DEPT PATHOL,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT INTERNAL MED,BIRMINGHAM,AL 35294. BIRMINGHAM VA MED CTR,DEPT PATHOL,BIRMINGHAM,AL. BIRMINGHAM VA MED CTR,MED SERV LAB,BIRMINGHAM,AL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A491 EP A491 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75401946 ER PT J AU SRIKANTH, S RADO, TA AF SRIKANTH, S RADO, TA TI ANALYSIS OF PU.1 INTERACTIONS IN DIFFERENTIATING MYELOID CELLS SO BLOOD LA English DT Meeting Abstract C1 UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. BIRMINGHAM VAMC,BIRMINGHAM,AL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A133 EP A133 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75400516 ER PT J AU SRIKANTH, S RADO, TA AF SRIKANTH, S RADO, TA TI PU.1 IS NECESSARY FOR TISSUE-SPECIFIC GENE-EXPRESSION FROM THE HNE PROMOTER SO BLOOD LA English DT Meeting Abstract C1 UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. BIRMINGHAM VAMC,BIRMINGHAM,AL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1994 VL 84 IS 10 SU 1 BP A133 EP A133 PG 1 WC Hematology SC Hematology GA PR754 UT WOS:A1994PR75400515 ER PT J AU PUGH, TD CHANG, CS UEMURA, H WEINDRUCH, R AF PUGH, TD CHANG, CS UEMURA, H WEINDRUCH, R TI PROSTATIC LOCALIZATION OF SPONTANEOUS EARLY INVASIVE-CARCINOMA IN LOBUND-WISTAR RATS SO CANCER RESEARCH LA English DT Note ID ANDROGEN RECEPTOR; CANCER; ANTIBODIES; NEOPLASIA; TUMORS AB Animal models of human prostate cancer are very limited in number but are of obvious importance to develop. Dr. Morris Pollard (M. Pollard, J. Natl. Cancer Inst., 51: 1235-1241, 1973) has reported that Lobund-Wistar rats develop spontaneous metastatic prostatic cancer when they become old(similar to 25% incidence after 25 months). A chemically-indnced form of the disease has also been described in Lobund-Wistar rats. However, recent reports suggest that most of the chemically induced adenocarcinomas are not prostatic in origin, with most arising in the seminal vesicle, and thereby raise questions about the origin of the spontaneous cancers. We herein report cancer spontaneously arising in the lateral lobes of the prostates in Lobund-Wistar rats. One of 8 rats killed at 16 months of age showed prostatic carcinoma in situ. Two of 39 rats killed at 20 months displayed early invasive adenocarcinomas with no signs of metastases. Because sectioning of the prostates in this study was limited to face sections from a single block for each rat, it is highly probable that the true incidence of dysplasias and carcinomas is underestimated by these data. Dysplastic or neoplastic changes were not seen in either the seminal vesicles or other portions of the prostatic complex. The nuclei of adenocarcinoma cells showed less labeling with antibody to the androgen hormone receptor than did normal cells. These data strongly support the validity of the Pollard model of spontaneous prostate cancer in Lobund-Wister rats. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT HUMAN ONCOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI 53705. FU NIA NIH HHS [R01 AG 10536] NR 21 TC 12 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 NOV 15 PY 1994 VL 54 IS 22 BP 5766 EP 5770 PG 5 WC Oncology SC Oncology GA PR217 UT WOS:A1994PR21700006 PM 7525050 ER PT J AU LI, ZG SUMIDA, M BIRCHBAUER, A SCHOTZ, MC REUE, K AF LI, ZG SUMIDA, M BIRCHBAUER, A SCHOTZ, MC REUE, K TI ISOLATION AND CHARACTERIZATION OF THE GENE FOR MOUSE HORMONE-SENSITIVE LIPASE SO GENOMICS LA English DT Article ID CHOLESTEROL ESTER HYDROLASE; ADIPOSE-TISSUE; CHROMOSOMAL LOCALIZATION; MESSENGER-RNA; RECEPTOR GENE; IDENTIFICATION; EXPRESSION; SEQUENCE; RAT; BINDING AB Hormone-sensitive lipase (HSL) is the rate-limiting enzyme in hydrolysis of triglycerides in adipose tissue and of cholesteryl esters in steroidogenic tissues and macrophages. The gene encoding mouse HSL has been isolated and characterized from two overlapping X clones, The gene spans approximately 10.4 kb and comprises 9 exons interrupted by 8 introns. The deduced amino acid sequence specifies a protein of 759 amino acids with a Mr of 83,297 in the absence of posttranslational modifications, The known functional domains of the HSL protein are encoded by discrete exons, with the putative catalytic site (Ser(423)) encoded by exon 6, and the basal and regulatory phosphorylation sites (Ser(557) and Ser(559)) encoded by exon 8, In addition, a putative lipid binding domain occurs in exon 9. The mouse protein shows 94% identity with the previously determined rat sequence and 85% identity with the recently determined human sequence. Interestingly, despite the high degree of similarity, the three species diverge significantly for a stretch of 16 amino acid residues upstream of the phosphorylation sites, In addition, an error was discovered in the carboxyl-terminal portion of the previously reported rat sequence, which produced a frame shift and premature termination of the coding sequence, The corrected rat sequence alters the identity of 12 amino acid residues and extends the protein an additional 11 residues, We have also examined the mouse HSL gene and 5' flanking region for nucleotide sequences that may modulate HSL gene transcription, Using primer extension, we identified a major transcription initiation site 593 nucleotides upstream of the protein coding sequence. Homologies with several known gene regulatory elements are present in the HSL 5' flanking region, including sequence motifs that appear to direct expression in adipose, testis, adrenal, and myeloid tissues. (C) 1994 Academic Press, Inc. C1 UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. RP LI, ZG (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,BLDG 113,ROOM 312,LOS ANGELES,CA 90073, USA. FU NHLBI NIH HHS [HL28481] NR 39 TC 41 Z9 44 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD NOV 15 PY 1994 VL 24 IS 2 BP 259 EP 265 DI 10.1006/geno.1994.1614 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA PX512 UT WOS:A1994PX51200008 PM 7698747 ER PT J AU ZITTEL, TT DEGIORGIO, R STERNINI, C RAYBOULD, HE AF ZITTEL, TT DEGIORGIO, R STERNINI, C RAYBOULD, HE TI FOS PROTEIN EXPRESSION IN THE NUCLEUS OF THE SOLITARY TRACT IN RESPONSE TO INTESTINAL NUTRIENTS IN AWAKE RATS SO BRAIN RESEARCH LA English DT Article DE NUCLEUS OF THE SOLITARY TRACT; FOS-LIKE IMMUNOREACTIVITY; IMMUNOCYTOCHEMISTRY; SMALL INTESTINE; LIPID; CARBOHYDRATE ID C-FOS; BRAIN-STEM; SPINAL-CORD; CHOLECYSTOKININ; REPRESENTATION; SUPPRESSION; STIMULATION; INDUCTION; STIMULUS; NEURONS AB Nutrients in the intestine inhibit food intake via an action on the vagal afferent pathway. The aim of the present study was to use immunochemical detection of Fos protein-like immunoreactivity (FLI) in the brainstem to trace the neuronal pathways activated by intestinal nutrients. Perfusion of the intestine of awake rats via an indwelling duodenal catheter with iso-osmotic mannitol, hydrochloric acid or casein hydrolysate had no effect on the number of FLI neurons in the nucleus of the solitary tract (NTS). Lipid emulsion (20%) and 2.7 M glucose significantly increased the number of immunopositive cells in the NTS. There was a significant increase in the number of immunopositive cells from caudal to rostral NTS. Nutrients effective at decreasing food intake (carbohydrate and fat) produced significant increases in Fos-like immunopositive cells in the NTS. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR GASTROCNTER BIOL,CURE,DEPT MED,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR GASTROCNTER BIOL,CURE,DEPT PHYSIOL,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR GASTROCNTER BIOL,CURE,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA. OI De Giorgio, Roberto/0000-0003-0867-5873 FU NIDDK NIH HHS [DK41004, DK41301] NR 26 TC 58 Z9 58 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 NOV 14 PY 1994 VL 663 IS 2 BP 266 EP 270 DI 10.1016/0006-8993(94)91272-6 PG 5 WC Neurosciences SC Neurosciences & Neurology GA PQ749 UT WOS:A1994PQ74900011 PM 7874510 ER PT J AU BOYAN, BD SCHWARTZ, Z PARKSNYDER, S DEAN, DD YANG, FM TWARDZIK, D BONEWALD, LF AF BOYAN, BD SCHWARTZ, Z PARKSNYDER, S DEAN, DD YANG, FM TWARDZIK, D BONEWALD, LF TI LATENT TRANSFORMING GROWTH-FACTOR-BETA IS PRODUCED BY CHONDROCYTES AND ACTIVATED BY EXTRACELLULAR-MATRIX VESICLES UPON EXPOSURE TO 1,25-(OH)(2)D-3 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID VITAMIN-D METABOLITES; ARACHIDONIC-ACID TURNOVER; MOLECULAR-WEIGHT COMPLEX; CARTILAGE CELLS-INVITRO; RESTING ZONE; ALKALINE-PHOSPHATASE; PLATE CHONDROCYTES; FACTOR-BETA-1 GENE; MESSENGER-RNA; BONE CULTURES AB Resting zone and growth zone (GC) costochondral chondrocytes constitutively release latent, but not active, transforming growth factor-beta (TGF-beta) into the culture medium. When exogenous TGF-beta is added to the culture medium, no autocrine effect is observed. However, when 1,25-(OH)(2)D-3 is added, a dose-dependent inhibition of latent TGF-beta release is found. Messenger RNA levels for TGF-beta 1 are unchanged by treatment with either 1,25-(OH)(2)D-3 or TGF-beta 1. Since active growth factor was not observed in the conditioned medium, we tested the hypothesis that latent TGF-beta could be activated in the matrix. GC matrix vesicles, extracellular organelles associated with matrix calcification, were able to activate latent TGF-beta 1 and TGF-beta 2 when preincubated with 1,25-(OH)(2)D-3. In contrast, GC plasma membranes activated latent TGF-beta, and addition of 1,25-(OH)(2)D-3 inhibited this activation. The 1,25-(OH)(2)D-3-dependent decrease in latent TGF-beta in the medium, with no detectable change in mRNA level, and the inhibition of plasma membrane activation of latent TGF-beta by 1,25-(OH)(2)D-3 suggest that 1,25-(OH)(2)D-3 may act through post-transcriptional and/or nongenomic mechanisms. The results also suggest that latent TGF-beta is activated in the matrix and that 1,25-(OH)(2)D-3 regulates this activation by a direct, non-genomic action on the matrix vesicle membrane. C1 UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PERIODONT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED ENDOCRINOL & METAB,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT STRUCT & CELLULAR BIOL,SAN ANTONIO,TX 78284. HEBREW UNIV JERUSALEM,HADASSAH FAC DENT MED,DEPT PERIODONT,JERUSALEM,ISRAEL. ADV TISSUE SCI,LA JOLLA,CA 92037. UNIV WASHINGTON,SCH MED,DEPT DERMATOL,SEATTLE,WA 98195. AUDIE MURPHY VET AFFAIRS MED CTR,SAN ANTONIO,TX 78284. RP BOYAN, BD (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT ORTHOPAED,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [DE05937, DE08569, DE08603] NR 69 TC 81 Z9 82 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 11 PY 1994 VL 269 IS 45 BP 28374 EP 28381 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PV772 UT WOS:A1994PV77200089 PM 7961777 ER PT J AU WEG, JG BALK, RA THARRATT, RS JENKINSON, SG SHAH, JB ZACCARDELLI, D HORTON, J PATTISHALL, EN AF WEG, JG BALK, RA THARRATT, RS JENKINSON, SG SHAH, JB ZACCARDELLI, D HORTON, J PATTISHALL, EN TI SAFETY AND POTENTIAL EFFICACY OF AN AEROSOLIZED SURFACTANT IN HUMAN SEPSIS-INDUCED ADULT-RESPIRATORY-DISTRESS-SYNDROME SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Note ID SYNTHETIC SURFACTANT; PULMONARY SURFACTANT; EXOGENOUS SURFACTANT; LUNG INJURY; MORTALITY; FAILURE; DELIVERY; SYSTEM AB Objective.-To evaluate the safety and potential efficacy of aerosolized surfactant in intubated patients with adult respiratory distress syndrome (ARDS). Design.-A prospective, double-blind, placebo-controlled, randomized, parallel, mutlicenter pilot clinical trial. Patients.-A total of 51 patients with sepsis-induced ARDS were entered into the study within 18 hours of developing sepsis or sepsis syndrome. Intervention.-Patients were randomized into four treatment groups in a 2:1:2:1 ratio, as follows: 12 hours of surfactant per day, 12 hours of 0.6% saline per day, 24 hours of surfactant per day, and 24 hours of 0.6% saline per day. Surfactant or saline was aerosolized continuously for up to 5 days using an in-line nebulizer that aerosolized only during inspiration. Main Outcome Measures.-Ventilatory data, arterial blood gases, and hemodynamic parameters were measured at baseline, every 4 or 8 hours during the 5 days of treatment, 24 hours after treatment, and 30 days after treatment, at which time mortality was also assessed. Safety was evaluated throughout the 30 days of the study. Results.-Surfactant was administered safely in ventilated patients when given continuously throughout the 5 days using the nebulizer system. Although there were no differences in any physiological parameter between the treatment groups, there was a dose-dependent trend in reduction of mortality from 47% in the combined placebo group to 41% and 35% in the groups treated with 12 hours and 24 hours of surfactant per day, respectively. Conclusions-Aerosolized surfactant was well tolerated when administered on a continuous basis for up to 5 days; however, at the doses given, it did not result in significant improvements in patients with sepsis-induced ARDS. C1 RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT PULM & CRIT CARE MED,CHICAGO,IL 60612. UNIV CALIF DAVIS,CTR MED,DIV PULM & CRIT CARE MED,SACRAMENTO,CA. AUDIE L MURPHY VET AFFAIRS HOSP,PULM DIS SECT,SAN ANTONIO,TX. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT ANESTHESIOL,RICHMOND,VA 23298. BURROUGHS WELLCOME CO,DIV CLIMATE RES,RES TRIANGLE PK,NC 27709. RP WEG, JG (reprint author), UNIV MICHIGAN,CTR MED,DEPT INTERNAL MED,DIV PULM & CRIT CARE MED,ROOM B1H245-0026,ANN ARBOR,MI 48109, USA. NR 37 TC 102 Z9 104 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD NOV 9 PY 1994 VL 272 IS 18 BP 1433 EP 1438 DI 10.1001/jama.272.18.1433 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA PP690 UT WOS:A1994PP69000031 PM 7933425 ER PT J AU CORNFORD, EM HYMAN, S LANDAW, EM AF CORNFORD, EM HYMAN, S LANDAW, EM TI DEVELOPMENTAL MODULATION OF BLOOD-BRAIN-BARRIER GLUCOSE-TRANSPORT IN THE RABBIT SO BRAIN RESEARCH LA English DT Article DE BLOOD-BRAIN BARRIER GLUCOSE TRANSPORTER; KINETIC CONSTANT; GLUT1 ISOFORM; QUANTITATIVE IMMUNOGOLD ELECTRON MICROSCOPY; LUMINAL AND ABLUMINAL MEMBRANE; NEONATE; SUCKLING; WEANLING AND ADULT; DEVELOPMENTAL UP-REGULATION; CEREBRAL BLOOD FLOW; PERMEABILITY SURFACE AREA PRODUCT ID RAT CEREBRAL-CORTEX; FLOW; METABOLISM; KINETICS; ACID; PHOSPHORYLATION; 2-DEOXYGLUCOSE; TRANSLOCATION; CAPILLARIES; EXPRESSION AB Blood-brain barrier (BBB) glucose transport rates were measured using the intracarotid injection method in newborn, 14-day-old suckling, 28-day-old weanling and adult rabbits, and compared with membrane transporter density. Light microscope immunochemistry confirmed the presence of the GLUT1 glucose transporter isoform in these rabbits. Quantitative electron microscopic immunogold analyses of GLUT1-immunoreactive sites per micrometer of capillary membrane indicated GLUT1 density increased with age, and correlated with in vivo measurements of V-max. Maximal transport velocities (V-max) of glucose transfer (an indicator of the activity and relative number of transporter proteins) increased significantly (P = 0.05) with age: in neonates V-max = 0.61 mu mol.min(-1).g(-1), in sucklings V-max = 0.68 mu mol.min(-1).g(-1), in weanlings V-max = 0.88 mu mol.min(-1).g(-1), and in adults Vmax = 1.01 mu mol.min(-1) g(-1). Cerebral blood flow (CBF) rates, increased with age from 0.19 and 0.26 ml.min(-1).g(-1) in neonates and sucklings to 0.51 (weanlings) and 0.70 (adults) ml.min(-1).g(-1). Non-linear regression analyses indicated the half-saturation constant (K-m) for glucose transport ranged from 13 mM in adult rabbits to 19 mM in 14-day-old sucklings: differences in K-m were not significant. Age-related changes in the Permeability-Surface Area product (PS +/-S.E.) of both water and glucose were also seen. At all ages studied, the diffusion component (K-d) of glucose uptake was not distinguishable from zero. We conclude developmental up-regulation of the rabbit BBB glucose transporter is characterized by no changes in transporter affinity, and provide the first demonstration of increased membrane transporter proteins correlating with an age-related increase (65%) in glucose transporter maximal velocity. C1 VET ADM MED CTR, W LOS ANGELES VET AFFAIRS MED CTR, SW REG VA EPILEPSY CTR, NEUROL SERV, 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 BRAIN RES INST, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT BIOMATH, LOS ANGELES, CA 90024 USA. RP CORNFORD, EM (reprint author), VET ADM MED CTR, W LOS ANGELES VET AFFAIRS MED CTR, SW REG VA EPILEPSY CTR, RES SERV, LOS ANGELES, CA 90073 USA. FU NCI NIH HHS [CA-16042]; NINDS NIH HHS [NS 25554] NR 60 TC 20 Z9 20 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 EI 1872-6240 J9 BRAIN RES JI Brain Res. PD NOV 7 PY 1994 VL 663 IS 1 BP 7 EP 18 DI 10.1016/0006-8993(94)90457-X PG 12 WC Neurosciences SC Neurosciences & Neurology GA PP616 UT WOS:A1994PP61600002 PM 7850472 ER PT J AU SLOAN, IS HOROWITZ, PM CHIRGWIN, JM AF SLOAN, IS HOROWITZ, PM CHIRGWIN, JM TI RAPID SECRETION BY A NONCLASSICAL PATHWAY OF OVEREXPRESSED MAMMALIAN MITOCHONDRIAL RHODANESE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN CATHEPSIN-D; MOLECULAR CHAPERONES; LIVER RHODANESE; PROTEINS; CELL; EXPRESSION; CDNA; THIOREDOXIN; MEMBRANES; SEQUENCE AB Rhodanese is a small (33 kDa) monomeric sulfurtransferase which is synthesized on cytoplasmic ribosomes and imported into the mitochondrial matrix without cleavage of its amino terminus. When we transfected mammalian cell lines with rhodanese cDNA under the control of an efficient viral promoter, up to 40% of the overexpressed protein was secreted into the medium. This secretion was not the result of cell lysis, did not occur via the endoplasmic reticulum, and did not require the amino-terminal mitochondrial import signal. Addition of a carboxyl-terminal peptide extension did not block secretion, nor did a number of inhibitors of cellular sorting processes. Rhodanese polypeptide is known to associate with chaperonin proteins. In the absence of available mitochondrial import sites, such a complex in the cytoplasm of transfected cells could deliver unfolded rhodanese to export pores on the inner surface of the plasma membrane. This mechanism could contribute to the nonclassical secretion of cytoplasmically synthesized interleukins, growth factors, and lectins. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV ENDOCRINOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. FU NIEHS NIH HHS [ES 05729]; NIGMS NIH HHS [GM 25177] NR 46 TC 17 Z9 17 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 4 PY 1994 VL 269 IS 44 BP 27625 EP 27630 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PV771 UT WOS:A1994PV77100072 PM 7961679 ER PT J AU GOODWIN, TM HERSHMAN, JM COLE, L AF GOODWIN, TM HERSHMAN, JM COLE, L TI INCREASED CONCENTRATION OF THE FREE BETA-SUBUNIT OF HUMAN CHORIONIC-GONADOTROPIN IN HYPEREMESIS GRAVIDARUM SO ACTA OBSTETRICIA ET GYNECOLOGICA SCANDINAVICA LA English DT Article DE FREE BETA HCG; HYPEREMESIS GRAVIDARUM ID HCG; PREGNANCY; NICKS AB Objective. The amount of free beta subunit hCG (free beta) has been reported to be increased in trophoblast disease and Down's syndrome, conditions also associated with high total hCG. increased total hCG has been reported in hyperemesis gravidarum. We sought to determine if sera from singleton gestations with hyperemesis gravidarum contained a higher proportion of free beta hCG compared to controls of comparable gestational age. Methods. Sera from 39 patients with hyperemesis gravidarum was compared with that from 23 control subjects of comparable gestational age with respect to beta hCG and its subunits (free beta and free alpha). Results. Hyperemesis patients and controls were comparable with respect to age, weight and gestational age. The concentration of hCG was greater in hyperemesis patients (9237 +/- 3613 ng/ml, mean +/- s.d.) compared to controls (5543 +/- 2290, p < 0.005) as was the concentration of free beta hCG (101 +/- 70 ng/ml vs. 31 + 31, p < 0.001). Free alpha did not differ between hyperemesis patients and controls (399 +/- 231 ng/ml vs. 377 +/- 214). A percent free beta greater than 0.6 was found in 33/39 hyperemesis patients (85%) compared to 5/23 controls (22%), p < 0.001. Conclusion. Increased free beta hCG is found in hyperemesis gravidarum. This finding strengthens the association of hyperemesis with abnormal metabolism of hCG. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA. YALE UNIV,DEPT OBSTET & GYNECOL,NEW HAVEN,CT 06520. RP GOODWIN, TM (reprint author), UNIV SO CALIF,WOMENS HOSP,DEPT OBSTET & GYNECOL,ROOM 5K-10,1240 N MISS RD,LOS ANGELES,CA 90033, USA. NR 12 TC 47 Z9 50 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-6349 J9 ACTA OBSTET GYN SCAN JI Acta Obstet. Gynecol. Scand. PD NOV PY 1994 VL 73 IS 10 BP 770 EP 772 DI 10.3109/00016349409072502 PG 3 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QA070 UT WOS:A1994QA07000006 PM 7817726 ER PT J AU HISNANICK, JJ AF HISNANICK, JJ TI CHANGES OVER TIME IN THE ADL STATUS OF ELDERLY US VETERANS SO AGE AND AGEING LA English DT Article ID ALL-CAUSE MORTALITY; COMPRESSION; MORBIDITY; DYNAMICS; POLICY; HEALTH AB The ageing of the US veteran population has greatly out-paced that of the general US population in the last decade and the demographics of this subgroup have changed relative to the US general population. To address the concerns of policy makers within the US Department of Veterans' Affairs (VA), data on elderly US male veterans and non-veterans from the Longitudinal Survey on Aging in 1984, 1986, 1988, and 1990 were used in a prospective study. Health status or well-being was assessed through changes over time in ADL status, according to the following five categories; (I) the presence of no ADL dependence and not developing a dependence between survey periods, (II) no change in ADL dependence between survey periods, (III) an increase in ADL dependence status between survey periods, (IV) a decrease in ADL dependence between survey periods, and (V) the occurrence of death between survey periods. Using a polytomous logistic regression model, these five categories were assessed in relation to a set of variables representing social, health-care utilization, and socioeconomic characteristics. The estimated coefficients from the model indicate that family income, having worked in the last 12 months, having an increase or no change in levels of physical activity in the past 12 months and the presence of Medicare coverage are inversely associated with moving, over time, into a lower state of health status or wellbeing. The prior existence of an ADL limitation, the number of doctor and hospital visits in the past 12 months, level of education, having been widowed in the past 12 months and veteran status were all proportionally associated with the likelihood of moving into a lower state of health status or well-being. These findings lead to the conclusion that being a veteran in the US does make a difference in regard to moving into various states of health status or well-being. This difference is supported by the estimated coefficient for veteran status being significant at a p value of 0.01 and through an evaluation of the estimated transition likelihood, controlling for veteran status. Veterans are less likely to die than their non-veteran counterparts, but have a greater likelihood of transition into levels of ADL dependence. Similarly, given the existence of a prior ADL limitation, over time, veterans are less likely to die, but more likely to move into a state of increased ADL limitations. RP HISNANICK, JJ (reprint author), US DEPT VET AFFAIRS,NATL CTR VET ANAL & STAT 008C12,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 34 TC 9 Z9 9 U1 1 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0002-0729 J9 AGE AGEING JI Age Ageing PD NOV PY 1994 VL 23 IS 6 BP 505 EP 511 DI 10.1093/ageing/23.6.505 PG 7 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA PT038 UT WOS:A1994PT03800013 PM 9231946 ER PT J AU ANTIMISIARIS, M SARMA, JSM SCHOENBAUM, MP SHARMA, PP VENKATARAMAN, K SINGH, BN CHRISTENSON, P AF ANTIMISIARIS, M SARMA, JSM SCHOENBAUM, MP SHARMA, PP VENKATARAMAN, K SINGH, BN CHRISTENSON, P TI EFFECTS OF AMIODARONE ON THE CIRCADIAN-RHYTHM AND POWER SPECTRAL CHANGES OF HEART-RATE AND QT INTERVAL - SIGNIFICANCE FOR THE CONTROL OF SUDDEN CARDIAC DEATH SO AMERICAN HEART JOURNAL LA English DT Article ID III ANTIARRHYTHMIC AGENTS; VENTRICULAR ARRHYTHMIAS; MYOCARDIAL-INFARCTION; THYROID-FUNCTION; LONG; TERM; ADRENOCEPTORS; MORTALITY; MUSCLE; DRUG AB Effects of chronic amiodarone therapy on the circadian rhythmicity and power spectral changes of heart rate and QT intervals from Holter recordings were evaluated in three groups of patients: group 1 baseline (n = 10); group 2, treated for 3 to 8 months (n = 11); and group 3, treated for >1 year(n = 13). Amiodarone reduced heart rate, which reached steady state at 3 to 6 months; bradycardia was evident during the entire 24 hours. The corrected QT (QT(c)) interval increased as a function of treatment duration. It was 457 +/- 39, 530 + 28 (p < 0.001), and 581 +/- 36 (p < 0.0002) msec for groups 1, 2, and 3, after 6 months, respectively. The circadian rhythmicity of QT, was abolished in group 3. Power spectral analysis showed a tendency for amiodarone to reduce both R-R and QT interval variabilities, suggesting inhibition of autonomic control on the heart by the drug. The effectiveness of amiodarone against ventricular arrhythmias may result in part from the sustained bradycardia in concert with continuous uniform prolongation of myocardial repolarization. C1 W LOS ANGELES VET AFFAIRS MED CTR,DIV CARDIOL,LOS ANGELES,CA 90073. CITY HOPE NATL MED CTR,DUARTE,CA 91010. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT BIOMATH,LOS ANGELES,CA. NR 36 TC 15 Z9 16 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD NOV PY 1994 VL 128 IS 5 BP 884 EP 891 DI 10.1016/0002-8703(94)90584-3 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PN864 UT WOS:A1994PN86400006 PM 7942479 ER PT J AU CUI, GG SEN, LY SAGER, P UPPAL, P SINGH, BN AF CUI, GG SEN, LY SAGER, P UPPAL, P SINGH, BN TI EFFECTS OF AMIODARONE, SEMATILIDE, AND SOTALOL ON QT DISPERSION SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID MYOCARDIAL-INFARCTION; ELECTROPHYSIOLOGY; PHARMACOLOGY; PROLONGATION; CHANNELS; CELLS AB To study the effects of class III agents on QT/QTc dispersion in patients with heart disease and cardiac arrhythmias, QT dispersion and QRS and RR intervals were compared in patients before and after treatment with amiodarone (n = 26), sematilide (n = 26), and sotalol (n = 26). QT, QRS, and RR intervals, and QTc values were calculated for each complex, and their mean values were calculated for each lead. QT and QTc dispersions were defined as differences between the minimal and maximal QT or QTc values in each of the 12 leads studied. Amiodarone, sematilide, and sotalol all significantly prolonged the QT interval and the QTc value. Significant reductions in QT and QTc dispersions were only found in the amiodarone group (QT dispersions: 79 +/- 13 vs 49 +/- 14 ms; p <0.001; QTc dispersions: 0.08 +/- 0.02 vs 0.05 +/- 0.01 s(1/2); p <0.001). The mean RR interval was significantly increased in patients after treatment with amiodarone (p <0.001) and sotalol (p <0.001), but not in patients receiving sematilide treatment (p >0.2). The baseline QT and QTc dispersions were significantly greater in patients with than without myocardial infarction before treatment (p <0.001). The mean baseline values for QT/QTc dispersions were not significantly different among all 3 groups. However, only amiodarone significantly reduced the QT dispersion (from 76 +/- 10 to 46 +/- 11 ms; p <0.001) and QTc dispersion (from 0.09 +/- 0.02 to 0.05 +/- 0.01 s(1/2); p <0.001) in patients with myocardial infarction. The reduction in the QT/QTc dispersion was significantly greater than that in patients without myocardial infarction (p <0.01). It is concluded that (1) antiarrhythmic agents that get by lengthening repolarization have differing effects on QT/QTc dispersion, most likely reflecting differences in their fundamental mechanisms whereby they prolong myocardial repolarization, and (2) the low reported incidence of torsades de pointes with amiodarone may in part be due to reduced dispersion of QT and QTc compared with other class III cents. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,DIV CARDIOVASC,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. NR 22 TC 81 Z9 85 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD NOV 1 PY 1994 VL 74 IS 9 BP 896 EP 900 DI 10.1016/0002-9149(94)90582-7 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PP130 UT WOS:A1994PP13000010 PM 7526675 ER PT J AU DEUTSCH, JC KOLLI, VR SANTHOSHKUMAR, CR KOLHOUSE, JF AF DEUTSCH, JC KOLLI, VR SANTHOSHKUMAR, CR KOLHOUSE, JF TI SERUM XYLOSE ANALYSIS BY GAS-CHROMATOGRAPHY MASS-SPECTROMETRY SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE XYLOSE; INTESTINAL MALABSORPTION; GAS CHROMATOGRAPHY; MASS SPECTROMETRY; SERUM ID MASS-SPECTROMETRY; ALPHA-TOCOPHEROL; MALABSORPTION; PLASMA; BLOOD; URINE AB A gas chromatography/mass spectrometric (GC/MS) isotope dilution assay for xylose was developed using tertbutyldimethylsilyl-derivatized xylose and [C-13](1) xylose, and applied to human serum samples. A calibration curve in serum using this assay showed <3% variation (<10 mg/L) for any given point. The correlation coefficient for xylose measurements made on 27 sera between a colorimetric method performed by a national commercial reference laboratory and the GC/MS method developed here was .952. However, xylose determinations of 10 of 27 samples differed by >10% (up to 150 mg/L) when colorimetric values were compared to GC/MS. Two of these samples had borderline-low xylose values by GC/MS, but were well within the normal range by colorimetric analysis. gas chromatography/mass spectrometric isotope dilution assay appears to be an accurate method to measure xylose in serum. These data also suggest that further prospective studies comparing GC/MS to colorimetric methods are indicated for subjects undergoing oral xylose testing. C1 DENVER VET AFFAIRS HOSP,DEPT MED,DIV GASTROENTEROL,DENVER,CO. DENVER VET AFFAIRS HOSP,DEPT MED,DIV HEMATOL,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,DIV HEMATOL,DENVER,CO. RP DEUTSCH, JC (reprint author), UNIV COLORADO,HLTH SCI CTR,DIV GASTROENTEROL,4200 E 9TH AVE,DENVER,CO 80262, USA. NR 19 TC 5 Z9 5 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD NOV PY 1994 VL 102 IS 5 BP 595 EP 599 PG 5 WC Pathology SC Pathology GA PQ162 UT WOS:A1994PQ16200008 PM 7942623 ER PT J AU LICHTENSTEIN, MJ GRIFFIN, MR CORNELL, JE MALCOLM, E RAY, WA AF LICHTENSTEIN, MJ GRIFFIN, MR CORNELL, JE MALCOLM, E RAY, WA TI RISK-FACTORS FOR HIP-FRACTURES OCCURRING IN THE HOSPITAL SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACCIDENTAL FALLS; AGED; HIP FRACTURES; HOSPITALS; PSYCHOTROPIC DRUGS; WOUNDS AND INJURIES ID FALLS; LONG; BENZODIAZEPINES; PREVENTION; ACCIDENTS; RESIDENTS; INJURIES AB Risk factors for in-hospital hip fractures among patients aged greater than or equal to 65 years were evaluated in a population-based case-control study conducted in the Canadian province of Saskatchewan from 1983 through 1985. There were 129 cases with confirmed in-hospital hip fractures and 234 controls, who were those controls from a previous study in this setting hospitalized on their assigned index date. Study variables were abstracted from the hospital chart. Six factors were independently associated with a significantly increased risk of in-hospital hip fracture: impaired vision (odds ratio = 1.97, 95% confidence interval (CI)1.18-3.30), assisted ambulation (odds ratio = 2.12, 95% CI 1.25-3.59), confusion (odds ratio = 2.48, 95% CI 1.37-4.48), psychotropic drug use (odds ratio = 2.02, 95% CI 1.22-3.33), lowest weight tertile (odds ratio = 2.86, 95% CI 1.38-5.92), and prior in-hospital fall (odds ratio = 2.71, 95% CI 1.52-4.82). The risk increased substantially with the number of factors present, from an odds ratio of 4.08 (95% CI 1.56-10.67) for one factor (reference group, no factors) to 82.84 (95% CI 18.6-368.7) for four or more factors (p < 0.001, test for trend). These data underscore the multifactorial etiology of in-hospital hip fracture and suggest that prevention programs need to target multiple risk factors. C1 VANDERBILT UNIV,SCH MED,DEPT PREVENT MED,DIV PHARMACOEPIDEMIOL,NASHVILLE,TN 37232. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX. LAB & DIS CONTROL SERV,REGINA,SK,CANADA. FU FDA HHS [FD-U-000073]; PHS HHS [CCR407306] NR 36 TC 51 Z9 51 U1 6 U2 9 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD NOV 1 PY 1994 VL 140 IS 9 BP 830 EP 838 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA PQ069 UT WOS:A1994PQ06900008 PM 7977293 ER PT J AU BARNWELL, SL CLARK, WM NGUYEN, TT ONEILL, OR WYNN, ML COULL, BM AF BARNWELL, SL CLARK, WM NGUYEN, TT ONEILL, OR WYNN, ML COULL, BM TI SAFETY AND EFFICACY OF DELAYED INTRAARTERIAL UROKINASE THERAPY WITH MECHANICAL CLOT DISRUPTION FOR THROMBOEMBOLIC STROKE SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE THROMBOLYSIS; THROMBOSIS, CEREBRAL; DRUGS, INTRAARTERIAL INJECTION; BRAIN, INFARCTION; INTERVENTIONAL NEURORADIOLOGY ID TISSUE PLASMINOGEN-ACTIVATOR; MIDDLE CEREBRAL-ARTERY; THROMBOLYTIC THERAPY; TERRITORY STROKE; ISCHEMIC STROKE AB PURPOSE: To evaluate safety and efficacy of delayed intraarterial urokinase therapy with mechanical disruption of clot to treat thromboembolic stroke. METHODS: Thirteen patients with cerebral thrombolic disease (10 carotid territory, 3 basilar territory) were treated with catheter-directed intraarterial urokinase therapy with mechanical disruption of the clots. All patients were excluded from a 6-hour multicenter thrombolytic trial by either time, recent surgery, age, seizure, or myocardial infarction. Time elapsed before treatment ranged from 3.5 to 48 hours (12 +/- 13 hours), with 200 000 to 900 000 U of urokinase used. RESULTS: Ten patients had successful vessel recanalization, confirmed by repeat angiography. Cases with distal branch vessel occlusions were less likely to recanalize. Asymptomatic hemorrhagic conversion occurred in 2 patients on repeat scans. Both acute neurologic and functional outcomes were assessed with significant improvement occurring in 9 (69%) of 13 patients at 48 hours (greater than four-point change on the National Institutes of Health scale) and in 100% of 3-month survivors. All patients who improved had normal initial CT scans. CONCLUSIONS: Intraarterial cerebral thrombolysis with mechanical disruption of clot seems to be a useful therapy in selected stroke cases even after 6 hours. C1 OREGON HLTH SCI UNIV,DEPT RADIOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DOTTER INTERVENT INST,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,OREGON STROKE CTR,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,NEUROL SERV,PORTLAND,OR. RP BARNWELL, SL (reprint author), OREGON HLTH SCI UNIV,DEPT NEUROSURG,L-472,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. NR 18 TC 133 Z9 136 U1 0 U2 0 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD NOV PY 1994 VL 15 IS 10 BP 1817 EP 1822 PG 6 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA PQ991 UT WOS:A1994PQ99100004 PM 7863929 ER PT J AU CHANG, A HAMMOND, TG SUN, TT ZEIDEL, ML AF CHANG, A HAMMOND, TG SUN, TT ZEIDEL, ML TI PERMEABILITY PROPERTIES OF THE MAMMALIAN BLADDER APICAL MEMBRANE SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE WATER PERMEABILITY; UREA; ENDOCYTOSIS; FLOW CYTOMETRY ID RABBIT URINARY-BLADDER; TRANSITIONAL EPITHELIAL-CELLS; EXPANSION-CONTRACTION CYCLE; PLASMA-MEMBRANE; NONELECTROLYTE PERMEABILITIES; SURFACE GLYCOSAMINOGLYCANS; WATER PERMEABILITY; LUMINAL MEMBRANE; COLLECTING DUCT; TRANSLOCATION AB The luminal surface of mammalian bladder is exposed to urine with a composition widely different from that of plasma that bathes the basolateral surface of epithelium. Therefore we predict that the bladder permeability barrier, which is likely located in the apical membrane (AM), will exhibit low permeabilities to water, urea, NH3, H+, and small nonelectrolytes. AM surface area increases as the bladder fills with urine and decreases during emptying, a process that involves cyclical endocytosis and reinsertion of membrane from a pool of AM endosomes (AME). Rigid-appearing plaques composed of three proteins, uroplakins, have been identified acid occupy 70-90% of AM surface area. To determine permeability properties of the AM permeability barrier, we purified AME and measured their permeabilities. Rabbit urinary bladders were removed, and their apical surface was exposed to carboxyfluorescein (CF) or horseradish peroxidase (HRP). Exposure to hypotonic and then isotonic basolateral solutions induced endocytosis of luminal CF or HRP into AME. Electron microscopy of bladders after this treatment revealed HRP entrapped within AME bordered by plaques. AME were purified by differential and sucrose-gradient centrifugation, and CF-containing AME were purified 17.0 +/- 3-fold (SD) with respect to homogenate. Analysis of purified AME by flow cytometry showed that > 95% of vesicles contained CF entrapped from luminal solution and were selectively labeled with anti-uroplakin antibody. AME osmotic water permeability averaged 2.3 +/- 0.66 x 10(-4) cm/s and exhibited a high activation energy, indicating that AM contains no water channels. Permeability to urea and NH3 averaged 7.8 +/- 3.7 x 10(-7) and 1.5 +/- 0.3 x 10(-3) cm/s, respectively, which are exceptionally low and similar to permeabilities of other water-tight membranes, including toad urinary bladder and gastric mucosa. AME behaved as a single population in all permeability studies, which will permit future characterization of protein and lipid structure responsible for these unique permeability properties. C1 VET AFFAIRS MED CTR, RES SERV, BOSTON, MA 02132 USA. UNIV WISCONSIN, DEPT MED, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53706 USA. NYU, MED CTR, DEPT DERMATOL, NEW YORK, NY 10003 USA. UNIV PITTSBURGH, SCH MED, DIV RENAL & ELECTROLYTE, PITTSBURGH, PA 15213 USA. UNIV PITTSBURGH, SCH MED, EPITHELIAL CELL BIOL LAB, PITTSBURGH, PA 15213 USA. VET AFFAIRS MED CTR, MED SERV, BOSTON, MA 02132 USA. FU NIDDK NIH HHS [DK-46117, R0-1-DK-47547, DK-43955] NR 42 TC 77 Z9 77 U1 2 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD NOV PY 1994 VL 267 IS 5 BP C1483 EP C1492 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA PW518 UT WOS:A1994PW51800037 PM 7977709 ER PT J AU GIORDANO, M CASTELLINO, P MCCONNELL, EL DEFRONZO, RA AF GIORDANO, M CASTELLINO, P MCCONNELL, EL DEFRONZO, RA TI EFFECT OF AMINO-ACID INFUSION ON RENAL HEMODYNAMICS IN HUMANS - A DOSE-RESPONSE STUDY SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE AMINO ACIDS; GLOMERULAR FILTRATION RATE; RENAL PLASMA FLOW; RENAL FUNCTIONAL RESERVE; GLUCAGON ID GLOMERULAR-FILTRATION RATE; GROWTH FACTOR-I; MEAT MEAL; INDUCED HYPERFILTRATION; GLUCAGON; INSULIN; PROTEIN; SOMATOMEDIN; KIDNEY; PROSTAGLANDINS AB We evaluated the dose-response relationship between the plasma amino acid (AA) concentration and renal hemodynamics in eight normal subjects. After an overnight fast, a balanced 10% AA solution was infused for 180 min at five separate infusion rates: 0.5 (group I), 1.0 (group 11), 2.0 (group III), 4.0 (group IV), and 6.0 (group V) ml.kg(-1).min(-1) on separate days. Basal plasma AA concentration was 1.87 +/- 0.1 mmol/l and increased to 2.26 +/- 0.1 (group 1), 2.66 +/- 0.2 (group II), 3.79 +/- 0.5 (group III), 5.81 +/- 0.4 (group IV), and 7.41 +/- 0.4 mmol/l (group V). Basal glomerular filtration rate (GFR) and renal plasma flow (RPF) averaged 95 +/- 4 and 476 +/- 29 ml.1.73 m(-2).min(-1), respectively, and rose to 98 +/- 5 and 506 +/- 40 (group I) [P = not significant (NS)], 102 +/- 3 and 533 +/- 30 (group II) (P < 0.05 vs. basal), 110 +/- 4 and 567 +/- 29 (group III), 115 +/- 7 and 610 +/- 55 (group IV), and 117 +/- 7 and 614 +/- 66 ml.1.73 m(-2).min(-1) (group V) (P = NS vs, group TV). Basal plasma glucagon concentration averaged 68 +/- 10 pg/ml and increased to 74 +/- 10 (group I), 83 +/- 11 (group II) (P < 0.05 vs. basal), 100 +/- 14 (group III), 121 +/- 14 (group IV), and 229 +/- 35 pg/ml (group V) (P < 0.01 vs. basal). Increases in plasma growth hormone (GH) and insulin levels were observed only during groups IV and V. Plasma insulin-like growth factor I (IGF-I) did not change significantly during AA infusion. These results indicate the following: 1) increases in plasma AA concentrations within the physiological range cause a dose-related rise in GFR and RPF (r = 0.94, P < 0.001); 2) pharmacological increases in plasma AA levels are not associated with any further rise in GFR and RPF above that observed with physiological hyperaminoacidemia; and 3) within the physiological range the increases in GFR and RPF are closely correlated with the elevation in plasma glucagon concentration (r = 0.98, P < 0.001) but not with changes in insulin, GH, or IGF-I levels. C1 UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV DIABET, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP GIORDANO, M (reprint author), UNIV NAPLES 2, IST MED INTERNA & NEFROL, DIV POLICLIN, CAPPELLA CANGIANI, VIA PANSINI, I-80131 NAPLES, ITALY. NR 33 TC 22 Z9 24 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrol. Physiol. PD NOV PY 1994 VL 267 IS 5 BP F703 EP F708 PG 6 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA PW546 UT WOS:A1994PW54600001 PM 7977774 ER PT J AU SILMAN, JB PETERS, JI LEVINE, SM JENKINSON, SG AF SILMAN, JB PETERS, JI LEVINE, SM JENKINSON, SG TI DEVELOPMENT OF INTRACRANIAL TUBERCULOMAS WHILE RECEIVING THERAPY FOR PULMONARY FIBROSIS SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Note ID CHEMOTHERAPY; MENINGITIS AB Development of tuberculomas on adequate tuberculosis therapy is an uncommon event. This case report describes a patient who developed multiple intracranial tuberculomas while receiving adequate supervised outpatient therapy for sensitive pulmonary tuberculosis who was documented to have no intracranial lesions prior to initiation of treatment. C1 AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. NR 17 TC 9 Z9 9 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD NOV PY 1994 VL 150 IS 5 BP 1439 EP 1440 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA PR664 UT WOS:A1994PR66400034 PM 7695703 ER PT J AU PELLEGRIN, KL FRUEH, BC AF PELLEGRIN, KL FRUEH, BC TI WHY PSYCHOLOGISTS DONT THINK LIKE PHILOSOPHERS SO AMERICAN PSYCHOLOGIST LA English DT Note C1 RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC. RP PELLEGRIN, KL (reprint author), MED UNIV S CAROLINA,CHARLESTON,SC 29425, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 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 NOV PY 1994 VL 49 IS 11 BP 970 EP 970 PG 1 WC Psychology, Multidisciplinary SC Psychology GA PQ622 UT WOS:A1994PQ62200010 ER PT J AU KINOSIAN, B GLICK, H GARLAND, G AF KINOSIAN, B GLICK, H GARLAND, G TI CHOLESTEROL AND CORONARY HEART-DISEASE - PREDICTING RISKS BY LEVELS AND RATIOS SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE CORONARY DISEASE; CHOLESTEROL; LIPOPROTEINS, HDL CHOLESTEROL; LIPOPROTEINS, LDL CHOLESTEROL; PRACTICE GUIDELINES ID DENSITY LIPOPROTEIN CHOLESTEROL; CARDIOVASCULAR-DISEASE; PREVALENCE; WOMEN; FAT AB Objective: Comparison of four measures of cholesterol for predicting men and women who will develop coronary heart disease within 8 to 10 years. Design: Cohort study. Patients: 1898 men who received placebo (the placebo group of the Lipid Research Clinics [LRC] Coronary Primary Prevention Trial [CPPT]), 1025 men and 1442 women who participated in the 1970-1971 Framingham Heart Study biennial examination, and 1911 men and 1767 women without coronary heart disease who were from the LRC Population Prevalence Study. Measurements: Total cholesterol, low-density lipoprotein (LDL) cholesterol, ratio of total cholesterol to high-density lipoprotein (HDL) cholesterol, and the ratio of LDL to HDL. Outcomes were coronary heart disease in the CPPT and Framingham studies and death from coronary heart disease in the Prevalence Study. Results: independent information in the total cholesterol/HDL ratio added risk-discriminating ability to total Cholesterol and LDL cholesterol measures (P < 0.02), but the reverse was not true. Among women, a high-risk threshold of 5.6 for the total cholesterol/HDL ratio identified a 0% to 15% larger group at 25% to 45% greater risk in the Prevalence and Framingham studies, respectively, than did current guidelines. Among men in the same studies, a risk threshold of 6.4 for the total cholesterol/HDL ratio identified a 69% to 95% larger group at 2% to 14% greater risk than did LDL cholesterol levels alone. Eight-year likelihood ratios for coronary heart disease ranged from 0.32 to 3.11 in men and from 0.59 to 2.98 in women for total cholesterol/HDL ratios (grouped from < 3 to greater than or equal to 9). Conclusions: The total cholesterol/HDL ratio is a superior measure of risk for coronary heart disease compared with either total cholesterol or LDL cholesterol levels. Current practice guidelines could be more efficient if risk stratification was based on this ratio rather than primarily on the LDL cholesterol level. C1 UNIV PENN,DEPT ECON,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. RP KINOSIAN, B (reprint author), UNIV PENN,RALSTON PENN CTR,DIV GEN INTERNAL MED,ROOM 230,3615 CHESTNUT ST,PHILADELPHIA,PA 19104, USA. FU NIA NIH HHS [NIA R29-AG09837-03] NR 27 TC 301 Z9 312 U1 1 U2 5 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD NOV 1 PY 1994 VL 121 IS 9 BP 641 EP 647 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA PN450 UT WOS:A1994PN45000002 PM 7944071 ER PT J AU COX, M HADDAD, JG AF COX, M HADDAD, JG TI LYMPHOMA, HYPERCALCEMIA, AND THE SUNSHINE VITAMIN SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material ID HORMONE-RELATED PROTEIN; CELL LEUKEMIA-LYMPHOMA; CULTURED ALVEOLAR MACROPHAGES; D ENDOCRINE SYSTEM; PARATHYROID-HORMONE; HUMORAL HYPERCALCEMIA; 1,25-DIHYDROXYVITAMIN-D3 PRODUCTION; TRANSFORMED LYMPHOCYTES; CALCITRIOL LEVELS; SERUM LEVELS C1 HOSP UNIV PENN,PHILADELPHIA,PA 19104. RP COX, M (reprint author), DEPT VET AFFAIRS MED CTR,MED SERV 111,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 44 TC 4 Z9 4 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD NOV 1 PY 1994 VL 121 IS 9 BP 709 EP 712 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA PN450 UT WOS:A1994PN45000012 PM 7944081 ER PT J AU MADDIX, DS TALLIAN, KB MEAD, PS AF MADDIX, DS TALLIAN, KB MEAD, PS TI RIFABUTIN - A REVIEW WITH EMPHASIS ON ITS ROLE IN THE PREVENTION OF DISSEMINATED MYCOBACTERIUM-AVIUM COMPLEX INFECTION SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; ANTIMICROBIAL AGENTS; PROPHYLAXIS; ANSAMYCIN; INVITRO; INTRACELLULARE; CYCLOSPORINE; INHIBITION; ABSORPTION AB OBJECTIVE: To discuss the mechanism of action, in vitro and in vivo activity, pharmacokinetics, clinical trials, adverse effects, drug interactions, and dosage guidelines of rifabutin. DATA SOURCES: Pertinent literature published between 1982 and 1993 was identified via a MEDLINE search. Published proceedings of selected conferences were also reviewed. STUDY SELECTION: Selected basic science, microbiologic, and pharmacokinetic articles were evaluated. Because only limited data regarding rifabutin were available in the literature, all clinical trials involving the use of rifabutin in the prevention of Mycobacterium avium complex (MAC) infection in AIDS patients were reviewed. DATA SYNTHESIS: Rifabutin is a rifamycin derivative that was approved recently for the prevention of disseminated MAC disease in patients with advanced HIV infection. The drug has in vitro and in vivo activity against gram-positive bacteria, gram-negative bacteria, and mycobacteria. Two prospective, randomized, double-blind, placebo-controlled, multicenter trials demonstrated that rifabutin decreased the progression to MAC bacteremia in AIDS patients by about 50 percent. Adverse effects that resulted in the discontinuation of rifabutin prophylaxis occurred in 16 percent of patients. Rifabutin induces hepatic enzymes to a lesser extent than does rifampin, but dosage adjustment of drugs that are known to interact with rifampin may be required. CONCLUSIONS: Rifabutin is the only drug shown to be effective in the prevention of MAC bacteremia in AIDS patients; therefore, it should be made available as a formulary agent. It may be reasonable to delay initiation of rifabutin prophylaxis until CD4 lymphocyte counts are less than 75-50/mm3. C1 UNIV CALIF SAN FRANCISCO,SCH PHARM,SAN FRANCISCO,CA 94143. SAN FRANCISCO VET AFFAIRS MED CTR,MED SERV,INFECT DIS SECT,SAN FRANCISCO,CA. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. RP MADDIX, DS (reprint author), SAN FRANCISCO VET AFFAIRS MED CTR,PHARM SERV 119,4150 CLEMENT ST,SAN FRANCISCO,CA 94121, USA. NR 33 TC 9 Z9 9 U1 0 U2 1 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD NOV PY 1994 VL 28 IS 11 BP 1250 EP 1254 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA PT259 UT WOS:A1994PT25900010 PM 7849340 ER PT J AU BARCHIESI, F COLOMBO, AL MCGOUGH, DA FOTHERGILL, AW RINALDI, MG AF BARCHIESI, F COLOMBO, AL MCGOUGH, DA FOTHERGILL, AW RINALDI, MG TI IN-VITRO ACTIVITY OF A NEW ANTIFUNGAL TRIAZOLE, D0870, AGAINST CANDIDA-ALBICANS ISOLATES FROM ORAL CAVITIES OF PATIENTS INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID AZOLE-RESISTANT; IN-VITRO; FLUCONAZOLE RESISTANCE; LIPID-COMPOSITION; EMERGENCE; GLABRATA; THERAPY; STRAINS; AIDS AB We investigated the in vitro activity of a new antifungal triazole, D0870, against 100 Candida albicans isolates from the oral cavities of patients infected,vith human immunodeficiency virus by using a broth macrodilution method following the recommendations provided by the National Committee for Clinical Laboratory Standards (document M27-P). All of the isolates were chosen from C. albicans isolates already tested for fluconazole susceptibility by the procedure of the National Committee for Clinical Laboratory Standards. Fifty isolates were considered fluconazole susceptible (MICs, less than or equal to 4 mu g/ml), and 50 isolates were considered fluconazole resistant (MICs, greater than or equal to 8 mu g/ml). The in vitro data demonstrated that D0870 had good activity against isolates tested; for 90% of all strains of C. albicans, MICs were 0.5 mu g/ml. However, the D0870 MICs for the fluconazole-susceptible isolates were lower than those for the fluconazole-resistant isolates; MICs for 50 and 90% of the isolates tested were less than or equal to 0.0078 and 0.06 mu g/ml, respectively, for fluconazole-susceptible isolates and 0.25 and 2 mu g/ml, respectively, for fluconazole-resistant isolates (P < 0.001). Our data suggest that this new triazole could represent a valid alternative in the treatment of oral candidiasis in human immunodeficiency virus-infected patients. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. ESCOLA PAULISTA MED,SAO PAULO,BRAZIL. UNIV ANCONA,IST MALATTIE INFETT & MED PUBBL,ANCONA,ITALY. RP BARCHIESI, F (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,FUNGUS TESTING LAB,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 21 TC 14 Z9 15 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 NOV PY 1994 VL 38 IS 11 BP 2553 EP 2556 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA PP222 UT WOS:A1994PP22200007 PM 7872746 ER PT J AU VALERO, G MORENO, F GRAYBILL, JR AF VALERO, G MORENO, F GRAYBILL, JR TI ACTIVITIES OF CLARITHROMYCIN, OFLOXACIN, AND CLARITHROMYCIN PLUS ETHAMBUTOL AGAINST MYCOBACTERIUM-SIMIAE IN MURINE MODEL OF DISSEMINATED INFECTION SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID INTRACELLULAR ACTIVITIES; AVIUM COMPLEX; ENHANCEMENT AB After 2 weeks of intravenous challenge with Mycobacterium simiae, ICR outbred mice were treated with clarithromycin, ofloxacin, or clarithromycin pins ethambutol for 4 weeks. All three therapy groups demonstrated a decrease in the level of infection in both the lungs and the spleen. There were no significant differences among the three treated groups in decreasing mycobacterial counts in the lungs; however, both ofloxacin and clarithromycin plus ethambutol were superior to clarithromycin alone in reducing the level of infection in the spleen. Results of the study suggest a potential role for these agents in the treatment of human M. simiae infection. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT INFECT DIS,SAN ANTONIO,TX 78284. NR 12 TC 22 Z9 22 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 NOV PY 1994 VL 38 IS 11 BP 2676 EP 2677 PG 2 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA PP222 UT WOS:A1994PP22200031 PM 7872769 ER PT J AU COLSTON, JT KUMAR, P CHAMBERS, JP FREEMAN, GL AF COLSTON, JT KUMAR, P CHAMBERS, JP FREEMAN, GL TI ALTERED SARCOLEMMAL CALCIUM-CHANNEL DENSITY AND CA2+-PUMP ATPASE ACTIVITY IN TACHYCARDIA HEART-FAILURE SO CELL CALCIUM LA English DT Article ID DIHYDROPYRIDINE RECEPTOR; MYOCARDIUM; BINDING; CA-2+; MODEL; DESENSITIZATION; NOREPINEPHRINE; DEPENDENCE; ACTIVATION; DOGS AB Whether sarcolemmal (SL) calcium handling is altered in endstage heart failure produced by chronic rapid pacing is not known. To investigate this we paced 7 rabbits at a rate of 400 beats/min for 35 +/- 11 days. 6 animals served as non-paced controls. Purified left ventricular SL membranes were then prepared and tested for [H-3]-nitrendipine binding and (Ca2++Mg2+)-dependent ATPase (Ca2+-pump) activity. Results show a 50% reduction in calcium channel antagonist binding sites with B-max values reduced from 450 +/- 40 to 230 +/- 8 fmoles/mg protein in response to chronic rapid pacing (P < 0.01). This change was accompanied by a modest decrease in K-d from 0.29 +/- 0.09 to 0.22 +/- 0.03 nM (not significant). V-max values for the SL Ca2+-pump ATPase were decreased from 387 to 164 nmoles/mg protein/min (P < 0.01) with K-Ca(2+) values reduced from 0.91 to 0.28 mu M Ca2+ (P < 0.05) in response to tachycardia induced failure as compared to controls. ATPase activity in both groups was very sensitive to 25 mu M calmidazolium and 5 mu M vanadate. Results from this study indicate that both a reduction in SL calcium channel density and decrease in SL Ca2+-pump ATPase activity are evident in tachycardia heart failure. We conclude that sarcolemmal calcium handling is altered in heart failure induced by chronic rapid pacing and that such changes may contribute to systolic dysfunction associated with this model of heart failure. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,DIV LIFE SCI,BRAIN RES LAB BIOCHEM,SAN ANTONIO,TX 78285. NR 28 TC 23 Z9 23 U1 0 U2 2 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0143-4160 J9 CELL CALCIUM JI Cell Calcium PD NOV PY 1994 VL 16 IS 5 BP 349 EP 356 DI 10.1016/0143-4160(94)90028-0 PG 8 WC Cell Biology SC Cell Biology GA PR183 UT WOS:A1994PR18300002 PM 7859249 ER PT J AU PURNER, MB BERENS, RL KRUG, EC CURIEL, TJ AF PURNER, MB BERENS, RL KRUG, EC CURIEL, TJ TI EPSTEIN-BARR VIRUS-TRANSFORMED B-CELLS, A POTENTIALLY CONVENIENT SOURCE OF AUTOLOGOUS ANTIGEN-PRESENTING CELLS FOR THE PROPAGATION OF CERTAIN HUMAN CYTOTOXIC T-LYMPHOCYTES SO CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY LA English DT Article ID ENVELOPE GLYCOPROTEIN; REVERSE-TRANSCRIPTASE; VIRAL HEMAGGLUTININ; SEQUENCE VARIATION; SOLUBLE-ANTIGEN; INFECTED CELLS; HLA-ANTIGEN; CLONES; LINES; INDUCTION AB Antigen-specific cytotoxic T cells (CTL) are generally elicited in vitro by incubation of effector cells with an appropriate major histocompatibility complex-matched antigen-presenting cell (APC). In the case of CTL derived from inbred rodents, spleen cells from an animal of the same strain serve as a ready source of autologous major histocompatibility complex-identical APC. In outbred human populations, however, a convenient source of human leukocyte antigen-matched APC is ordinarily difficult to obtain, and for that reason human antigen-specific CTL may be difficult to propagate. We describe a method whereby Epstein-Barr virus-transformed human B cells (B-LCL) serve as a convenient source of efficient APC for the propagation of human antigen-specific CTL. B-LCL are produced by using B cells from the donor under study and are thus human leukocyte antigen identical to the donor. Using this method, we have propagated human CD4+ Toxoplasma gondii-specific CTL for up to 9 months in vitro, during which time the cells retained their functional capability. C1 UNIV COLORADO,HLTH SCI CTR,DIV INFECT DIS,BOX B-168,4200 E 9TH AVE,DENVER,CO 80262. DENVER VET AFFAIRS MED CTR,DIV INFECT DIS,DENVER,CO 80220. NR 39 TC 5 Z9 5 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 1071-412X J9 CLIN DIAGN LAB IMMUN JI Clin. Diagn. Lab. Immunol. PD NOV PY 1994 VL 1 IS 6 BP 696 EP 700 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PV209 UT WOS:A1994PV20900014 PM 8556523 ER PT J AU TALAL, N AF TALAL, N TI HISTORICAL OVERVIEW OF SJOGRENS-SYNDROME SO CLINICAL AND EXPERIMENTAL RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 4th Breton Workshop on Autoimmunity CY APR 14-16, 1994 CL BREST, FRANCE SP CONSEIL REG BRETAGNE, CONSEIL GEN FINISTERE, FRENCH NAVY, UNIV BRETAGNE OCCIDENTALE 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. NR 8 TC 0 Z9 0 U1 0 U2 0 PU CLINICAL & EXPER RHEUMATOLOGY PI PISA PA VIA SANTA MARIA 31, 56126 PISA, ITALY SN 0392-856X J9 CLIN EXP RHEUMATOL JI Clin. Exp. Rheumatol. PD NOV-DEC PY 1994 VL 12 SU 11 BP S3 EP S4 PG 2 WC Rheumatology SC Rheumatology GA QN123 UT WOS:A1994QN12300002 PM 7768047 ER PT J AU LOPESVIRELLA, MF VIRELLA, G AF LOPESVIRELLA, MF VIRELLA, G TI ATHEROSCLEROSIS AND AUTOIMMUNITY SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Review ID LOW-DENSITY-LIPOPROTEIN; CIRCULATING IMMUNE-COMPLEXES; MONOCYTE-DERIVED MACROPHAGES; HUMAN-ENDOTHELIAL-CELLS; SMOOTH-MUSCLE CELLS; CHOLESTERYL ESTER ACCUMULATION; SYSTEMIC LUPUS-ERYTHEMATOSUS; POLYMORPHONUCLEAR LEUKOCYTES; MONOCLONAL-ANTIBODIES; VASCULAR DISEASES AB The possible involvement of immunological mechanisms in the pathogenesis of atherosclerosis has been suggested intermittently since the early 1970s. Both humoral and cellular mechanisms have been proposed to participate in the onset and/or progression of atheromatous lesions, but the theories postulating the involvement of autoantibodies and immune complexes have met with considerable experimental support. Modified lipoproteins, particularly different forms of oxidized LDL, have been reported to elicit humoral immune responses in both experimental animals and humans. Oxidized LDL has been demonstrated in atheromatous lesions, anti-oxidized LDL antibodies have been detected in circulation and in atheromatous plaques, and immune complexes formed with LDL and anti-LDL have been isolated from the serum of patients with manifestations of atherosclerosis. In addition, in vitro-formed LDL-IC and IC isolated from patients have been demonstrated to cause intracellular accumulation of cholesteryl esters (CE) in human macrophages and fibroblasts. The accumulation of CE in macrophages exposed to LDL-IC is unique to this type of IC and is associated with a paradoxical overexpression of the native LDL receptor and with increase synthesis and release of interleukin 1 and TNF-alpha. The release of these cytokines in the subendothelial space may have a significant role in promoting the interaction of endothelial cells with mononuclear cells, causing endothelial cell damage directly or indirectly, and also in inducing smooth muscle cell proliferation. Thus, several lines of evidence suggest that humoral autoimmunity may play a significant role in the pathogenesis of atherosclerosis. (C) 1994 Academic Press, Inc. C1 MED UNIV S CAROLINA,DEPT MED,DIV METAB ENDOCRINOL & NUTR,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT MICROBIOL & IMMUNOL,CHARLESTON,SC 29425. RP LOPESVIRELLA, MF (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29403, USA. NR 97 TC 49 Z9 52 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD NOV PY 1994 VL 73 IS 2 BP 155 EP 167 DI 10.1006/clin.1994.1184 PG 13 WC Immunology; Pathology SC Immunology; Pathology GA PN333 UT WOS:A1994PN33300001 PM 7923923 ER PT J AU ZHANEL, GG CRAIG, WA AF ZHANEL, GG CRAIG, WA TI PHARMACOKINETIC CONTRIBUTIONS TO POSTANTIBIOTIC EFFECTS - FOCUS ON AMINOGLYCOSIDES SO CLINICAL PHARMACOKINETICS LA English DT Review ID BETA-LACTAM ANTIBIOTICS; GRAM-NEGATIVE BACTERIA; EXPERIMENTAL PSEUDOMONAS ENDOCARDITIS; KILLING-CURVE METHOD; ESCHERICHIA-COLI; ENTEROCOCCUS-FAECALIS; STAPHYLOCOCCUS-AUREUS; SUBINHIBITORY CONCENTRATIONS; ANTIMICROBIAL ACTIVITY; INVITRO ACTIVITY AB The postantibiotic effect (PAE) refers to a period of time after complete removal of an antimicrobial during which there is no growth of the target organism. The PAE appears to be a feature of most antimicrobial agents and has been documented with a variety of common bacterial pathogens. Various factors influence the presence or duration of the PAE including the type of organism, type of antimicrobial, concentration of antimicrobial, duration of antimicrobial exposure, antimicrobial combinations, and inoculum and medium used. beta-Lactams demonstrate a PAE against Gram-positive cocci, but produce only a short PAE with Gram-negative bacilli. Antimicrobial agents that inhibit RNA or protein synthesis have a PAE against Gram-positive cocci and Gram-negative bacilli. In vivo studies of aminoglycosides suggest that area under the plasma concentration-time curve is the pharmacokinetic parameter that best correlates with clinical efficacy. This is thought to be due to the concentration-dependent killing and PAE possessed by these antimicrobials. Animal and human studies have reported that once-daily administration of aminoglycoside is as effective as, or more effective than, and possibly less toxic than traditional multiple daily administration. C1 UNIV MANITOBA, FAC MED, DEPT MED MICROBIOL, WINNIPEG, MB, CANADA. UNIV MANITOBA, FAC PHARM, WINNIPEG R3T 2N2, MB, CANADA. UNIV WISCONSIN, WILLIAM S MIDDLETON MEM VET HOSP, MADISON, WI USA. UNIV WISCONSIN, FAC MED, MADISON, WI USA. NR 123 TC 39 Z9 48 U1 1 U2 3 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 0312-5963 J9 CLIN PHARMACOKINET JI Clin. Pharmacokinet. PD NOV PY 1994 VL 27 IS 5 BP 377 EP 392 DI 10.2165/00003088-199427050-00005 PG 16 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA PQ553 UT WOS:A1994PQ55300005 PM 7851055 ER PT J AU NORMAN, DC YOSHIKAWA, TT AF NORMAN, DC YOSHIKAWA, TT TI INFECTIONS OF THE BONE, JOINT, AND BURSA SO CLINICS IN GERIATRIC MEDICINE LA English DT Article AB Septic arthritis caused by Neisseria gonorrhoeae is an infection almost exclusively of patients younger than 40(21,39); rarely is the infection reported in elderly patients.(14,16) Therefore, this discussion on septic arthritis in the geriatric population is on nongonococcal septic arthritis. When several studies of nongonococcal septic arthritis (hereafter referred to as septic arthritis) in adults are analyzed, approximately 40% of these cases occur in patients aged 60 years and older.(26,38) This high proportion of joint infection with increased age appears to have occurred primarily during the recent antibiotic era.(35) Moreover, an increasing number of reports on septic arthritis in older patients have appeared in the literature during the past decade.(9,24,31,34,51,60) Mortality caused by septic arthritis in the general adult population is approximately 10%.(26) In contrast, elderly patients with joint infections experience death rates ranging from 19% to 33%.(24,31,51) Morbidity or complications associated with septic arthritis (e.g., osteomyelitis, loss of joint function, osteoarthritis, duration of immobility) also appear to increase with age.(9,24,31,51) C1 DEPT VET AFAIRS,OFF GERIATR & EXTENDED CARE 114,WASHINGTON,DC 20420. W LOS ANGELES DEPT VET AFFAIRS MED CTR,LOS ANGELES,CA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0749-0690 J9 CLIN GERIATR MED JI Clin. Geriatr. Med. PD NOV PY 1994 VL 10 IS 4 BP 703 EP 718 PG 16 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA PU744 UT WOS:A1994PU74400011 PM 7850698 ER PT J AU NEW, AS TRESTMAN, RL SIEVER, LJ AF NEW, AS TRESTMAN, RL SIEVER, LJ TI THE PHARMACOTHERAPY OF BORDERLINE PERSONALITY-DISORDER SO CNS DRUGS LA English DT Article ID IMPULSIVE AGGRESSIVE-BEHAVIOR; DSM-III; DIAGNOSTIC INTERVIEW; DOUBLE-BLIND; HALOPERIDOL; FLUOXETINE; PLACEBO; PHENELZINE; EFFICACY; LITHIUM AB Pharmacotherapy is used increasingly as a helpful adjunct to psychotherapeutic interventions in the treatment of borderline personality disorder. Clinical trials have been performed to investigate drug treatment of the 3 symptom clusters associated with borderline personality disorder - impulsivity, affective lability and psychotic-like symptoms. Although no single agent ameliorates all the symptoms of this diagnosis, and patients vary considerably in their response to medication, pharmacological strategies for each symptom can be delineated. Impulsivity and aggression can be treated with selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs), lithium, beta-adrenoceptor blockers or antipsychotics. Affective symptomology has also been found to respond to MAOIs, SSRIs and lithium. Interestingly, patients with borderline personality disorder do not seem to respond to tricyclic antidepressants. As would be expected, antipsychotics are the most effective medications for the treatment of the psychotic symptoms of borderline personality disorder. Various techniques to improve compliance and enhance the treatment alliance with the patient can be suggested, including patient education about the role of the pharmacologist (and therapist) in treatment and about the nature of agents prescribed. In addition, if possible, patients should be allowed to play an active part in the selection of drugs. C1 BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,NEW YORK,NY. MT SINAI MED CTR,NEW YORK,NY 10029. RP NEW, AS (reprint author), WESTERN PSYCHIAT INST & CLIN,RM 1175,3811 OHARA ST,PITTSBURGH,PA 15243, USA. NR 56 TC 4 Z9 4 U1 1 U2 3 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PD NOV PY 1994 VL 2 IS 5 BP 347 EP 354 DI 10.2165/00023210-199402050-00003 PG 8 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA PQ781 UT WOS:A1994PQ78100003 ER PT J AU ERSHLER, WB SUN, WH BINKLEY, N AF ERSHLER, WB SUN, WH BINKLEY, N TI THE ROLE OF INTERLEUKIN-6 IN CERTAIN AGE-RELATED DISEASES SO DRUGS & AGING LA English DT Review ID MYELOMA-CELL-GROWTH; ACUTE PHASE RESPONSE; ALZHEIMERS-DISEASE; MULTIPLE-MYELOMA; CYTOKINE EXPRESSION; SIGNAL TRANSDUCER; PRECURSOR PROTEIN; HODGKINS-DISEASE; BONE-RESORPTION; IL-6 AB Interleukin-6 (IL-6) is a pro-inflammatory cytokine with a wide range of functions. Perhaps the most important physiologically is its role as a mediator of the acute phase inflammatory response. Normally, there is little measurable IL-6 in the circulation, but levels increase abruptly to nanogram amounts during an inflammatory process. During aging, it has been proposed that the tight regulation of IL-6 gene expression becomes less effective and levels are measurable even when there is no evidence for inflammation. Several investigators have identified this cytokine as being involved in the pathogenesis of various disease processes and we have suggested that certain age-associated diseases are directly related. Among these are late-life lymphoma and myeloma, osteoporosis and possibly Alzheimer's disease. RP ERSHLER, WB (reprint author), UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,CTR GERIATR RES EDUC & CLIN,DEPT MED,MADISON,WI 53706, USA. FU NIA NIH HHS [AG00451, AG00213] NR 68 TC 64 Z9 64 U1 0 U2 1 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1170-229X J9 DRUG AGING JI Drugs Aging PD NOV PY 1994 VL 5 IS 5 BP 358 EP 365 PG 8 WC Geriatrics & Gerontology; Pharmacology & Pharmacy SC Geriatrics & Gerontology; Pharmacology & Pharmacy GA PQ371 UT WOS:A1994PQ37100005 PM 7833589 ER PT J AU CARNES, M GOODMAN, BM LENT, SJ VO, H JAECKELS, R AF CARNES, M GOODMAN, BM LENT, SJ VO, H JAECKELS, R TI COINCIDENT PLASMA ACTH AND CORTICOSTERONE TIME-SERIES - COMPARISONS BETWEEN YOUNG AND OLD RATS SO EXPERIMENTAL GERONTOLOGY LA English DT Article DE ACTH; GLUCOCORTICOIDS; AGING; TIME SERIES ANALYSIS; CHRONOBIOLOGY ID CORTICOTROPIN-RELEASING-FACTOR; PITUITARY-ADRENOCORTICAL AXIS; DIMINISHED DIURNAL SECRETION; AGE-RELATED-CHANGES; CIRCADIAN-RHYTHM; SYSTEM; CORTISOL; HORMONE; RESPONSIVENESS; PLASTICITY AB Senescence is accompanied by a reduced ability to respond to a variety of physical acid behavioral stressors. A sizable literature has been devoted to the interplay between hypothalamic-pituitary-adrenocortical axis dysfunction and senescence; yet, the precise interactions remain an enigma. Adrenocorticotropic hormone (ACTH) is secreted in pulsatile bursts generating complex signals in the plasma compartment that must be ''read'' by adrenocortical cells in order to initiate appropriate secretory responses. We have previously demonstrated subtle differences between young and old rats in the pattern of fluctuations in plasma ACTH concentrations over time, despite no difference in mean levels. The present work addressed the physiological significance of these differences in the plasma ACTH Signal by analyzing the corresponding plasma corticosterone concentration time series and the relationship between these two hormones over time. Time series of integrated 10-min ACTH and corticosterone concentrations were collected over 4 h at the time of diurnal activation and analyzed in the time and frequency domains. The time of onset of the diurnal surge occurred 20 min later in old rats, and the ratio of corticosterone to ACTH was less at the time of onset and peak of the diurnal surge. Corticosterone levels were lower in old rats and mean ACTH and corticosterone levels were correlated in young but not old rats, as were maximum levels of the two hormones. Cross-correlation of ACTH and corticosterone time series and comparison of spectra were consistent with smoother fluctuations in plasma corticosterone in old animals with less variability at time scales less than 55 min. We conclude that age may be associated with a delay in diurnal activation of the HPA axis, a loss of sensitivity of adrenal corticosterone secretion to plasma ACTH levels, and a relative loss of high frequency variability in the corticosterone signal, as seen in many physiological systems with age. RP CARNES, M (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,GRECC,2500 OVERLOOK TERRACE,ROOM B-2091,MADISON,WI 53705, USA. FU NIDDK NIH HHS [DK-40759] NR 68 TC 15 Z9 15 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD NOV-DEC PY 1994 VL 29 IS 6 BP 625 EP 643 DI 10.1016/0531-5565(94)90075-2 PG 19 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA PU887 UT WOS:A1994PU88700003 PM 9435915 ER PT J AU ZIMMERMAN, M LISH, JD FARBER, NJ HARTUNG, J LUSH, D KUZMA, MA PLESCIA, G AF ZIMMERMAN, M LISH, JD FARBER, NJ HARTUNG, J LUSH, D KUZMA, MA PLESCIA, G TI SCREENING FOR DEPRESSION IN MEDICAL PATIENTS - IS THE FOCUS TOO NARROW SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article ID DIAGNOSTIC INTERVIEW SCHEDULE; HEALTH-CARE UTILIZATION; PANIC DISORDER; SELF-REPORT; PSYCHIATRIC-DISORDERS; SOMATIZATION DISORDER; ADDICTIVE-DISORDERS; MENTAL-DISORDERS; SOCIAL MORBIDITY; CHEST PAIN AB There is growing consensus that depression is a major public health problem causing significant psychosocial morbidity and mortality which should be addressed by casefinding efforts in primary care settings. A large amount of literature has examined the ability of self-report questionnaires to detect depression in medical patients and the results have been encouraging. However, studies of general population and psychiatric patient samples indicate that depression is frequently comorbid with other psychiatric disorders, and that psychiatric disorders other than depression are also associated with significant morbidity and mortality. Consequently, we believe that psychiatric screening in primary care should be broad based. We administered a newly developed, multidimensional questionnaire (the SCREENER), that simultaneously screens for a range of DSM-III-R psychiatric disorders, to 508 medical outpatients attending a VA general medical clinic. Compared with nondepressed cases, the depressed patients significantly more often reported all of the nondepressive symptoms. Nine of the ten nondepressive disorders screened for by the SCREENER were significantly more frequent in the depressed group. Most patients who screened positive for depression also screened positive for at least one nondepressive disorder. Compared with patients who only screened positive for depression, those who screened positive for both depression and a nondepressive disorder rated their physical and emotional health more poorly and made more visits to the doctor. Compared with patients who did not screen positive for any disorder, those who only screened positive for a nondepressive disorder rated their physical and emotional health more poorly, and more frequently had a history of mental health treatment. C1 MED COLL PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19129. MED COLL PENN,DIV GEN MED,PHILADELPHIA,PA 19129. PHILADELPHIA VET AFFAIRS MED CTR,DEPT INTERNAL MED,PHILADELPHIA,PA. NR 59 TC 20 Z9 20 U1 4 U2 6 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD NOV PY 1994 VL 16 IS 6 BP 388 EP 396 DI 10.1016/0163-8343(94)90114-7 PG 9 WC Psychiatry SC Psychiatry GA PR841 UT WOS:A1994PR84100003 PM 7843575 ER PT J AU AZIZASHUSTER, E AF AZIZASHUSTER, E TI A CHILD AT ALL COSTS - POSTHUMOUS REPRODUCTION AND THE MEANING OF PARENTHOOD SO HUMAN REPRODUCTION LA English DT Article DE ASSISTED REPRODUCTION; CRYOPRESERVATION OF SPERM AND EMBRYOS; GAMETE DONATION; POSTHUMOUS REPRODUCTION AB The creation of babies by assisted and collaborative techniques of reproduction, such as in-vitro fertilization or cryopreservation of gametes and embryos, stimulates strong emotions and fantasies about life, death, sexuality and immortality. Particularly, the cryopreservation of spermatozoa for post-mortem reproduction forces us to come to terms with the meaning of human reproduction, and the extent of individual rights to procreate using artificial means. RP AZIZASHUSTER, E (reprint author), DEPT VET AFFAIRS MED CTR,ETH PROGRAM,PHILADELPHIA,PA 19104, USA. NR 11 TC 16 Z9 16 U1 0 U2 1 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 NOV PY 1994 VL 9 IS 11 BP 2182 EP 2185 PG 4 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA PU209 UT WOS:A1994PU20900043 PM 7868695 ER PT J AU CHIAPPELLI, F FROST, P MANFRINI, E LEE, P PHAM, L GARCIA, C DALEY, S KUNG, M VILLANUEVA, P AF CHIAPPELLI, F FROST, P MANFRINI, E LEE, P PHAM, L GARCIA, C DALEY, S KUNG, M VILLANUEVA, P TI COCAINE BLUNTS HUMAN CD4(+) CELL ACTIVATION SO IMMUNOPHARMACOLOGY LA English DT Article DE COCAINE; HUMAN T LYMPHOCYTE; CD4(+) CELL ACTIVATION ID BLOOD T-LYMPHOCYTES; BETA-ENDORPHIN; PROLIFERATION; INVITRO; EXPRESSION; MOLECULE; SURFACE; MICE AB Cocaine is reported to be immunotoxic. The biochemical mechanisms responsible for the immunopharmacological outcomes of cocaine in vivo and in vitro remain, however, to be fully elucidated. Our experimental data confirm that exposure of normal human T cells to micromolar concentrations of cocaine modulates T-cell responses to stimulation by a variety of stimuli, and indicate that cocaine impairs early activation events during CD4(+) but not CD4(-) T-cell stimulation. Pre-incubation of enriched CD4(+) T-cell subpopulations that express the homing receptor CD62L with nanomolar concentrations of the endogenous opioid peptide beta-endorphin leads to a more severe impairment of activation than that noted following pre-incubation with micromolar concentrations of cocaine alone. These findings begin to elucidate the molecular and cellular mechanisms of the immunopathology of cocaine. Our data support the proposition that cocaine abuse may place cocaine-abuser HIV-seropositive individuals at increased risk of opportunistic infections. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,HUMAN IMMUNOL & PSYCHONEUROIMMUNOL LAB,LOS ANGELES,CA 90073. UNIV ANCONA,ANCONA,ITALY. UNIV CALIF LOS ANGELES,DEPT BIOL,LOS ANGELES,CA 90024. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES,SCH DENT,HUMAN ORAL & MOLEC IMMUNOL LAB,LOS ANGELES,CA 90024, USA. OI Frost, Patrick/0000-0003-3348-5983 FU NIDA NIH HHS [NIDA-07683]; PHS HHS [GR 6773-01] NR 35 TC 12 Z9 12 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0162-3109 J9 IMMUNOPHARMACOLOGY JI Immunopharmacology PD NOV-DEC PY 1994 VL 28 IS 3 BP 233 EP 240 DI 10.1016/0162-3109(94)90059-0 PG 8 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA PN500 UT WOS:A1994PN50000008 PM 7852054 ER PT J AU IGIETSEME, JU MAGEE, DM WILLIAMS, DM RANK, RG AF IGIETSEME, JU MAGEE, DM WILLIAMS, DM RANK, RG TI ROLE FOR CD8(+) T-CELLS IN ANTICHLAMYDIAL IMMUNITY DEFINED BY CHLAMYDIA-SPECIFIC T-LYMPHOCYTE CLONES SO INFECTION AND IMMUNITY LA English DT Note ID FEMALE GUINEA-PIGS; TUMOR NECROSIS FACTOR; GENITAL-INFECTION; INCLUSION CONJUNCTIVITIS; GAMMA INTERFERON; HOST DEFENSE; ROLE INVIVO; TRACHOMATIS; MICE; RESOLUTION AB The role of CD8(+). T cells in antichlamydial immunity was investigated in a murine model of chlamydial genital infection by using T-cell clones generated against the Chlamydia trachomatis agent of mouse pneumonitis (MoPn). Two CD8(+) T-cell clones tested (2.1F and 2.14-9) were chlamydia antigen specific and MHC restricted and reacted against MoPn as well as the Chlamydia psittaci agent of guinea pig inclusion conjunctivitis and C. trachomatis serovar E, suggesting the recognition of a genus-specific antigen. Upon adoptive transfer into persistently MoPn-infected nu/nu mice, 55.6% of the recipients of clone 2.1F (15 of 27) resolved the infection but recipients of clone 2.14-9 did not. The ability to resolve the MoPn infection correlated with the capacity of clone 2.1F to elaborate a combination of gamma interferon and tumor necrosis factor alpha. The results suggested that in addition to CD4(+) T cells, CD8(+) T cells may also contribute to anti-chlamydial T-cell immunity in vivo. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP IGIETSEME, JU (reprint author), UNIV ARKANSAS MED SCI HOSP,DEPT IMMUNOL & MICROBIOL,4301 MARKHAM ST,SLOT 511,LITTLE ROCK,AR 72205, USA. FU NIAID NIH HHS [AI26328] NR 29 TC 90 Z9 92 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 NOV PY 1994 VL 62 IS 11 BP 5195 EP 5197 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA PN304 UT WOS:A1994PN30400073 PM 7927806 ER PT J AU LEONG, GB SILVA, JA GARZATREVINO, ES OLIVA, D FERRARI, MM KOMANDURI, RV CALDWELL, JCB AF LEONG, GB SILVA, JA GARZATREVINO, ES OLIVA, D FERRARI, MM KOMANDURI, RV CALDWELL, JCB TI THE DANGEROUSNESS OF PERSONS WITH THE OTHELLO SYNDROME SO JOURNAL OF FORENSIC SCIENCES LA English DT Article; Proceedings Paper CT 46th Annual Meeting of the American-Academy-of-Forensic-Sciences CY FEB 14-19, 1994 CL SAN ANTONIO, TX SP AMER ACAD FORENSIC SCI DE PSYCHIATRY; DANGEROUSNESS; DELUSIONS; MENTAL DISORDER; OTHELLO SYNDROME; ORGANIC DELUSIONAL DISORDER ID PATHOLOGICAL JEALOUSY; MORBID JEALOUSY; SEXUAL JEALOUSY; PIMOZIDE; FLUOXETINE AB The Othello syndrome, or delusional jealousy, often raises significant forensic issues, particularly dangerousness. Dangerous patients suffering from the Othello delusion may present with hostility ranging from verbal threats to homicidal acts. We present three cases of individuals suffering from Othello syndrome associated with significant hostility and organic mental factors. We analyze these cases along with Othello syndrome cases culled from the recent anglophonic literature, especially in terms of implications for domestic and public safety. C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP LEONG, GB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV 116AA,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 35 TC 12 Z9 13 U1 0 U2 4 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD NOV PY 1994 VL 39 IS 6 BP 1445 EP 1454 PG 10 WC Medicine, Legal SC Legal Medicine GA PV998 UT WOS:A1994PV99800012 PM 7815024 ER PT J AU SILVA, JA LEONG, GB GARZATREVINO, ES LEGRAND, J OLIVA, D WEINSTOCK, R BOWDEN, CL AF SILVA, JA LEONG, GB GARZATREVINO, ES LEGRAND, J OLIVA, D WEINSTOCK, R BOWDEN, CL TI A COGNITIVE MODEL OF DANGEROUS DELUSIONAL MISIDENTIFICATION SYNDROMES SO JOURNAL OF FORENSIC SCIENCES LA English DT Article; Proceedings Paper CT 46th Annual Meeting of the American-Academy-of-Forensic-Sciences CY FEB 14-19, 1994 CL SAN ANTONIO, TX SP AMER ACAD FORENSIC SCI DE PSYCHIATRY; DANGEROUSNESS; VIOLENCE; DELUSIONS; MISIDENTIFICATION; MENTAL DISORDER ID CAPGRAS SYNDROME; SUBJECTIVE DOUBLES; PREFRONTAL CORTEX; FREGOLI SYNDROME; SCHIZOPHRENIA; VIOLENCE; INTERMETAMORPHOSIS; PERSPECTIVE; EROTOMANIA; TOMOGRAPHY AB The hallmark of the delusional misidentification syndromes is the presence of a misidentification delusion of the self or others. Delusional misidentification may present with an increased risk for dangerous behaviors. Individuals suffering from delusional misidentification syndromes may express hostility in ways ranging from serious verbal threats to homicidal acts. The causes of dangerous misidentification delusions remain for the most part undetermined. In this article, we report a series of six cases of individuals who harbored dangerous misidentification delusions. These individuals were studied phenomenologically and forensically. They were also studied biologically, including neuropsychological testing. A cognitive hypothesis aimed at explaining dangerousness and delusional misidentification is proposed. Implications of the hypothesis for further research are briefly outlined. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 64 TC 14 Z9 14 U1 1 U2 7 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD NOV PY 1994 VL 39 IS 6 BP 1455 EP 1467 PG 13 WC Medicine, Legal SC Legal Medicine GA PV998 UT WOS:A1994PV99800013 PM 7815025 ER PT J AU LIVINGSTON, EH AF LIVINGSTON, EH TI BLOOD-FLOW, CONTRACTIONS AND ISCHEMIA-REPERFUSION - A POSSIBLE PATHOGENETIC MECHANISM FOR ULCERS SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY LA English DT Editorial Material ID INDUCED GASTRIC-LESIONS; MUCOSAL INJURY; RAT; ACID; DISTENSION; ISCHEMIA; MOTILITY; STOMACH; DAMAGE C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SURG SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,RES SERV,LOS ANGELES,CA. CTR ULCER RES & EDUC,LOS ANGELES,CA. NR 19 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL AUSTR PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON 3053, AUSTRALIA SN 0815-9319 J9 J GASTROEN HEPATOL JI J. Gastroenterol. Hepatol. PD NOV-DEC PY 1994 VL 9 IS 6 BP 652 EP 653 DI 10.1111/j.1440-1746.1994.tb01580.x PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PY131 UT WOS:A1994PY13100026 PM 7865728 ER PT J AU LEUCHTER, AF DUNKIN, JJ LUFKIN, RB ANZAI, Y COOK, IA NEWTON, TF AF LEUCHTER, AF DUNKIN, JJ LUFKIN, RB ANZAI, Y COOK, IA NEWTON, TF TI EFFECT OF WHITE-MATTER DISEASE ON FUNCTIONAL CONNECTIONS IN THE AGING BRAIN SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID SOMATOSENSORY EVOKED-POTENTIALS; HEALTHY ELDERLY SUBJECTS; MAGNETIC-RESONANCE; ALZHEIMERS-DISEASE; LEUKO-ARAIOSIS; EEG COHERENCE; PERIVENTRICULAR HYPERINTENSITY; DIFFERENTIAL-DIAGNOSIS; MULTIINFARCT DEMENTIA; SENILE DEMENTIA AB Periventricular white matter hyperintensities (PVHs) seen on T2 weighted MRI studies are common in elderly people and often represent demyelination of fibres. Damage to these fibres could lead to functional disconnection between brain regions. Electroencephalographic coherence, a measure of shared electrical activity between regions, was examined to determine if there was evidence for such disconnection. Twenty two subjects with clinically diagnosed dementia of the Alzheimer's type, 16 with multi-infarct dementia, and 18 normal controls were studied. It was hypothesised that coherence between areas presumably linked by fibres that traverse the periventricular region would be decreased in subjects with PVHs, and that PVHs would have a stronger association with decreased coherence than clinical diagnosis. It was also hypothesised that coherence between areas presumably connected by long corticocortical tracts that are neuroanatomically separated from the ventricles would be low in patients with Alzheimer's disease because of pyramidal cell death in this group, but would not be affected by the presence of PVHs. Patients with PVHs in fact had lower coherence than those without PVHs in the pre-Rolandic and post-Rolandic areas, where connecting fibres traverse the periventricular region. There was no effect of PVHs, however, on coherence between areas separated by the Rolandic fissure that were connected by long corticocortical tracts; this coherence was lowest among the patients with Alzheimer's disease. These patterns of association suggest that coherence may detect different types of neurophysiological ''disconnection,'' and may be sensitive to selective damage to different fibre pathways. C1 UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,DEPT PSYCHIAT,QEEG LAB,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,DEPT BIOBEHAV SCI,QEEG LAB,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT RADIOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA 90073. OI newton, thomas/0000-0002-3198-5901 FU NIA NIH HHS [P30 AG10123]; NIMH NIH HHS [MH 40705] NR 63 TC 50 Z9 50 U1 0 U2 3 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 NOV PY 1994 VL 57 IS 11 BP 1347 EP 1354 DI 10.1136/jnnp.57.11.1347 PG 8 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA PQ919 UT WOS:A1994PQ91900009 PM 7964810 ER PT J AU YOSHIKAWA, TT AF YOSHIKAWA, TT TI A TRIBUTE TO SOLOMON,DAVID,H., MD SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Letter RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,WASHINGTON,DC 20422, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD NOV PY 1994 VL 42 IS 11 BP 1219 EP 1219 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA PQ005 UT WOS:A1994PQ00500019 PM 7963216 ER PT J AU HARDIN, TC JENNINGS, TS AF HARDIN, TC JENNINGS, TS TI CEFEPIME SO PHARMACOTHERAPY LA English DT Article ID BROAD-SPECTRUM CEPHALOSPORIN; BETA-LACTAM ANTIBIOTICS; GRAM-NEGATIVE BACTERIA; CYSTIC-FIBROSIS PATIENTS; PSEUDOMONAS-AERUGINOSA; INVITRO ACTIVITY; HOSPITALIZED-PATIENTS; ENTEROBACTER-CLOACAE; TISSUE PENETRATION; ESCHERICHIA-COLI AB Cefepime is a potent, broad-spectrum, fourth-generation cephalosporin with enhanced activity against most gram-positive aerobic bacterial pathogens and many gram-negative aerobic bacteria that are resistant to other cephalosporins. The drug's zwitterionic structure contributes to more rapid penetration of gram-negative bacterial cell membranes, and its low affinity for most type I beta-lactamases leads to significantly reduced enzymatic degradation compared with other cephalosporins. Cefepime has a good toxicity profile, with minor gastrointestinal and central nervous system symptoms being most prevalent. At dosages ranging from 1-2 g every 8-12 hours, it is an alternative option for infections of the lower respiratory tract, urinary tract, and skin and skin structures, as well as febrile episodes in neutropenic patients with cancer, and bacteremia or septicemia in critically ill patients. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. RP HARDIN, TC (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PHARM SERV 119,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 82 TC 17 Z9 18 U1 0 U2 0 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER BOX 806 171 HARRISON AVE, BOSTON, MA 02111 SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD NOV-DEC PY 1994 VL 14 IS 6 BP 657 EP 668 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA PU104 UT WOS:A1994PU10400002 PM 7885968 ER PT J AU RUDKIN, GH MILLER, TA AF RUDKIN, GH MILLER, TA TI LIPEDEMA - A CLINICAL ENTITY DISTINCT FROM LYMPHEDEMA SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article AB In a review of 250 cases of lymphedema of the lower extremity, 9 patients were noted to share unique similarities in their history and physical findings. Although these patients had mild swelling in their pretibial areas and were all referred with a diagnosis of lymphedema of the legs, their findings differed significantly from the usual patient with either congenital or acquired lymphedema. Notably, the lower extremity swelling was always bilateral and symmetrical in nature and never involved the feet. Skin changes characteristic of lymphedema were not found, and consistent fat pads were present anterior to the lateral malleoli in each patient. These findings are representative of a clinical entity known as lipedema, which is distinct from lymphedema and for which treatment may be different. C1 UNIV CALIF LOS ANGELES,MED CTR,DIV PLAST SURG,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,PLAST SURG SECT,LOS ANGELES,CA 90073. NR 8 TC 52 Z9 53 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD NOV PY 1994 VL 94 IS 6 BP 841 EP 847 DI 10.1097/00006534-199411000-00014 PG 7 WC Surgery SC Surgery GA PP248 UT WOS:A1994PP24800014 PM 7972431 ER PT J AU SILVA, JA LEONG, GB AF SILVA, JA LEONG, GB TI DELUSIONS OF PSYCHOLOGICAL CHANGE OF THE SELF SO PSYCHOPATHOLOGY LA English DT Article ID CAPGRAS SYNDROME; MISIDENTIFICATION SYNDROMES; LYCANTHROPY; TOMOGRAPHY AB Delusions of psychological change of the self are becoming increasingly appreciated as a type of misidentification delusions. Most available knowledge on delusions of psychological change of the self derives from single case studies. In this article, we present a study encompassing 30 cases of this delusion. Diagnostic and phenomenologic aspects of this delusion are discussed as well as its relation to other types of misidentification delusions. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA 90073. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 28 TC 13 Z9 13 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD NOV-DEC PY 1994 VL 27 IS 6 BP 285 EP 290 PG 6 WC Psychiatry SC Psychiatry GA PQ634 UT WOS:A1994PQ63400004 PM 7846252 ER PT J AU CONNOR, MJ NANTHUR, J PUHVEL, SM AF CONNOR, MJ NANTHUR, J PUHVEL, SM TI INFLUENCE OF 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (TCDD) ON TNF-ALPHA-LEVELS IN THE SKIN OF CONGENIC HAIRED AND HAIRLESS MICE SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID LANGERHANS CELLS; ENDOTOXIN; KERATINOCYTES; AH AB It has been proposed that TNF-alpha mediates TCDD-induced toxicity. TCDD induces a chloracne-like response in the skin of hairless HRS/J mice but not in congenic haired animals. Using an ELISA, we measured TNF-alpha levels in the skin of TCDD-treated haired and hairless HRS/J mice to test the hypothesis that TNF-alpha mediates the cutaneous toxicity of TCDD. TNF-(a)lpha levels in the skin of haired mice were at or below minimal detectable levles and were unchanged by TCDD exposure. In contrast, TNF-alpha levels were significantly higher in the skin of hairless mice after exposure. The bulk of the induced TNF-alpha was present in the dermis, although detectable amounts were present in the epidermis. To determine if murine skin cells were producing TNF-alpha in direct response to TCDD, cultures of neonatal epidermak keratinocytes and dermal fibroblasts were treated with varying biologically active doses of TCDD or vehicle (DMSO) or with lipopolysaccharide (LPS) as a positive control. Within 24 hr of exposure to LPS, TNF-alpha levels were increased in the culture media of cells tested. In contrast, TCDD treatment (10(-11) M to 10(-7) M) failed to induce detectable TNF-alpha release from either fibroblasts or keratinocytes over a comparable time frame or when measured for up to 6 days following exposure. The failure of TCDD to stimulate TNF-alpha production by keratinocytes or fibroblasts suggests that the rise in dermal TNF-alpha levels seen in vivo is unlikely to be a primary component of the mechanism of toxicity. We suggest that the source of the dermal TNF-alpha in TCDD-treated hairless mouse skin is probably component cells of the inflammatory response. (C) 1994 Academic Press, Inc. C1 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,VET ADM,LOS ANGELES,CA 90073. RP CONNOR, MJ (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,DIV DERMATOL,LOS ANGELES,CA 90024, USA. FU NIEHS NIH HHS [ES 03597] NR 20 TC 4 Z9 4 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD NOV PY 1994 VL 129 IS 1 BP 12 EP 15 DI 10.1006/taap.1994.1223 PG 4 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA PQ822 UT WOS:A1994PQ82200002 PM 7974484 ER PT J AU KOWLURU, A METZ, SA AF KOWLURU, A METZ, SA TI CHARACTERIZATION OF NUCLEOSIDE DIPHOSPHOKINASE ACTIVITY IN HUMAN AND RODENT PANCREATIC BETA-CELLS - EVIDENCE FOR ITS ROLE IN THE FORMATION OF GUANOSINE TRIPHOSPHATE, A PERMISSIVE FACTOR FOR NUTRIENT-INDUCED INSULIN-SECRETION SO BIOCHEMISTRY LA English DT Article ID GTP-BINDING PROTEINS; DIPHOSPHATE KINASE; RAT ISLETS; HISTIDINE-RESIDUES; ADENYLATE-CYCLASE; ACTIVATION; MASTOPARAN; RELEASE; GUANINE; INTACT AB We have recently demonstrated a permissive role for GTP in nutrient-induced insulin secretion. One of the possible loci at which GTP might exert its regulatory effects include one (or more) of the GTP-binding proteins which we have identified in subcellular fractions (including secretory granules) of pancreatic islets. Herein, we characterize nucleoside diphosphokinase (NDP kinase) activity, which catalyzes the transphosphorylation of nucleotide diphosphate (e.g., GDP) to nucleotide triphosphates (e.g., GTP) in insulin-secreting cells. The presence of NPP kinase activity in normal rat and human islets, and pure beta (RIN and HIT) cells, was verified by three distinct approaches: first, its catalytic activity (formation of GTP or GTP gamma S from GDP and ATP or ATP gamma S); secondly, by immunologic detection; and third, by quantitating the phosphoenzyme intermediate of NDP kinase, which is involved in a ping-pong phosphotransfer mechanism. Subcellularly, NDP kinase is predominantly cytosolic (with a tetrameric molecular mass of 85-90 kDa) and requires divalent metal ions and thiols for its activity. UDP, which forms an abortive complex with the enzyme, inhibited its activity in a Concentration-dependent manner (K-i = 2 mM). The phosphorylated intermediate of NDP kinase was differentially sensitive to heat, acidic pH, and a histidine-selective reagent, diethyl pyrocarbonate, suggesting that (one of) the phosphoamino acid(s) may be histidine. These data demonstrate that in beta cells NDP kinase undergoes transient phosphorylation and suggest that this phosphate, in turn, is transferred to GDP. If the GTP which is formed thereby is bound to, or channelled to, relevant GTP-binding proteins, it would facilitate the formation of active form of these proteins. NDP kinase might therefore couple mitochondrial oxidative events to extramitochondrial sites critical to stimulus-secretion coupling. C1 UNIV WISCONSIN, SCH MED, ENDOCRINOL SECT, MADISON, WI 53792 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. RP UNIV WISCONSIN, SCH MED,CTR CLIN SCI H4568,DEPT MED, DIV ENDOCRINOL, 600 HIGHLAND AVE, MADISON, WI 53792 USA. FU NIDDK NIH HHS [DK37312] NR 57 TC 52 Z9 53 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 18 PY 1994 VL 33 IS 41 BP 12495 EP 12503 DI 10.1021/bi00207a017 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PM582 UT WOS:A1994PM58200017 PM 7918472 ER PT J AU STEELE, R SCHUNA, AA SCHREIBER, R AF STEELE, R SCHUNA, AA SCHREIBER, R TI CALCIUM-CHANNEL ANTAGONISTS AND GINGIVAL HYPERPLASIA - RESPONSE SO ANNALS OF INTERNAL MEDICINE LA English DT Letter ID OVERGROWTH; PLAQUE C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,CHICAGO,IL 60612. RP STEELE, R (reprint author), COOK CTY HOSP,CHICAGO,IL 60612, 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 15 PY 1994 VL 121 IS 8 BP 625 EP 625 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA PL486 UT WOS:A1994PL48600019 ER PT J AU YU, XF MCLANE, MF RATNER, L OBRIEN, W COLLMAN, R ESSEX, M LEE, TH AF YU, XF MCLANE, MF RATNER, L OBRIEN, W COLLMAN, R ESSEX, M LEE, TH TI KILLING OF PRIMARY CD4(+) T-CELLS BY NON-SYNCYTIUM-INDUCING MACROPHAGE-TROPIC HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AIDS; CD4(+) T LYMPHOCYTES ID ENVELOPE PROTEIN; MONONUCLEAR PHAGOCYTES; BIOLOGICAL PHENOTYPE; PRIMARY INFECTION; HTLV-III; HIV-1; AIDS; PROGRESSION; VARIANTS; IDENTIFICATION AB Understanding the mechanism by which human immunodeficiency virus type 1 (HIV-1) kills CD4(+) T lymphocytes is important to the development of therapeutic and prophylactic strategies. Recent studies have indicated that, in some cases, progression to AIDS is associated with the appearance of syncytium-inducing, T cell line-tropic HIV-1 variants. Nevertheless, approximately 50% of subjects with AIDS harbor only non-syncytium-inducing, macrophage-tropic (NSI-M) variants of HIV-1. In most asymptomatic patients, NSI-M HIV-1 isolates are the predominant virus type found. We report here that cytopathicity of NSI-M HIV-1 for primary CD4(+) T lymphocytes can be directly detected in vitro. The extent of CD4(+) T-cell killing was not completely correlated with the rate of viral replication, suggesting that other characteristics of HIV-1 contribute to its cytopathicity. Our findings suggest that: (i) direct killing by NSI-M HIV-1 may contribute to CD4(+) T-lymphocyte depletion in vivo, and (ii) the determinants of HIV-1 cytopathicity for CD4(+) T lymphocytes and cell tropism or syncytia-forming ability are not necessarily tightly linked. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,DEPT MED & MOLEC MICROBIOL,ST LOUIS,MO 63110. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,DEPT MED,DIC INFECT DIS,LOS ANGELES,CA 90073. UNIV PENN,SCH MED,DEPT MED,DIV PULM & CRIT CARE,PHILADELPHIA,PA 19104. NR 29 TC 30 Z9 30 U1 2 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 OCT 11 PY 1994 VL 91 IS 21 BP 10237 EP 10241 DI 10.1073/pnas.91.21.10237 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA PM138 UT WOS:A1994PM13800117 PM 7937869 ER PT J AU SIEGLER, EL STINEMAN, MG MAISLIN, G AF SIEGLER, EL STINEMAN, MG MAISLIN, G TI DEVELOPMENT OF COMPLICATIONS DURING REHABILITATION SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID CO-MORBIDITY; LENGTH; STAY; PREDICTORS; UNIT AB Background and Methods: Although studies have demonstrated that medical rehabilitation patients have many complications that warrant attention, none has attempted to categorize complications by severity. This retrospective cohort study examined the incidence, types, and severity of problems that interrupt rehabilitation and the major risk factors for these events. Results: Of 1075 patients, 359 (33.4%) had acute medical complications on rehabilitation considered severe enough to interrupt treatment. Of the 359 patients, 158 (44%) required an unexpected transfer off rehabilitation. The most common reasons for unexpected transfer were surgical causes (22.8%), followed by infection or fever (17.1%) and by thromboembolic events (16.5%). Logistic regression revealed that major risk factors for complications requiring transfer were a primary diagnosis of deconditioning or nontraumatic spinal cord injury (adjusted odds ratio, 2.7; confidence interval, 1.8 to 4.2), severity of initial disability (adjusted odds ratio, 1.2; confidence interval, 1.1 to 1.3 for every 10-point drop in a Modified Barthel Index), and number of comorbid conditions (adjusted odds ratio, 1.1; confidence interval, 1.0 to 1.2). Risk factors for any complication were similar, but there was an interaction between comorbidity and the degree of functional impairment; in patients who were severely functionally impaired, the number of comorbidities was not as strongly associated with the risk of complications as it was in patients who were less functionally impaired. Conclusion: There is a complex relationship among the type of underlying medical impairment, severity of functional limitation, comorbidity, and unanticipated medical or surgical complications that interrupt rehabilitation. The interruptions vary both in type and in severity. C1 UNIV PENN,DIV GERIATR MED REHABIL MED & BIOSTAT MED,PHILADELPHIA,PA. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA. OI Siegler, Eugenia/0000-0001-9449-5873 FU NIA NIH HHS [K08-AG00487] NR 12 TC 31 Z9 31 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 OCT 10 PY 1994 VL 154 IS 19 BP 2185 EP 2190 DI 10.1001/archinte.154.19.2185 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA PK696 UT WOS:A1994PK69600008 PM 7944839 ER PT J AU HERBERT, V KASDAN, TS AF HERBERT, V KASDAN, TS TI ALFALFA, VITAMIN-E, AND AUTOIMMUNE DISORDERS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Letter ID SYSTEMIC LUPUS-ERYTHEMATOSUS; AMINO-ACID; INGESTION C1 BRONX VET AFFAIRS MED CTR,HEMATOL & NUTR RES LABS,BRONX,NY 10468. RP HERBERT, V (reprint author), MT SINAI MED CTR,HEMATOL & NUTR RES LABS,BRONX,NY 10468, USA. NR 11 TC 9 Z9 9 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD OCT PY 1994 VL 60 IS 4 BP 639 EP 640 PG 2 WC Nutrition & Dietetics SC Nutrition & Dietetics GA PJ930 UT WOS:A1994PJ93000026 PM 8092103 ER PT J AU PRINZ, C SCOTT, DR HURWITZ, D HELANDER, HF SACHS, G AF PRINZ, C SCOTT, DR HURWITZ, D HELANDER, HF SACHS, G TI GASTRIN EFFECTS ON ISOLATED RAT ENTEROCHROMAFFIN-LIKE CELLS IN PRIMARY CULTURE SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE CHOLECYSTOKININ B RECEPTOR; HISTAMINE; HISTIDINE DECARBOXYLASE; DEOXYRIBONUCLEIC ACID SYNTHESIS; SIGNAL TRANSDUCTION ID HISTIDINE-DECARBOXYLASE GENE; SELF-REPLICATION RATE; PLASMA GASTRIN; HYPERGASTRINEMIC RATS; TYROSINE KINASES; ENDOCRINE-CELLS; ANTIULCER DRUGS; MUCOSAL CELLS; CHOLECYSTOKININ; STOMACH AB The hormone gastrin stimulates acid secretion by releasing histamine from gastric enterochromaffin-like (ECL) cells and induces ECL cell proliferation in vivo. This study uses a > 90% pure ECL cell preparation in culture to compare gastrin effects on histamine release, histidine decarboxylase (HDC) activity, and DNA synthesis. Gastrin and the cholecystokinin octapeptide (CCK-8, nonsulfated) induced histamine release from ECL cells (24-96 h of primary culture) within 5 min of incubation [concentration eliciting 50% of maximal response (EC(50)), 4 and 2 x 10-(11) M, respectively]. The CCK-B antagonist L-365,260 inhibited this effect [concentration inhibiting 50% of maximal response (IC50), 2 x 10(-8) M], whereas the CCK-A antagonist L-364,718 (10(-8) M) and the tyrosine kinase inhibitor genistein (10(-4) M) had no effect. Histamine release was associated with a biphasic elevation of intracellular Ca2+. Gastrin stimulated HDC activity two- to threefold after 60 min of incubation (EC(50), 10(-10) M). Gastrin also increased DNA synthesis in ECL cells, with an EC(50) of 1.7 x 10(-12) M as measured by the incorporation of 5-bromo-2'deoxyuridine (BrdU). Positive nuclear immunostaining increased two- to threefold in up to 20% of ECL cells after 48-96 h of incubation. This effect was inhibited by L-365,260 (IC50, 5 x 10(-9) M) and by genistein (10(-4) M) but was not altered by L-364,718 (10(-8) M). The antisecretory drugs omeprazole, lansoprazole, and pantoprazole did not affect BrdU incorporation in isolated ECL cells. In conclusion, acute and chronic gastrin effects on the ECL cell are mediated via CCK-B receptors but differ in apparent receptor affinity and signal transduction pathways. C1 UNIV CALIF LOS ANGELES, DEPT PHYSIOL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, DEPT MED, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, CTR ULCER RES, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, CTR EDUC GASTROENTER, LOS ANGELES, CA 90073 USA. FU NIDDK NIH HHS [DK-41301, DK-17294, DK-40615] NR 49 TC 125 Z9 125 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD OCT PY 1994 VL 267 IS 4 BP G663 EP G675 PG 13 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA PW598 UT WOS:A1994PW59800023 PM 7524350 ER PT J AU GRANDALIANO, G CHOUDHURY, GG BISWAS, P ABBOUD, HE AF GRANDALIANO, G CHOUDHURY, GG BISWAS, P ABBOUD, HE TI MITOGENIC SIGNALING OF THROMBIN IN MESANGIAL CELLS - ROLE OF TYROSINE PHOSPHORYLATION SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE GROWTH FACTORS; SIGNAL TRANSDUCTION; GLOMERULUS ID PROTEIN KINASE-C; HUMAN-PLATELETS; RECEPTOR ACTIVATION; PERTUSSIS TOXIN; PATHWAYS; VASOPRESSIN; COAGULATION; ENDOTHELIN; GENISTEIN; INHIBITOR AB Thrombin elicits multiple biological effects on a variety of cells. We have previously shown that thrombin is a potent mitogen for human glomerular mesangial cells. This mitogenic effect of thrombin is associated with activation of phospholipase C (PLC) and induction of platelet-derived growth factor (PDGF) gene expression. The thrombin receptor, which belongs to the guanine nucleotide binding protein (G protein)-coupled receptor family, has recently been shown to induce rapid tyrosine phosphorylation of cellular proteins. In the present study, we investigated the role of protein-tyrosine phosphorylation in mediating the cellular responses elicited by thrombin in human glomerular mesangial cells. Amino acid labeling followed by immunoprecipitation with phosphotyrosine antibodies demonstrate that thrombin stimulates tyrosine phosphorylation of a set of cellular proteins. Treatment of mesangial cells with thrombin followed by immunoblotting with phosphotyrosine antibodies showed three major bands of tyrosine-phosphorylated proteins similar to 130, 70, and 44-42 kDa. Phosphorylation of these proteins was inhibited by two tyrosine kinase inhibitors, herbimycin A and genistein. Both compounds inhibited DNA synthesis and PDGF B-chain gene expression but had no effect on inositol phosphates production or increases in cytosolic calcium in response to thrombin. These data demonstrate that protein-tyrosine phosphorylation is not required for thrombin-induced PLC activation with inositol phosphate formation and subsequent intracellular calcium release, but it is an absolute requirement for thrombin-induced DNA synthesis and PDGF B-chain gene expression. C1 UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV NEPHROL, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET AFFAIRS HOSP, SAN ANTONIO, TX 78284 USA. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK-43988, DK-33665] NR 31 TC 15 Z9 15 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrol. Physiol. PD OCT PY 1994 VL 267 IS 4 BP F528 EP F536 PG 9 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA PW545 UT WOS:A1994PW54500003 PM 7524356 ER PT J AU HOHNLOSER, SH KLINGENHEBEN, T SINGH, BN AF HOHNLOSER, SH KLINGENHEBEN, T SINGH, BN TI AMIODARONE-ASSOCIATED PROARRHYTHMIC EFFECTS - A REVIEW WITH SPECIAL REFERENCE TO TORSADE-DE-POINTES TACHYCARDIA SO ANNALS OF INTERNAL MEDICINE LA English DT Review ID SUSTAINED VENTRICULAR-TACHYCARDIA; ARRHYTHMIA SUPPRESSION TRIAL; ANTIARRHYTHMIC DRUG-THERAPY; ACUTE MYOCARDIAL-INFARCTION; PLACEBO-CONTROLLED TRIAL; SUDDEN CARDIAC DEATH; LOW-DOSE AMIODARONE; LONG QT SYNDROME; TERM FOLLOW-UP; DE-POINTES AB Purpose: To assess the incidence of amiodarone-mediated aggravation of ventricular tachyarrhythmias or the development of new arrhythmias, such as torsade de pointes, in patients with cardiac disease. Data Sources and Study Selection: A MEDLINE literature search was done to identify articles published during the last 20 years that presented data on amiodarone-associated proarrhythmic events. The articles were divided into three categories: case reports, uncontrolled retrospective studies, and prospective controlled trials. In addition, articles were identified that examined the effects of amiodarone in patients with previously documented drug-induced torsade de pointes. Results: 65 English-language case reports dealing with torsade de pointes during amiodarone therapy were found in the literature. In many of these cases, other predisposing factors for the development of torsade de pointes were reported. Seventeen studies each reported data from at least 50 patients who were treated with amiodarone for at least 6 months. Of 2878 patients included in these trials, 57 were reported to have a proarrhythmic event while exposed to the drug (an overall incidence of 2%). Torsade de pointes was observed in one third of these patients (an overall incidence of 0.7%). In seven placebo-controlled trials in which the drug was given as monotherapy, amiodarone was not associated with the development of a proarrhythmic event in any patient. Finally, in three reports, 31 patients with previous drug-mediated torsade de pointes were exposed to amiodarone during short- and long-term therapy. In none of these patients did a recurrent episode of torsade de pointes develop, despite the amiodarone-induced prolongation of the QTc interval, which was equivalent to that observed at the time of torsade de pointes during exposure to previous drugs. Conclusions: Amiodarone appears to be associated with a remarkably low frequency of proarrhythmic events and an incidence of torsade de pointes of less than 1.0%. This low arrhythmogenicity and the negligible negative inotropic effect of the compound constitute properties that make amiodarone particularly useful in treating high-risk patients prone to sudden cardiac death. Its potential to reduce this risk is currently being evaluated in several large prospective trials. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP HOHNLOSER, SH (reprint author), UNIV FREIBURG,DEPT CARDIOL,HUGSTETTER STR 55,D-79106 FREIBURG,GERMANY. NR 79 TC 236 Z9 239 U1 0 U2 4 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 1994 VL 121 IS 7 BP 529 EP 535 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA PJ102 UT WOS:A1994PJ10200009 PM 8067651 ER PT J AU OROURKE, TJ WEISS, GR NEW, P BURRIS, HA RODRIGUEZ, G ECKHARDT, J HARDY, J KUHN, JG FIELDS, S CLARK, GM VONHOFF, DD AF OROURKE, TJ WEISS, GR NEW, P BURRIS, HA RODRIGUEZ, G ECKHARDT, J HARDY, J KUHN, JG FIELDS, S CLARK, GM VONHOFF, DD TI PHASE-I CLINICAL-TRIAL OF ORMAPLATIN (TETRAPLATIN, NSC-363812) SO ANTI-CANCER DRUGS LA English DT Article DE NEUROTOXICITY; ORMAPLATIN; PHASE I TRIAL ID CARCINOMA CELL-LINES; OVARIAN-CANCER; PERIPHERAL NEUROTOXICITY; CISPLATIN NEUROTOXICITY; PLATINUM ANALOGS; SENSITIVITY; RESISTANCE; NEUROPATHY; COMPLEXES; TOXICITY AB Ormaplatin is a platinum analog that was developed because of an altered toxicity profile and non-cross resistance to cisplatin in both in vitro and in vivo models. To determine the toxicities and maximum tolerated dose of ormaplatin on a daily times five schedule, patients with refractory solid tumors received ormaplatin on five consecutive days at nine dose levels ranging from 1.0 to 15.0 mg/m(2)/day. A total of 35 patients received 70 cycles of therapy. Nausea and vomiting and myelosuppression were moderate and not dose-limiting. Dose-limiting neurotoxicity, consisting of a sensory peripheral neuropathy, was seen in all five patients who received cumulative doses greater than or equal to 165 mg/m(2). This neurotoxicity was symptomatic in all patients and caused significant functional impairment in four patients with inability to walk in two patients. A sensitive atomic absorption spectroscopy analysis performed for one patient at the 13.0 mg/m(2)/day dose level showed a Cp(max) of 163 ng/ml and a t(1/2) of 10.9 min for free platinum. A phase II dose could not be determined due to the onset of peripheral neuropathy at low cumulative doses and not at absolute dose levels. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. CANC THERAPY & RES CTR S TEXAS,SAN ANTONIO,TX 78229. RP OROURKE, TJ (reprint author), BROOKE ARMY MED CTR,HEMATOL ONCOL SERV,FT SAM HOUSTON,TX 78234, USA. FU NCI NIH HHS [CM 07305-01, P01-CA54-174-02]; NCRR NIH HHS [5M01RR01346-09] NR 27 TC 33 Z9 33 U1 1 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4973 J9 ANTI-CANCER DRUG JI Anti-Cancer Drugs PD OCT PY 1994 VL 5 IS 5 BP 520 EP 526 DI 10.1097/00001813-199410000-00002 PG 7 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA PM436 UT WOS:A1994PM43600002 PM 7858283 ER PT J AU TALAL, N AF TALAL, N TI ONCOGENES, AUTOGENES, AND RHEUMATIC DISEASES SO ARTHRITIS AND RHEUMATISM LA English DT Editorial Material ID AUTOIMMUNE-DISEASE; SALIVARY-GLAND; FAS ANTIGEN; LPR MICE; APOPTOSIS; INFECTION; CELLS; GENE; LYMPHOCYTES; EXPRESSION C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. 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 NIDCR NIH HHS [DEO9311-03] NR 21 TC 16 Z9 16 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 OCT PY 1994 VL 37 IS 10 BP 1421 EP 1422 DI 10.1002/art.1780371003 PG 2 WC Rheumatology SC Rheumatology GA PM444 UT WOS:A1994PM44400002 PM 7945465 ER PT J AU RAHMAN, MU KLEYMAN, TR MCENTEE, CM HUDSON, AP AF RAHMAN, MU KLEYMAN, TR MCENTEE, CM HUDSON, AP TI REGULATION OF MITOCHONDRIAL CAMP-DEPENDENT PROTEIN-KINASE ACTIVITY IN YEAST SO BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL LA English DT Article ID AMP RECEPTOR PROTEIN; CYCLIC-AMP; SACCHAROMYCES-CEREVISIAE; BINDING PROTEIN; TRANSCRIPTION FACTOR; STRINGENT RESPONSE; PHOSPHORYLATION; SUBUNIT; IMPORT; GENES AB We have shown that transcription of the yeast (S. cerevisiae) mitochondrial (mt) genome is cAMP-sensitive, via a mt cAMP-dependent protein kinase (cAPK). In relation to that work, we examined whether the BCY1 gene product functions as regulatory subunit for mt cAPK, as it does for the cytoplasmic enzyme. We demonstrate that mt protein extracts from a bcy1 strain show no cAPK activity, whereas similar extracts from an otherwise isochromosomal BCY1 strain show high levels of such activity. Partial purification of mt cAPK from each strain confirms this difference. Photoaffinity labeling with 8-N-3[P-32]cAMP and highly-purified mt protein extracts from the BCY1 strain identifies one cAMP-binding protein (M(r) approximate to 47000), while similar mt extracts from the bcy1 strain lack all cAMP-binding proteins. These data suggest that BCY1 regulates yeast mt cAPK, and that inactivation of BCY1 removes that mt activity from cAMP control. C1 UNIV PENN,SCH MED,COLL MED,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PHYSIOL,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,MED RES SERV,PHILADELPHIA,PA 19104. NR 36 TC 11 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 1039-9712 J9 BIOCHEM MOL BIOL INT JI Biochem. Mol. Biol. Int. PD OCT PY 1994 VL 34 IS 4 BP 745 EP 753 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PT217 UT WOS:A1994PT21700013 PM 7866301 ER PT J AU PALUMBO, CL FITZPATRICK, PM NAESER, MA MIMURA, M PRETE, MN SAMARAWEERA, R ALBERT, ML AF PALUMBO, CL FITZPATRICK, PM NAESER, MA MIMURA, M PRETE, MN SAMARAWEERA, R ALBERT, ML TI INCREASE IN LESION SIZE ON CT SCAN IN CHRONIC APHASIA PATIENTS WITH IMPROVED NAMING ABILITY SO BRAIN AND LANGUAGE LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT NEUROL,APHASIA RES CTR,BOSTON,MA 02118. VET AFFAIRS MED CTR,NEUROL SERV,BOSTON,MA. VET AFFAIRS MED CTR,RADIOL SERV,BOSTON,MA. TUFTS UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02111. VET AFFAIRS MED CTR,SPEECH PATHOL SERV,BOSTON,MA. US DEPT VET AFFAIRS,MED RES SERV,WASHINGTON,DC. NR 8 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT PY 1994 VL 47 IS 3 BP 491 EP 493 PG 3 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA PM042 UT WOS:A1994PM04200062 ER PT J AU HAESSLER, R KUZUME, K CHIEN, GL WOLFF, RA DAVIS, RF VANWINKLE, DM AF HAESSLER, R KUZUME, K CHIEN, GL WOLFF, RA DAVIS, RF VANWINKLE, DM TI ANESTHETICS ALTER THE MAGNITUDE OF INFARCT LIMITATION BY ISCHEMIC PRECONDITIONING SO CARDIOVASCULAR RESEARCH LA English DT Article DE MYOCARDIAL INFARCTION; ANESTHETICS; RABBIT ID A1 ADENOSINE RECEPTORS; ISCHEMIC MYOCARDIUM; COLLATERAL FLOW; CONSCIOUS DOGS; K+ CHANNEL; SIZE; RABBIT; REPERFUSION; HALOTHANE; BLOCKADE AB Objective: The aim was to determine whether three commonly used animal anaesthetics alter the magnitude of infarct limitation achieved with ischaemic preconditioning. Methods: Eighty four anaesthetised nonpreconditioned and preconditioned open chest rabbits underwent a 30 min coronary occlusion followed by 3 h reperfusion. Ischaemic preconditioning was achieved with 5 min coronary occlusion beginning 15 min before the 30 min coronary occlusion. The anaesthetics studied were: pentobarbitone (30 mg.kg(-1) intravenously + 30-50 mg.kg(-1).h(-1) intravenously), isoflurane (1.5-2.5% end expiratory), and ketamine/xylazine (cocktail of 67 mg ketamine and 6.7 mg xylazine.ml(-1), 1 ml.kg(-1) intramuscularly + 0.3-1.3 ml.kg(-1).h(-1) intramuscularly). Area at risk was delineated with ZnCdS particles and infarction assessed with tetrazolium. Results: There were no significant differences in area at risk, heart rate, arterial pressure, and temperature between non-preconditioned and preconditioned hearts. Although infarct size was not significantly different among non-preconditioned hearts for each anaesthetic regimen (p = NS), the magnitude of infarct limitation with preconditioning varied with the anaesthetic employed (decrease in infarct size from control values of 81%, 44%, and 33% for pentobarbitone, isoflurane and ketamine/xylazine, respectively, p = 0.0145 for comparison of the three magnitudes, two factor ANOVA). Conclusion: Anaesthetic regimens affect the degree of infarct size limitation seen with ischaemic preconditioning. C1 PORTLAND VA MED CTR,DEPT ANESTHESIOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT ANESTHESIOL,PORTLAND,OR 97201. UNIV MUNICH,MUNICH,GERMANY. EHIME UNIV,MATSUYAMA,EHIME 790,JAPAN. NR 40 TC 66 Z9 66 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6363 J9 CARDIOVASC RES JI Cardiovasc. Res. PD OCT PY 1994 VL 28 IS 10 BP 1574 EP 1580 DI 10.1093/cvr/28.10.1574 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PL800 UT WOS:A1994PL80000018 PM 8001048 ER PT J AU OHLIN, AK MARLAR, RA AF OHLIN, AK MARLAR, RA TI USING PCR-SSCP, A MUTATION IN THE THROMBOMODULIN GENE IS IDENTIFIED IN A 45-YEAR-OLD MALE PRESENTING WITH THROMBOEMBOLIC DISEASE SO CIRCULATION LA English DT Meeting Abstract C1 UNIV LUND HOSP,DEPT CLIN CHEM,S-22185 LUND,SWEDEN. UNIV COLORADO,SCH MED,DEPT PATHOL,DENVER,CO 80202. DENVER VET AFFAIRS MED CTR,LAB SERV,DENVER,CO. 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 1994 VL 90 IS 4 BP 132 EP 132 PN 2 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA PN417 UT WOS:A1994PN41700742 ER PT J AU SAGER, PT FOLLMER, C UPPAL, P PRUITT, C GODFREY, R AF SAGER, PT FOLLMER, C UPPAL, P PRUITT, C GODFREY, R TI THE EFFECTS OF BETA-ADRENERGIC STIMULATION ON THE FREQUENCY-DEPENDENT ELECTROPHYSIOLOGIC ACTIONS OF AMIODARONE AND SEMATILIDE IN HUMANS SO CIRCULATION LA English DT Article DE AMIODARONE; SEMATILIDE; ACTION POTENTIAL DURATION; ISOPROTERENOL ID ACTION-POTENTIAL DURATION; TRANSIENT OUTWARD CURRENT; III ANTIARRHYTHMIC AGENT; RECTIFIER K+-CURRENT; VENTRICULAR-TACHYCARDIA; MYOCARDIAL-INFARCTION; REFRACTORY PERIOD; SODIUM CURRENT; GUINEA-PIG; ISOPROTERENOL AB Background The autonomic nervous system appears to play an important role in the development of clinical ventricular arrhythmias, and beta-adrenergic sympathetic stimulation may be important in modulating the electrophysiologic effects of class III antiarrhythmic agents. This study prospectively determined the effects of isoproterenol on the frequency-dependent actions of sematilide (a pure class III agent that selectively blocks the delayed rectifier potassium current) and amiodarone (a class III agent with a complex pharmacologic profile) on ventricular repolarization, refractoriness, and conduction. Methods and Results The frequency-dependent electrophysiologic effects of sematilide (n=11) and amiodarone (n=22) were determined at (1) drug-free baseline, (2) during steady state (>48 hours) dosing with sematilide (455+/-5 mg/d [mean+/-SEM]) or after 10.5 days of amiodarone loading (1618+/-32 mg/d), and (3) during isoproterenol administration (35 ng/kg per minute) to patients receiving sematilide or amiodarone. Electrophysiologic determinations were made at paced cycle lengths of 300 to 500 ms. The two groups were similar in all clinical characteristics. The ventricular action potential duration at 90% repolarization (APD(90)) was significantly prolonged by sematilide (mean increase, 7+/-1%, P<.01 by ANOVA) and amiodarone (mean increase, 12+/-1%, P<.001). However, while sematilide-induced APD(90) prolongation was fully reversed to baseline values during isoproterenol infusion, the APD(90) in patients receiving amiodarone remained significantly prolonged by a mean of 6+/-1% compared with baseline (P=.005). The reduction in the APD(90) was frequency dependent for both agents, with a greater reduction at longer than shorter paced cycle lengths (P<.02). During isoproterenol infusion the right ventricular effective refractory period (RVERP) in patients receiving sematilide was significantly reduced to mean values of 8+/-2% below baseline (P<.05), whereas the RVERP in patients receiving amiodarone remained significantly prolonged by a mean of 7+/-1% above baseline values (P=.01). Sematilide and sematilide/isoproterenol had no effect on ventricular conduction. Amiodarone increased the QRS duration by 14+/-4% (paced cycle length, 500 ms) to 32+/-5% (paced cycle length, 300 ms) compared with baseline values. Isoproterenol attenuated amiodarone-induced QRS prolongation by a mean of 5+/-1% (P=.005), without frequency-dependent effects, consistent with isoproterenol-induced increases in the sodium current. During isoproterenol infusion there was a trend for the sustained VT cycle length to be reduced below baseline in patients receiving sematilide (275+/-16 versus 298+/-55 ms, P=.06), whereas it remained significantly prolonged compared with baseline in patients receiving amiodarone (327+/-17 versus 257+/-12 ms, P<.001). Conclusions Isoproterenol fully reversed the effects of selective potassium channel block with sematilide on the APD(90) and further reduced the RVERP to values significantly below baseline; it partially attenuated but did not fully reverse amiodarone-induced prolongation of the APD(90) and RVERP, which remained significantly prolonged beyond baseline values. Isoproterenol exerted frequency-dependent effects in both patient groups on the APD(90); it modestly attenuated amiodarone-induced conduction slowing without frequency-dependent actions; and the sustained VT cycle length remained significantly prolonged during isoproterenol administration to patients receiving amiodarone but not in those receiving sematilide. These findings may have important clinical implications regarding protection from arrhythmia development in patients receiving pure class III agents or amiodarone. C1 UNIV CALIF LOS ANGELES, DEPT MED, LOS ANGELES, CA USA. RP SAGER, PT (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, DIV CARDIOL, 691-W111E, WILSHIRE & SAWTELLE BLVD, LOS ANGELES, CA 90073 USA. NR 56 TC 42 Z9 43 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0009-7322 EI 1524-4539 J9 CIRCULATION JI Circulation PD OCT PY 1994 VL 90 IS 4 BP 1811 EP 1819 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA PM632 UT WOS:A1994PM63200026 PM 7923666 ER PT J AU THET, LA ALLEN, PL KUCKEN, AM KAYSEN, JH AF THET, LA ALLEN, PL KUCKEN, AM KAYSEN, JH TI CHANGES IN THYROID TRANSCRIPTION FACTOR-I GENE-EXPRESSION DURING LUNG DEVELOPMENT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV WISCONSIN,DEPT MED,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. 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 1994 VL 42 IS 3 BP A427 EP A427 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA PD505 UT WOS:A1994PD50500440 ER PT J AU HARMS, BA MYERS, GA ROSENFELD, DJ STARLING, JR AF HARMS, BA MYERS, GA ROSENFELD, DJ STARLING, JR TI MANAGEMENT OF FULMINANT ULCERATIVE-COLITIS BY PRIMARY RESTORATIVE PROCTOCOLECTOMY SO DISEASES OF THE COLON & RECTUM LA English DT Article DE FULMINANT; ULCERATIVE COLITIS; ILEAL POUCH ID POUCH-ANAL ANASTOMOSIS; TOXIC MEGACOLON; ILEAL RESERVOIR; ILEOSTOMY; COLECTOMY; SURGERY AB Severe acute ulcerative colitis unresponsive to medical management is characterized by multiple associated risk factors including anemia, hypoproteinemia, and high steroid requirements when urgent surgery is required. Current surgical options include use of primary ileal pouch-anal anastomosis (IPAA) vs. historic trends favoring colectomy with ileostomy. PURPOSE: To evaluate the efficacy of primary IPAA in patients with severe colitis, we reviewed our own experience in 20 patients with this condition. METHODS: Patients undergoing primary restorative proctocolectomy included 13 males and 7 females (mean age, 30.5 +/- 2.4 years). Exclusion criteria for primary reconstruction included septic patients and patients with associated medical conditions such as pulmonary or cardiovascular disease. History of ulcerative colitis averaged 3.1 +/- 1.1 years (range, 1 month to 19 years). Preoperative mean total serum protein concentration was 5.0 +/- 0.2 g/dl, and mean albumin concentration was 2.1 +/- 0.2 g/dl, reflecting disease severity. The average daily steroid requirement at the time of urgent colectomy was 58.0 +/- 4.4 mg of prednisone (or intravenous equivalent). Primary IPAA included 18 ''W'' reservoirs, 1 ''S'' reservoir, and 1 ''J'' reservoir. RESULTS: Major surgical complications included mild pancreatitis (10 percent), anastomotic leak (5 percent), adrenal insufficiency (15 percent), an upper gastrointestinal bleed (5 percent), and small bowel obstruction (15 percent). There were no deaths, and no patients developed pelvic sepsis or required IPAA removal. At three and twelve months, 24-hr stool frequency averaged 7.3 +/- 0.4 and 4.9 +/- 0.3, respectively. Overall day and night continence was excellent and not different from patients who underwent elective IPAA procedures for ulcerative colitis. CONCLUSIONS: Improved options such as primary IPAA may be safely used in selected patients requiring urgent surgery for severe or fulminant ulcerative colitis. Medical management should be abbreviated when disease control cannot be promptly achieved. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP HARMS, BA (reprint author), UNIV WISCONSIN,DEPT SURG,H4-740,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 25 TC 16 Z9 16 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0012-3706 J9 DIS COLON RECTUM JI Dis. Colon Rectum PD OCT PY 1994 VL 37 IS 10 BP 971 EP 978 DI 10.1007/BF02049307 PG 8 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA PM204 UT WOS:A1994PM20400002 PM 7924717 ER PT J AU PRINZ, C SACHS, G WALSH, JH COY, DH WU, SV AF PRINZ, C SACHS, G WALSH, JH COY, DH WU, SV TI THE SOMATOSTATIN RECEPTOR SUBTYPE ON RAT ENTEROCHROMAFFIN-LIKE CELLS SO GASTROENTEROLOGY LA English DT Article ID G-PROTEIN; MOLECULAR-CLONING; ENDOCRINE-CELLS; AFFINITY; STOMACH; BRAIN; ANTIBODIES; EXPRESSION; INHIBITION; HISTAMINE AB Background/Aims: Gastric enterochromaffinlike (ECL) cells play an important role in peripheral regulation of acid secretion. This study investigated the somatostatin receptor subtype on ECL cells. Methods: ECL cells were isolated from rat fundic mucosa to a purity of 90%-95% by combining enzymatic digestion, elutriation, density gradient centrifugation, and culture. Results: Polymerase chain reaction performed with templates from an ECL cell complementary DNA library and primers specific to each of the five known somatostatin receptor subtypes showed that the somatostatin receptor type 2 was significantly enriched in ECL complementary DNA. Single cell videoimaging of highly purified ECL cells in culture showed that only the somatostatin receptor type 2 selective agonist, DC 32-87, inhibited the gastrin-induced calcium signal at 10(-11) mol/L. The type 3 and type 4 selective agonists, DC 25-12 and DC 32-92, and also somatostatin 14 required 100-1000 times higher concentrations (10(-8) mol/L). The somatostatin receptor type 2 analogue also inhibited gastrin-stimulated histamine release with a 50% inhibitory concentration (IC50 value of 2 x 10(-12) mol/L, whereas somatostatin 14 and the type 3 and 4 analogues showed IC50 values of 1 to 5 x 10(-9) mol/L. Conclusions: The predominant somatostatin receptors on rat gastric ECL cells are of the somatostatin receptor 2 subtype; they inhibit histamine secretion by interfering with the gastrin-induced calcium signal. C1 UNIV CALIF LOS ANGELES,CTR ULCER RES & EDUC,CTR GASTROENTER BIOL,DEPT MED,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. TULANE UNIV,DEPT MED,NEW ORLEANS,LA 70118. FU NIDDK NIH HHS [DK17294, DK40615, DK41301] NR 27 TC 116 Z9 116 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD OCT PY 1994 VL 107 IS 4 BP 1067 EP 1074 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PJ586 UT WOS:A1994PJ58600019 PM 7523214 ER PT J AU MARRA, F CHOUDHURY, GG PINZANI, M ABBOUD, HE AF MARRA, F CHOUDHURY, GG PINZANI, M ABBOUD, HE TI REGULATION OF PLATELET-DERIVED GROWTH-FACTOR SECRETION AND GENE-EXPRESSION IN HUMAN LIVER FAT-STORING CELLS SO GASTROENTEROLOGY LA English DT Article ID SIMIAN SARCOMA-VIRUS; FACTOR-A-CHAIN; RAT HEPATIC LIPOCYTES; EXTRACELLULAR-MATRIX; ITO CELLS; CONDITIONED MEDIUM; MESSENGER-RNA; PDGF-B; V-SIS; FIBROSIS AB Background/Aims: Liver fat-storing cells (FSCs) actively proliferate and secrete extracellular matrix during liver injury. Platelet-derived growth factor (PDGF) is a potent mitogen for cultured FSCs. In the present study, we investigated the regulation of PDGF gene expression and production in cultured human liver FSCs. Methods: PDGF A-chain and B-chain expression was analyzed by Northern blotting and ribonuclease protection assay, respectively. Secretion of PDGF was evaluated by immunoprecipitation and immunoblotting of conditioned medium and metabolic labeling of FSC followed by immunoprecipitation. Results: Three PDGF A-chain transcripts were detectable. Stimulation of FSC with phorbol myristate acetate (10(-7) mol/L) or PDGF BB (20 ng/mL) increased steady-state levels of PDGF A-chain and B-chain messenger RNA. PDGF AA had a small stimulatory effect on A-chain but not B-chain messenger RNA levels. FSCs secrete PDGF in the conditioned medium. The secreted protein is bioactive, because concentrated conditioned medium induced an increase in thymidine incorporation that was inhibited by anti-PDGF antibodies. Conclusions: This study shows that cultured FSCs express PDGF A- and B-chain genes and release bioactive PDGF in the culture medium. These data raise the possibility of an autocrine or short-loop paracrine effect of PDGF in FSCs as a mechanism contributing to the maintenance of the proliferative state during liver injury. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET AFFAIRS HOSP,SAN ANTONIO,TX. UNIV FLORENCE,MED CLIN 2,FLORENCE,ITALY. RI Marra, Fabio/K-7263-2016 OI Marra, Fabio/0000-0001-8629-0878 FU NIDDK NIH HHS [DK-33665, DK-43988] NR 40 TC 45 Z9 45 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 1994 VL 107 IS 4 BP 1110 EP 1117 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PJ586 UT WOS:A1994PJ58600024 PM 7926460 ER PT J AU SCHARRE, DW MAHLER, ME AF SCHARRE, DW MAHLER, ME TI PARKINSONS-DISEASE - MAKING THE DIAGNOSIS, SELECTING DRUG THERAPIES SO GERIATRICS LA English DT Article ID LEVODOPA AB Parkinson's disease is a progressive neurodegenerative condition of unknown cause and with no known cure. The diagnosis is based on clinical findings of rest tremor, muscle rigidity, bradykinesia, and gait instability. Over 40% of patients develop a dementia syndrome that is largely distinct from Alzheimer's disease. Depression is common, also occurring in more than 40% of patients with PD. Careful evaluation is necessary to help distinguish Parkinson's disease from secondary causes of parkinsonism. Carbidopa/levodopa, dopamine agonists, and monoamine oxidase type B inhibitors are the main-stays of treatment. Anticholinergics and other agents may also be useful. Pharmacologic treatment must be carefully titrated to control symptoms and to avoid side effects. In advanced disease, dose-related dyskinesias, end-of-dose wearing-off effect, and unpredictable sudden motor fluctuations become very disabling and difficult to manage. C1 UNIV CALIF LOS ANGELES, SCH MED, REED NEUROL RES CTR, LOS ANGELES, CA USA. W LOS ANGELES VA MED CTR, NEUROBEHAV UNIT, LOS ANGELES, CA USA. NR 21 TC 6 Z9 6 U1 0 U2 2 PU ADVANSTAR COMMUNICATIONS INC PI DULUTH PA 131 W 1ST STREET, DULUTH, MN 55802 USA SN 0016-867X J9 GERIATRICS JI Geriatrics PD OCT PY 1994 VL 49 IS 10 BP 14 EP + PG 0 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA PL101 UT WOS:A1994PL10100002 PM 7926845 ER PT J AU GERETY, MB AF GERETY, MB TI HEALTH-CARE REFORM FROM THE VIEW OF A GERIATRICIAN SO GERONTOLOGIST LA English DT Article ID CONTROLLED TRIAL; MEDICINE; UNIT; WILL C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78285. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,SAN ANTONIO,TX 78285. RP GERETY, MB (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 28 TC 4 Z9 4 U1 2 U2 2 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 OCT PY 1994 VL 34 IS 5 BP 590 EP 597 PG 8 WC Gerontology SC Geriatrics & Gerontology GA PX801 UT WOS:A1994PX80100006 PM 7959123 ER PT J AU ALVAREZ, O MALDONADO, AL SPEEG, KV AF ALVAREZ, O MALDONADO, AL SPEEG, KV TI EFFECT OF BILE-DUCT OBSTRUCTION AND STENTING ON P-GLYCOPROTEIN CONTENT AND FUNCTION STUDIED IN-VIVO IN THE RAT SO HEPATOLOGY LA English DT Meeting Abstract C1 UT,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL,SAN ANTONIO,TX. AL MURPHY VET ADM HOSP,SAN ANTONIO,TX. 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 1994 VL 20 IS 4 BP A187 EP A187 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PM556 UT WOS:A1994PM55600362 ER PT J AU DUPONTVERSTEEGDEN, EE MCCARTER, RJ KATZ, MS AF DUPONTVERSTEEGDEN, EE MCCARTER, RJ KATZ, MS TI VOLUNTARY EXERCISE DECREASES PROGRESSION OF MUSCULAR-DYSTROPHY IN DIAPHRAGM OF MDX MICE SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE CONTRACTILE PROPERTIES; MUSCLES; RESPIRATORY MUSCLE; ENDURANCE TRAINING; DUCHENNE MUSCULAR DYSTROPHY ID CONTRACTILE PROPERTIES; SKELETAL-MUSCLE; DUCHENNE; MOUSE; ENDURANCE; EXPRESSION; WEAKNESS AB Effects of voluntary wheel running on contractile properties of diaphragm (DIA) and soleus (SOL) of dystrophic (mdx) and control (C57BL/10SNJ) mice were evaluated. In particular, we tested the hypothesis that daily voluntary running is not deleterious to muscle function in mdx mice. Both groups of mice ran extensively (control mice similar to 7 km/day, mdx mice similar to 5 km/day). Exercise increased maximal specific tetanus tension of mdx DIA from 1.02 +/- 0.04 to 1.33 +/- 0.06 kg/cm(2) but did not restore it to the control level (2.55 +/- 0.17 kg/cm(2)). Maximal tetanus tension of sedentary mdx SOL (2.41 +/- 0.17 kg/cm(2)) was reduced compared with control (3.10 +/- 0.15 kg/cm(2)) and was not altered by running activity. Optimal length was significantly lower in DIA of mdx mice, and exercise did not change this. Fatigability and contractile properties of muscles measured in vitro were not altered by running activity with the exception of increased contraction time in mdx DIA. In conclusion, extensive wheel running is not deleterious to muscle function in mdx mice contrary to predictions of the ''work overload'' theory of muscular dystrophy. Rather, this exercise is beneficial for active tension generation of melt DIA, the muscle most closely resembling muscles of patients with Duchenne muscular dystrophy. 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,GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX 78284. NR 32 TC 76 Z9 77 U1 1 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 OCT PY 1994 VL 77 IS 4 BP 1736 EP 1741 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA PL694 UT WOS:A1994PL69400024 PM 7836193 ER PT J AU FLEET, JC HOCK, JM AF FLEET, JC HOCK, JM TI IDENTIFICATION OF OSTEOCALCIN MESSENGER-RNA IN NONOSTEOID TISSUE OF RATS AND HUMANS BY REVERSE TRANSCRIPTION-POLYMERASE CHAIN-REACTION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID GAMMA-CARBOXYGLUTAMIC ACID; CALCIUM-BINDING PROTEINS; K-DEPENDENT PROTEIN; MESSENGER-RNA; BONE; GENE; EXPRESSION; SEQUENCES; 1,25-DIHYDROXYVITAMIN-D; CALCIFICATION AB Diseased or necrotic tissue can become calcified in a way that resembles bone. We examined soft tissues for the presence and regulation of the mRNA for the bone-associated protein, osteocalcin (OC). RNA was isolated from liver, kidney, lung, brain, muscle, and bone of young (2 months) male SD rats and analyzed for beta-actin, IGF-I, metallothionein IIa, alpha(1) collagen, calbindin-D-9k (CaBP), and OC mRNA by reverse transcription-polymerase chain reaction (RT-PCR). All PCR products but CaBP were found in bone; CaBP was present only in duodenum, kidney, and lung. OC product was detected in all tissues; the identity of the PCR product was confirmed by sequencing. Bone OC mRNA levels were calculated to be 1000-fold higher than duodenal levels. Rats fed a 0.8% strontium diet for 7 days to drive down serum 1,25-dihydroxyvitamin D-3 levels [1,25(OH)(2)D-3] and then injected with 300 ng 1,25(OH)(2)D-3/100 body weight had increased duodenal CaBP (2.5-fold) and femur OC mRNA (2.2-fold) 24 h after treatment. Duodenal OC mRNA was unchanged. OC mRNA was found in nondiseased human aortae, and the amount of message was elevated in calcified aorta and calcified aortic plaques. These results demonstrate that (1) tissues other than bone have low basal expression of OC mRNA, (2) OC mRNA is not regulated by vitamin D in nonosteoid tissue, and (3) expression of OC mRNA in atherosclerotic aorta reflects a role for bone-forming cells in ectopic bone formation observed in certain disease conditions. C1 TUFTS UNIV,SCH DENT MED,BOSTON,MA 02111. US DEPT VET AFFAIRS,OUTPATIENT CLIN,BOSTON,MA. RP FLEET, JC (reprint author), TUFTS UNIV,USDA,HUMAN NUTR RES CTR AGING,824 HNRCA,711 WASHINGTON ST,BOSTON,MA 02111, USA. FU NHLBI NIH HHS [P01-HL48743] NR 33 TC 80 Z9 83 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD OCT PY 1994 VL 9 IS 10 BP 1565 EP 1573 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PJ111 UT WOS:A1994PJ11100008 PM 7817802 ER PT J AU BARCHIESI, F COLOMBO, AL MCGOUGH, DA RINALDI, MG AF BARCHIESI, F COLOMBO, AL MCGOUGH, DA RINALDI, MG TI COMPARATIVE-STUDY OF BROTH MACRODILUTION AND MICRODILUTION TECHNIQUES FOR IN-VITRO ANTIFUNGAL SUSCEPTIBILITY TESTING OF YEASTS BY USING THE NATIONAL-COMMITTEE-FOR-CLINICAL-LABORATORY-STANDARDS PROPOSED STANDARD SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID FLUCONAZOLE-RESISTANT CANDIDA; HUMAN-IMMUNODEFICIENCY-VIRUS; INOCULUM SIZE; INVITRO SUSCEPTIBILITIES; CRYPTOCOCCUS-NEOFORMANS; MULTICENTER EVALUATION; IN-VITRO; ALBICANS; AIDS; TRIAZOLE AB A comparative study of broth macro- and microdilution methods for susceptibility testing of fluconazole, itraconazole, flucytosine, and amphotericin B was conducted with 273 yeasts. The clinical isolates included 100 Candida albicans, 28 Candida tropicalis, 25 Candida parapsilosis, 15 Candida lusitaniae, 15 Candida krusei, 50 Cryptococcus neoformans var. neoformans, 25 Torulopsis (Candida) glabrata, and 15 Trichosporon beigelii strains. Both methods were performed according to the National Committee for Clinical Laboratory Standards' (NCCLS) recommendations (document M27-P). For fluconazole, itraconazole, and flucytosine, the endpoint was the tube that showed 80% growth inhibition compared,vith the growth control for the macrodilution method and the well with slightly hazy turbidity (score I) compared with the growth control for the microdilution method. For amphotericin B, the endpoint was the tube and/or well in which there was absence of growth. For the reference macrodilution method, the MICs were determined after 48 h of incubation for Candida spp., T. glabrata, and T. beigelii and after 72 h for C. neoformans var. neoformans. For the microdilution method, either the first-day MICs (24 h for all isolates other than C. neoformans var. neoformans and 48 h for C. neoformans var. neoformans) or the second-day MICs (48 and 72 h, respectively) were evaluated. The agreement within one doubling dilution of the macrodilution reference for all drugs,vas higher with the second-day MICs than with the first-day MICs for the microdilution test for most of the tested strains. General agreement was 92% for fluconazole, 85.7% for itraconazole, 98.3% for flucytosine, and 96.4% for amphotericin B. For C. neoformans var. neoformans and T. beigelii, the agreement of the first-day reading was higher than that of the second-day reading for fluconazole (94 versus 92%, respectively, for C. neoformans var. neoformans, and 86.7 versus 80%, respectively, for T. beigelii). Our studies indicate that the microdilution technique performed following the NCCLS guidelines with a second-day reading is a valid alternative method for testing fluconazole, itraconazole, flucytosine, and amphotericin B against these eight species of yeasts. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV ANCONA,IST MALATTIE INFETT & MED PUBL,ANCONA,ITALY. ESCOLA PAULISTA MED,BR-04023 SAO PAULO,BRAZIL. RP BARCHIESI, F (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,FUNGUS TESTING LAB,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 40 TC 91 Z9 94 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD OCT PY 1994 VL 32 IS 10 BP 2494 EP 2500 PG 7 WC Microbiology SC Microbiology GA PG912 UT WOS:A1994PG91200028 PM 7814488 ER PT J AU SAPICO, FL REEVES, D WEXLER, HM DUNCAN, J WILSON, KH FINEGOLD, SM AF SAPICO, FL REEVES, D WEXLER, HM DUNCAN, J WILSON, KH FINEGOLD, SM TI PRELIMINARY-STUDY USING SPECIES-SPECIFIC OLIGONUCLEOTIDE PROBE FOR RIBOSOMAL-RNA OF BILOPHILA-WADSWORTHIA SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID RIBOSOMAL DNA; SPECIMENS; RNA AB Portions of the 16S RNA from a urease-positive Bilophila wadsworthia strain were sequenced, and a probe was constructed. The probe was end labeled with [P-32]ATP and polynucleotide kinase and hybridized on a nylon filter (by dot blot hybridization) to the immobilized rRNA of 12 B. wadsworthia strains and eight other anaerobic isolates. The probe efficiently?v hybridized only to the Bilophila strains. Cross-reactivity at high RNA levels (2,000 ng) was observed with one strain of Bacteroides thetaiotaomicron and one strain of Bacteroides fragilis (with 10X SET buffer [20x SET buffer is 0.5 M NaCl, 0.03 M Tris, and 2 mM EDTA]) but was not seen at lower RNA levels or with 5x SET buffer. When tested against mixed cultures of aerobic and anaerobic isolates representative of appendiceal abscess flora, the probe did not react with mixed cultures containing no Bilophila cells and could detect greater than or equal to 10(5) Bilophila CFU/ml when the mixture was seeded with Bilophila cells. This probe is of potential use in the rapid identification of pure isolates and in the direct identification of B. wadsworthia in clinical specimens. C1 W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,MED SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. UNIV SO CALIF,RANCHO LOS AMIGOS MED CTR,DEPT MED,DOWNEY,CA 90242. UNIV SO CALIF,SCH MED,DEPT MED,LOS ANGELES,CA 90033. VET AFFAIRS MED CTR,DIV INFECT DIS,DURHAM,NC 27705. VET AFFAIRS MED CTR,MED SERV,DURHAM,NC 27705. VET AFFAIRS MED CTR,RES SERV,DURHAM,NC 27705. DUKE UNIV,MED CTR,DURHAM,NC 27705. RP SAPICO, FL (reprint author), UNIV SO CALIF,RANCHO LOS AMIGOS MED CTR,DIV INFECT DIS,7601 E IMPERIAL HWY,244 HB,DOWNEY,CA 90242, USA. NR 22 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD OCT PY 1994 VL 32 IS 10 BP 2510 EP 2513 PG 4 WC Microbiology SC Microbiology GA PG912 UT WOS:A1994PG91200031 PM 7529241 ER PT J AU SPARANO, JA FISHER, RI WEISS, GR MARGOLIN, K ARONSON, FR HAWKINS, MJ ATKINS, MB DUTCHER, JP GAYNOR, ER BOLDT, DH DOROSHOW, JH ERNEST, ML SZNOL, M MIER, JW AF SPARANO, JA FISHER, RI WEISS, GR MARGOLIN, K ARONSON, FR HAWKINS, MJ ATKINS, MB DUTCHER, JP GAYNOR, ER BOLDT, DH DOROSHOW, JH ERNEST, ML SZNOL, M MIER, JW TI PHASE-II TRIALS OF HIGH-DOSE INTERLEUKIN-2 AND LYMPHOKINE-ACTIVATED KILLER-CELLS IN ADVANCED BREAST-CARCINOMA AND CARCINOMA OF THE LUNG, OVARY, AND PANCREAS AND OTHER TUMORS SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE INTERLEUKIN-2; LAK CELLS; ADVANCED CARCINOMA; BREAST CARCINOMA; PHASE II TRIAL ID NECROSIS-FACTOR-ALPHA; NON-HODGKINS-LYMPHOMA; RECOMBINANT INTERLEUKIN-2; ADVANCED CANCER; ADOPTIVE IMMUNOTHERAPY; CONTINUOUS-INFUSION; THERAPY; COMBINATION; HEAD; NECK AB Treatment with interleukin-2 (IL-2) used alone or in combination with lymphokine-activated killer (LAK) cells is known to be an active therapy for patients with advanced renal cell carcinoma and melanoma. To further explore the activity of IL-2/LAK cell therapy in patients with advanced cancer of various primary sites, the Extramural IL-2/LAK Working Group (ILWG) initiated two phase II trials of high-dose IL-2/LAK therapy: one in patients with advanced breast carcinoma, and one in patients with advanced cancer arising in other sites. Patients with advanced renal cell carcinoma, melanoma, colorectal carcinoma, and lymphoma (Hodgkin's and B-cell non-Hodgkin's) were not eligible for the latter trial, but were treated on other ILWG trials that have been reported previously. Sixty-nine patients received high-dose IL-2 (600,000 IU/kg administered by a 15-min intravenous infusion every 8 h) on days 1-5 and days 11-15. Leukapheresis was performed for collection and ex vivo expansion of LAK cells on days 7-10, and the LAK cells were reinfused on days 11, 12, and 14. The studies were designed to determine whether treatment with IL-2/LAK resulted in at least a 40% response rate, a level of activity that was believed to be sufficient to justify the toxicity and cost of IL-2/LAK therapy. An adequate number of patients with carcinoma of the breast (N = 12), pancreas (N = 8), ovary (N = 7), and lung (non-small cell; N = 6) were accrued to assess response; most of these patients had prior chemotherapy that had failed. In addition, 32 patients with a variety of other tumor types were accrued, but accrual was not adequate to assess response in other primary tumor sites. One patient with adenocarcinoma of the breast had a partial response of 17 weeks' duration. Two patients had minor tumor regression (adenocarcinoma of the lung and spindle cell sarcoma of the lung). We conclude that high-dose IL-2/LAK is not likely to be associated with a response rate exceeding 40% for patients with carcinomas arising in the breast, pancreas, ovary, and lung (non-small cell). C1 LOYOLA UNIV,MED CTR,MAYWOOD,IL. UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. CITY HOPE NATL MED CTR,DUARTE,CA. UNIV CALIF SAN FRANCISCO,MED CTR,SAN FRANCISCO,CA. NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA. RP SPARANO, JA (reprint author), ALBERT EINSTEIN COLL MED,MONTEFIORE MED CTR,CTR CANC,111 E 210TH ST,BRONX,NY 10467, USA. FU NCI NIH HHS [N01-CM73703, N01-CM73702, N01-CM73704] NR 53 TC 21 Z9 21 U1 0 U2 3 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 1994 VL 16 IS 3 BP 216 EP 223 DI 10.1097/00002371-199410000-00006 PG 8 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA PM631 UT WOS:A1994PM63100006 PM 7834121 ER PT J AU CONRAD, AJ CHIANG, EY ANDEEN, LE AVOLIO, C WALKER, SM BAUMHEFNER, RW MIRZAYAN, R TOURTELLOTTE, WW AF CONRAD, AJ CHIANG, EY ANDEEN, LE AVOLIO, C WALKER, SM BAUMHEFNER, RW MIRZAYAN, R TOURTELLOTTE, WW TI QUANTITATION OF INTRATHECAL MEASLES-VIRUS IGG ANTIBODY-SYNTHESIS RATE - SUBACUTE SCLEROSING PANENCEPHALITIS AND MULTIPLE-SCLEROSIS SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE MEASLES; SUBACUTE SCLEROSING PANENCEPHALITIS; MULTIPLE SCLEROSIS; INTRATHECAL SYNTHESIS RATE; ANTIBODY INDEX; ENZYME-LINKED IMMUNOSORBENT ASSAY; QUANTITATION; IMMUNOGLOBULIN G ID CENTRAL NERVOUS-SYSTEM; BLOOD-BRAIN-BARRIER; CEREBROSPINAL-FLUID; HIV ANTIBODIES; AIDS; QUANTIFICATION; ENCEPHALITIS; MENINGITIS; INFECTION; DIAGNOSIS AB A method for quantitating specific anti-viral antibodies in serum and cerebrospinal fluid (CSF) is established using enzyme-linked immunosorbent assay (ELISA). Quantitated antibody levels are used to determine intrathecal specific IgG synthesis rate for the particular antibody. Measles virus was used as a model for validating this quantitative technique: a mutated form of measles virus is a cause of subacute sclerosing panencephalitis (SSPE) and there is a possibility that measles virus is related to the cause of multiple sclerosis (MS). Matched serum and CSF samples were assayed. Concentration of anti-measles IgG was determined and intrathecal measles-specific IgG synthesis rate was calculated. For the SSPE samples, measles-specific IgG synthesis rate was elevated and comprised > 20% of the total intrathecal IgG synthesis rate; these results are consistent with the literature. The ELISA method can be performed routinely, providing a quick, simple, reproducible means of quantitating specific antibody concentrations, with sensitivity greater than 1 nanogram per milliliter. With this method, quantitation of IgG antibodies to any other viral antigen can be reliably and precisely determined. C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. CHILDRENS HOSP LOS ANGELES,DEPT PEDIAT,LOS ANGELES,CA 90027. UNIV SO CALIF,SCH MED,DEPT MICROBIOL,LOS ANGELES,CA 90027. UNIV CALIF LOS ANGELES,SCH MED,BRAIN RES INST,LOS ANGELES,CA 90024. NR 27 TC 29 Z9 31 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD OCT PY 1994 VL 54 IS 1-2 BP 99 EP 108 DI 10.1016/0165-5728(94)90236-4 PG 10 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA PL703 UT WOS:A1994PL70300012 PM 7929807 ER PT J AU KEATING, PA LINDBLOM, B LUBKER, J KREIMAN, J AF KEATING, PA LINDBLOM, B LUBKER, J KREIMAN, J TI VARIABILITY IN JAW HEIGHT FOR SEGMENTS IN ENGLISH AND SWEDISH VCVS SO JOURNAL OF PHONETICS LA English DT Article ID SPEECH; DYNAMICS AB This study compares the extent of coarticulatory influences of vowels on consonants and consonants on vowels in VCV utterances from English and Swedish speakers. Three vowels and ten consonants form the VCV utterances, with V1 = V2 and the nuclear stress on the second vowel. The measure of coarticulation is the vertical height of the jaw, which was determined using the Stockholm University Movetrack magnetometer system. Results of the experiment indicate that the two languages behave similarly overall, and that vowels are overall more open and overall more variable than are consonants. However, little of the variation in vowel height is attributable to consonant context, whereas much of the variation in consonant height is attributable to vowel context, and the effect of vowel context on consonant height is statistically reliable whereas the effect of consonant context on vowel height is not. These results support the proposal by Lindbolm (1983) that consonant segments may accommodate their jaw heights to those of neighboring vowels. The results also weakly support his proposal that consonants differ in their propensity to coarticulate, with alveolar consonants showing less effect of vowel context and /h/ the most. C1 UNIV STOCKHOLM,DEPT LINGUIST,STOCKHOLM,SWEDEN. UNIV VERMONT,COLL ARTS & SCI,BURLINGTON,VT 05405. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP KEATING, PA (reprint author), UNIV CALIF LOS ANGELES,DEPT LINGUIST,PHONET LAB,LOS ANGELES,CA 90024, USA. NR 26 TC 36 Z9 36 U1 0 U2 1 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0095-4470 J9 J PHONETICS JI J. Phon. PD OCT PY 1994 VL 22 IS 4 BP 407 EP 422 PG 16 WC Linguistics; Language & Linguistics SC Linguistics GA QB576 UT WOS:A1994QB57600004 ER PT J AU ZWEBEN, JE CLARK, HW AF ZWEBEN, JE CLARK, HW TI TRAUMATIC EXPERIENCES AND SUBSTANCE-ABUSE - INTRODUCTION SO JOURNAL OF PSYCHOACTIVE DRUGS LA English DT Article C1 UNIV CALIF SAN FRANCISCO,SCH MED,SAN FRANCISCO,CA 94143. SAN FRANCISCO VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBSTANCE ABUSE SERV,SAN FRANCISCO,CA. RP ZWEBEN, JE (reprint author), FOURTEENTH ST CLIN & MED GRP & E BAY COMMUNITY RECOVERY PROJECT,OAKLAND,CA, USA. NR 0 TC 0 Z9 0 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 1994 VL 26 IS 4 BP 323 EP 325 PG 3 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA PY835 UT WOS:A1994PY83500001 ER PT J AU ZWEBEN, JE CLARK, HW SMITH, DE AF ZWEBEN, JE CLARK, HW SMITH, DE TI TRAUMATIC EXPERIENCES AND SUBSTANCE-ABUSE - MAPPING THE TERRITORY SO JOURNAL OF PSYCHOACTIVE DRUGS LA English DT Article DE ADDICTION; RECOVERY-ORIENTED THERAPY; SUBSTANCE ABUSE; TRAUMATIC EXPERIENCES; POSTTRAUMATIC STRESS DISORDER ID POSTTRAUMATIC-STRESS-DISORDER; VIETNAM VETERANS; DISSOCIATIVE EXPERIENCES; GENERAL-POPULATION; PHYSICAL ABUSE; VICTIMIZATION; INPATIENTS; SYMPTOMS; RECOVERY AB This article examines the relationships between various types of traumatic experiences and addictive behavior, with an eye to formulating effective treatment strategies. Interventions in the posttraumatic stress disorder (PTSD) and related fields are reviewed in an effort to understand how best to integrate them into substance abuse treatment. The recovery-oriented therapy model is used as a framework to define treatment tasks at each stage of the recovery process: how one addresses painful issues depends on the objective, given the recovery stage at hand. These tasks include making a commitment to abstinence, stopping alcohol and other drug use, consolidating abstinence and changing lifestyles, and addressing short- and long-term psychosocial issues. The article focuses on the clinical features of PTSD in an effort to enhance the practitioner's ability to address this disorder within the context of substance abuse treatment. Finally, recommendations are offered for training practitioners at varying skill levels in the addiction treatment field. C1 FOURTEENTH ST CLIN & MED GRP & E BAY COMMUNITY RECOVERY PROJECT,OAKLAND,CA. UNIV CALIF SAN FRANCISCO,SCH MED,SAN FRANCISCO,CA 94143. HAIGHT ASHBURY FREE MED CLIN INC,SAN FRANCISCO,CA. MERRITH PERALTA INST,OAKLAND,CA. SAN FRANCISCO VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBSTANCE ABUSE SERV,SAN FRANCISCO,CA. NR 64 TC 53 Z9 54 U1 1 U2 7 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 1994 VL 26 IS 4 BP 327 EP 344 PG 18 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA PY835 UT WOS:A1994PY83500002 PM 7884595 ER PT J AU GERETY, MB WILLIAMS, JW MULROW, CD CORNELL, JE KADRI, AA ROSENBERG, J CHIODO, LK LONG, M AF GERETY, MB WILLIAMS, JW MULROW, CD CORNELL, JE KADRI, AA ROSENBERG, J CHIODO, LK LONG, M TI PERFORMANCE OF CASE-FINDING TOOLS FOR DEPRESSION IN THE NURSING-HOME - INFLUENCE OF CLINICAL AND FUNCTIONAL-CHARACTERISTICS AND SELECTION OF OPTIMAL THRESHOLD SCORES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID RESEARCH DIAGNOSTIC-CRITERIA; MAJOR DEPRESSION; MEDICAL OUTCOMES; ALZHEIMER TYPE; SCALE; DEMENTIA; COMMUNITY; CARE; MORTALITY; INVENTORY AB OBJECTIVE: To compare case-finding tools for depression in the nursing home setting and to evaluate effects of subject function, cognition, and disease number on test performance. DESIGN: Cross-sectional survey. SETTING: One academic and four community homes. SUBJECTS: One hundred thirty-four randomly selected, mildly cognitively impaired, functionally dependent residents. METHODS AND MEASURES: The Geriatric Depression Scale (GDS), Short Geriatric Depression Scale (SGDS), Center for Epidemiologic Studies Depression Scale (CES-D), and Brief Carrol Depression Rating Scale (BCDRS) were administered. The Structured Clinical Interview for DSM-III-R diagnoses was administered independently,. Operating characteristics and the effects of subject characteristics on test performance were evaluated using McNemar's test and logistic regression. Selection of ''optimal'' threshold scores was guided by Kraemer's quality indices and clinical judgment. RESULTS: Thirty-five subjects (26%) had major depression. No differences were found among the instruments in sensitivity (range 0.74-0.89), specificity (range 0.62-0.77), or area under the receiver operating curve (ROC) (range 0.85-0.91). Resident characteristics did not affect test performance. Quality indices showed the GDS and BCDRS met criteria for moderate to substantial agreement with the criterion standard, whereas the SGDS and the CES-D achieved only fair agreement. No change in threshold scores was warranted. CONCLUSIONS: The GDS and BCDRS performed well in the nursing home. As the GDS can serve as a both a case-finding and severity instrument, it is preferred. Use of brief, interviewer-administered tools may improve detection of depression in the nursing home. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. RP GERETY, MB (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 FU AHRQ HHS [1-U01-HS07397-02]; NIA NIH HHS [NIA UO1AG09117] NR 48 TC 120 Z9 121 U1 0 U2 3 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 OCT PY 1994 VL 42 IS 10 BP 1103 EP 1109 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA PK179 UT WOS:A1994PK17900012 PM 7930337 ER PT J AU GERETY, MB AF GERETY, MB TI ADVERSE EVENTS - RELATED TO DRUGS OR IATROGENIC - REPLY SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Letter C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. RP GERETY, MB (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD OCT PY 1994 VL 42 IS 10 BP 1132 EP 1133 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA PK179 UT WOS:A1994PK17900020 ER PT J AU KREISBERG, JI GARONI, JA RADNIK, R AYO, SH AF KREISBERG, JI GARONI, JA RADNIK, R AYO, SH TI HIGH GLUCOSE AND TGF-BETA(1), STIMULATE FIBRONECTIN GENE-EXPRESSION THROUGH A CAMP RESPONSE ELEMENT SO KIDNEY INTERNATIONAL LA English DT Article ID GROWTH-FACTOR-BETA; SIGNAL TRANSDUCTION PATHWAYS; MESANGIAL CELLS; TRANSCRIPTIONAL ACTIVATION; CYCLIC-AMP; INDUCED BINDING; PROTEINS; FAMILY; PHOSPHORYLATION; INCREASE AB Previously, we reported that mesangial cells increased fibronectin, laminin and type IV collagen synthesis when cultured in the presence of high glucose (30 mM). Although mRNA levels for all three extracellular matrix (ECM) proteins were also increased in high glucose conditions, the mechanism for this increase was not known. In order to determine whether increased transcription was involved in the observed increase in fibronectin mRNA levels mesangial cells were transfected with a construct containing the 5'-flanking region of the fibronectin (FN) gene [position +69 to -510 base pairs (bp)] fused to the coding region of the chloramphenicol acetyltransferase (CAT) gene [FN-CAT (-510)]. Cells were transiently and stably transfected with this construct. Under serum-free conditions, high glucose increased CAT activity only in the presence of TGF beta(1) (referred to as TGF beta). The experiments were performed without serum because FN-CAT (-510) contains a serum responsive element. The increase in CAT was approximately twofold in transiently transfected cells and threefold in stably transfected cells. TGF beta alone increased CAT activity approximately 30%. Stimulation of fibronectin gene expression appeared to occur at the level of a cAMP response element (CRE) located -170 bp of the FN gene because cells transfected with a construct containing an oligonucleotide encoding for this CRE fused to a minimal fibronectin promoter (-56 bp) and a CAT reporter gene [CRE (-170) FN-CAT] displayed similar increments of CAT activity after treatment with high glucose and TGF beta. Gel shift mobility assays with a CRE oligonucleotide revealed multiple complexes with mesangial cell nuclear proteins. No differences in the mobility or abundance of complexes were observed in the different conditions tested. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP KREISBERG, JI (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 37 TC 48 Z9 49 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD OCT PY 1994 VL 46 IS 4 BP 1019 EP 1024 DI 10.1038/ki.1994.362 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA PH786 UT WOS:A1994PH78600009 PM 7861696 ER PT J AU ABSHER, JR SULTZER, DL MAHLER, ME FISHMAN, J AF ABSHER, JR SULTZER, DL MAHLER, ME FISHMAN, J TI P(C) ANALYSIS FACILITATES DEMENTIA DIAGNOSIS SO MEDICAL DECISION MAKING LA English DT Article DE DEMENTIA; MULTIINFARCT; ALZHEIMERS DISEASE; DIAGNOSTIC TESTS; ROC ANALYSIS ID MULTI-INFARCT DEMENTIA; ADRDA WORK GROUP; ALZHEIMERS-DISEASE; CLINICAL-DIAGNOSIS; DIFFERENTIATION; ACCURACY; SCALE; TESTS AB A modified receiver operating characteristic (ROC) analysis technique was applied to a sample of 161 consecutive volunteers seen in a dementia clinic. Clinical, imaging, neuropsychological, and laboratory evaluation guided experienced clinicians in clinical diagnosis, taken as the ''gold standard.'' Two symptom inventories, the Hachinski Ischemic Score and the Dementia of the Alzheimer's Type Inventory, were obtained by clinicians who were blind to final clinical diagnosis; scores on these inventories correlate with the likelihoods of multiinfarct dementia and Alzheimer's disease, respectively. A disjunctive sequential testing strategy was analyzed such that subthreshold scores on the first test identified patients for whom the second test was considered. Both tests were analyzed at all possible cutoff-point combinations and in both possible testing sequences. Diagnoses based on these tests were compared with the clinical ''gold standard'' diagnoses to determine the accuracy of the testing procedures. The best strategy correctly classified 154/161 (95.6%) of the dementia patients and required cutoff points (5 for the HIS and 10 for the Dementia of the Alzheimer's Type Inventory) that were lower than those usually recommended for either test used alone (i.e., 7 and 14, respectively). The Hachinski Ischemic Score-then Dementia of the Alzheimer's Type inventory testing sequence was superior to the reverse strategy. A sensitivity analysis (varying prevalences of Alzheimer's disease, multi-infarct dementia, and other dementias) revealed similar test Performances across a wide range of prevalences. These data suggest. that simple clinical tests that take approximately 30 minutes to administer can produce diagnostic classifications of dementia that are similar to those of clinicians experienced in dementia diagnosis. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,BEHAV NEUROSCI SECT,PSYCHIAT SERV,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,NEUROBEHAV PROGRAM,LOS ANGELES,CA. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. FU NIA NIH HHS [AG00172, AG00260]; NIMH NIH HHS [MH00910] NR 30 TC 2 Z9 2 U1 0 U2 0 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 OCT-DEC PY 1994 VL 14 IS 4 BP 393 EP 402 DI 10.1177/0272989X9401400410 PG 10 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA PL433 UT WOS:A1994PL43300010 PM 7808214 ER PT J AU CUMMINGS, JL AF CUMMINGS, JL TI DEPRESSION IN NEUROLOGIC DISEASES SO PSYCHIATRIC ANNALS LA English DT Article ID STROKE C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHIAT SERV, BEHAV NEUROSCI SECT, LOS ANGELES, CA USA. NR 25 TC 8 Z9 8 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD OCT PY 1994 VL 24 IS 10 BP 525 EP 531 PG 7 WC Psychiatry SC Psychiatry GA PP675 UT WOS:A1994PP67500006 ER PT J AU CASTELLON, SA ASARNOW, RF GOLDSTEIN, MJ MARDER, SR AF CASTELLON, SA ASARNOW, RF GOLDSTEIN, MJ MARDER, SR TI PERSISTING NEGATIVE SYMPTOMS AND INFORMATION-PROCESSING DEFICITS IN SCHIZOPHRENIA - IMPLICATIONS FOR SUBTYPING SO PSYCHIATRY RESEARCH LA English DT Article DE SPAN OF APPREHENSION TEST; PROGNOSIS; DEFICIT SYNDROME OF SCHIZOPHRENIA; ATTENTION ID POSITIVE SYMPTOMS; NONDEFICIT FORMS; BACKWARD-MASKING; VULNERABILITY; FLUPHENAZINE; DEFINITION AB To test the hypothesis that schizophrenic patients with persisting negative symptoms have stable information-processing impairments compared with schizophrenic patients without persisting negative symptoms, 20 chronic schizophrenic outpatients were trichotomously subgrouped on the basis of the level of negative symptoms that they displayed across multiple rating periods over a 1-year period. Brief Psychiatric Rating Scale assessments of negative symptoms were used to assign subjects into either an operationally defined persisting negative symptom (PNS), transient negative symptom (TNS), or no negative symptom (NNS) subgroup. The level and pattern of these subgroups' performance on a visual information-processing task, the Span of Apprehension Test (SPAN), were compared. Although the three groups did not differ statistically in level of SPAN performance during a drug-free baseline, the PNS group had significantly poorer SPAN performance than the other two groups at the 1-year followup assessment. The SPAN performance of the TNS and NNS groups improved while the SPAN performance of the PNS group did not improve over the 1-year followup period. C1 UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,PSYCHIAT SPECIAL PROGRAMS,LOS ANGELES,CA. FU NIMH NIH HHS [MH-45112] NR 31 TC 7 Z9 8 U1 0 U2 0 PU ELSEVIER SCI PUBL 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 OCT PY 1994 VL 54 IS 1 BP 59 EP 69 DI 10.1016/0165-1781(94)90065-5 PG 11 WC Psychiatry SC Psychiatry GA QC481 UT WOS:A1994QC48100006 PM 7701029 ER PT J AU FRUEH, BC MIRABELLA, RF CHOBOT, K FOSSEY, MD AF FRUEH, BC MIRABELLA, RF CHOBOT, K FOSSEY, MD TI CHRONICITY OF SYMPTOMS IN COMBAT VETERANS WITH PTSD TREATED BY THE VA MENTAL-HEALTH SYSTEM SO PSYCHOLOGICAL REPORTS LA English DT Article; Proceedings Paper CT 9th Annual Meeting of the International-Society-for-Traumatic-Stress-Studies CY OCT 24-27, 1993 CL SAN ANTONIO, TX SP Int Soc Traumat Stress Studies ID POSTTRAUMATIC-STRESS-DISORDER; VIETNAM COMBAT; RELIABILITY; VALIDITY; SCALE AB Self-report questionnaire data, collected at two stages of treatment, are presented for a group of 40 combat veterans with PTSD treated within the VA mental health system. Patients completed the Beck Depression Inventory, Mississippi Scale, and Dissociative Experiences Scale prior to treatment at a PTSD outpatient clinic and at midtreatment follow-up. Patients' symptom reports at follow-up were not correlated with length of time in treatment. Further, results suggest that patients' self-reported symptoms on these measures do not show evidence of improvement after entry into the VA mental health system. Explanations for this apparent chronicity of symptoms are discussed. RP FRUEH, BC (reprint author), RALPH H JOHNSON VET AFFAIRS MED CTR,PSYCHOL SERV 116B,109 BEE ST,CHARLESTON,SC 29401, USA. NR 20 TC 9 Z9 9 U1 1 U2 1 PU PSYCHOLOGICAL REPORTS PI MISSOULA PA P O BOX 9229, MISSOULA, MT 59807 SN 0033-2941 J9 PSYCHOL REP JI Psychol. Rep. PD OCT PY 1994 VL 75 IS 2 BP 843 EP 848 PG 6 WC Psychology, Multidisciplinary SC Psychology GA PR104 UT WOS:A1994PR10400024 PM 7862794 ER PT J AU KENNEDY, EM HARMS, BA STARLING, JR AF KENNEDY, EM HARMS, BA STARLING, JR TI ABSENCE OF MALADAPTIVE NEURONAL PLASTICITY AFTER GENITOFEMORAL-ILIOINGUINAL NEURECTOMY SO SURGERY LA English DT Article; Proceedings Paper CT 51st Annual Meeting of the Central-Surgical-Association CY MAR 03-05, 1994 CL CHICAGO, IL SP CENT SURG ASSOC ID NEURALGIA; PAIN; DIAGNOSIS AB Background. Pain (neuralgia) and paresthesia in the inguinal region after lower abdominal of various medications. The management of chronic pain syndromes is often coordinated by anesthesiologists. Neurolytic therapy is seldom recommended, on the basis of the theory of Methods. Twenty-three patients underwent genitofemoral neurectomy at our institution between 1981 and 1990. Records were reviewed to determine preoperative symptoms, evaluation, and treatment. Patients were contacted and questioned about current symptoms and disability. Results. All records were reviewed. Sixteen (70%) of the patients were located for long-term follow-up. Patients were symptomatic for an average of 3.3 years and underwent 3.1 operations before referral. Inguinal herniorrhaphy was the most common initial surgery (14 of 16 patients). All patients underwent multidisciplinary evaluation. Fifteen underwent L(1-2) paraspinous nerve block, and 13 had total pain relief Postoperative follow-up ranged from 36 to 144 months. Ten patients reported significant pain relief and three patients reported slight improvement. Three of the six patients who had persistent neuralgia had significant orchialgia. None of the patients who had significant relief had preoperative testicular pain. Conclusions. Genitofemoral neurectomy provided long-term relief in 62.5% of patients with genitofemoral neuralgia. Severe testicular pain indicated a less favorable outcome. These data do not support the maladaptive neuronal plasticity theory but do support early referral of some patients for neurectomy. C1 UNIV WISCONSIN HOSP & CLIN,DEPT SURG,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,SURG SERV,MADISON,WI. NR 14 TC 14 Z9 14 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 1994 VL 116 IS 4 BP 665 EP 671 PG 7 WC Surgery SC Surgery GA PK681 UT WOS:A1994PK68100011 PM 7940164 ER PT J AU LAWRENCE, VA BIRCH, S GAFNI, A AF LAWRENCE, VA BIRCH, S GAFNI, A TI IMPACT OF NEW CLINICAL GUIDELINES ON THE NORTH-AMERICAN BLOOD ECONOMY SO TRANSFUSION MEDICINE REVIEWS LA English DT Article ID PHARMACEUTICAL MANUFACTURING APPROACH; TRANSFUSION MEDICINE; CELL TRANSFUSION; UNITED-STATES; COLLECTION; CONTROVERSIES; STRATEGIES; SURGERY; BANKS C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. MCMASTER UNIV,HLTH SCI CTR,CTR HLTH ECON & POLICY ANAL,DEPT CLIN EPIDEMIOL & BIOSTAT,HAMILTON,ON,CANADA. RP LAWRENCE, VA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 40 TC 5 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0887-7963 J9 TRANSFUS MED REV JI Transf. Med. Rev. PD OCT PY 1994 VL 8 IS 4 BP 232 EP 241 DI 10.1016/S0887-7963(94)70115-2 PG 10 WC Hematology SC Hematology GA PL840 UT WOS:A1994PL84000002 PM 7841667 ER PT J AU MANTHEY, CL PERERA, PY HENRICSON, BE HAMILTON, TA QURESHI, N VOGEL, SN AF MANTHEY, CL PERERA, PY HENRICSON, BE HAMILTON, TA QURESHI, N VOGEL, SN TI ENDOTOXIN-INDUCED EARLY GENE-EXPRESSION IN C3H/HEJ (LPS(D)) MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CHEMOTYPE LIPOPOLYSACCHARIDE PREPARATIONS; PERMEABILITY-INCREASING PROTEIN; AMINO-TERMINAL FRAGMENT; LIPID-A; MURINE MACROPHAGES; TYROSINE PHOSPHORYLATION; GAMMA-INTERFERON; MONONUCLEAR PHAGOCYTES; PERITONEAL-MACROPHAGES; C3H-HEJ LYMPHOCYTES AB C3H/HeJ (Lps(d)) macrophages have been shown to respond to certain LPSs, especially from rough mutant bacteria. C3H/OuJ (Lps(n)) macrophages are induced by wild-type LPS, rough LPS, or lipid A to express many genes, including TNF-alpha, TNFR-2, IL-1 beta, IP-10, D3, and D8. C3H/HeJ macrophages failed to induce any of these genes when cultured with wild-type LPS or synthetic lipid A, even when pretreated with IFN-gamma. However, rough mutant Salmonella minnesota Ra, Rc, and Rd LPS, and Escherichia coli D31 m3 Rd LPS induced Lps(d) macrophages to express a subset of genes within the gene panel. Because bioactive preparations contained trace quantities of endotoxin protein(s), a deoxycholate-modified, phenol-water method was used to repurify rough LPS into an aqueous phase, and extract endotoxin proteins into a phenol phase. Repurified LPS failed to stimulate Lps(d) macrophages; however, phenol fractions were similar to 10% as potent in Lps(d) macrophages as crude rough LPS. Full potency was restored in C3H/HeJ macrophages when aqueous phase LPS and phenol-phase proteins were coprecipitated, suggesting that LPS and endotoxin proteins interact synergistically. Endotoxin proteins alone induced TNF-alpha, TNFR-2, and IL-1 beta, but not IP-10, D3, and D8 genes in both Lps(d) and Lps(n) macrophages. Tyrosine phosphorylation of three 41- to 47-kDa proteins was induced by endotoxin proteins, but not by LPS, in Lps(d) macrophages. Thus, endotoxin proteins seem to activate a signaling pathway(s) that converges (distal to the Lps gene product) with a subset of LPS-signaling pathways. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL & IMMUNOL,BETHESDA,MD 20814. CLEVELAND CLIN FDN,RES INST,CLEVELAND,OH 44195. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,SCH AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NCI NIH HHS [CA39621]; NIAID NIH HHS [AI-08451, AI-18797] NR 47 TC 106 Z9 106 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 SEP 15 PY 1994 VL 153 IS 6 BP 2653 EP 2663 PG 11 WC Immunology SC Immunology GA PF189 UT WOS:A1994PF18900031 PM 7521367 ER PT J AU KALIN, NH TAKAHASHI, LK CHEN, FL AF KALIN, NH TAKAHASHI, LK CHEN, FL TI RESTRAINT STRESS INCREASES CORTICOTROPIN-RELEASING HORMONE MESSENGER-RNA CONTENT IN THE AMYGDALA AND PARAVENTRICULAR NUCLEUS SO BRAIN RESEARCH LA English DT Note DE STRESS; CORTICOTROPIN RELEASING HORMONE; MESSENGER-RNA; AMYGDALA; HYPOTHALAMUS ID FACTOR-LIKE IMMUNOREACTIVITY; MESSENGER RIBONUCLEIC-ACID; RAT-BRAIN REGIONS; DIFFERENTIAL REGULATION; FACTOR RECEPTORS; RNA; RESPONSES; CATECHOLAMINES; HYPOTHALAMUS; ANTAGONISM AB Corticotropin-releasing hormone (CRH) neurons located in the paraventricular nucleus (PVN) of the hypothalamus are implicated in regulating the endocrine response to stress. The amygdala is an established component of the neural circuitry mediating the stress response, To obtain information concerning the effects of stress on amygdala CRH neurons, a time-course study was conducted to examine, in rats, whether a 1-h restraint period increases CRH mRNA levels. The effects of restraint were also measured in the PVN. Using a sensitive RNase protection assay, we found that CRH mRNA levels in both the amygdala and paraventricular nucleus were significantly elevated 1 h after cessation of restraint. CRH mRNA levels in the paraventricular nucleus, but not the amygdala, remained elevated at the 3-h post-stress interval. 48 h after the termination of restraint, CRH mRNA levels in both brain structures returned to control levels. These data provide the first direct evidence that stress activates amygdala CRH neurons. C1 UNIV WISCONSIN,DEPT PSYCHOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. RP KALIN, NH (reprint author), UNIV WISCONSIN,DEPT PSYCHIAT,MADISON,WI 53792, USA. FU NIMH NIH HHS [MH-40855] NR 24 TC 169 Z9 172 U1 1 U2 7 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 5 PY 1994 VL 656 IS 1 BP 182 EP 186 DI 10.1016/0006-8993(94)91382-X PG 5 WC Neurosciences SC Neurosciences & Neurology GA PD957 UT WOS:A1994PD95700023 PM 7804835 ER PT J AU RABENECK, L AF RABENECK, L TI BECAUSE ITS THERE - IT WAS MALLORY, NOT HILLARY SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Letter RP RABENECK, L (reprint author), DEPT VET AFFAIRS MED CTR,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD SEP PY 1994 VL 89 IS 9 BP 1601 EP 1601 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PE994 UT WOS:A1994PE99400054 PM 8079958 ER PT J AU LEUCHTER, A SIMON, SL DALY, KA ABRAMS, M ROSENBERGTHOMPSON, S DUNKIN, JJ COOK, IA NEWTON, TF SPAR, JE AF LEUCHTER, A SIMON, SL DALY, KA ABRAMS, M ROSENBERGTHOMPSON, S DUNKIN, JJ COOK, IA NEWTON, TF SPAR, JE TI QUANTITATIVE EEG CORRELATES OF OUTCOME IN OLDER PSYCHIATRIC-PATIENTS .2. 2-YEAR FOLLOW-UP OF PATIENTS WITH DEPRESSION SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article ID LATE-LIFE DEPRESSION; GERIATRIC DEPRESSION; COGNITIVE IMPAIRMENT; REVERSIBLE DEMENTIA; PROGNOSIS; AGE; RELAPSE; ILLNESS AB The authors examined quantitative electroencephalographic (QEEG) coherence in 3 7 depressed elderly patients and performed 2-year follow-up evaluations. All subjects had equivocal cognitive impairment, but none had delirium or dementia. More than 40% (16/37) recovered from depression, and 38% (14/37) remained well for 2 years. Twenty-four percent (n = 9) had died within 2 years, most from cardiac causes. Low trans-Rolandic coherence from the left hemisphere was strongly associated with mortality: 44% (7/16) of those with low coherence died, and 78% (7/9) of those who died had low coherence. Among survivors (n = 28) at follow-up, low coherence was significantly associated with lower functional status. These findings suggest that the coherence variable measures actual neurophysiologic differences between groups of depressed patients and these differences are associated with the heterogeneous outcomes of depression in elderly patients. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. W LOS ANGELES VA MED CTR, PSYCHIAT SERV, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, NEUROPSYCHIAT INST & HOSP, QUANTITAT EEG LAB, LOS ANGELES, CA USA. NR 46 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD FAL PY 1994 VL 2 IS 4 BP 290 EP 299 PG 10 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA PJ695 UT WOS:A1994PJ69500004 ER PT J AU BARNES, JL HASTINGS, RR DELAGARZA, MA AF BARNES, JL HASTINGS, RR DELAGARZA, MA TI SEQUENTIAL EXPRESSION OF CELLULAR FIBRONECTIN BY PLATELETS, MACROPHAGES, AND MESANGIAL CELLS IN PROLIFERATIVE GLOMERULONEPHRITIS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HABU SNAKE-VENOM; SMOOTH-MUSCLE ACTIN; GROWTH-FACTOR-BETA; EXTRACELLULAR-MATRIX; GENE-EXPRESSION; GLOMERULAR-DISEASES; HUMAN-KIDNEY; RAT; LOCALIZATION; RECEPTORS AB Fibronectin (Fn) regulates cell migration, proliferation, and extracellular matrix formation during embryogenesis, angiogenesis, and wound healing. Fn also promotes mesangial cell migration and proliferation in vitro and contributes to extracellular matrix formation and tissue remodeling during glomerular disease. In this study, we examined, by immunohistochemistry and in situ hybridization, the temporal glomerular localization and cellular sources of Fn in Habu snake venom (HSV)-induced proliferative glomerulonephritis. Early HSV-induced glomerular lesions consisted of microaneurysms devoid of resident glomerular cells and filled with platelets, leukocytes, and erythrocytes. Over the course of the disease, mesangial cells migrated into the lesions, proliferated, and formed a confluent cellular mass. Fn was present in lesions beginning at 8 hours, with highest intensity at 72 hours and diminishing at 2 weeks after HSV. Staining for Fn at 8 and 24 hours after HSV was attributed to platelets and macrophages. In situ hybridization and phenotypic identification of cell types within lesions revealed macrophages as the predominant source of cellular Fn mRNA at these times. At 48 hours after HSV, Fn mRNA was expressed in proliferating mesangial cells in addition to macrophages. Most cells in lesions at 72 hours after HSV were mesangial, at a time when expression of Fn mRNA peaked. Cellular expression for Fn mRNA and translated protein declined at 2 weeks after HSV. These studies support the hypothesis that Fn, derived from platelets and macrophages, provides a provisional matrix involved with mesangial cell migration into glomerular lesions. Fn produced by mesangial cells might contribute to the formation of a stable extracellular matrix. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP BARNES, JL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK38758] NR 56 TC 57 Z9 58 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 1994 VL 145 IS 3 BP 585 EP 597 PG 13 WC Pathology SC Pathology GA PG110 UT WOS:A1994PG11000012 PM 8080041 ER PT J AU LIN, CM MUSCH, M MEO, P ZEBROWITZ, J CHANG, E KLEYMAN, TR AF LIN, CM MUSCH, M MEO, P ZEBROWITZ, J CHANG, E KLEYMAN, TR TI ANTIIDIOTYPIC ANTIBODIES TO DELINEATE EPITOPE SPECIFICITY OF ANTI-AMILORIDE ANTIBODIES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MONOCLONAL ANTIBODIES; SODIUM ION/HYDROGEN ION EXCHANGE ID DISTINCT EPITOPES; NA+ CHANNELS; RECEPTOR; ANALOG AB Amiloride and related compounds have found widespread use as cation transport inhibitors. We have previously raised a series of polyclonal anti-amiloride antibodies using different amiloride-protein conjugates as immunogens, where amiloride was coupled to protein either through its guanidino moiety or through its 5-aminopyrazinyl moiety. The anti-amiloride antibodies recognized distinct sites on amiloride, and the site of attachment of amiloride to carrier protein was a critical factor in determining which part of the amiloride molecule was recognized by the anti-amiloride antibody. The specificity of binding of amiloride analogues to these polyclonal anti-amiloride antibodies mimicked the specificity of binding of amiloride analogues to selected isoforms of the epithelial Na+ channel or the Na+/H+ exchanger, suggesting that antigen binding site of these antibodies might be similar in structure to amiloride binding sites on selected Nai transport proteins. We previously generated monoclonal antiidiotypic antibodies RA2.4 and RA6.3 by an auto-anti-idiotypic approach, using amiloride coupled to albumin through the guanidinium moiety (amiloride-A1). We have now raised a series of monoclonal anti-idiotypic antibodies, T6, T26, T40, and T181, using amiloride coupled to keyhole limpet hemocyanin through the 5-aminopyrazinyl moiety (amiloride-A5) as an immunogen with the same auto-anti-idiotypic approach. These monoclonal anti-idiotypic antibodies recognized both polyclonal anti-amiloride-Al and anti-amiloride-A5 antibodies, suggesting that idiotype-anti-idiotype interaction was not epitope restricted. Competitive inhibition studies demonstrated that the binding of monoclonal antibodies T6 and T40 to the anti-amiloride-A5 antibody is inhibited by amiloride and 5-(N-ethyl-N-isopropyl)amiloride, suggesting that T6 and T40 bind at or near the amiloride binding site of the anti-amiloride-A5 antibody. The monoclonal antibody T6 inhibited Na+/H+ exchange activity of the brush border of chicken enterocytes by 19%, suggesting that this antibody might interact with the amiloride binding site on the Na+/H+ exchanger. C1 UNIV PENN,VET AFFAIRS MED CTR,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,VET AFFAIRS MED CTR,DEPT PHYSIOL,PHILADELPHIA,PA 19104. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. FU NIDDK NIH HHS [DK-42086, DK-38510] NR 16 TC 3 Z9 3 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD SEP PY 1994 VL 267 IS 3 BP C821 EP C826 PN 1 PG 6 WC Physiology SC Physiology GA PH382 UT WOS:A1994PH38200019 PM 7524337 ER PT J AU LONDON, MJ SHROYER, AL GROVER, FL SETHI, GK MARSHALL, G MORITZ, T TOBLER, HG MCCARTHY, MJ HENDERSON, W HAMMERMEISTER, KE AF LONDON, MJ SHROYER, AL GROVER, FL SETHI, GK MARSHALL, G MORITZ, T TOBLER, HG MCCARTHY, MJ HENDERSON, W HAMMERMEISTER, KE TI EVALUATING ANESTHESIA HEALTH-CARE-DELIVERY FOR CARDIAC-SURGERY - THE ROLE OF PROCESS AND STRUCTURE VARIABLES SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 UNIV COLORADO,HLTH SCI CTR,DENVER VAMC,DEPT ANESTHESIOL,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DENVER VAMC,DEPT CARDIOL,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DENVER VAMC,DEPT CARDIAC SURG,DENVER,CO 80220. RI Shroyer, Annie Laurie/B-8836-2016 OI Shroyer, Annie Laurie/0000-0001-6461-0623 NR 1 TC 0 Z9 0 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 SEP PY 1994 VL 81 IS 3A SU S BP A1255 EP A1255 PG 1 WC Anesthesiology SC Anesthesiology GA PJ091 UT WOS:A1994PJ09101254 ER PT J AU DHAUNSI, GS SINGH, I ORAK, JK SINGH, AK AF DHAUNSI, GS SINGH, I ORAK, JK SINGH, AK TI ANTIOXIDANT ENZYMES IN CIPROFIBRATE-INDUCED OXIDATIVE STRESS SO CARCINOGENESIS LA English DT Article ID RAT-LIVER PEROXISOMES; PROLIFERATOR-INDUCED HEPATOCARCINOGENESIS; SUPEROXIDE-DISMUTASE; ENDOPLASMIC-RETICULUM; BETA-OXIDATION; GLUTATHIONE-PEROXIDASE; HYPOLIPIDEMIC DRUGS; FATTY-ACIDS; PROTEIN; CLOFIBRATE AB To understand the mechanism of peroxisome proliferator-induced oxidative stress in non-mutagenic carcinogenesis, the effect of ciprofibrate, a peroxisome proliferator, on the activities and protein amounts of various antioxidant enzymes in different subcellular compartments was examined. Ciprofibrate treatment for short-term (3 weeks) as well as long-term (12 weeks) duration increased the total cellular catalase activity, whereas superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were decreased significantly. Withdrawal of ciprofibrate from the diet did not normalize these activities. The observed decreases in total cellular SOD and GPX activities following ciprofibrate treatment were due to significant decreases in cytosolic CuZn SOD and GPX, whereas mitochondrial levels of Mn SOD and GPX were relatively unchanged. The peroxisomal CuZn SOD acid GPX activities were increased significantly after both short- and long-term treatment, whereas catalase activity was reduced. Western blot analysis of cytoplasm for GPX and CuZn SOD showed a significant decrease in GPX and CuZn SOD proteins. Mitochondrial GPX protein was found to be slightly decreased, whereas Mn SOD protein levels did not show any significant change. The excessive production of H2O2 by oxidases and O-2(-) by the cytochrome P450 enzyme system, along with the observed loss of antioxidant protection by loss of activities of catalase in peroxisomes and GPX and CuZn SOD in cytoplasm, may be the critical factors in peroxisomal proliferator-induced oxidative stress and initiation and promotion of carcinogenesis by this class of non-mutagenic agents. Both enzyme activities, as well as protein amounts of GPX and CuZn SOD, were higher in peroxisomes but lower in cytoplasm in ciprofibrate-treated liver as compared to control liver. The Mn SOD protein was decreased in peroxisomes, whereas mitochondrial Mn SOD was relatively unaffected in ciprofibrate-treated liver as compared to control. These observations suggest that the regulation of expression of peroxisomal CuZn SOD and Mn SOD is different from their counterparts in other cellular compartments. C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VET AFFAIRS MED CTR,DEPT PATHOL & LAB MED,CHARLESTON,SC 29403. FU NINDS NIH HHS [NS-22576] NR 60 TC 34 Z9 36 U1 0 U2 0 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 SEP PY 1994 VL 15 IS 9 BP 1923 EP 1930 DI 10.1093/carcin/15.9.1923 PG 8 WC Oncology SC Oncology GA PJ846 UT WOS:A1994PJ84600024 PM 7923586 ER PT J AU IMAMURA, T MCDERMOTT, PJ KENT, RL NAGATSU, M COOPER, G CARABELLO, BA AF IMAMURA, T MCDERMOTT, PJ KENT, RL NAGATSU, M COOPER, G CARABELLO, BA TI ACUTE CHANGES IN MYOSIN HEAVY-CHAIN SYNTHESIS RATE IN PRESSURE VERSUS VOLUME OVERLOAD SO CIRCULATION RESEARCH LA English DT Article DE HYPERTROPHY; MYOSIN SYNTHESIS RATE; PRESSURE OVERLOAD; VOLUME OVERLOAD ID LEFT-VENTRICULAR FUNCTION; AORTIC-VALVE REPLACEMENT; CHRONIC MITRAL REGURGITATION; PROTEIN-SYNTHESIS; CONTRACTILE FUNCTION; CARDIAC-HYPERTROPHY; ULTRAMICRO METHOD; PERFORMANCE; STENOSIS; HEART AB The left ventricular hypertrophy that develops with the volume overload of mitral regurgitation is relatively less than that which develops with the pressure overload of aortic stenosis even when both lesions are severe, The hypertrophy that develops must be the sum of changes in the rate of myocardial protein synthesis and degradation. In the present canine study, we explored early changes in the synthesis rate of myosin heavy chain in response to severe acute pressure overload versus that of the severe acute volume overload of mitral regurgitation. We tested the hypothesis that in acute overload, the rate of protein synthesis would increase less in the volume-overload model than in the pressure-overload model, a potential partial mechanism for the discrepancy in the eventual total amount of hypertrophy that develops in these two lesions. Acute pressure overload was produced by inflating a balloon in the descending aorta, and acute volume overload was produced by using our closed-chest mitral chordal rupture technique. In both models, the hemodynamic lesion that was created was severe. In eight dogs with pressure overload, the average gradient across the balloon wa 119.8 +/- 6.1 mm Hg. In six dogs with volume overload, the average regurgitant fraction was 0.67 +/- 0.06. Six other dogs served as controls. The average rate of myosin heavy chain synthesis in control dogs was 2.7 +/- 0.2% per day, virtually identical to the rate we found in the severe volume-overload model. In contrast, the rate was increased in the pressure-overload model by 30% to 3.5 +/- 0.3% per day (P<.05). We conclude that the rate of myocardial protein synthesis increases measurably after 6 hours of severe pressure overload but does not after 6 hours of severe volume overload. If these early qualitative differences persisted, they would help explain the relative lack of hypertrophy in the volume overload of mitral regurgitation. C1 MED UNIV S CAROLINA,DEPT MED,DIV CARDIOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. FU NHLBI NIH HHS [NHLBI R01 HL-38185] NR 39 TC 56 Z9 59 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 SEP PY 1994 VL 75 IS 3 BP 418 EP 425 PG 8 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA PC935 UT WOS:A1994PC93500003 PM 8062416 ER PT J AU ELZAATARI, FAK ENGSTRAND, L HACHEM, CY GRAHAM, DY NASER, SA AF ELZAATARI, FAK ENGSTRAND, L HACHEM, CY GRAHAM, DY NASER, SA TI IDENTIFICATION AND CHARACTERIZATION OF MYCOBACTERIUM-PARATUBERCULOSIS RECOMBINANT PROTEINS EXPRESSED IN ESCHERICHIA-COLI SO CURRENT MICROBIOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; CROHNS-DISEASE; IMMUNOLOGICAL ANALYSIS; SEQUENCE DETERMINATION; 65-KILODALTON PROTEIN; PARA-TUBERCULOSIS; CONTROL TISSUES; JOHNES DISEASE; BOVIS BCG; FIBRONECTIN AB Mycobacterium paratuberculosis is the causative agent of Johne's disease, a chronic enteritis in ruminants, and it has also been isolated and identified from patients with Crohn's disease, an inflammatory bowel disease. The control of Johne's disease has been hampered by the lack of a reliable diagnostic test because of the large degree of antigenic cross-reactivity between mycobacterial and non-mycobacterial species. To help identify specific antigen(s) or epitope(s), an M. paratuberculosis expression library was screened with antibodies and DNA probes. In total, 54 clones were randomly picked, purified, and characterized by DNA probes and monoclonal antibodies with known specificity to individual mycobacterial antigens. Four clones carrying the heat shock protein 65K-, two representing the secreted protein 32K-, three representing the 21K-, and 20 clones representing the specific insertion element of M. paratuberculosis (IS900)-encoding genes and their gene products were identified and characterized. Well-defined recombinant antigens and/or epitopes representing M. paratuberculosis may facilitate the development of specific diagnostic tests and the investigation of their role in these chronic diseases. C1 BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. RP ELZAATARI, FAK (reprint author), VET AFFAIRS MED CTR 111D,DEPT MED,INFLAMMATORY BOWEL DIS LAB,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 36 TC 31 Z9 31 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0343-8651 J9 CURR MICROBIOL JI Curr. Microbiol. PD SEP PY 1994 VL 29 IS 3 BP 177 EP 184 DI 10.1007/BF01570760 PG 8 WC Microbiology SC Microbiology GA NX667 UT WOS:A1994NX66700009 PM 7765093 ER PT J AU LYONS, TJ LI, W WELLSKNECHT, MC JOKL, R AF LYONS, TJ LI, W WELLSKNECHT, MC JOKL, R TI TOXICITY OF MILDLY MODIFIED LOW-DENSITY LIPOPROTEINS TO CULTURED RETINAL CAPILLARY ENDOTHELIAL-CELLS AND PERICYTES SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; MONOCYTE-DERIVED MACROPHAGES; CHOLESTERYL ESTER SYNTHESIS; MAILLARD REACTION-PRODUCTS; GLYCEMIC CONTROL; SKIN COLLAGEN; CYTO-TOXICITY; RISK-FACTORS; RETINOPATHY; INSULIN AB To investigate the role of modified low-density lipoproteins (LDL) in the pathogenesis of diabetic retinopathy, we studied the cytotoxicity of normal and mildly modified human LDL to bovine retinal capillary endothelial cells and pericytes in vitro. Pooled LDL was incubated (in phosphate-buffered saline-EDTA, 3 days, 37 degrees C) under 1) nitrogen with additional chelating agents and 2) air, to prepare normal and minimally oxidized LDL, respectively. Similar conditions, but with the addition of 50 mM D-glucose, were used to prepare glycated and glycoxidized LDL. None of the LDL preparations was recognized by the macrophage scavenger receptor, confirming Limited modification. Retinal capillary endothelial cells and pericytes were grown to confluence and then exposed for 2 or 3 days to serum-free medium (1% albumin) supplemented with normal or modified LDL (100 mg/l) or to serum-free medium alone. Cytotoxicity was assessed by cell counting (live and total cells) and by cell protein determination. Compared with normal LDL, modified LDL were cytotoxic to both cell types at both time points, causing highly significant decreases in live and total cell counts (P < 0.001) (analysis of variance). Reductions in cell protein also were significant for pericytes at day 3 (P = 0.016) and of borderline significance for endothelial cells at day 2 (P = 0.05) and day 3 (P = 0.063). Cytotoxicity increased as follows: normal < glycated less than or equal to minimally oxidized < glycoxidized LDL. We conclude that, in diabetes, mild modification of LDL resulting from separate or combined processes of glycation and oxidation may contribute to chronic retinal capillary injury and thus to the development of diabetic retinopathy. C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. UNIV S CAROLINA,DEPT CHEM & BIOCHEM,COLUMBIA,SC 29208. RP LYONS, TJ (reprint author), MED UNIV S CAROLINA,DIV ENDOCRINOL DIABET & METAB,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. FU NIDDK NIH HHS [DK-19971] NR 47 TC 81 Z9 82 U1 0 U2 6 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD SEP PY 1994 VL 43 IS 9 BP 1090 EP 1095 DI 10.2337/diabetes.43.9.1090 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PC974 UT WOS:A1994PC97400002 PM 8070608 ER PT J AU CHERUBIN, CE STRATTON, CW AF CHERUBIN, CE STRATTON, CW TI ASSESSMENT OF THE BACTERICIDAL ACTIVITY OF SPARFLOXACIN, OFLOXACIN, LEVOFLOXACIN, AND OTHER FLUOROQUINOLONES COMPARED WITH SELECTED AGENTS OF PROVEN EFFICACY AGAINST LISTERIA-MONOCYTOGENES SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Article ID INVITRO ACTIVITY; QUINOLONE; SULFAMETHOXAZOLE; TRIMETHOPRIM; MENINGITIS AB The search for alternative therapeutic agents for listeriosis includes the quinolone group. Accordingly, the bactericidal activity of ciprofloxacin, levofloxacin, lomefloxacin, ofloxacin, sparfloxacin, and temofloxacin, in comparison with that of ampicillin and sulfamethoxazole-trimethoprim, was evaluated against Listeria monocytogenes at 24 and 48 h of incubation using time-kill kinetic methodology. The inhibitory concentrations for each agent fell into a narrow range comparable with ampicillin. For example, the minimum inhibitory concentration (MIC) ranges, MIC(90) (24 h), and MIC(90) (48 h) of the most active quinolone, sparfloxacin, were 0.25-2, 2, and 2 mu g/ml, respectively, with 4 mu g/ml achieving greater than or equal to 99.9% killing of the inoculum at 24 h with no regrowth by 48 h. At 2-4 times the MIC, bactericidal activity for all quinolones tested was noted at 24 h, unlike the action of ampicillin, which only becomes bactericidal at 48 h. These concentrations are within the achievable range of serum concentrations for a number of these agents. Because selected new fluoroquinolones at two to four times the MIC show bactericidal activity at 24 h, these agents may prove useful as therapeutic alternatives for the treatment of listeriosis. C1 W LOS ANGELES VET AFFAIRS MED CTR,INFECT DIS SECT,WILKES BARRE,PA. VANDERBILT UNIV,SCH MED,NASHVILLE,TN 37212. NR 21 TC 8 Z9 8 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD SEP PY 1994 VL 20 IS 1 BP 21 EP 25 DI 10.1016/0732-8893(94)90014-0 PG 5 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA PT229 UT WOS:A1994PT22900004 PM 7867294 ER PT J AU HANDFORTH, A TREIMAN, DM AF HANDFORTH, A TREIMAN, DM TI EFFICACY AND TOLERANCE OF LONG-TERM, HIGH-DOSE GABAPENTIN - ADDITIONAL OBSERVATIONS SO EPILEPSIA LA English DT Article DE EPILEPSY; PARTIAL-ONSET SEIZURES; GABAPENTIN; ANTIEPILEPTIC DRUGS; PSYCHOSTIMULATION; ADVERSE EVENTS; TOLERANCE ID SEIZURES AB Gabapentin (GBP) has shown antiepileptic efficacy and good tolerance in clinical trials. Much remains to be learned about its clinical use. As a participating center in the US Gabapentin Study Group, we report observations that have practical implications for patient management. Twenty-three patients with intractable partial-onset seizures initiated open-label treatment after a blinded placebo-controlled add-on dose efficacy study. In the titration phase, GBP and concurrent antiepileptic drugs (AEDs) were adjusted to achieve optimal efficacy on maximally tolerated GBP doses. Nine patients had no significant improvement in seizure control and discontinued GBP. The remaining 14 patients were observed while treated long-term with stable-dose GBP and concurrent AEDs. Improvement was maintained as long as patients were followed: less than or equal to 4 years. The protocol-allowed upper dose limit, 2,400 mg/day, was well tolerated by 16 of 23 patients, indicating that higher doses may be tolerated. GBP discontinuation did net cause rebound increases in seizure frequency. The most common adverse events (AEs) (in 14 of 23) were similar to those induced by concurrent AEDs and responded to reduction of concurrent AEDs. Many patients reported positive psychostimulatory effects. These observations extend previous findings indicating that GBP is an effective and well-tolerated drug for treatment of partial-onset seizures. C1 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. RP HANDFORTH, A (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 13 TC 46 Z9 46 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD SEP-OCT PY 1994 VL 35 IS 5 BP 1032 EP 1037 DI 10.1111/j.1528-1157.1994.tb02551.x PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA PP612 UT WOS:A1994PP61200019 PM 7925148 ER PT J AU HANDFORTH, A TREIMAN, DM AF HANDFORTH, A TREIMAN, DM TI A NEW, NONPHARMACOLOGICAL MODEL OF CONVULSIVE STATUS EPILEPTICUS INDUCED BY ELECTRICAL-STIMULATION - BEHAVIORAL/ELECTROENCEPHALOGRAPHIC OBSERVATIONS AND RESPONSE TO PHENYTOIN AND PHENOBARBITAL SO EPILEPSY RESEARCH LA English DT Article DE STATUS EPILEPTICUS; EXPERIMENTAL SEIZURES; PHENYTOIN; PHENOBARBITAL; TREATMENT ID RODENT MODEL; KAINIC ACID; PILOCARPINE; SEIZURES; RATS; PATHOLOGY; LITHIUM AB Much remains to be learned about mechanisms underlying entry into, and temporal progression of, status epilepticus (SE). This report describes a non-pharmacologic model of generalized convulsive SE in rat. Pulsed trains of suprathreshold electric current were administered bilaterally to either of four rostral forebrain sites: orbital cortex, medial precentral cortex, deep prepiriform cortex, or rostral caudate-putamen (n=8 per site). This induction method resulted in 30/32 animals attaining limb-clonic convulsive SE within a mean of 30-35 min for each forebrain site, with no differences between sites. Subsequent SE proceeded without further interventions, permitting observation of the natural course of progression. A stereotyped behavioral/electrographic sequence occurred, characterized by devolution. Behaviorally, animals progressed from predominantly limb clonus to head clonus, then to subtle twitching, and finally to electrical SE before cessation of spikes. The corresponding electrographic progression was from fast and slow spiking to periodic epileptiform discharges (PEDs). In 20 animals surviving to 48 h, pathologic damage affected mainly limbic sites; damage was related to total convulsive time rather than to clonic activity. High-dose phenobarbital but not phenytoin suppressed SE when given during orbital cortex-induced limb-clonic SE. These findings are compatible with human observations and indicate that this model will enable investigations of generalized SE mechanisms and evaluation of new therapeutic agents for refractory SE. C1 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. RP HANDFORTH, A (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,NEUROL SERV,WILSHIRE & SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. NR 33 TC 11 Z9 11 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-1211 J9 EPILEPSY RES JI Epilepsy Res. PD SEP PY 1994 VL 19 IS 1 BP 15 EP 25 DI 10.1016/0920-1211(94)90084-1 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA PE965 UT WOS:A1994PE96500002 PM 7813410 ER PT J AU KIRIKAE, T SCHADE, FU KIRIKAE, F QURESHI, N TAKAYAMA, K RIETSCHEL, ET AF KIRIKAE, T SCHADE, FU KIRIKAE, F QURESHI, N TAKAYAMA, K RIETSCHEL, ET TI DIPHOSPHORYL LIPID-A DERIVED FROM THE LIPOPOLYSACCHARIDE (LPS) OF RHODOBACTER-SPHAEROIDES ATCC-17023 IS A POTENT COMPETITIVE LPS INHIBITOR IN MURINE MACROPHAGE-LIKE J774.1 CELLS SO FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY LA English DT Article DE LIPOPOLYSACCHARIDE; LIPOPOLYSACCHARIDE RECEPTOR; RHODOBACTER SPHAEROIDES LIPID A; MACROPHAGE-LIKE CELL LINE ID TUMOR-NECROSIS-FACTOR; RHODOPSEUDOMONAS-SPHAEROIDES; NONTOXIC LIPOPOLYSACCHARIDE; HUMAN-MONOCYTES; FATTY-ACIDS; BINDING; ATCC-17023; ENDOTOXIN; ACTIVATION; INDUCTION AB Pentaacyl diphosphoryl lipid A derived from the nontoxic lipopolysaccharide (LPS) of Rhodobacter sphaeroides ATCC 17023 (RsDPLA) did not induce tumour necrosis factor-alpha nor interleukin-6 release in the murine macrophage-like cell line J774.1. However, it effectively inhibited the induction of these two cytokines by LPS of Salmonella minnesota Re mutant R595 (ReLPS) in a concentration-dependent manner. Maximal inhibition and half-maximal inhibition occurred when the ReLPS to RsDPLA mass ratio was 1:30 and 1:1, respectively. A binding study was performed in the presence of serum to determine whether RsDPLA is competing with ReLPS for LPS binding sites on J774.1 cells. This assay allows the determination of LPS binding to J774.1 cells via a mechanism involving CD14, a receptor for complexes of LPS with LPS binding protein (LBP), and its possible inhibition. The results show that RsDPLA strongly inhibits the binding of(125) I-labelled ReLPS to J774.1 cells. Maximal and one-half maximal inhibition of binding occurred when the ReLPS to RsDPLA mass ratios were 1:2.5 and 1:0.5, respectively. It was found that the inhibition of binding by RsDPLA was much stronger than that by unlabelled ReLPS. These results suggest that RsDPLA is competing with ReLPS for CD14-dependent recognition of LPS on J774.1 cells. C1 FORSCHUNGSINST BORSTEL,INST EXPTL BIOL & MED,D-23845 BORSTEL,GERMANY. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NIGMS NIH HHS [GM-36054] NR 24 TC 27 Z9 28 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0928-8244 J9 FEMS IMMUNOL MED MIC JI FEMS Immunol. Med. Microbiol. PD SEP PY 1994 VL 9 IS 3 BP 237 EP 243 DI 10.1111/j.1574-695X.1994.tb00499.x PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PH574 UT WOS:A1994PH57400010 PM 7812271 ER PT J AU MUSE, KE OBERLEY, TD SEMPF, JM OBERLEY, LW AF MUSE, KE OBERLEY, TD SEMPF, JM OBERLEY, LW TI IMMUNOLOCALIZATION OF ANTIOXIDANT ENZYMES IN ADULT HAMSTER-KIDNEY SO HISTOCHEMICAL JOURNAL LA English DT Article ID GLUTATHIONE-S-TRANSFERASE; CUZN-SUPEROXIDE-DISMUTASE; HUMAN CELL-LINES; COPPER-ZINC; IMMUNOHISTOCHEMICAL LOCALIZATION; RAT HEPATOCYTES; SYRIAN-HAMSTER; XANTHINE-OXIDASE; FREE-RADICALS; HUMAN-TISSUES AB Immunoperoxidase and immunogold techniques were used to localize the following antioxidant enzyme systems in the adult hamster kidney at the light and ultrastructural levels: superoxide dismutases, catalases, peroxidases and glutathione S-transferases. Each cell type in the kidney showed specific patterns of labelling of these enzymes. For example, proximal and distal tubular and transitional epithelial cells showed significant staining for all of these enzymes, while glomerular cells and cells of the thin loop of Henle did not show significant staining at the light microscope level. In addition, high levels of glutathione peroxidase were found in smooth muscle cells of renal arteries. At the ultrastructural level, each enzyme was found in a specific subcellular location. Manganese superoxide dismutase was found in mitochondria, catalase was localized in peroxisomes, while copper, zinc superoxide dismutase and glutathione S-transferase (liver and placental forms) were found in both the nucleus and cytoplasm. Glutathione peroxidase was found to have a broad intracellular distribution, with localization in mitochondria, peroxisomes, nucleus, and cytoplasm. Microvilli of tubular cells were labelled by antibodies to catalase, copper, zinc superoxide dismutase, glutathione peroxidase, and glutathione S-transferases. Cell types that were negative by light microscopy immunoperoxidase studies showed definite labelling with immunogold post-embedding ultrastructural techniques (glomerular cells and cells of the loop of Henle), demonstrating the greater sensitivity of the latter technique. These observations demonstrate that there are large variations in the levels of antioxidant enzymes in different cell types, and that even within a distinct cell type, the levels of these enzymes vary in different subcellular locations. Our results demonstrate for the first time the overall antioxidant enzyme status of individual kidney cell types, thereby explaining why different cell types have differing susceptibilities to oxidant stress. Possible physiological and pathological consequences of these findings are discussed. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL & LAB MED SERV,ELECTRON MICROSCOPY SECT,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53706. UNIV IOWA,COLL MED,RADIAT RES LAB,IOWA CITY,IA 52242. FU NCI NIH HHS [CA 41267] NR 55 TC 73 Z9 74 U1 0 U2 1 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0018-2214 J9 HISTOCHEM J JI Histochem.J. PD SEP PY 1994 VL 26 IS 9 BP 734 EP 753 DI 10.1007/BF00158205 PG 20 WC Cell Biology SC Cell Biology GA PH500 UT WOS:A1994PH50000005 PM 7843985 ER PT J AU KLEIN, BS JONES, JM AF KLEIN, BS JONES, JM TI PURIFICATION AND CHARACTERIZATION OF THE MAJOR ANTIGEN WI-1 FROM BLASTOMYCES-DERMATITIDIS YEASTS AND IMMUNOLOGICAL COMPARISON WITH A-ANTIGEN SO INFECTION AND IMMUNITY LA English DT Article ID HISTOPLASMA-CAPSULATUM; POLYACRYLAMIDE GELS; PROTEINS; ELECTROPHORESIS; DIAGNOSIS; ACID AB The lack of well-defined antigens from Blastomyces dermatitidis has hampered the ability to reliably diagnose human infection and study the immunobiology of blastomycosis. We recently discovered a novel surface protein on B. dermatitidis yeasts, designated WI-1, and demonstrated it to be a key antigenic target of humoral and cellular responses during infection. In the present article, we purified acid characterized WI-1 and cbmpared it immunologically with the only Blastomyces antigen commercially available, A antigen. WI-1 was purified by high-performance liquid chromatography over a DEAE cellulose column. It eluted from the column at a point on the salt gradient corresponding to 460 to 490 mM NaCI, reflecting its acidic pi of congruent to 5.2. Purified WI-1 had a molecular mass of 120 kDa and contained a large amount of cysteine (85 residues) and aromatic amino acids but undetectable carbohydrate. In contrast, A antigen had a molecular mass of 135 kDa and contained 37% carbohydrate. Immunological comparison of the two antigens showed that, when radiolabeled, WI-1 was more reactive with anti-Blastomyces antisera than A antigen but did not cross-react with anti-Histoplasma antisera. Proteinase digestion of WI-1 eliminated its recognition by anti-WI-1 and anti-Blastomyces antisera. Proteinase treatment of A antigen had no effect on its recognition by anti-Blastomyces or anti-Histoplasma antisera, but periodate treatment abolished recognition by anti-Histoplasma antisera, indicating that the cross-reactive determinant(s) of A antigen is displayed on the accompanying carbohydrate. In further studies, anti-WI-1 antiserum reacted with A antigen and, conversely, anti-A antiserum and monoclonal antibodies (MAbs) reacted with WI-1, indicating a shared determinant on the two antigens. A recombinant 25-amino-acid repeat, recently cloned from WI-1 and found to be the major target of antibody recognition of WI-1, reacted strongly with anti-A antiserum and MAbs. In MAb competition tests, MAbs specific for the 25-residue repeat abolished binding of anti-A antiserum to A antigen. In antigen inhibition tests, the recombinant repeat abolished binding of anti-a antiserum to A antigen. These results demonstrate that the repeat is the major site of antibody recognition of both WI-1 and A antigen and that the recombinant, nonglycosylated peptide could replace either native antigen in formatting better diagnostic tests for blastomycosis. Moreover, they suggest that producing fungal protein antigens as nonglycosylated peptides in a procaryotic expression system may circumvent problems of antigen cross-reactivity that are due to posttranslational modification. C1 UNIV WISCONSIN HOSP & CLIN,SCH MED,DEPT INTERNAL MED,MADISON,WI 53705. UNIV WISCONSIN HOSP & CLIN,SCH MED,DEPT MED MICROBIOL & IMMUNOL,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. RP KLEIN, BS (reprint author), UNIV WISCONSIN HOSP & CLIN,SCH MED,DEPT PEDIAT,INFECT DIS SECT,K4-434,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU PHS HHS [A100905, A131479] NR 32 TC 37 Z9 38 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 1994 VL 62 IS 9 BP 3890 EP 3900 PG 11 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA PC836 UT WOS:A1994PC83600039 PM 7520423 ER PT J AU OGAWA, M AF OGAWA, M TI HEMATOPOIESIS SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article; Proceedings Paper CT New Trends in Immunopharmacology 1993 Conference CY JUL 17, 1993 CL TOKYO, JAPAN DE HEMATOPOIETIC STEM CELLS; HEMATOPOIETIC PROGENITORS; DIFFERENTIATION OF STEM CELLS; CYTOKINES; INTERLEUKIN; GROWTH FACTORS ID COLONY-STIMULATING FACTOR; MURINE LYMPHOHEMATOPOIETIC PROGENITORS; PRIMITIVE STEM-CELLS; PAIRED PROGENITORS; GROWTH-FACTORS; FACTOR-I; INTERLEUKIN-3-DEPENDENT PROLIFERATION; HUMAN MEGAKARYOCYTOPOIESIS; DISPARATE DIFFERENTIATION; RECOMBINANT HUMAN AB Cellular turnover of the hematopoietic system is supported by a small population of cells termed hematopoietic stem cells. Stem cells are capable of self-renewal and differentiation into individual lymphomyeloid lineages. Available evidence indicates that the decision of a stem cell to self-renew or differentiate and the decision of a multipotential progenitor to select a lineage pathway during differentiation (commitment) are intrinsic to the progenitors and are stochastic in nature. In contrast, proliferative kinetics of the progenitors, namely survival and expansion of the progenitors, appear to be controlled by a number of interacting cytokines. Whereas proliferation and maturation of committed progenitors are controlled by late-acting factors such as erythropoietin, macrophage colony-stimulating factor, granulocyte colony-stimulating factor, and interleukin-5, progenitors at earlier stages of development are controlled by a group of several overlapping cytokines. Interleukin-3, granulocyte/macrophage colony-stimulating factor, and interleukin-4 regulate proliferation of multipotential progenitors only after they are triggered to exit from dormancy state. Triggering of cycling of dormant primitive progenitors and proliferation of lymphohemopoietic primitive progenitors appear to require interactions of early acting cytokines including interleukin-6 granulocyte colony-stimulating factor, interleukin-11, interleukin-12 leukemia inhibitory factor and steel factor. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. RP OGAWA, M (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. FU NIDDK NIH HHS [DK32294] NR 65 TC 35 Z9 35 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 1994 VL 94 IS 3 SU S BP 645 EP 650 DI 10.1016/0091-6749(94)90142-2 PN 2 PG 6 WC Allergy; Immunology SC Allergy; Immunology GA PH235 UT WOS:A1994PH23500011 PM 8083474 ER PT J AU IDA, R LEE, A HUANG, J BRANDI, ML YAMAGUCHI, DT AF IDA, R LEE, A HUANG, J BRANDI, ML YAMAGUCHI, DT TI PROSTAGLANDIN-STIMULATED 2ND MESSENGER SIGNALING IN BONE-DERIVED ENDOTHELIAL-CELLS IS DEPENDENT ON CONFLUENCY IN CULTURE SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID ARACHIDONIC-ACID METABOLISM; CYTOSOLIC FREE CALCIUM; OSTEOBLAST-LIKE CELLS; PARATHYROID-HORMONE; BOVINE BONE; CYCLIC-AMP; RELEASE; CAMP; MOBILIZATION; TRANSDUCTION AB New bone formation is associated with an increase in blood flow by the invasion of capillaries. Endothelial cells that line the capillaries can produce paracrine factors that affect bone growth and development, and in turn, could be affected by products produced by bone cells, in particular the osteoblasts. Since osteoblasts produce prostaglandins E(2) and F-2 alpha (PGE(2), PGF(2 alpha)), it was investigated if these PGs were agonists to bone-derived endothelial cells (BBE) by assessing changes in cAMP and free cytosolic calcium concentration ([Ca2+]i) second messenger generation. We found that confluent cultures of BBE cells, a clonal endothelial cell line derived from bovine sternal bone, responded to 1 mu M PGE(2) by an increase in cAMP. PGF(2 alpha) at the same concentration was less potent in stimulating an increase in cAMP production in confluent BBE cells. Subconfluent cells with a morphology similar to that of fibroblastic cells were not as sensitive to PGE(2)-stimulated cAMP generation. PGF(2 alpha) failed to elicit any cAMP production in subconfluent cultures. PGE(2) and PGF(2 alpha) both stimulated an increase in [Ca2+]i concentration in a dose-dependent manner. The potency of PGE(2) was similar to that of PGF(2 alpha) in stimulating an increase in [Ca2+]i. The Ca2+ response was mostly independent of extracellular Ca+, was unchanged even with prior indomethacin treatment, was unaffected by caffeine pretreatment, but was abolished subsequent to thapsigargin pretreatment. The PG-induced increase in [Ca2+]i was also dependent on the confluency oi the cells. In a subconfluent state, the responses to PGE(2) or PGF(2 alpha) were either negligible, or only small increases in [Ca2+]i were noted with high concentrations of these two PGs. Consistent, dose-dependent increases in [Ca2+]i were stimulated by these PGs only when the cells were confluent and had a cobblestoned appearance. Since it was previously demonstrated that BBE cells respond to parathyroid hormone (PTH) by the production of cAMP, we tested if bovine PTH(1-34) amide [bPTH(1-34) also increased [Ca2+]i in these cells. No change in [Ca2+]i was found in response to bPTH (1-34), although bPTH (1-34) stimulated a nine to tenfold increase in cAMP. We conclude that BBE cells respond to PGE(2) and PGF(2 alpha) but not to bPTH(1-34) by an increase in [Ca2+]i probably secondary to stimulation of phospholipase C and that the cAMP and [Ca2+]i second messenger responses in BBE cells are dependent on the state of confluency of the cells. (C) 1994 Wiley-Liss, Inc. C1 W LOS ANGELES VET AFFAIRS MED CTR,DENT SERV,LOS ANGELES,CA 90073. UNIV FLORENCE,ENDOCRINE UNIT,FLORENCE,ITALY. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN 11G,LOS ANGELES,CA 90073. NR 42 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD SEP PY 1994 VL 160 IS 3 BP 585 EP 595 DI 10.1002/jcp.1041600322 PG 11 WC Cell Biology; Physiology SC Cell Biology; Physiology GA PF218 UT WOS:A1994PF21800021 PM 8077296 ER PT J AU RABENECK, L AF RABENECK, L TI AIDS ENTEROPATHY - WHATS IN A NAME SO JOURNAL OF CLINICAL GASTROENTEROLOGY LA English DT Article DE HIV; ACQUIRED IMMUNODEFICIENCY SYNDROME; SMALL INTESTINE ID HUMAN IMMUNODEFICIENCY VIRUS; CHRONIC DIARRHEA; HIV ENTEROPATHY; INFECTIONS AB The term acquired immunodeficiency syndrome (AIDS) enteropathy was first used in 1984 to refer to changes in intestinal structure and function in human immunodeficiency virus (HIV)-infected patients. Since then, confusion has arisen regarding the meaning of the term. To identify the sources of this confusion we performed a methodologic critique of published clinical research on the topic. We carried out a literature search to identify clinical studies that included at least 20 subjects. Among the six cross-sectional studies we identified, no consensus exists regarding the term itself, to whom it applies, the elements on which it is based, and the criteria for its definition. Further, methodologic problems pertaining to the selection of cases and controls limited the conclusions that could be drawn from these studies. Alterations of mucosal structure and function occur in some HIV-infected patients. However, the nature of these alterations and their relationships to symptoms (diarrhea), immune function, and enteric pathogens remain unclear. Further research is needed to develop a taxonomy for AIDS enteropathy. In carrying out this research, attention to methodologic issues will be important. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. RP RABENECK, L (reprint author), VET AFFAIRS MED CTR 111D,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 21 TC 9 Z9 9 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-0790 J9 J CLIN GASTROENTEROL JI J. Clin. Gastroenterol. PD SEP PY 1994 VL 19 IS 2 BP 154 EP 157 DI 10.1097/00004836-199409000-00017 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PD968 UT WOS:A1994PD96800016 PM 7963365 ER PT J AU ADKINS, DR SALZMAN, D BOLDT, D KUHN, J IRVIN, R ROODMAN, GD LYONS, R SMITH, L FREYTES, CO LEMAISTRE, CF AF ADKINS, DR SALZMAN, D BOLDT, D KUHN, J IRVIN, R ROODMAN, GD LYONS, R SMITH, L FREYTES, CO LEMAISTRE, CF TI PHASE-I TRIAL OF DACARBAZINE WITH CYCLOPHOSPHAMIDE, CARMUSTINE, ETOPOSIDE, AND AUTOLOGOUS STEM-CELL TRANSPLANTATION IN PATIENTS WITH LYMPHOMA AND MULTIPLE-MYELOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; RELAPSED HODGKINS-DISEASE; METASTATIC MALIGNANT-MELANOMA; HIGH-DOSE CYCLOPHOSPHAMIDE; 5-(3,3-DIMETHYL-1-TRIAZENO)IMIDAZOLE-4-CARBOXAMIDE NSC-45388; COMBINATION CHEMOTHERAPY; REFRACTORY MALIGNANCIES; MAMMALIAN-CELLS; ALKYLTRANSFERASE; CANCER AB Purpose: We investigated the feasibility of escalating doses of dacarbazine (DTIC) in combination with high-dose cyclophosphamide, carmustine, and etoposide (CBV) given with autologous stem-cell transplantation in 33 patients with relapsed or refractory lymphoma or multiple myeloma. Patients and Methods: Eligible patients were treated in this phase I study with cyclophosphamide (7.2 g/m(2)), carmustine (BCNU) (600 mg/m(2)), etoposide (2.4 g/m(2)), and escalating doses of DTIC (3,000 to 6,591 mg/m(2)) administered either as a 2- (in 23 patients) or a 6- (in 10 patients) hour infusion to determine the maximum-tolerated dose (MTD) of DTIC and the toxicity profile of this combination. Results: The MTD of DTIC infused over 2 hours and given with the CBV regimen was 3,900 mg/m(2), with the dose-limiting toxicity being hypotension. Seven patients experienced transient acute hypocalcemia in association with the DTIC infusion. Prolonging the DTIC infusion to 6 hours or administration of supplemental calcium did not allow further dose escalation of DTIC to occur. Other non-hematologic toxicities observed with this regimen have been reported with CBV alone. Of 25 patients assessable for tumor response at first evaluation posttransplant, 13 (52%) were in complete remission (CR), four (16%) were in partial remission (PR), five (20%) had stable disease (SD), and three (12%) had progressive disease (PROG). Of 31 patients assessable for relapse-free survival, 22 are alive with 13 in CR, one in PR, two with SD, and six with FROG at a median follow-up duration of 313 days (range, 35 to 749+). Treatment-related mortality occurred in six patients (18%). Conclusion: The feasibility of combining DTIC in high doses with the CBV regimen has been demonstrated. Dose-limiting hypotension is transient and reversible when DTIC is administered at 3,900 mg/m(2) with CBV. Future trials to evaluate the effect of the addition of DTIC to the CBV regimen on response rate and relapse-free survival are encouraged. (C) 1994 by American Society of Clinical Oncology. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 43 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD SEP PY 1994 VL 12 IS 9 BP 1890 EP 1901 PG 12 WC Oncology SC Oncology GA PG300 UT WOS:A1994PG30000022 PM 7916039 ER PT J AU SOKOLSKI, KN CUMMINGS, JL ABRAMS, BI DEMET, EM KATZ, LS COSTA, JF AF SOKOLSKI, KN CUMMINGS, JL ABRAMS, BI DEMET, EM KATZ, LS COSTA, JF TI EFFECTS OF SUBSTANCE-ABUSE ON HALLUCINATION RATES AND TREATMENT RESPONSES IN CHRONIC PSYCHIATRIC-PATIENTS SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT 144th Annual Meeting of the American-Psychiatric-Association CY MAY 07-12, 1991 CL NEW ORLEANS, LA SP AMER PSYCHIAT ASSOC ID AUDITORY HALLUCINATIONS; TEMPORAL-LOBE; VISUAL HALLUCINATIONS; CLINICAL COURSE; SCHIZOPHRENIA; ABNORMALITIES; DIAGNOSIS; PSYCHOSIS; PERFUSION; DISORDER AB Background: Few data systematically document the effects of illicit drug exposure on psychotic illness. We examined the effect of substance abuse on rates and treatment responses of hallucinations in a chronic psychiatric population. Method: 113 cooperative patients consecutively admitted to a state psychiatric hospital were administered the Structured Clinical Diagnostic Interview for DSM-III-R, a Hallucination Interview, and an inventory of past and current substances of abuse. Demographic information was obtained on 104 of 108 patients who declined interview. Medication dosage was analyzed for one third of the interviewed sample; hospital records, nursing reports, contacts with relatives, and urine drug screens were used to confirm information from patient interviews. Hallucination rates and response were compared by diagnositic groups (chi-square). Results: Noninterviewed patients had more frequent hospitalizations, more patients diagnosed with psychosis not otherwise specified or schizoaffective disorder, and fewer females with comorbid substance abuse than the study population. Among interviewed subjects, those with substance abuse and psychiatric illness had first admissions at an earlier age than patients with no substance abuse (p = .005). Schizophrenics experienced higher rates of visual (p = .04) and olfactory (p = .05) hallucinations when using illicit drugs. Substance abuse was associated with decreased treatment responsiveness of auditory (p < .03) and tactile (p < .004) hallucinations in schizophrenic or manic patients. Compared with nonparanoid patients, there was a trend for paranoid schizophrenics with substance abuse to experience more frequent visual (p = .09) and tactile (p = .06) and more refractory auditory (p = .08) hallucinations. No differences in medication dosages were found between patients with treatment-responsive and treatment-refractory hallucinations. Conclusion: Abused substances may interact selectively with primary psychiatric illness to increase rates and treatment resistance of specific hallucination modalities; etiologies are discussed. C1 METROPOLITAN STATE HOSP,NORWALK,CA. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF IRVINE,DEPT PSYCHIAT & HUMAN BEHAV,IRVINE,CA 92717. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. RP SOKOLSKI, KN (reprint author), LONG BEACH VA MED CTR,DEPT PSYCHIAT 116A,5901 E 7TH ST,LONG BEACH,CA 90822, USA. NR 41 TC 20 Z9 20 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD SEP PY 1994 VL 55 IS 9 BP 380 EP 387 PG 8 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA PQ172 UT WOS:A1994PQ17200002 PM 7929017 ER PT J AU OBRIEN, WA AF OBRIEN, WA TI HIV-1 ENTRY AND REVERSE TRANSCRIPTION IN MACROPHAGES SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE CD4; GP120; ENVELOPE; NEUTRALIZATION; NUCLEOTIDES ID HUMAN-IMMUNODEFICIENCY-VIRUS; RECOMBINANT SOLUBLE CD4; AIDS-RELATED COMPLEX; ENVELOPE V3 LOOP; T-CELLS; MONONUCLEAR PHAGOCYTES; GLYCOPROTEIN GP120; HUMAN MONOCYTES; TYPE-1 VIRIONS; HTLV-III/LAV AB Although CD4 is required for efficient virus entry, it is not sufficient for entry of all primary HIV-1 strains. There may be additional virus-cell interactions, possibly involving the V3 region of the extracellular envelope protein, gp120, that occur following conformational changes induced by CD4 binding. This second interaction would precede fusion events and entry of the virus core. Primary HIV-1 strains appear to have a higher virion envelope density and retain gp120 better than HIV-1 strains adapted to growth in T cell lines in culture. These properties may confer a growth advantage in vivo to primary strains on the basis of less well exposed CD4 binding and neutralization domains. HIV-1 entry into both activated and quiescent T cells, as well as macrophages, is efficient for most primary strains, but there are different patterns of reverse transcription. Productive infection of activated T cells is associated with cell proliferation and accumulation of full-length reverse transcripts within 4 to 6 h. In resting, nondividing T cells, reverse transcription is aborted prior to full-length viral DNA formation. A third pattern of reverse transcription is seen in nondividing cultured macrophages with slow kinetics and accumulation of full-length viral DNA between 36 and 48 h. This rate can be increased by adding exogenous nucleotides, but still not to the rate seen in activated T cells. Future antiretroviral therapies may involve interference with cell-specific functions involved in reverse transcription. C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA. RP OBRIEN, WA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,WILSHIRE & SAWTELLE BLVD,691-111F,LOS ANGELES,CA 90073, USA. FU NIAID NIH HHS [AI 29894] NR 51 TC 20 Z9 20 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD SEP PY 1994 VL 56 IS 3 BP 273 EP 277 PG 5 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA PF341 UT WOS:A1994PF34100010 PM 8083599 ER PT J AU CACCIOLA, JS RUTHERFORD, MJ ALTERMAN, AI SNIDER, EC AF CACCIOLA, JS RUTHERFORD, MJ ALTERMAN, AI SNIDER, EC TI AN EXAMINATION OF THE DIAGNOSTIC-CRITERIA FOR ANTISOCIAL PERSONALITY-DISORDER IN SUBSTANCE-ABUSERS SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID INTERVIEW SCHEDULE; BEHAVIOR; VALIDITY; ALCOHOL AB In this article, we compare problem severity and adult antisocial behavior among three groups of cocaine- or alcohol-dependent patients: those with antisocial personality disorder (APD), those who met adult but not childhood APD criteria (A-APD), and those who met neither (non-APD) in order to determine the clinical utility of the A-APD category. Subjects were 269 male veterans admitted for substance abuse treatment. The Addiction Severity Index was used to determine problem severity and the NIMH Diagnostic Interview Schedule was used to obtain positive DSM-III APD criteria and APD diagnoses. More APD subjects reported arrests, illegal behavior, and chronic lying than A-APD and non-APD subjects. On several variables (recent family/social problems, trouble controlling violent behavior, and time incarcerated), A-APD subjects were intermediate in severity. Overall, the non-APD subjects had the least severe problem status. When the APD and A-APD groups were equated on number of positive adult APD criteria, the only differences that consistently remained were difficulty controlling violent behavior and commission of criminal acts, which were endorsed more frequently in the APD group. It appears that the unique contribution of the early onset criteria for the APD diagnosis is that it identifies individuals more likely to engage in criminal and violent behavior. The more general irresponsibility and disregard for the rights of others characteristic of APD is equally evident in both antisocial groups. This work indicates that the APD versus non-APD distinction may not be fine grained enough for clinical or research purposes. C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP CACCIOLA, JS (reprint author), UNIV PENN,CTR STUDIES ADDICT,3900 CHESTNUT ST,PHILADELPHIA,PA 19104, USA. NR 24 TC 32 Z9 32 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD SEP PY 1994 VL 182 IS 9 BP 517 EP 523 DI 10.1097/00005053-199409000-00007 PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA PH205 UT WOS:A1994PH20500007 PM 8083681 ER PT J AU MEGA, MS CUMMINGS, JL AF MEGA, MS CUMMINGS, JL TI FRONTAL-SUBCORTICAL CIRCUITS AND NEUROPSYCHIATRIC DISORDERS SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; RHESUS-MONKEY; PARKINSONS-DISEASE; SUBSTANTIA-NIGRA; SQUIRREL-MONKEY; CAUDATE-NUCLEUS; NIGROSTRIATAL PROJECTIONS; EFFERENT PROJECTIONS; MEDIODORSAL NUCLEUS AB Five parallel anatomic circuits link regions of the frontal cortex to the striatum, globus pallidus/substantia nigra, and thalamus. The circuits originate in the supplmentary motor area, frontal eye fields, dorsolateral prefrontal region, lateral orbitofrontal area, and anterior cingulate cortex. Open loop structures that provide input to or receive output from specific circuits share functions, cytoarchitectural features, and phylogenetic histories with the relevant circuits. The circuits mediate motor and oculomotor function as well as executive functions, socially responsive behavior, and motivation. Neuropsychiatric disorders of frontal-subcortical circuits include impaired executive function, disinhibition, and apathy; indicative mood disorders include depression, mania, and lability. Transmitters, modulators, receptor subtypes, and second messengers within the circuits provide a chemoarchitecture that can inform pharmacotherapy. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL & PSYCHIAT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT BIOBEHAV SCI, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, BEHAV NEUROSCI SECT, LOS ANGELES, CA USA. FU NIA NIH HHS [AG11012-3] NR 65 TC 463 Z9 469 U1 4 U2 17 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD FAL PY 1994 VL 6 IS 4 BP 358 EP 370 PG 13 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA PN731 UT WOS:A1994PN73100004 PM 7841807 ER PT J AU STONE, CK CHRISTIAN, BT NICKLES, RJ PERLMAN, SB AF STONE, CK CHRISTIAN, BT NICKLES, RJ PERLMAN, SB TI TECHNETIUM 94M-LABELED METHOXYISOBUTYL ISONITRILE - DOSIMETRY AND RESTING CARDIAC IMAGING WITH POSITRON EMISSION TOMOGRAPHY SO JOURNAL OF NUCLEAR CARDIOLOGY LA English DT Article DE POSITRON EMISSION TOMOGRAPHY; NITROGEN 13-LABELED AMMONIA; TECHNETIUM 94M-LABELED SESTAMIBI; MYOCARDIAL INFARCTION ID HEXAKIS 2-METHOXYISOBUTYL ISONITRILE; MYOCARDIAL BLOOD-FLOW; N-13 AMMONIA; PERFUSION; QUANTIFICATION; TL-201; PET; INFARCTION; DEPENDENCE; THALLIUM AB Background. Development of a positron-emitting form of technetium has allowed the imaging of technetium radiopharmaceuticals with positron emission tomography (PET). We used Tc-94m to compare the distribution of the myocardial perfusion agent sestamibi at rest with the conventional PET perfusion tracer N-13-labeled ammonia (N-13-ammonia). Methods and Results. Dosimetry calculations were performed with the known whole-body distribution of Tc-99m-labeled sestamibi. Dynamic PET imaging of N-13-ammonia and Tc-94m-labeled sestamibi (Tc-94m-sestamibi) for 32 minutes was performed in eight patients with previous myocardial infarction. Initial myocardial and extramyocardial distribution of Tc-94m-sestamibi was compared with that of N-13-ammonia by qualitative and quantitative analysis. Quantitative comparison of the two tracers was performed with region-of-interest analysis and circumferential profiles. Qualitatively, the cardiac distribution of the tracers was similar in normal and infarcted myocardium. A decrease in the definition of the epicardial and endocardial borders of the heart was seen with Tc-94m-sestamibi, presumably because of the lower dose of radionuclide injected. Quantitatively, there was no difference in infarct size, defined prospectively as tracer activity less than 20% of maximum activity for the section, between the two tracers. Circumferential profile analysis with 12-degree radial sections similarly demonstrated no difference in regional cardiac distribution of the tracers. Conclusions. These results revealed no significant difference in myocardial uptake compared with N-13-ammonia suggesting that the myocardial uptake of sestamibi correlates with that of myocardial perfusion. C1 UNIV WISCONSIN,SCH MED,DEPT RADIOL,NUCL MED SECT,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,DEPT MED PHYS,MADISON,WI 53792. UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET ADM HOSP,CTR POSITRON EMISS TOMOG,MADISON,WI 53792. RP STONE, CK (reprint author), UNIV WISCONSIN,SCH MED,CTR CLIN SCI,DEPT MED,CARDIOL SECT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NHLBI NIH HHS [R29 HL47003] NR 30 TC 20 Z9 21 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1071-3581 J9 J NUCL CARDIOL JI J. Nucl. Cardiol. PD SEP-OCT PY 1994 VL 1 IS 5 BP 425 EP 433 DI 10.1007/BF02961596 PN 1 PG 9 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA PU851 UT WOS:A1994PU85100002 PM 9420726 ER PT J AU KAPUR, KK DEUPREE, R DENT, RJ HASSE, AL AF KAPUR, KK DEUPREE, R DENT, RJ HASSE, AL TI A RANDOMIZED CLINICAL-TRIAL OF 2 BASIC REMOVABLE PARTIAL DENTURE DESIGNS .1. COMPARISONS OF 5-YEAR SUCCESS RATES AND PERIODONTAL HEALTH SO JOURNAL OF PROSTHETIC DENTISTRY LA English DT Article ID COOPERATIVE-DENTAL-IMPLANT; BLADE-VENT IMPLANTS; ABUTMENT TEETH; PLACEMENT; MOBILITY; MOVEMENT AB A randomized clinical trial was undertaken to compare the effectiveness of two partial denture designs, one with I-bar (bar) and the other with circumferential retainers (circumferential), in 134 patients with Kennedy class I and class II edentulous conditions. A total of 30 partial dentures were considered failures, five because of abutment failures and 25 because of the lack of removable partial denture use for eating. The 5-year success rate of 71.3% for the circumferential design did not differ significantly from the 76.6% for the bar design (p > 0.05). There were no discernible changes in the nine periodontal health components of abutment teeth with either of the two designs after 60 months. The results indicate that the two designs do not differ significantly in terms of success rates, maintenance care, and effects on abutment teeth. A well-constructed removable partial denture of either design, supported by favorable abutments and accompanied by a regular recall program offers a satisfactory treatment modality. C1 UNIV CALIF LOS ANGELES,SCH DENT,LOS ANGELES,CA 90024. RP KAPUR, KK (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 34 TC 37 Z9 40 U1 2 U2 14 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-3913 J9 J PROSTHET DENT JI J. Prosthet. Dent. PD SEP PY 1994 VL 72 IS 3 BP 268 EP 282 DI 10.1016/0022-3913(94)90340-9 PG 15 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA PD992 UT WOS:A1994PD99200009 PM 7965900 ER PT J AU KREIMAN, J GERRATT, BR BERKE, GS AF KREIMAN, J GERRATT, BR BERKE, GS TI THE MULTIDIMENSIONAL NATURE OF PATHOLOGICAL VOCAL QUALITY SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID ROUGHNESS SEVERITY RATINGS; SPECTRAL NOISE-LEVELS; ABNORMAL VOICE QUALITIES; RELIABILITY; BREATHINESS; PERCEPTION; HOARSENESS; DYSPHONIA AB Although the terms ''breathy'' and ''rough'' are frequently applied to pathological voices, widely accepted definitions are not available and the relationship between these qualities is not understood. To investigate these matters, expert listeners judged the dissimilarity of pathological voices with respect to breathiness and roughness. A second group of listeners rated the voices on unidimensional scales for the same qualities. Multidimensional scaling analyses suggested that breathiness and roughness are related, multidimensional constructs. Unidimensional ratings of both breathiness and roughness were necessary to describe patterns of similarity with respect to either quality. Listeners differed in the relative importance given to different aspects of voice quality, particularly when judging roughness. The presence of roughness in a voice did not appear to influence raters' judgments of breathiness; however, judgments of roughness were heavily influenced by the degree of breathiness, the particular nature of the influence varying from listener to listener. Differences in how listeners focus their attention on the different aspects of multidimensional perceptual qualities apparently are a significant source of interrater unreliability (noise) in voice quality ratings. C1 W LOS ANGELES VET AFFAIRS MED CTR,AUDIOL & SPEECH PATHOL 126,LOS ANGELES,CA 90073. RP KREIMAN, J (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DIV HEAD & NECK SURG,CHS 62-132,LOS ANGELES,CA 90024, USA. FU NIDCD NIH HHS [NIDCD DC 01797] NR 46 TC 77 Z9 79 U1 0 U2 0 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD SEP PY 1994 VL 96 IS 3 BP 1291 EP 1302 DI 10.1121/1.410277 PG 12 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA PG307 UT WOS:A1994PG30700005 PM 7962996 ER PT J AU MAHONEY, J DRINKA, TJK ABLER, R GUNTERHUNT, G MATTHEWS, C GRAVENSTEIN, S CARNES, M AF MAHONEY, J DRINKA, TJK ABLER, R GUNTERHUNT, G MATTHEWS, C GRAVENSTEIN, S CARNES, M TI SCREENING FOR DEPRESSION - SINGLE QUESTION VERSUS GDS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Note ID POPULATION C1 UNIV WISCONSIN,DEPT MED GERIATR,MADISON,WI. ROCKY MT REHABIL INST,AURORA,CO. UNIV WISCONSIN,SCH SOCIAL WORK,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED NEUROL,MADISON,WI. RP MAHONEY, J (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,GRECC,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. RI Gravenstein, Stefan/G-1681-2011 NR 17 TC 139 Z9 139 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 SEP PY 1994 VL 42 IS 9 BP 1006 EP 1008 PG 3 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA PE832 UT WOS:A1994PE83200019 PM 8064088 ER PT J AU WENZEL, UO FOUQUERAY, B KARAMITSOS, C BHANDARI, B VALENTE, AJ ABBOUD, HE AF WENZEL, UO FOUQUERAY, B KARAMITSOS, C BHANDARI, B VALENTE, AJ ABBOUD, HE TI THROMBIN INDUCES MONOCYTE CHEMOTACTIC PROTEIN-1 (MCP-1) PRODUCTION IN VASCULAR SMOOTH-MUSCLE CELLS (VSMC) DERIVED FROM HUMAN RENAL-ARTERIES SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Meeting Abstract 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,SAN ANTONIO,TX 78284. NR 0 TC 1 Z9 1 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 SEP PY 1994 VL 5 IS 3 BP 553 EP 553 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77101230 ER PT J AU CHOUDHURY, GG ABBOUD, HE AF CHOUDHURY, GG ABBOUD, HE TI VANADATE ACTIVATES PHOSPHATIDYLINOSITOL-3 KINASE (PI3 KINASE) VIA ENHANCED TYROSINE PHOSPHORYLATION OF PLATELET-DERIVED GROWTH-FACTOR RECEPTOR TYPE-BETA (PDGFR-BETA) IN HUMAN MESANGIAL CELLS (HMC) SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 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 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 SEP PY 1994 VL 5 IS 3 BP 690 EP 690 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77101775 ER PT J AU MARRA, F BONEWALD, LF PARK, IS PARKSNYDER, S WOODRUFF, KA ABBOUD, HE AF MARRA, F BONEWALD, LF PARK, IS PARKSNYDER, S WOODRUFF, KA ABBOUD, HE TI SECRETION OF MULTIPLE FORMS OF LATENT TRANSFORMING GROWTH-FACTOR-BETA BY HUMAN MESANGIAL CELLS SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Meeting Abstract C1 UT,HSCSA,DEPT MED,SAN ANTONIO,TX. 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 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD SEP PY 1994 VL 5 IS 3 BP 697 EP 697 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77101802 ER PT J AU AMEDTRADUEGE, AM MAJEWSKI, RR VERROUST, PJ HAMMOND, TG AF AMEDTRADUEGE, AM MAJEWSKI, RR VERROUST, PJ HAMMOND, TG TI HETEROTRIMERIC G-PROTEINS MEDIATE STIMULATION OF RENAL CORTICAL ENDOSOMAL FUSION BY SCAVENGER PATHWAY RECEPTORS SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. HOP TENON,INSERM,U64,F-75970 PARIS 20,FRANCE. NR 2 TC 1 Z9 1 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 SEP PY 1994 VL 5 IS 3 BP 706 EP 706 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77101839 ER PT J AU KIYOMOTO, H ABBOUD, HE FOUQUERAY, BL CHOUDHURY, GG AF KIYOMOTO, H ABBOUD, HE FOUQUERAY, BL CHOUDHURY, GG TI PHORBOL-MYRISTATE ACETATE (PMA)-INDUCED INHIBITION OF THE CYTOPLASMIC TYROSINE PHOSPHATASE PTP1B ENHANCES TYROSINE PHOSPHORYLATION IN HUMAN MESANGIAL CELLS (HMC) SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 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 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 SEP PY 1994 VL 5 IS 3 BP 719 EP 719 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77101891 ER PT J AU KREISBERG, J GARONI, J RADNIK, R KREISBERG, S AF KREISBERG, J GARONI, J RADNIK, R KREISBERG, S TI PHORBOL-MYRISTATE ACETATE (PMA) INCREASES FIBRONECTIN (FN) GENE-EXPRESSION THROUGH A CAMP-RESPONSIVE ELEMENT (CRE) IN MESANGIAL CELL-CULTURES SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Meeting Abstract C1 UT,HSCSA,DEPT PATHOL,SAN ANTONIO,TX. 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 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD SEP PY 1994 VL 5 IS 3 BP 720 EP 720 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77101894 ER PT J AU FOUQUERAY, B GRANDALIANO, G WENZEL, U BHANDARI, B WOODRUFF, K VALENTE, A ABBOUD, HE AF FOUQUERAY, B GRANDALIANO, G WENZEL, U BHANDARI, B WOODRUFF, K VALENTE, A ABBOUD, HE TI CYTOKINES AND THROMBIN REGULATE MCP-1 GENE-EXPRESSION IN BOVINE GLOMERULAR ENDOTHELIAL-CELLS SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Grandaliano, Giuseppe/G-2963-2012 NR 0 TC 5 Z9 5 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 SEP PY 1994 VL 5 IS 3 BP 747 EP 747 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77102002 ER PT J AU KASINATH, BS GRELLIER, P TERHUNE, WC MALDONADO, R CHOUDHURY, GG ABBOUD, SL AF KASINATH, BS GRELLIER, P TERHUNE, WC MALDONADO, R CHOUDHURY, GG ABBOUD, SL TI HIGH GLUCOSE MEDIUM REDUCES GLOMERULAR-BASEMENT-MEMBRANE (GBM) HEPARAN-SULFATE PROTEOGLYCAN (HSPG) CORE PROTEIN GENE-EXPRESSION IN GLOMERULAR EPITHELIAL-CELLS (GEC) SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 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 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 SEP PY 1994 VL 5 IS 3 BP 967 EP 967 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77102877 ER PT J AU KIYOMOTO, H CHOUDHURY, GG FOUQUERAY, BL ABBOUD, HE AF KIYOMOTO, H CHOUDHURY, GG FOUQUERAY, BL ABBOUD, HE TI ACTIVATION OF GLOMERULAR PHOSPHOTYROSINE PHOSPHATASE IN STREPTOZOTOCIN-INDUCED DIABETES (STZD) IN THE RAT SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 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 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 SEP PY 1994 VL 5 IS 3 BP 967 EP 967 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77102879 ER PT J AU PARK, IS KIYOMOTO, H BARNES, JL WOODRUFF, K ABBOUD, HE AF PARK, IS KIYOMOTO, H BARNES, JL WOODRUFF, K ABBOUD, HE TI GLOMERULAR MONOCYTE INFILTRATION IN EARLY STREPTOZOTOCIN-INDUCED DIABETES (STZD) IS ASSOCIATED WITH INCREASED EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) AND CELLULAR FIBRONECTIN (CFN) SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 8 Z9 8 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 SEP PY 1994 VL 5 IS 3 BP 971 EP 971 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PG771 UT WOS:A1994PG77102894 ER PT J AU KAO, YH SORENSON, JA BAHN, MM WINKLER, SS AF KAO, YH SORENSON, JA BAHN, MM WINKLER, SS TI DUAL-ECHO MRI SEGMENTATION USING VECTOR DECOMPOSITION AND PROBABILITY TECHNIQUES - A 2-TISSUE MODEL SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE SEGMENTATION; VOLUME MEASUREMENT; FRACTIONAL VOLUME; IMAGE PROCESSING ID MAGNETIC-RESONANCE IMAGES; CEREBROSPINAL-FLUID SPACES; TEMPORAL-LOBE; GRAY-MATTER; MULTISPECTRAL ANALYSIS; FIELD INHOMOGENEITIES; HIPPOCAMPAL-FORMATION; VOLUME MEASUREMENTS; BRAIN; NOISE AB We combined a vector decomposition technique with Gaussian probability thresholding in feature space to segment normal brain tissues, tumors, or other abnormalities on dual-echo MR images. The vector decomposition technique assigns to each voxel a fractional volume for each of two tissues. A probability threshold, based on an assumed Gaussian probability density function describing random noise, isolates a region in feature space for fractional volume calculation that minimizes contamination from other tissues. The calculated fractional volumes are unbiased estimates of the true fractional volumes. The contrast-to-noise ratio (CNR) between tissues on the segmented images is the same as the Euclidean norm of CNRs in the original images. The method is capable of segmenting more than two tissues from a set of dual-echo images by sequentially analyzing different pairs of tissues. The model is analyzed mathematically and in experiments with a phantom. Two clinical examples are presented. C1 UNIV WISCONSIN,DEPT PHYS,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED PHYS,MADISON,WI 53706. UNIV WISCONSIN,DEPT RADIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,SERV RADIOL,MADISON,WI. NR 68 TC 13 Z9 13 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD SEP PY 1994 VL 32 IS 3 BP 342 EP 357 DI 10.1002/mrm.1910320310 PG 16 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA PE259 UT WOS:A1994PE25900009 PM 7984067 ER PT J AU ROSS, S RICHARDSON, MD GRAYBILL, JR AF ROSS, S RICHARDSON, MD GRAYBILL, JR TI ASSOCIATION BETWEEN MALASSEZIA-FURFUR COLONIZATION AND SEBORRHEIC DERMATITIS IN AIDS PATIENTS SO MYCOSES LA English DT Article DE MALASSEZIA FURFUR; SEBORRHEIC DERMATITIS; HIV; AIDS ID ACQUIRED IMMUNODEFICIENCY SYNDROME; PITYROSPORUM-ORBICULARE; KETOCONAZOLE; PREVALENCE; DISEASE; SCALP AB A total of 180 HIV-positive patients were assessed for seborrhoeic dermatitis (SD) and colonization with Malassezia species. Diseased skin of patients with seborrhoeic dermatitis were sampled selectively for Malassezia. In patients without SD, uninvolved skin was sampled. The prevalence of SD was 19%. Of the 34 SD patients, 16 were positive for Malassezia. Of the 146 patients without SD, only 27 were culture positive for Malassezia. Analysis of the largest HIV-positive patient population studied thus far yielded only a weak correlation between SD and Malassezia colonization. C1 AUDIE L MURPHY MEM VET ADM MED CTR,INFECT DIS SECT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV GLASGOW,DEPT DERMATOL,REG MYCOL REFERENCE LAB,GLASGOW G12 8QQ,LANARK,SCOTLAND. NR 20 TC 3 Z9 4 U1 0 U2 0 PU BLACKWELL WISSENSCHAFTS VERLAG GMBH PI BERLIN PA KURFURSTENDAMM 57, D-10707 BERLIN, GERMANY SN 0933-7407 J9 MYCOSES JI Mycoses PD SEP-OCT PY 1994 VL 37 IS 9-10 BP 367 EP 370 PG 4 WC Dermatology; Mycology SC Dermatology; Mycology GA QN784 UT WOS:A1994QN78400012 PM 7746298 ER PT J AU DENT, CD DEBOOM, GW HAMLIN, ML AF DENT, CD DEBOOM, GW HAMLIN, ML TI PROLIFERATIVE MYOSITIS OF THE HEAD AND NECK - REPORT OF A CASE AND REVIEW OF THE LITERATURE SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS LA English DT Note ID MASSETER MUSCLE AB A case of proliferative myositis arising in the tongue is described. Light and electron micrographs revealed the characteristic infiltrative growth pattern and cellular pleomorphism of this lesion. A review of the literature disclosed 50 reported cases of proliferative myositis, including 10 that originated in the head and neck. The rapid growth rate and unusual gross and histologic appearance of this infiltrative lesion have contributed to its relatively frequent misdiagnosis and inappropriate treatment. Consequently it is hoped that this report will help clarify its benign nature. C1 W LOS ANGELES VA MED CTR,WESTERN DENT EDUC CTR,LOS ANGELES,CA. RP DENT, CD (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,COLL DENT,DEPT ORAL & MAXILLOFACIAL SURG,RICHMOND,VA 23298, USA. NR 13 TC 13 Z9 15 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1079-2104 J9 ORAL SURG ORAL MED O JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. PD SEP PY 1994 VL 78 IS 3 BP 354 EP 358 DI 10.1016/0030-4220(94)90068-X PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA PG827 UT WOS:A1994PG82700016 PM 7970598 ER PT J AU HU, ZQ HENDERSON, GI MOCK, DM SCHENKER, S AF HU, ZQ HENDERSON, GI MOCK, DM SCHENKER, S TI BIOTIN UPTAKE BY BASOLATERAL MEMBRANE-VESICLES OF HUMAN PLACENTA - NORMAL CHARACTERISTICS AND ROLE OF ETHANOL SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID TRANSPORT; RAT; LIVER AB This study assessed the mechanism of uptake of biotin by the fetal-facing (basolateral) membrane of the term human placenta. Using membrane vesicles, we showed that most of the uptake was attributable to transfer of the vitamin Into the vesicle and that the uptake was saturable, Na-dependent, carrier-mediated, and electroneutral. The rate of uptake was less than for biotin uptake by the maternal-facing (apical) membrane of the human placenta. Because ethanol inhibits biotin uptake by the apical membrane, the effect of ethanol on uptake by basolateral vesicles was investigated. With 10-hr exposure at a concentration of 2 and 3 mg/ml, but not 1 mg/ml, ethanol modestly inhibited biotin uptake. The mechanism of inhibition by alcohol is not known. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL & NUTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV ARKANSAS MED SCI HOSP,DEPT PEDIAT,LITTLE ROCK,AR 72202. ARKANSAS CHILDRENS HOSP,DIV DIGEST ENDOCRINE GENET & NUTR DISORDERS,LITTLE ROCK,AR 72202. UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,DIV GASTROENTEROL & NUTR,SAN ANTONIO,TX 78284. FU NIAAA NIH HHS [NIAAA RO1 AA07514]; NIDDK NIH HHS [NIDDK RO1-36823] NR 18 TC 11 Z9 12 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 SEP PY 1994 VL 206 IS 4 BP 404 EP 408 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA PE330 UT WOS:A1994PE33000009 PM 7521055 ER PT J AU LEUCHTER, AF COOK, IA MENA, I DUNKIN, JJ CUMMINGS, JL NEWTON, TF MIGNECO, O LUFKIN, RB WALTER, DO LACHENBRUCH, PA AF LEUCHTER, AF COOK, IA MENA, I DUNKIN, JJ CUMMINGS, JL NEWTON, TF MIGNECO, O LUFKIN, RB WALTER, DO LACHENBRUCH, PA TI ASSESSMENT OF CEREBRAL PERFUSION USING QUANTITATIVE EEG CORDANCE SO PSYCHIATRY RESEARCH-NEUROIMAGING LA English DT Article DE ELECTROENCEPHALOGRAPHY; SINGLE PHOTON EMISSION COMPUTED TOMOGRAPHY; DEMENTIA; STROKE; CORDANCE ID ALZHEIMERS-DISEASE; BLOOD-FLOW; SCHIZOPHRENIA; DEMENTIA; SPECT; HIPPOCAMPUS; INFARCTION; CORTICES AB Brain electrical activity is related to cerebral perfusion. The nature of this relationship is unclear, however, and surface-recorded activity has not been a reliable indicator of brain perfusion. We studied 27 subjects, all of whom were examined with single photon emission tomography (SPECT) and quantitative electroencephalography (QEEG), to assess associations between QEEG cordance and relative brain perfusion. Cordance has two indicator states: concordance, which may indicate high perfusion; and discordance, which may indicate low perfusion. We used multiple linear regression to assess the association between cordance and SPECT values, and found that cordance values were strongly associated with tissue perfusion. Concordance in the a band was associated both with mean tissue perfusion and the volume of normally perfused tissue, and it had a stronger association with perfusion than any other QEEG variable. Discordance in the beta(1) band was associated with mean perfusion, and it had a stronger association than did relative but not absolute power. These data suggest that cordance may be useful for the noninvasive assessment of brain perfusion. C1 UNIV CALIF LOS ANGELES,HARBOR MED CTR,DIV NUCL MED,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 RADIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT BIOSTAT,LOS ANGELES,CA 90024. RP LEUCHTER, AF (reprint author), UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,QUANTITAT EEG LAB,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. OI newton, thomas/0000-0002-3198-5901 FU NIA NIH HHS [P30 AG10123]; NIMH NIH HHS [MH-40705] NR 40 TC 25 Z9 25 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0925-4927 J9 PSYCHIAT RES-NEUROIM JI Psychiatry Res. Neuroimaging PD SEP PY 1994 VL 55 IS 3 BP 141 EP 152 DI 10.1016/0925-4927(94)90022-1 PG 12 WC Clinical Neurology; Neuroimaging; Psychiatry SC Neurosciences & Neurology; Psychiatry GA PR489 UT WOS:A1994PR48900003 PM 7870854 ER PT J AU EMERSON, J PANKRATZ, L JOOS, S SMITH, S AF EMERSON, J PANKRATZ, L JOOS, S SMITH, S TI PERSONALITY-DISORDERS IN PROBLEMATIC MEDICAL PATIENTS SO PSYCHOSOMATICS LA English DT Article ID DSM-III; DIFFICULT PATIENT; CARE; COMORBIDITY; PHYSICIANS; DIAGNOSIS AB To better understand problematic medical patients, the psychiatric diagnoses of 448 patients referred to a behavioral medicine clinic were examined. Forty-two percent met DSM-III-R personality disorder criteria. Analysis of the comorbidity of Axis I and Axis II diagnoses revealed a statistically significant co-occurrence between somatoform and personality disorders (P < 0.0001). Some of the difficulties in making a personality disorder diagnosis are reviewed, as are reasons why knowledge of personality disorder diagnoses is important to medical providers. C1 PORTLAND VA MED CTR,MED SERV,HLTH SERV RES & DEV PROGRAM,PSYCHIAT SERV,PSYCHOL SERV,PORTLAND,OR. OREGON HLTH SCI UNIV,DEPT PSYCHIAT,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED PSYCHOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. NR 29 TC 14 Z9 14 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SEP-OCT PY 1994 VL 35 IS 5 BP 469 EP 473 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA PD412 UT WOS:A1994PD41200007 PM 7972662 ER PT J AU HERSHMAN, JM AF HERSHMAN, JM TI HIGHLIGHTS OF THIS ISSUE SO THYROID LA English DT Editorial Material RP HERSHMAN, JM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BLDG 114,ROOM 200,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD FAL PY 1994 VL 4 IS 3 BP 237 EP 237 DI 10.1089/thy.1994.4.237 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PH851 UT WOS:A1994PH85100001 ER PT J AU HERSHMAN, JM AF HERSHMAN, JM TI ASTWOOD,TED INTELLECTUAL LEGACY - SOME PERSONAL VIEWPOINTS SO THYROID LA English DT Article C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90073. RP HERSHMAN, JM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,BLDG 114,ROOM 200,WILSHIRE & SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. NR 19 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD FAL PY 1994 VL 4 IS 3 BP 313 EP 317 DI 10.1089/thy.1994.4.313 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PH851 UT WOS:A1994PH85100015 PM 7833669 ER PT J AU LAM, HC KOMINSKI, GF PETZ, LD SOFAER, S AF LAM, HC KOMINSKI, GF PETZ, LD SOFAER, S TI FACTORS AFFECTING THE LABOR EFFICIENCY OF HOSPITAL-BASED BLOOD-BANK LABORATORIES SO TRANSFUSION LA English DT Article AB Background: A variety of financing mechanisms and managerial innovations have been developed in the past decade to control hospital costs. Some evidence suggests that those changes have not produced substantial improvements in labor efficiency among employees in the hospital's technical level, such as in the blood bank laboratories. Study Design and Methods: This study measured labor efficiency in 40 hospital-based blood bank laboratories in Southern California during the year from July 1989 to June 1990 and explored the impact of financial, managerial, and operational factors on labor efficiency. Results: With standardized output measures used in all blood bank laboratories, a wide variation of labor efficiency was found. Multivariate analyses indicate that the labor efficiency of blood bank employees was not influenced by organizational financial incentives, but was affected by the managerial styles of blood bank managers. Conclusion: Interpretation of the findings suggests that labor efficiency is affected by operational designs intended to improve responses to variable workloads and reduce slack time. C1 UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT HLTH SCI,LOS ANGELES,CA 90025. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. GEORGE WASHINGTON UNIV,SCH MED,DEPT HLTH SCI,WASHINGTON,DC. RP LAM, HC (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,2134 PARNELL AVE,LOS ANGELES,CA 90025, USA. NR 7 TC 6 Z9 6 U1 1 U2 3 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD SEP PY 1994 VL 34 IS 9 BP 811 EP 817 DI 10.1046/j.1537-2995.1994.34994378284.x PG 7 WC Hematology SC Hematology GA PJ636 UT WOS:A1994PJ63600014 PM 8091472 ER PT J AU LIN, EY BRUNICARDI, FC AF LIN, EY BRUNICARDI, FC TI HIV-INFECTION AND SURGEONS SO WORLD JOURNAL OF SURGERY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HEALTH-CARE WORKERS; INTRAVENOUS-DRUG-USERS; OPERATING-ROOM; BLOOD CONTACT; RISK-FACTORS; AIDS; TRANSMISSION; SEROPREVALENCE; EPIDEMIOLOGY AB The human immunodeficiency virus (HIV) causes acquired immunodeficiency syndrome, which remains uniformly fatal in affected individuals. A common route of HIV transmission is via inoculation of contaminated blood, which may occur during surgical procedures. Surgeons may estimate their risk of HIV infection over a 30-year surgical career based on HIV prevalence among surgical patients, percutaneous injury rate per operation, and seroconversion rate. Surgeons can reduce their risk by various means, but the most pragmatic is by reducing the rate of percutaneous injury through optimal surgical technique and proper precautions. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DEPT SURG,LOS ANGELES,CA 90073. NR 48 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2313 J9 WORLD J SURG JI World J.Surg. PD SEP-OCT PY 1994 VL 18 IS 5 BP 753 EP 757 PG 5 WC Surgery SC Surgery GA PJ239 UT WOS:A1994PJ23900020 PM 7975695 ER PT J AU SLICE, LW WONG, HC STERNINI, C GRADY, EF BUNNETT, NW WALSH, JH AF SLICE, LW WONG, HC STERNINI, C GRADY, EF BUNNETT, NW WALSH, JH TI THE CONSERVED NPX(N)Y MOTIF PRESENT IN THE GASTRIN-RELEASING PEPTIDE RECEPTOR IS NOT A GENERAL SEQUESTRATION SEQUENCE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SWISS 3T3 CELLS; BETA-ADRENERGIC-RECEPTOR; MEDIATED INTERNALIZATION; DOWN-REGULATION; BOMBESIN; RAT; BINDING; IMMUNOREACTIVITY; DESENSITIZATION; PHOSPHORYLATION AB Exposure of the gastrin-releasing peptide (GRP) receptor to agonists causes a rapid desensitization of the receptor-stimulated mobilization of intracellular calcium. Homologous desensitization occurs by uncoupling the G-proteins from the receptor and by ligand induced internalization. The molecular determinants of desensitization of the GRP receptor are not well known. The importance of tyrosine 324 which is located in a highly conserved NPX(2-3)Y motif of the GRP receptor was investigated. Kirsten murine sarcoma virus-transformed rat kidney (KNRK) cells were transfected with expression vectors encoding either the wild type or the mutant (tyrosine 324 to alanine 324) rat GRP receptor. The wild type and mutant GRP receptors were expressed at a high level in the KNRK cells, 2.0 x 10(6) and 0.5 x 10(6) receptors per cell, respectively. The wild type and mutant GRP receptors bound GRP with the same affinity (K-d = 6-7 nM). KNRK cells expressing the wild type or mutant GRP receptor had similar [Ca2+](i) dose response to GRP. KNRK cells expressing the GRP receptor rapidly internalized bound I-125-GRP at 37 degrees C. Internalization was inhibited at 4 degrees C and by 0.45 nl sucrose. The internalization of bound I-125-GRP by the mutant GRP receptor was identical to the wild type receptor. Fluorescent microscopy was used to directly observe the GRP receptor expressed on the surface of the KNRK cells and to visualize its ligand induced internalization. There was no difference in the pattern of internalization between the wild type and mutant GRP receptors expressed in KNRK cells. Therefore, the highly conserved tyrosine 324 does not have a role in GRP binding, receptor-G-protein interaction, or initial events of ligand induced receptor internalization. The NPX(n)Y motif is not a general sequestration sequence for seven transmembrane G-protein linked receptors. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR GASTROENTER BIOL,DEPT PHYSIOL,LOS ANGELES,CA 90073. UNIV CALIF SAN FRANCISCO,DEPT SURG,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94143. RP SLICE, LW (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR GASTROENTER BIOL,DEPT MED,LOS ANGELES,CA 90073, USA. FU NIDDK NIH HHS [DK 35740, DK 39957, DK 17294] NR 25 TC 66 Z9 66 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 26 PY 1994 VL 269 IS 34 BP 21755 EP 21761 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PK973 UT WOS:A1994PK97300057 PM 8063819 ER PT J AU MARSHALL, G GROVER, FL HENDERSON, WG HAMMERMEISTER, KE AF MARSHALL, G GROVER, FL HENDERSON, WG HAMMERMEISTER, KE TI ASSESSMENT OF PREDICTIVE MODELS FOR BINARY OUTCOMES - AN EMPIRICAL-APPROACH USING OPERATIVE DEATH FROM CARDIAC-SURGERY SO STATISTICS IN MEDICINE LA English DT Article ID PROGNOSTIC PREDICTION; REGRESSION-MODELS; RISK ASSESSMENT; ADVANTAGES AB Predictive models in medical research have gained popularity among physicians as an important tool in medical decision making. Eight methodological strategies for creating predictive models are compared in a large, complex data base consisting of preoperative risk and operative outcome data on 12,712 patients undergoing coronary artery bypass grafting and entered into the Department of Veterans Affairs Cardiac Surgery Risk Assessment Program between April 1987 and March 1990. The models under consideration were developed to predict operative death (any death within 30 days following the surgical procedure or later if the result of a perioperative complication). The two strategies with the best predictive power among the eight examined were stepwise logistic regression done and data reduction by cluster analysis combined with clinical judgement followed by a logistic regression model. The additive model based on unadjusted relative risks, the model based on Bayes' Theorem, and the logistic model using all candidate variables were good alternatives. Whether or not we imputed values did not have a significant impact on the predictive power of the models. C1 US DEPT VET AFFAIRS,COOPERAT STUDIES PROGRAM,HINES,IL 60141. RP MARSHALL, G (reprint author), UNIV COLORADO,SCH MED,DEPT VET AFFAIRS MED CTR,1055 CLEMONT ST,DENVER,CO 80220, USA. RI Marshall, Guillermo/F-2302-2011 NR 15 TC 33 Z9 33 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD AUG 15 PY 1994 VL 13 IS 15 BP 1501 EP 1511 DI 10.1002/sim.4780131502 PG 11 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA PF482 UT WOS:A1994PF48200001 PM 7973229 ER PT J AU TAKAHASHI, LK AF TAKAHASHI, LK TI ORGANIZING ACTION OF CORTICOSTERONE ON THE DEVELOPMENT OF BEHAVIORAL-INHIBITION IN THE PREWEANLING RAT SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE PREWEANLING RAT; BEHAVIORAL INHIBITION; FREEZING; ULTRASONIC VOCALIZATION; CONSPECIFIC THREAT; SOCIAL ISOLATION; ADRENAL STEROID; CORTICOSTERONE; ADRENALECTOMY ID REGULATE POSTNATAL-DEVELOPMENT; DENTATE GYRUS; SEXUAL-DIFFERENTIATION; PREOPTIC AREA; BRAIN; GLUCOCORTICOIDS; ADRENALECTOMY; RESPONSES; RECEPTOR; STEROIDS AB Altricial rat pups develop the ability to freeze and to terminate their emission of ultrasonic vocalizations when exposed to an unfamiliar adult male rat. This developmental competence in expressing behavioral inhibition is impaired when rat pups are adrenalectomized (ADX) on postnatal day 10, a period prior to the emergence of behavioral inhibition. Adrenalectomy, however, fails to induce similar behavioral deficits when performed after behavioral inhibition has developed. Results suggest that adrenal steroids are involved in promoting the development but not the activation of behavioral inhibition. To critically test this hypothesis, four groups of rats were adrenalectomized on day 10 and tested for behavioral inhibition on day 18. Prior to testing, one group of rats received daily s.c. injections of vehicle whereas another group was treated with daily injections of 3.0 mg/kg of corticosterone (B). The other two groups of rats received daily B injections on only days 10-13 or days 14-17. Results indicated that ADX rats treated with B only on days 10-13 as well as throughout exhibited significantly higher levels of freezing than the other two treatment groups. In order to evaluate whether the behavioral inhibitory deficits produced by ADX at 10 days of age are due to a delayed insensitivity to the 3.0 mg/kg dose of B, day 10 pups were ADX and injected on days 14-17 with doses of B as high as 12 mg/kg. When tested for behavioral inhibition on day 18, these high doses of B were found to be ineffective in potentiating freezing above the level of vehicle-treated rats. Together, results suggest that prior to the end of the second postnatal week endogenous adrenal steroids and in particular B, are critically involved in developmental changes necessary for the eventual species typical expression of behavioral inhibition. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 46 TC 51 Z9 51 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD AUG 12 PY 1994 VL 81 IS 1 BP 121 EP 127 DI 10.1016/0165-3806(94)90074-4 PG 7 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA PB770 UT WOS:A1994PB77000013 ER PT J AU PHARR, PN OGAWA, M HOFBAUER, A LONGMORE, GD AF PHARR, PN OGAWA, M HOFBAUER, A LONGMORE, GD TI EXPRESSION OF AN ACTIVATED ERYTHROPOIETIN OR A COLONY-STIMULATING FACTOR-1 RECEPTOR BY PLURIPOTENT PROGENITORS ENHANCES COLONY FORMATION BUT DOES NOT INDUCE DIFFERENTIATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID BLAST CELL COLONIES; HEMATOPOIETIC PROGENITORS; CSF-1 RECEPTOR; LINEAGE COMMITMENT; POINT MUTATION; GROWTH-FACTOR; PROLIFERATION; ONCOGENE; SUPERFAMILY; DOMAIN AB Whether the presence of specific receptors on the surface of developing cells is the cause of consequence of lineage restriction is not known. If activation of specific receptors is the driving event in differentiation, the premature expression of specific receptors would promote differentiation along that pathway. In this study pluripotent progenitors, obtained from blast cell colonies (pooled or individual) of 5-flurouracil-treated mice, were infected with retroviral vectors containing either an activated receptor for erythropoietin (EPO), an erythroid progenitor growth factor, or the receptor for colony-stimulating factor 1 (CSF-1), a macrophage growth factor. These receptors exhibit expression patterns restricted to committed progenitors. The developmental potential of infected pluripotent progenitors was not changed, although they expressed the exogenous genes, suggesting that in these cells activation of lineage-specific receptors does not induce differentiation. Acquisition of a constitutively activated EPO receptor allowed erythroid development in mixed colonies in the absence of EPO, as expected. Infection of progenitors with a virus containing the CSF-1 receptor promoted the development of granulocyte/macrophage (GM) colonies but did not alter the differentiation potential of either colony-forming unit (CFU)-GM or CFU-mix. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29401. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT CELL BIOL,ST LOUIS,MO 63110. RP PHARR, PN (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401, USA. FU NCI NIH HHS [CA 50244]; NIDDK NIH HHS [DK 32294] NR 31 TC 43 Z9 44 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 2 PY 1994 VL 91 IS 16 BP 7482 EP 7486 DI 10.1073/pnas.91.16.7482 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA PA376 UT WOS:A1994PA37600022 PM 8052607 ER PT J AU JOHNSON, VA AF JOHNSON, VA TI COMBINATION THERAPY - MORE EFFECTIVE CONTROL OF HIV TYPE-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 2nd Annual Optimal Management of HIV Disease; Clinical Conference - 10th Anniversary Perspectives on Aids: Clinical Investigation of HIV Disease CY JAN, 1994 CL FT LAUDERDALE, FL ID HUMAN-IMMUNODEFICIENCY-VIRUS; RECOMBINANT INTERFERON-ALPHA; RO 31-8959; IN-VITRO; SYNERGISTIC INHIBITION; REVERSE-TRANSCRIPTASE; MULTIDRUG-RESISTANCE; ZIDOVUDINE; INVITRO; REPLICATION AB The rationale for combining anti-HIV-1 agents is to provide more complete viral suppression, to limit the emergence of drug resistance during chronic viral replication, and to provide more effective antiretroviral treatment even when mixtures of drug-resistant and drug-sensitive strains are present. In vitro experiments reveal increased suppression with multiple-drug therapy, but viral breakthrough occurs after prolonged time in culture even during triple-drug therapy. Clinical results available to date indicate that drugs should be given simultaneously for optimal benefit. There appears to be a rationale for early initiation of combination therapy before the onset of increased viral burden and the emergence of syncytium-inducing viral variants. The results of ACTG protocol 155 revealed benefit of zidovudine and zalcitabine over monotherapy with either agent in patients with CD4(+) cell counts greater than or equal to 150 cells/mm(3). However, further clinical studies will be necessary before firm recommendations can be made about the indications for combination antiretroviral therapy in HIV-l-infected individuals at different stages of disease. Ultimately, we need better drugs, in combination, which significantly impact on HIV-1 burden to achieve more complete viral suppression and to reduce selection of drug-resistant viral variants. C1 UNIV ALABAMA,CTR AIDS RES,DEPT MICROBIOL,BIRMINGHAM,AL 35294. BIRMINGHAM VET AFFAIRS MED CTR,BIRMINGHAM,AL 35294. RP JOHNSON, VA (reprint author), UNIV ALABAMA,CTR AIDS RES,DEPT MED,DIV INFECT DIS,229 TINSLEY HARRISON TOWER,1900 UNIV BLVD,BIRMINGHAM,AL 35294, USA. FU NIAID NIH HHS [AI 32794, AI 32775] NR 32 TC 15 Z9 15 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1994 VL 10 IS 8 BP 907 EP 912 DI 10.1089/aid.1994.10.907 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PE522 UT WOS:A1994PE52200006 PM 7811541 ER PT J AU OGAWA, M HIRAYAMA, F AF OGAWA, M HIRAYAMA, F TI CYTOKINE REGULATION OF LYMPHOHEMATOPOIETIC PROGENITORS IN CULTURE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29401. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1994 VL 10 SU 1 BP S110 EP S110 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PF066 UT WOS:A1994PF06600330 ER PT J AU ALASSI, MT GENTA, RM KARTTUNEN, TJ GRAHAM, DY AF ALASSI, MT GENTA, RM KARTTUNEN, TJ GRAHAM, DY TI CLARITHROMYCIN AMOXICILLIN THERAPY FOR HELICOBACTER-PYLORI INFECTION SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Article ID METRONIDAZOLE RESISTANCE; DUODENAL-ULCER; CAMPYLOBACTER-PYLORI; TRIPLE THERAPY; ERADICATION; SUSCEPTIBILITY; AMOXICILLIN; COMBINATION; EFFICACY AB Background: More convenient therapies are needed to treat Helicobacter pylori infection successfully. Clarithromycin and amoxycillin are effective against H. pylori both in vivo and in vitro. Recent success with a high dose amoxycillin-metronidazole combination therapy led us to evaluate clarithromycin-amoxycillin dual therapy for H. pylori infection. Methods: We tested the combination of clarithromycin 500 mg t.d.s. with meals plus amoxycillin 750 mg t.d.s. with meals for 10 days for its effect on H. pylori infection in 29 patients with documented H. pylori peptic ulcers. There were 27 men and 2 women, ranging in age from 23 to 77 years. H. pylori and ulcer status were evaluated at entry and at least 4 weeks after ending antimicrobial therapy. For ulcer healing, ranitidine 300 mg was given each evening for 6 weeks. H. pylori status was determined by CLOtest and histology. Results: H. pylori infection was cured in 86% (95% CI = 78-99%). Compliance averaged 93% by pill count. Ten patients (34%) experienced mild side effects: eight reported dysgeusia and two had mild diarrhoea; none discontinued therapy because of side effects. Conclusion: We conclude that dual therapy with clarithromycin and amoxycillin is a safe and effective alternative regimen for the successful treatment of H. pylori infections. C1 VET AFFAIRS MED CTR 111D,DEPT PATHOL,HOUSTON,TX 77030. VET AFFAIRS MED CTR 111D,DIV MOLEC VIROL,HOUSTON,TX 77030. BAYLOR COLL MED,,HOUSTON,TX 77030. RP GRAHAM, DY (reprint author), VET AFFAIRS MED CTR 111D,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 42 TC 38 Z9 38 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-2813 J9 ALIMENT PHARM THERAP JI Aliment. Pharmacol. Ther. PD AUG PY 1994 VL 8 IS 4 BP 453 EP 456 PG 4 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA PB417 UT WOS:A1994PB41700011 PM 7986970 ER PT J AU DENNING, DW LEE, JY HOSTETLER, JS PAPPAS, P KAUFFMAN, CA DEWSNUP, DH GALGIANI, JN GRAYBILL, JR SUGAR, AM CATANZARO, A GALLIS, H PERFECT, JR DOCKERY, B DISMUKES, WE STEVENS, DA AF DENNING, DW LEE, JY HOSTETLER, JS PAPPAS, P KAUFFMAN, CA DEWSNUP, DH GALGIANI, JN GRAYBILL, JR SUGAR, AM CATANZARO, A GALLIS, H PERFECT, JR DOCKERY, B DISMUKES, WE STEVENS, DA TI NIAID MYCOSES STUDY-GROUP MULTICENTER TRIAL OF ORAL ITRACONAZOLE THERAPY FOR INVASIVE ASPERGILLOSIS SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID PULMONARY ASPERGILLOSIS; DIAGNOSIS; EPIDEMIOLOGY; INVITRO AB BACKGROUND: Invasive aspergillosis is the most common invasive mould infection and a major cause of mortality in immunocompromised patients. Response to amphotericin B, the only antifungal agent licensed in the United States for the treatment of aspergillosis, is suboptimal. METHODS: A multicenter open study with strict entry criteria for invasive aspergillosis evaluated oral itraconazole (600 mg/d for 4 days followed by 400 mg/d) in patients with various underlying conditions. Response was based on clinical and radiologic criteria plus microbiology, histopathology, and autopsy data. Responses were categorized as complete, partial, or stable. Failure was categorized as an itraconazole failure or overall failure. RESULTS: Our study population consisted of 76 evaluable patients. Therapy duration varied from 0.3 to 97 weeks (median 46). At the end of treatment, 30 (39%) patients had a complete or partial response, and 3 (4%) had a stable response, and in 20 patients (26%), the protocol therapy was discontinued early (at 0.6 to 54.3 weeks) because of a worsening clinical course or death due to aspergillosis (itraconazole failure). Twenty-three (30%) patients withdrew for other reasons including possible toxicity (7%) and death due to another cause but without resolution of aspergillosis (20%). Itraconazole failure rates varied widely according to site of disease and underlying disease group: 14% for pulmonary and tracheobronchial disease, 50% for sinus disease, 63% for central nervous system disease, and 44% for other sites; 7% in solid organ transplant, 29% in allogeneic bone marrow transplant patients, and 14% in those with prolonged granulocytopenia (median 19 days), 44% in AIDS patients, and 32% in other host groups. The relapse rates among those who completed therapy and those who discontinued early for possible toxicity were 12% and 40%, respectively; all were still immunosuppressed. CONCLUSION: Oral itraconazole is a useful alternative therapy for invasive aspergillosis with response rates apparently comparable to amphotericin B. Relapse in immunocompromised patients may be a problem. Controlled trials are necessary to fully assess the role of itraconazole in the treatment of invasive aspergillosis. C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,SAN JOSE,CA 95128. CALIF INST MED RES,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,DIV INFECT DIS & GEOG MED,STANFORD,CA 94305. UNIV ALABAMA,CTR COMPREHENS CANC,DIV BIOSTAT,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MED,DIV INFECT DIS,BIRMINGHAM,AL 35294. UNIV MICHIGAN,SCH MED,VET AFFAIRS MED CTR,DEPT INTERNAL MED,DIV INFECT DIS,ANN ARBOR,MI. VET AFFAIRS MED CTR,MED SERV,DIV INFECT DIS,TUCSON,AZ. UNIV ARIZONA,DEPT MED,TUCSON,AZ. AUDIE L MURPHY MEM VET ADM MED CTR,DIV INFECT DIS,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. BOSTON UNIV,SCH MED,DEPT MED,DIV INFECT DIS,BOSTON,MA 02118. UNIV CALIF SAN DIEGO,DEPT MED,DIV PULM MED,SAN DIEGO,CA 92103. DUKE UNIV,DEPT MED,DIV INFECT DIS,DURHAM,NC. OI Denning, David/0000-0001-5626-2251 FU NIAID NIH HHS [N01-AI-15082] NR 20 TC 370 Z9 376 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD AUG PY 1994 VL 97 IS 2 BP 135 EP 144 DI 10.1016/0002-9343(94)90023-X PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA PB686 UT WOS:A1994PB68600006 PM 8059779 ER PT J AU GLASSMAN, PA BELL, RM TRANQUADA, RE AF GLASSMAN, PA BELL, RM TRANQUADA, RE TI THE 1966 ENACTMENT OF MEDICARE - ITS EFFECT ON DISCHARGES FROM LOS-ANGELES COUNTY-OPERATED HOSPITALS SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note AB The effect of Medicare on two public hospitals in Los Angeles County was analyzed by examining the percentage of patients 65 years of age and older among all discharges from 1958 through 1971. At Harbor General Hospital, discharges of elderly patients had dropped from 21.7% to 7.9% by late 1966; at Los Angeles County General Hospital, discharges decreased from 15.3% to 10.7% between 1966 and 1967. Monitoring public hospitals' demographic changes after enacting a national health plan may provide information on patients' and providers' acceptance of insurance and on resources needed by public hospitals to care for those left without coverage. C1 RAND CORP,SANTA MONICA,CA. UNIV SO CALIF,SCH MED,LOS ANGELES,CA. UNIV SO CALIF,SCH PUBL ADM,LOS ANGELES,CA 90089. RP GLASSMAN, PA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DIV GEN INTERNAL MED 691-W111G,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 10 TC 1 Z9 1 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD AUG PY 1994 VL 84 IS 8 BP 1325 EP 1327 DI 10.2105/AJPH.84.8.1325 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA PC266 UT WOS:A1994PC26600026 PM 8059897 ER PT J AU LEVINE, SM ANZUETO, A PETERS, JI CRONIN, T SAKO, EY JENKINSON, SC BRYAN, CL AF LEVINE, SM ANZUETO, A PETERS, JI CRONIN, T SAKO, EY JENKINSON, SC BRYAN, CL TI MEDIUM-TERM FUNCTIONAL RESULTS OF SINGLE-LUNG TRANSPLANTATION FOR END-STAGE OBSTRUCTIVE LUNG-DISEASE SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID PULMONARY-DISEASE; EMPHYSEMA; EXERCISE; CORTICOSTEROIDS; RESPONSES; DIAPHRAGM; MYOPATHY; HEART AB Controversy has surrounded the use of single-lung transplantation (SLT) for the treatment of endstage obstructive lung disease. In recent years, several transplant centers have performed SLT for such indications. In this report, we describe functional results in patients undergoing SLT for obstructive lung disease, twenty-two followed over one year and 10 over two years. Data include pulmonary function testing, gas exchange, quantitative ventilation and perfusion to the lung graft, and results of symptom-limited graded cycle exercise testing after SLT. Our results show improvement in obstructive dysfunction FEV(1) 0.49 +/- 0.13 L (16 +/- 4% predicted) pre-SLT to 1.71 +/- 0.43 L (57 +/- 12% predicted) 3 mo after SLT, FEV(1)/FVC 0.30 +/- 0.07 pre-SLT to 0.75 +/- 0.09 3 mo after SLT, and improvement in arterial oxygenation, PaO2 58 +/- 10 mm Hg pre SLT to PaO2 86 +/- 13 mm Hg 3 mo post-SLT. In addition, these improvements were sustained up to 1 to 2 yr post-SLT. The majority of ventilation and perfusion go to the new lung graft. After SLT, patients have reduced maximum oxygen consumption (VO(2)max 40 to 60% predicted) but do not have ventilatory limitation to exercise and can carry out daily activities without compromise. We conclude that SLT is a viable medium-term therapeutic option for endstage obstructive lung disease. The long-term future of this technique remains to be determined. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED PULM DIS CRIT CARE,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. RP LEVINE, SM (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT 111E,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 39 TC 55 Z9 56 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD AUG PY 1994 VL 150 IS 2 BP 398 EP 402 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA PB286 UT WOS:A1994PB28600017 PM 8049821 ER PT J AU MOHSENIFAR, Z STEIN, M DELILLY, J MAHLER, ME MANDELKERN, M WILLIAMS, AJ AF MOHSENIFAR, Z STEIN, M DELILLY, J MAHLER, ME MANDELKERN, M WILLIAMS, AJ TI REGIONAL METABOLIC DEPENDENCY IN OBSTRUCTIVE SLEEP-APNEA SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Article DE SLEEP APNEA; OXYGEN-SUPPLY DEPENDENCY; POSITRON-EMISSION TOMOGRAPHY SCANNING ID POSITIVE AIRWAY PRESSURE; GLUCOSE-UTILIZATION; HEMODYNAMICS AB Abnormalities of oxygen use occur in obstructive sleep apnea, as do impaired cerebral perfusion and alterations of cerebral function. In this case study, the authors quantitated the local cerebral glucose metabolic rate in two patients with obstructive sleep apnea (one with and one without oxygen supply dependency) and assessed cerebral glucose use by increasing oxygen delivery through passive leg elevation. Obstructive sleep apnea was confirmed by visual analysis of nocturnal pulse oximetry traces in two patients and its severity assessed from the respiratory disturbance index and minimum oxygen saturation. Awake local cerebral glucose metabolic rate (mu M/min/100 g) was determined by positron-emission tomography using [18F]2-Fluoro-2-Deoxy-D-Glucose at baseline and on the following day during passive leg elevation. Conditions otherwise were unchanged. The patient with global oxygen supply dependency exhibited a significant increase in the local cerebral glucose metabolic rate. In contrast, the patient without global supply dependency had no change in the local cerebral glucose metabolic rate. These case studies demonstrate the first evidence of improvement in regional metabolic consumption in response to increased oxygen delivery and in the presence of global oxygen supply dependency. C1 W LOS ANGELES VA MED CTR,MED SERV,LOS ANGELES,CA. W LOS ANGELES VA MED CTR,RES SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. UNIV CALIF IRVINE,DEPT PHYS,IRVINE,CA 92717. RP MOHSENIFAR, Z (reprint author), CEDARS SINAI MED CTR,DIV PULM MED,8700 BEVERLY BLVD,ROOM 6732,LOS ANGELES,CA 90048, USA. NR 21 TC 2 Z9 2 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 1994 VL 308 IS 2 BP 75 EP 78 DI 10.1097/00000441-199408000-00001 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA PA658 UT WOS:A1994PA65800001 PM 8042657 ER PT J AU LEE, PY FLETCHER, WS SULLIVAN, ES VETTO, JT AF LEE, PY FLETCHER, WS SULLIVAN, ES VETTO, JT TI COLORECTAL-CANCER IN YOUNG-PATIENTS - CHARACTERISTICS AND OUTCOME SO AMERICAN SURGEON LA English DT Article; Proceedings Paper CT 36th Annual Meeting of the Midwest-Surgical-Association CY AUG 08-11, 1993 CL LINCOLNSHIRE, IL SP MIDWEST SURG ASSOC ID PATIENTS LESS; CARCINOMA; COLON; RECTUM; AGE; ADENOCARCINOMA; SURVEILLANCE; PROGNOSIS; COLITIS; ADULTS AB Controversy still exists regarding the features and prognosis of colorectal cancer in young patients. We reviewed the records of 62 patients 40 years of age and younger with adenocarcinoma of the colon and rectum, treated and followed at our institution between 1968 and 1991. These patients represented 3.1 per cent of our total colorectal patient population during that time period. Their mean age was 34.5 years old, with the youngest patient being 18 years of age. Modified Dukes stages at presentation were 8 per cent A, 20 per cent B, 23 per cent C, and 48 per cent 15. Underlying inflammatory bowel disease was present in 21 per cent of patients and was proportionately distributed between high (C and D) and low (A and B) stages. Half of the stage D patients had high grade lesions, compared with only 20 per cent of lower stage patients (P = 0.037). All but two patients had operative exploration; 36 (60%) had complete resection Of all gross disease. With a mean follow-up of 98.2 months, the 5-year overall survival for stage A disease was 100 per cent, but dropped to 85, 40, and 7 per cent for stages B, C and D, respectively. Compared to published figures for the general population, younger patients with colon and rectal cancer tend to present at a more advanced stage, but have similar stage-related survival. C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 33 TC 62 Z9 66 U1 0 U2 0 PU SOUTHEASTERN SURGICAL CONGRESS PI ATLANTA PA 1776 PEACHTREE RD, NW., SUITE 410N, ATLANTA, GA 30309-2352 SN 0003-1348 J9 AM SURGEON JI Am. Surg. PD AUG PY 1994 VL 60 IS 8 BP 607 EP 612 PG 6 WC Surgery SC Surgery GA NY413 UT WOS:A1994NY41300011 PM 8030817 ER PT J AU FOLLIS, F MILLER, K SCREMIN, OU PETT, S KESSLER, R WERNLY, J AF FOLLIS, F MILLER, K SCREMIN, OU PETT, S KESSLER, R WERNLY, J TI NMDA RECEPTOR BLOCKADE AND SPINAL-CORD ISCHEMIA DUE TO AORTIC CROSS-CLAMPING IN THE RAT MODEL SO CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Article ID CARDIAC-ARREST; MK-801; INJURY; BRAIN; PARAPLEGIA; ANTAGONIST; GLUTAMATE; PROTECTS; DAMAGE; PAPAVERINE AB Recent brain research proposes that, during ischemia, synaptically released excitatory amino acid neurotransmitters accumulate at toxic concentrations with ensuing neuronal death. Their action is mediated by the receptor subtype N-methyl-D-aspartate (NMDA). The protective effect of NMDA receptor blockade with intrathecal MgSO4 and MK-801 was investigated during spinal cord ischemia induced by aortic occlusion of 12 minutes. Male Sprague-Dawley rats, 250-300g, underwent intrathecal administration of 20 mu L of normal saline (SA n = 16), MgSO4 1M (MG n = 16), or MK-801, 25 mM solutions (MK n = 16) in a randomized order. After 2 hours, the animals underwent occlusion of the thoracic aorta and subclavian arteries for 12 min. An additional control group (CO n = 16) underwent occlusion for 12 minutes, without intrathecal injection. The animals were scored according to their functional performance (LS = lesion score) each day for four days by a blinded observer. Mean LS were calculated for each group at a given day. Treatment and control groups were not different at day 1 (P = 0.302). Group MG was improved from groups SA (P = < 0.0039) and CO (P = < 0.0048) at day 4. This study demonstrates that although intrathecal NMDA receptor blockade with MgSO, or MK-801 does not prevent paraplegia due to spinal cord ischemia in the rat, it could however influence the rate of recovery after ischemic injury. C1 UNIV NEW MEXICO,DEPT THORAC & CARDIOTHORAC SURG,ALBUQUERQUE,NM 87131. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHYSIOL,LOS ANGELES,CA 90024. FU NCRR NIH HHS [SO7 RR-05583-25, MO1 RR00997] NR 31 TC 24 Z9 26 U1 0 U2 0 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 1994 VL 21 IS 3 BP 227 EP 232 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA PC596 UT WOS:A1994PC59600007 PM 8000978 ER PT J AU DUBINETT, SM HUANG, M LICHTENSTEIN, A MCBRIDE, WH WANG, JY MARKOVITZ, G KELLEY, D GRODY, WW MINTZ, LE DHANANI, S AF DUBINETT, SM HUANG, M LICHTENSTEIN, A MCBRIDE, WH WANG, JY MARKOVITZ, G KELLEY, D GRODY, WW MINTZ, LE DHANANI, S TI TUMOR-NECROSIS-FACTOR-ALPHA PLAYS A CENTRAL ROLE IN INTERLEUKIN-2-INDUCED PULMONARY VASCULAR LEAK AND LYMPHOCYTE ACCUMULATION SO CELLULAR IMMUNOLOGY LA English DT Article ID ALVEOLAR MACROPHAGES; RECOMBINANT INTERLEUKIN-2; PASSIVE-IMMUNIZATION; HEMODYNAMIC-CHANGES; ENDOTHELIAL-CELLS; INTERFERON-GAMMA; GENE-EXPRESSION; ADVANCED CANCER; SEPTIC SHOCK; LUNG INJURY AB Administration of interleukin-2 (IL-2) leads to pulmonary vascular leak. This form of pulmonary edema has previously been postulated to be due to the in vivo induction of tumor necrosis factor-alpha (TNF-alpha). To determine whether TNF-alpha plays a role in IL-2-induced pulmonary vascular leak, we performed in situ hybridization of lung sections and reverse transcriptase-polymerase chain reaction of bronchoalveolar lavage macrophages from IL-2-challenged mice. The results confirm an in situ upregulation of TNF-alpha mRNA expression in the lungs associated with vascular leak. In addition, a significant increase in TNF-alpha protein production was found in the lung following IL2 administration, as measured by TNF-alpha-specific ELISA of lung supernatants (P = 0.028). Intravenous administration ofa soluble TNF receptor significantly diminished 1L-2-induced pulmonary vascular leak (P = 0.006). These findings confirm a central role for TNF-alpha in mediating the pulmonary vascular leak associated with IL-2 toxicity, (C) 1994 Academic Press, Inc. C1 UNIV CALIF LOS ANGELES,DIV MED ONCOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DIV RADIAT ONCOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DIV MOLEC PATHOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,MED RES SERV,LOS ANGELES,CA 90073. RP DUBINETT, SM (reprint author), UNIV CALIF LOS ANGELES,DIV PULM & CRIT CARE MED,WADSWORTH PULM IMMUNOL LAB,LOS ANGELES,CA 90024, USA. FU NCI NIH HHS [CA09120] NR 40 TC 45 Z9 46 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD AUG PY 1994 VL 157 IS 1 BP 170 EP 180 DI 10.1006/cimm.1994.1214 PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA NZ093 UT WOS:A1994NZ09300015 PM 8039244 ER PT J AU WINKELMAN, J ALTSCHULER, C GLENN, G LAESSIG, R GOLDSTEIN, D WERNER, M WILDING, P SILVERSTEIN, M KAMPA, I FIREMAN, B DAWSON, N MALKUS, H WITTE, D ROSMAN, A GARBER, C HOLTZMAN, N AF WINKELMAN, J ALTSCHULER, C GLENN, G LAESSIG, R GOLDSTEIN, D WERNER, M WILDING, P SILVERSTEIN, M KAMPA, I FIREMAN, B DAWSON, N MALKUS, H WITTE, D ROSMAN, A GARBER, C HOLTZMAN, N TI JAPANESE HEALTH-CARE SYSTEM - IN-VITRO DIAGNOSTIC-TESTS AND REIMBURSEMENTS - DISCUSSION SO CLINICAL CHEMISTRY LA English DT Discussion C1 ST JOSEPHS HOSP,MILWAUKEE,WI. MED COLL WISCONSIN,MILWAUKEE,WI 53226. WISCONSIN STATE LAB HYG,MADISON,WI. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20052. HOSP UNIV PENN,PHILADELPHIA,PA 19104. MAYO CLIN & MAYO FDN,DEPT MED,DIV AREA GEN INTERNAL MED,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DEPT HLTH SCI RES,CLIN EPIDEMIOL SECT,ROCHESTER,MN 55905. CASE WESTERN RESERVE UNIV,CLEVELAND,OH. YALE NEW HAVEN MED CTR,NEW HAVEN,CT 06504. BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY 10468. CUNY MT SINAI SCH MED,NEW YORK,NY 10468. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. KAISER PERMANENTE MED CTR,LOS ANGELES,CA. RP WINKELMAN, J (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT CLIN LABS,ADM LAB,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD AUG PY 1994 VL 40 IS 8 BP 1668 EP 1670 PG 3 WC Medical Laboratory Technology SC Medical Laboratory Technology GA PA073 UT WOS:A1994PA07300052 ER PT J AU TALAL, N AF TALAL, N TI CONCLUDING REMARKS - AUTOGENES AND ONCOGENES SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Editorial Material ID FAS MESSENGER-RNA; LPR MICE; AUTOIMMUNE-DISEASE; APOPTOSIS; EXPRESSION; INSERTION; ANTIGEN; GENES; ETN C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP TALAL, N (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [DEO 9311] NR 15 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD AUG PY 1994 VL 72 IS 2 BP 208 EP 209 DI 10.1006/clin.1994.1132 PG 2 WC Immunology; Pathology SC Immunology; Pathology GA PB324 UT WOS:A1994PB32400013 PM 8050195 ER PT J AU HUQUE, T BRAND, JG AF HUQUE, T BRAND, JG TI NITRIC-OXIDE SYNTHASE ACTIVITY OF THE TASTE ORGAN OF THE CHANNEL CATFISH, ICTALURUS-PUNCTATUS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY LA English DT Article DE NITRIC OXIDE SYNTHASE; TASTE ORGAN; ICTALURUS PUNCTATUS ID L-ARGININE; BINDING; CEREBELLUM; CYCLASE; SYSTEM; CELLS AB The constitutive nitric oxide synthase activity of the catfish taste organ (barbel) was characterized, using the conversion of L-[H-3]arginine to L-[H-3]citrulline as the index of enzyme activity. The enzyme was dependent on Ca2+ (but not calmodulin) and NADPH (but not FAD). Activity was moderately enhanced by tetrahydrobiopterin. Kinetic parameters were K-m = 22 mu M and V-max = 25 pmol/min/mg. The enzyme was inhibited by N-G-monomethyl-L-arginine (half-maximally at 3 mu M) and N-G-nitro-L-arginine (half-maximally at 50 mu M), and also by sodium nitroprusside and superoxide dismutase. In the presence of millimolar levels of the taste stimulus L-alanine, nitric oxide synthase activity was increased by up to 3-fold, with activation of the enzyme being reversed by N-G-monomethyl-L-arginine. There was no activation of guanylyl cyclase by L-alanine. These data indicate that a constitutive nitric oxide synthase activity is present in the catfish taste organ and that, therefore, nitric oxide may have a role in the biochemical mechanisms underlying taste perception. C1 UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. UNIV PENN,SCH DENT MED,DEPT BIOCHEM,PHILADELPHIA,PA 19104. RP HUQUE, T (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. NR 23 TC 11 Z9 12 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0305-0491 J9 COMP BIOCHEM PHYS B JI Comp. Biochem. Physiol. B-Biochem. Mol. Biol. PD AUG PY 1994 VL 108 IS 4 BP 481 EP 486 DI 10.1016/0305-0491(94)90101-5 PG 6 WC Biochemistry & Molecular Biology; Zoology SC Biochemistry & Molecular Biology; Zoology GA PK631 UT WOS:A1994PK63100010 ER PT J AU HOO, GWS SANTIAGO, S WILLIAMS, AJ AF HOO, GWS SANTIAGO, S WILLIAMS, AJ TI NASAL MECHANICAL VENTILATION FOR HYPERCAPNIC RESPIRATORY-FAILURE IN CHRONIC OBSTRUCTIVE PULMONARY-DISEASE - DETERMINANTS OF SUCCESS AND FAILURE SO CRITICAL CARE MEDICINE LA English DT Article DE ARTIFICIAL RESPIRATION; CHRONIC OBSTRUCTIVE PULMONARY DISEASE; HYPERCAPNIA; INTENSIVE CARE UNITS; INTERMITTENT POSITIVE PRESSURE VENTILATION; MECHANICAL VENTILATION; RESPIRATORY INSUFFICIENCY; TIDAL VOLUME; CRITICAL ILLNESS; PULMONARY EMERGENCIES; SEVERITY OF ILLNESS INDEX ID POSITIVE PRESSURE VENTILATION; FACE MASK; ACUTE EXACERBATIONS; COPD; COMPLICATIONS; SUPPORT; SYSTEM AB Objectives: To evaluate the efficacy of nasal mechanical ventilation in patients with chronic obstructive pulmonary disease and hypercapnic respiratory failure and to identify predictors of success or failure of nasal mechanical ventilation. Design: Prospective case series. Setting: Medical intensive care unit in Veterans Administration Medical Center. Patients: Twelve chronic obstructive pulmonary disease patients treated during 14 episodes of hypercapnic respiratory failure. Interventions: Nasal mechanical ventilation in addition to conventional therapy to treat hypercapnic respiratory failure. Patients underwent nasal mechanical ventilation for at least 30 mins, or longer if the therapy was tolerated. Responses to therapy and arterial blood gases were monitored. Measurements and Main Results: Half of the episodes were successfully treated with nasal mechanical ventilation. There were no differences in age, prior pulmonary function, baseline arterial blood gases, admission arterial blood gases, or respiratory rate between those patients successfully treated and those patients who failed nasal mechanical ventilation. Unsuccessfully treated patients appeared to have a greater severity of illness than successfully treated patients, as indicated by a higher Acute Physiology and Chronic Health Evaluation II score (mean 21 +/- 4 [SD] vs. 15 +/- 4; p = .02). Unsuccessfully treated patients were edentulous, had pneumonia or excess secretions, and had pursed-lip breathing, factors that prevented adequate mouth seal and contributed to greater mouth leaks than in successfully treated patients (the mean volume of the mouth leak was 314 +/- 107 vs. 100 +/- 70 mL; p < .01). Successfully treated patients were able to adapt more rapidly to the nasal mask and ventilator, with greater and more rapid reduction in Paco(2), correction of pH, and reduction in respiratory rate. Conclusions: Patients who failed nasal mechanical ventilation appeared to have a greater severity of illness; they were unable to minimize the amount of mouth leak (because of lack of teeth, secretions, or breathing pattern) and were unable to coordinate with the ventilator. These features may allow identification of poor candidates for nasal mechanical ventilation, avoiding unnecessary delays in endotracheal intubation and mechanical ventilation. C1 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. RP HOO, GWS (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,PULM & CRIT CARE SECT W111Q,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 23 TC 92 Z9 96 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD AUG PY 1994 VL 22 IS 8 BP 1253 EP 1261 PG 9 WC Critical Care Medicine SC General & Internal Medicine GA PA247 UT WOS:A1994PA24700009 ER PT J AU DULGEROFF, AJ HERSHMAN, JM AF DULGEROFF, AJ HERSHMAN, JM TI MEDICAL THERAPY FOR DIFFERENTIATED THYROID-CARCINOMA SO ENDOCRINE REVIEWS LA English DT Review ID TUMOR-NECROSIS-FACTOR; DOXORUBICIN PLUS CISPLATIN; CELL-MEDIATED-IMMUNITY; SERUM THYROGLOBULIN; RADIOACTIVE IODINE; CONCISE COMMUNICATION; I-131 THERAPY; IMMUNOLOGICAL ASPECTS; PAPILLARY CARCINOMA; HOSPITAL EXPERIENCE C1 W LOS ANGELES VET AFFAIRS MED CTR,DIV ENDOCRINOL & METAB W111D,LOS ANGELES,CA 90073. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 121 TC 56 Z9 58 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0163-769X J9 ENDOCR REV JI Endocr. Rev. PD AUG PY 1994 VL 15 IS 4 BP 500 EP 515 PG 16 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PD217 UT WOS:A1994PD21700007 PM 7988483 ER PT J AU PHARR, PN OGAWA, M HOFBAUER, A LONGMORE, G AF PHARR, PN OGAWA, M HOFBAUER, A LONGMORE, G TI NEITHER AN ACTIVATED ERYTHROPOIETIN NOR A CSF-1 RECEPTOR-INDUCED THE DIFFERENTIATION OF PLURIPOTENT PROGENITORS SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 VET AFFAIRS MED CTR,RALPH H JOHNSON DEPT,CHARLESTON,SC 29403. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. WASHINGTON UNIV,SCH MED,DIV HEMATOL ONCOL,ST LOUIS,MO 63110. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD AUG PY 1994 VL 22 IS 8 BP 685 EP 685 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA PB368 UT WOS:A1994PB36800030 ER PT J AU REDDY, SV SINGER, FR ROODMAN, GD AF REDDY, SV SINGER, FR ROODMAN, GD TI HEMATOPOIETIC PRECURSORS FROM PATIENTS WITH PAGETS-DISEASE (PD) OF BONE EXPRESS MEASLES-VIRUS NUCLEOCAPSID (MVN) MESSENGER-RNA SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. ST JOHNS MED CTR, SANTA MONICA, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0301-472X EI 1873-2399 J9 EXP HEMATOL JI Exp. Hematol. PD AUG PY 1994 VL 22 IS 8 BP 686 EP 686 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA PB368 UT WOS:A1994PB36800034 ER PT J AU CAREY, K AF CAREY, K TI COST ALLOCATION PATTERNS BETWEEN HOSPITAL INPATIENT AND OUTPATIENT DEPARTMENTS SO HEALTH SERVICES RESEARCH LA English DT Article DE COST ALLOCATION; OUTPATIENT SERVICE; COST FUNCTION ID PROSPECTIVE PAYMENT SYSTEM; PERFORMANCE; COMPETITION; PRODUCTIVITY; CONTAINMENT; OWNERSHIP; OUTPUT; LABOR AB Objective. This study examines changes in hospitals' cost allocation patterns between inpatient and outpatient departments in response to the implementation of the prospective payment system. Data Sources and Study Settings. The analysis was carried out using data for 3,961 hospitals obtained from the Medicare Cost Reports and from the American Hospital Association for the years 1984 through 1988. Study Design. A total operating cost function was estimated on the two outputs of discharges and outpatient visits. The estimation results were instrumental in disaggregating costs into inpatient and outpatient components. This was done cross sectionally for each of the five years. Principal Findings. Comparison of this cost breakdown with that of hospital revenue provides evidence of distinct patterns in which nonteaching, rural, and small hospitals increasingly allocated greater costs to outpatient departments than did large, urban, and teaching hospitals. Conclusions. The results suggest that small rural hospitals turned to the outpatient side in the face of tough economic challenges over the period of study. Because differences in cost allocation patterns occur by particular hospital category, analyses that rely on accounting cost or revenue data in order to identify cost differences among those same categories may come to erroneous conclusions. In particular, because teaching hospitals apportion costs more heavily on the inpatient side, cost allocation differences cause upward bias in the PPS medical education adjustment. RP CAREY, K (reprint author), US DEPT VET AFFAIRS,MANAGEMENT SCI GRP,200 SPRINGS RD,BEDFORD,MA 01730, USA. NR 42 TC 8 Z9 8 U1 2 U2 5 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 AUG PY 1994 VL 29 IS 3 BP 275 EP 292 PG 18 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA PD813 UT WOS:A1994PD81300002 PM 8063566 ER PT J AU GILL, JI GULLEY, ML AF GILL, JI GULLEY, ML TI IMMUNOGLOBULIN AND T-CELL RECEPTOR GENE REARRANGEMENT SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; POLYMERASE CHAIN-REACTION; MINIMAL RESIDUAL DISEASE; B-CELLS; LYMPHOPROLIFERATIVE DISORDERS; CLONAL REARRANGEMENT; HODGKINS-DISEASE; MALIGNANT-LYMPHOMA; REGION GENES; BETA-GENE C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. FU NCI NIH HHS [KO8-CA01615] NR 66 TC 19 Z9 19 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD AUG PY 1994 VL 8 IS 4 BP 751 EP 770 PG 20 WC Oncology; Hematology SC Oncology; Hematology GA PD162 UT WOS:A1994PD16200012 PM 7961289 ER PT J AU CLARE, N HANSEN, K AF CLARE, N HANSEN, K TI CYTOGENETICS IN THE DIAGNOSIS OF HEMATOLOGIC MALIGNANCIES SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; ACUTE NONLYMPHOCYTIC LEUKEMIA; ACUTE MYELOID-LEUKEMIA; ACUTE PROMYELOCYTIC LEUKEMIA; BONE-MARROW TRANSPLANTATION; NON-HODGKINS-LYMPHOMA; DENOVO MYELODYSPLASTIC SYNDROME; ACUTE MEGAKARYOCYTIC LEUKEMIA; POLYMERASE CHAIN-REACTION C1 AUDIE L MURPHY MEM VET ADM MED CTR,HEMATOL LAB,SAN ANTONIO,TX 78284. RP CLARE, N (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,CYTOGENET LAB,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 99 TC 9 Z9 9 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD AUG PY 1994 VL 8 IS 4 BP 785 EP 807 PG 23 WC Oncology; Hematology SC Oncology; Hematology GA PD162 UT WOS:A1994PD16200014 PM 7961291 ER PT J AU NISHIZAKI, Y KAUNITZ, JD ODA, M GUTH, PH AF NISHIZAKI, Y KAUNITZ, JD ODA, M GUTH, PH TI IMPAIRMENT OF GASTRIC-MUCOSAL DEFENSES MEASURED IN-VIVO IN CIRRHOTIC RATS SO HEPATOLOGY LA English DT Article ID ALKALINE-PHOSPHATASE ACTIVITY; PORTAL-HYPERTENSION; BLOOD-FLOW; INTRACELLULAR PH; LIVER-CIRRHOSIS; VASCULAR ECTASIAS; HUMAN-SERUM; INJURY; CELL; PROSTAGLANDIN-E2 AB Patients with cirrhosis have an increased incidence of gastric ulcers and erosions. We evaluated the effect of carbon tetrachloride-induced cirrhosis on rat gastric mucosal defense mechanisms using our recently developed in vivo fluorescence microscopy technique. Cirrhotic rats had increased portal vein pressure, increased serum aminotransferase concentrations and decreased serum albumin concentrations. We noted significantly more spontaneous gross gastric lesions in the cirrhotic rats. In vivo microscopic measurements revealed that cirrhotic rats had (a) a significantly thinner gastric mucous gel layer, (b) a much greater decrease in surface mucosal cell intracellular pH in response to an acid load, (c) decreased gastric mucosal blood how and (d) decreased surface cell viability. We conclude that spontaneous gastric mucosal lesions in cirrhotic rats may be related to more rapid penetration of acid through a thinner gastric mucous gel layer and a lower mucosal blood flow. These changes are associated with a decreased ability of the surface cells to maintain intracellular pH homeostasis, increased initial gastric surface cell acidification, decreased surface cell viability and a lower blood flow that probably is inadequate to remove the increased acid. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,CTR ULCER RES & EDUC,DEPT MED,LOS ANGELES,CA 90073. KEIO UNIV,SCH MED,DEPT INTERNAL MED,TOKYO 160,JAPAN. NR 45 TC 18 Z9 18 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD AUG PY 1994 VL 20 IS 2 BP 445 EP 452 DI 10.1016/0270-9139(94)90198-8 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PA130 UT WOS:A1994PA13000025 PM 8045506 ER PT J AU TYAN, ML AF TYAN, ML TI H-2-ASSOCIATED CLEFT-PALATE (CP) SUSCEPTIBILITY GENES SO IMMUNOGENETICS LA English DT Letter ID CHROMOSOME-17; MAPS; H-2 RP TYAN, ML (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD AUG PY 1994 VL 40 IS 4 BP 315 EP 315 PG 1 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA PE479 UT WOS:A1994PE47900017 PM 8082901 ER PT J AU KLEIN, BS CHATURVEDI, S HOGAN, LH JONES, JM NEWMAN, SL AF KLEIN, BS CHATURVEDI, S HOGAN, LH JONES, JM NEWMAN, SL TI ALTERED EXPRESSION OF SURFACE PROTEIN WI-1 IN GENETICALLY RELATED STRAINS OF BLASTOMYCES-DERMATITIDIS THAT DIFFER IN VIRULENCE REGULATES RECOGNITION OF YEASTS BY HUMAN MACROPHAGES SO INFECTION AND IMMUNITY LA English DT Article ID HISTOPLASMA-CAPSULATUM; PHASE VARIATION; POLYACRYLAMIDE GELS; ANTIGENIC VARIATION; MECHANISM; MUTATION; INVITRO; INVIVO; CELLS; GENES AB The molecular basis for pathogenicity and virulence of the dimorphic fungus Blastomyces dermatitidis remains unknown. WI-1 is a major cell wall protein of B. dermatitidis yeasts and is a recognition target of both humoral and cell-mediated immunity. As an initial study to determine if WI-1 might be linked to virulence of B. dermatitidis, we quantified WI-1 expression on three genetically related strains that differ in their virulence for mice: wild-type virulent ATCC strain 26199, mutant ATCC strain 60915 (which is 10,000-fold reduced in virulence), and mutant ATCC strain 60916 (which is avirulent). Two principal alterations in WI-1 expression were observed in the mutants. First, the mutants express more WI-1 on their surface, as quantified by flow cytometry with monoclonal antibody to WI-1 and by radioimmunoassay, but the WI-1 on their cell wall is less extractable than that on the wild-type strain. Second, the mutants shed less WI-1 during culture and demonstrate impaired professing of shed WI-1. Surface alterations in WI-1 were accompanied by significant differences in the binding of the virulent and mutant strains to human monocyte-derived macrophages. Attachment of yeasts to macrophages paralleled and was proportional to the expression of WI-1. Compared with wild-type yeasts, both mutants bound to macrophages more rapidly and in two- to threefold-greater magnitude. Furthermore, about 75% of yeast binding to macrophages was inhibited by a Fab anti-WI-1 monoclonal antibody. These results suggest that altered WI-1 expression on attenuated and avirulent mutant B. dermatitidis yeasts greatly facilitates macrophage recognition and binding of yeasts and, in turn, may contribute to more rapid ingestion and killing in the host. C1 UNIV WISCONSIN HOSP & CLIN,SCH MED,DEPT INTERNAL MED,MADISON,WI 53792. UNIV WISCONSIN HOSP & CLIN,SCH MED,DEPT MED MICROBIOL & IMMUNOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. UNIV CINCINNATI,COLL MED,DEPT INTERNAL MED,DIV INFECT DIS,CINCINNATI,OH 45267. RP KLEIN, BS (reprint author), UNIV WISCONSIN HOSP & CLIN,SCH MED,DEPT PEDIAT,600 HIGHLAND AVE,K4-434,MADISON,WI 53792, USA. FU NIAID NIH HHS [AI-31479, AI-23985, AI-00905] NR 28 TC 29 Z9 29 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 1994 VL 62 IS 8 BP 3536 EP 3542 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NY872 UT WOS:A1994NY87200064 PM 8039924 ER PT J AU HEFLE, SL LEMANSKE, RF BUSH, RK AF HEFLE, SL LEMANSKE, RF BUSH, RK TI ADVERSE REACTION TO LUPINE-FORTIFIED PASTA SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article DE LEGUME; HYPERSENSITIVITY; CROSS-REACTION; LUPINE ID MAJOR COMPONENT PROTEINS; LEGUME BOTANICAL FAMILY; ATOPIC-DERMATITIS; FOOD HYPERSENSITIVITY; CROSS-ALLERGENICITY; PEANUT ALLERGEN; CHILDREN; IDENTIFICATION; CHALLENGES; SERA AB A 5-year-old girl with peanut sensitivity experienced urticaria and angioedema after ingesting a spaghetti-like pasta fortified with sweet lupine seed flour The pasta was extracted and used in immunologic studies in patients with peanut sensitivity to determine whether such individuals are at similar risk. Results of skin prick tests with the lupine pasta extract were positive in five of seven subjects; these patients also reported a history of adverse reactions to green peas. In direct RAST studies IgE binding from pooled sera from patients with peanut sensitivity to the lupine pasta extract was 7 times that of a nonallergic control serum, and individual serum samples demonstrated binding from 1 to 6 times that of the negative control. Direct RAST studies of lupine seed flour with serum samples from patients with peanut allergy demonstrated IgE binding 1 to 11 times that of the negative control. Immunoblotting studies of electrophoretically separated pasta extract and lupine seed flour proteins showed IgE-binding protein bands at approximately 21 kd and in the range of 35 to 55 kd molecular weight We conclude that some peanut-sensitive patients may be at risk for adverse reactions to lupine. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,CTR CLIN SCI,DEPT MED,MADISON,WI. UNIV WISCONSIN,FOOD RES INST,MADISON,WI 53706. NR 26 TC 80 Z9 82 U1 0 U2 1 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 1994 VL 94 IS 2 BP 167 EP 172 DI 10.1016/0091-6749(94)90036-1 PG 6 WC Allergy; Immunology SC Allergy; Immunology GA PC926 UT WOS:A1994PC92600005 PM 8064069 ER PT J AU ATKINS, MB OBOYLE, KR SOSMAN, JA WEISS, GR MARGOLIN, KA ERNEST, ML KAPPLER, K MIER, JW SPARANO, JA FISHER, RI ECKARDT, JR PEREIRA, C ARONSON, FR AF ATKINS, MB OBOYLE, KR SOSMAN, JA WEISS, GR MARGOLIN, KA ERNEST, ML KAPPLER, K MIER, JW SPARANO, JA FISHER, RI ECKARDT, JR PEREIRA, C ARONSON, FR TI MULTIINSTITUTIONAL PHASE-II TRIAL OF INTENSIVE COMBINATION CHEMOIMMUNOTHERAPY FOR METASTATIC MELANOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACTIVATED KILLER-CELLS; HIGH-DOSE CISPLATIN; MALIGNANT-MELANOMA; ALPHA-INTERFERON; INTERLEUKIN-2; CHEMOTHERAPY; DACARBAZINE; TAMOXIFEN; THERAPY; REGIMEN C1 CYTOKINE WORKING GRP,BOSTON,MA. ALBERT EINSTEIN MED CTR,MONTEFIORE MED CTR,NEW YORK,NY. LOYOLA UNIV,MED CTR,MAYWOOD,IL 60153. UNIV TEXAS,AUDIE L MURPHY MEM VET ADM MED CTR,CTR HLTH SCI,SAN ANTONIO,TX. CITY HOPE NATL MED CTR,DUARTE,CA. UNIV CALIF SAN FRANCISCO,MED CTR,SAN FRANCISCO,CA 94143. RP ATKINS, MB (reprint author), TUFTS UNIV,NEW ENGLAND MED CTR,DIV HEMATOL ONCOL,BOX 245,BOSTON,MA 02111, USA. FU NCRR NIH HHS [M01-RR00054, M01-RR00079] NR 39 TC 106 Z9 107 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD AUG PY 1994 VL 12 IS 8 BP 1553 EP 1560 PG 8 WC Oncology SC Oncology GA PA257 UT WOS:A1994PA25700006 PM 8040667 ER PT J AU ALTSHULER, LL PIERRE, JM WIRSHING, WC AMES, D AF ALTSHULER, LL PIERRE, JM WIRSHING, WC AMES, D TI SERTRALINE AND AKATHISIA SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter ID FLUOXETINE RP ALTSHULER, LL (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 7 TC 22 Z9 22 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD AUG PY 1994 VL 14 IS 4 BP 278 EP 279 DI 10.1097/00004714-199408000-00010 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA NX836 UT WOS:A1994NX83600010 PM 7962686 ER PT J AU AMES, D WIRSHING, WC COKELY, HT LO, LL AF AMES, D WIRSHING, WC COKELY, HT LO, LL TI THE NATURAL COURSE OF PSEUDOTUMOR CEREBRI IN LITHIUM-TREATED PATIENTS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter ID CARBONATE C1 W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,MED CTR,LOS ANGELES,CA 90024. RP AMES, D (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024, USA. NR 6 TC 5 Z9 5 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD AUG PY 1994 VL 14 IS 4 BP 286 EP 287 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA NX836 UT WOS:A1994NX83600016 PM 7962691 ER PT J AU CHEMTOB, CM HAMADA, RS ROITBLAT, HL MURAOKA, MY AF CHEMTOB, CM HAMADA, RS ROITBLAT, HL MURAOKA, MY TI ANGER, IMPULSIVITY, AND ANGER CONTROL IN COMBAT-RELATED POSTTRAUMATIC-STRESS-DISORDER SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY LA English DT Article ID VIETNAM-ERA VETERANS; GENERAL-POPULATION; DEPRESSION; SCALE AB Empirical evidence of a relationship between combat-related PTSD and increased anger is lacking. In this study, 24 veterans of the Vietnam War with posttraumatic stress disorder (PTSD) scored significantly higher on an Anger factor comprising multiple measures of anger than did comparison groups of 23 well-adjusted Vietnam combat veterans and 12 noncombat Vietnam-era veterans with psychiatric diagnoses. In contrast, the 3 groups did not differ significantly on orthogonal factors, one of which comprised cognitive impulsivity measures and the other of which reflected motor impulsivity. Changes in heart rate in response to provocation loaded positively on the Anger factor and negatively on the 2 Impulsivity factors. Concurrent depression and trait anxiety did not have an effect on level of anger in individuals with PTSD. These empirical findings support and extend the clinical evidence regarding PTSD and anger. C1 UNIV HAWAII,HONOLULU,HI 96822. RP CHEMTOB, CM (reprint author), US DEPT VET AFFAIRS,RES & DEV 151,STRESS DISORDERS RES LAB,POB 50188,HONOLULU,HI 96850, USA. NR 34 TC 104 Z9 105 U1 0 U2 6 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0022-006X J9 J CONSULT CLIN PSYCH JI J. Consult. Clin. Psychol. PD AUG PY 1994 VL 62 IS 4 BP 827 EP 832 DI 10.1037/0022-006X.62.4.827 PG 6 WC Psychology, Clinical SC Psychology GA PD281 UT WOS:A1994PD28100020 PM 7962887 ER PT J AU GROVER, FL COHEN, DJ OPRIAN, C HENDERSON, WG SETHI, G HAMMERMEISTER, KE JOHNSON, R BIRDWELL, A SETHI, GK HALUZA, M KIM, T VITEK, ME CRAWFORD, M FOLLAND, ED KHURI, S HWANG, M MILLER, DC RAHIMTOOLA, S DEYKIN, D GOLD, J HUANG, P AF GROVER, FL COHEN, DJ OPRIAN, C HENDERSON, WG SETHI, G HAMMERMEISTER, KE JOHNSON, R BIRDWELL, A SETHI, GK HALUZA, M KIM, T VITEK, ME CRAWFORD, M FOLLAND, ED KHURI, S HWANG, M MILLER, DC RAHIMTOOLA, S DEYKIN, D GOLD, J HUANG, P TI DETERMINANTS OF THE OCCURRENCE OF AND SURVIVAL FROM PROSTHETIC VALVE ENDOCARDITIS - EXPERIENCE OF THE VETERANS AFFAIRS COOPERATIVE STUDY ON VALVULAR HEART-DISEASE SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID MANAGEMENT; REPLACEMENT AB For the determination of the risk factors associated with the development of and death caused by prosthetic valve endocarditis, data were reviewed from 66 patients who were prospectively entered into the Veterans Affairs Cooperative Study on Valvular Heart Disease and in whom prosthetic valve endocarditis subsequently developed. Data were recorded at 13 medical centers between October 1977 and September 1982 in patients randomized to receive a mechanical valve (Bjork-Shiley spherical disc, n = 510 patients) or a bioprosthetic valve (Hancock porcine heterograft, n = 522 patients). The average rate of prosthetic valve endocarditis development was 0.8% per year over an average follow-up period of 7.7 years. Of the 66 patients in whom prosthetic valve endocarditis developed (5.8%), 15 cases occurred within 2 months of operation (early) and 51 occurred after operation Gate). The most significant preoperative predictor of prosthetic valve endocarditis was active endocarditis at the time of operation (7.4% versus 0.9%) (p = 0.001). Early prosthetic valve endocarditis occurred more frequently in patients who underwent operation for multivalvular disease (p = 0.023). Significantly related perioperative variables were coma, prolonged mechanical ventilation, deep postoperative wound infection, postoperative jaundice, ventricular tachycardia, ventricular fibrillation, and replacement of more than one valve (p < 0.05). Multivariate predictors were hypoxia (p = 0.001), preoperative endocarditis (p = 0.003), preoperative valve lesion (p = 0.020), and resident surgeon (p = 0.05). Significant preoperative variables predictive of late prosthetic valve endocarditis were mitral stenosis and mixed mitral stenosis-regurgitation. The only multivariate predictor of late prosthetic valve endocarditis was superficial wound infection (p = 0.004). Of deaths attributable to prosthetic valve endocarditis, 41% occurred in patients treated with antibiotics alone, 48% occurred in patients treated with surgical intervention and antibiotics, and death resulted in both patients who received no treatment. No difference was found in the risk of early or late postoperative prosthetic valve endocarditis developing in patients receiving the mechanical valve versus those receiving the bioprosthetic valve. C1 UNIV COLORADO,HLTH SCI CTR,DEPT VET AFFAIRS MED CTR,CARDIOTHORAC SURG SECT,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,DEPT VET AFFAIRS MED CTR,CARDIOL SECT,DENVER,CO. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV ARIZONA,HLTH SCI CTR,DEPT VET AFFAIRS MED CTR,TUCSON,AZ. DEPT VET AFFAIRS MED CTR,COOPERAT STUDIES PROGRAM,COORDINATING CTR,HINES,IL. NR 27 TC 77 Z9 81 U1 0 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD AUG PY 1994 VL 108 IS 2 BP 207 EP 214 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA PB114 UT WOS:A1994PB11400002 PM 8041168 ER PT J AU OBRIEN, WA MAO, SH CAO, YZ MOORE, JP AF OBRIEN, WA MAO, SH CAO, YZ MOORE, JP TI MACROPHAGE-TROPIC AND T-CELL LINE-ADAPTED CHIMERIC STRAINS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 DIFFER IN THEIR SUSCEPTIBILITIES TO NEUTRALIZATION BY SOLUBLE CD4 AT DIFFERENT TEMPERATURES SO JOURNAL OF VIROLOGY LA English DT Note ID ENVELOPE V3 LOOP; GLYCOPROTEIN GP120; HOST-RANGE; HIV-1; IDENTIFICATION; DETERMINANT; INFECTION; AFFINITY; GENE; SENSITIVITY AB Molecular clones of three macrophage-tropic and three T-cell line-adapted strains of human immunodeficiency virus type 1 (HIV-1) were used to explore the mechanism of HIV-1 resistance to neutralization by soluble CD4 (sCD4). The three macrophage-tropic viruses, each possessing the V3 and flanking regions of JR-FL, were all resistant to sCD4 neutralization under the standard conditions of a short preincubation of the virus and sCD4 at 37 degrees C prior to inoculation of peripheral blood mononuclear cells. In contrast, the three T-cell line-adapted viruses, NL4-3 and two chimeras possessing the V3 and flanking regions of NL4-3 in the envelope background of JR-FL, were all sCD4 sensitive under these conditions. Sensitivity to sCD4 neutralization at 37 degrees C corresponded with rapid, sCD4-induced gp120 shedding from the viruses. However, when the incubation temperature of the sCD4 and virus was reduced to 4 degrees C, the three macrophage-tropic viruses shed gp120 and became more sensitive to sCD4 neutralization. In contrast, the rates of sCD4 induced gp120 shedding and virus neutralization were reduced for the three T-cell line-adapted viruses at 4 degrees C. Thus, HIV resistance to sCD4 is a conditional phenomenon; macrophage-tropic and T-cell line-adapted strains can be distinguished by the temperature dependencies of their neutralization by sCD4. The average density of gp120 molecules on the macrophage-tropic viruses exceeded by about fourfold that on the T-cell line-adapted viruses, suggesting that HIV growth in T-cell lines may select for a destabilized envelope glycoprotein complex. Further studies of early events in HIV-1 infection should focus on primary virus strains. C1 NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY. RP OBRIEN, WA (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,691-111F,WILTSHIRE & SAWTELLE,LOS ANGELES,CA 90073, USA. FU NIAID NIH HHS [AI 28697-03, AI27742-04, AI 29894-04] NR 34 TC 56 Z9 56 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD AUG PY 1994 VL 68 IS 8 BP 5264 EP 5269 PG 6 WC Virology SC Virology GA NW978 UT WOS:A1994NW97800062 PM 8035523 ER PT J AU STRACK, S AF STRACK, S TI RELATING MILLONS BASIC PERSONALITY STYLES AND HOLLANDS OCCUPATIONAL TYPES SO JOURNAL OF VOCATIONAL BEHAVIOR LA English DT Article ID ADJECTIVE CHECK LIST; SAMPLE; SCALES AB This study examined the relation between Millon's (1983) basic personality styles and Holland's (1985a) occupational types. Subjects were 75 men and 77 women college students who completed the Personality Adjective Check List (Strack, 1987, 1991b), a measure of Millon's basic personalities designed for use with normal adults, and the Self-Directed Search (SDS; Holland, 1985c, 1987). Pearson and canonical correlation analyses were conducted separately for men and women. Bivariate correlations were typically modest, ranging from -.34 to .46 across sexes. Two significant canonical variates emerged for both men and women. Meaningful associations were found for essentially all of Millon's basic personalities and Holland's types, although the pattern was different for men and women. Millon and Holland appeared most similar along dimensions of social dominance-submissiveness and emotionality (neuroticism)-restraint (conscientiousness). RP STRACK, S (reprint author), US DEPT VET AFFAIRS,PSYCHOL SERV 116B,OUTPATIENT CLIN,351 E TEMPLE ST,LOS ANGELES,CA 90012, USA. NR 38 TC 10 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0001-8791 J9 J VOCAT BEHAV JI J. Vocat. Behav. PD AUG PY 1994 VL 45 IS 1 BP 41 EP 54 DI 10.1006/jvbe.1994.1025 PG 14 WC Psychology, Applied SC Psychology GA PA234 UT WOS:A1994PA23400003 ER PT J AU PRIVITERA, MD TREIMAN, DM PLEDGER, GW SAHLROOT, JT HANDFORTH, A LINDE, MS FRANCE, CR CEREGHINO, JJ MCCUTCHEN, CB WOOD, JH AF PRIVITERA, MD TREIMAN, DM PLEDGER, GW SAHLROOT, JT HANDFORTH, A LINDE, MS FRANCE, CR CEREGHINO, JJ MCCUTCHEN, CB WOOD, JH TI DEZINAMIDE FOR PARTIAL SEIZURES - RESULTS OF AN N-OF-1 DESIGN TRIAL SO NEUROLOGY LA English DT Article ID CIGARETTE-SMOKING AB Background. Dezinamide (DZM, ADD 94057) is a potential antiepileptic drug that binds to the voltage-sensitive sodium channel and showed preliminary evidence of efficacy and safety in an open-label study. Methods. Our double-blind, placebo-controlled trial at two sites used an n-of-1 (single-patient) design. All 15 patients had medically intractable partial-onset seizures and were comedicated with phenytoin (PHT) only. Treatment was for six and week periods (three active paired with three placebo in random sequence). Assuming nonlinear kinetics, we used an initial pharmacokinetic profile to estimate dosages for reaching target plasma concentrations of DZM. Results. Statistically significant seizure reduction was found by both a randomization test (p = 0.0025) and a signed rank test (p = 0.048). Median seizure frequency decreased 37.9%, and 40% of patients had >50% seizure reduction, both compared with placebo. Pharmacokinetic predictions were not accurate; mean plasma concentrations fell well below target values. Plasma PHT concentrations increased (mean = 17.1%) during DZM treatment. The most common adverse experiences were fatigue, light-headedness, and abnormal gait; five patients required DZM dosage reductions. Conclusions. DZM showed minimal clinical toxicity and significant efficacy despite lower plasma concentrations than predicted by pharmacokinetics. This trial establishes the suitability of the n-of-1 design to investigational antiepileptie drug trials. C1 UNIV CALIF LOS ANGELES,MED CTR,DEPT NEUROL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,LOS ANGELES,CA. NINCDS,EPILEPSY BRANCH,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARM,RICHMOND,VA 23298. RP PRIVITERA, MD (reprint author), UNIV CINCINNATI,MED CTR,DEPT NEUROL 525,CINCINNATI,OH 45267, USA. FU NINDS NIH HHS [NINDS N01-NS-7-2328, NINDS N01-NS-8-2306] NR 12 TC 10 Z9 10 U1 1 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD AUG PY 1994 VL 44 IS 8 BP 1453 EP 1458 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA PB152 UT WOS:A1994PB15200018 PM 8058148 ER PT J AU TAKAHASHI, LK KIM, H AF TAKAHASHI, LK KIM, H TI INTRACRANIAL ACTION OF CORTICOSTERONE FACILITATES THE DEVELOPMENT OF BEHAVIORAL-INHIBITION IN THE ADRENALECTOMIZED PREWEANLING RAT SO NEUROSCIENCE LETTERS LA English DT Article DE PREWEANLING RAT; BEHAVIORAL INHIBITION; FREEZING; ULTRASONIC VOCALIZATION; DEVELOPMENT; CONSPECIFIC THREAT; ADRENAL STEROID; CORTICOSTERONE ID REGULATE POSTNATAL-DEVELOPMENT; DENTATE-GYRUS; GLUCOCORTICOID RECEPTOR; ONTOGENY; BRAIN; HIPPOCAMPUS; PITUITARY; STRESS; MATURATION; EXPRESSION AB We tested the hypothesis that in preweanling rats central administration of exogenous corticosterone (CORT) is sufficient to facilitate the development of behavioral inhibition. 28-gauge cannulae containing varying concentrations of CORT (0, 25, 50 and 100%) were implanted unilaterally into the lateral ventricles of 9-day-old rat pups. After a 24-h postoperative recovery period, pups were adrenalectomized. At 14 days of age, pups were tested for behavioral inhibition which consisted of removing the pup from the nest and exposing it to an unfamiliar adult male rat. Pups implanted with cannulae containing 0, 25 and 50% concentrations of CORT spent significantly less time in freezing postures than pups implanted with cannulae containing 100% CORT. These freezing pups also tended to emit fewer ultrasonic vocalizations than pups in the other three implant conditions, albeit the level obtained was not statistically significant. RIAs indicated that, in general, hormone-filled cannulae produced no detectable concentrations of plasma CORT on the day of the test or on days preceding testing. Results suggest that in the early postnatal period endogenous CORT acts centrally to facilitate the development of neural pathways involved in the ontogenetic expression of behavioral inhibition. 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 42 TC 10 Z9 11 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD AUG 1 PY 1994 VL 176 IS 2 BP 272 EP 276 DI 10.1016/0304-3940(94)90099-X PG 5 WC Neurosciences SC Neurosciences & Neurology GA PE808 UT WOS:A1994PE80800034 PM 7830963 ER PT J AU CORRIGAN, PW GREEN, MF TOOMEY, R AF CORRIGAN, PW GREEN, MF TOOMEY, R TI COGNITIVE CORRELATES TO SOCIAL CUE PERCEPTION IN SCHIZOPHRENIA SO PSYCHIATRY RESEARCH LA English DT Article DE SOCIAL SKILLS TRAINING; REHABILITATION; INFORMATION PROCESSING; PSYCHIATRIC SYMPTOMS ID PREFRONTAL CORTEX; SKILLS; PERFORMANCE; DISORDER; MEMORY AB Previous research has examined social skill learning in schizophrenic patients in relation to information-processing deficits and psychiatric symptoms. Relationships were examined in the current report between social cue perception, thought to be an early and necessary component of skill learning, and various information-processing deficits and psychiatric symptoms. Twenty-six inpatients with DSM-III-R diagnoses of schizophrenia completed measures of social cue perception, cognitive functioning, and psychiatric symptoms. Results showed that cue perception was significantly related to measures of early visual processing, recognition memory, and psychiatric symptoms of withdrawal/retardation. Implications of these findings for future research into the social-perceptual deficits of schizophrenic patients are discussed. C1 UNIV CHICAGO,PRITZKER SCH MED,CHICAGO,IL 60637. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. BOSTON UNIV,BOSTON,MA 02215. VET ADM MED CTR,HARVARD UNIV,DEPT PSYCHIAT,BROCKTON,MA 02401. FU NIMH NIH HHS [MH-30911, MH-43292] NR 45 TC 59 Z9 59 U1 0 U2 5 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 AUG PY 1994 VL 53 IS 2 BP 141 EP 151 DI 10.1016/0165-1781(94)90105-8 PG 11 WC Psychiatry SC Psychiatry GA PJ157 UT WOS:A1994PJ15700004 PM 7824674 ER PT J AU ORWOLL, ES BLIZIOTES, M AF ORWOLL, ES BLIZIOTES, M TI HETEROGENEITY IN OSTEOPOROSIS - MEN VERSUS WOMEN SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID BONE-MINERAL DENSITY; AGE-RELATED-CHANGES; CORTICOSTEROID-INDUCED OSTEOPOROSIS; RADIAL PHOTON-ABSORPTIOMETRY; HIP FRACTURE INCIDENCE; SEX-RELATED CHANGES; TRABECULAR BONE; SPINAL OSTEOPOROSIS; DIETARY CALCIUM; HEALTHY-MEN C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. RP ORWOLL, ES (reprint author), PORTLAND VET AFFAIRS MED CTR,BONE & MINERAL RES UNIT,3710 SW US VET HOSP RD,PORTLAND,OR 97201, USA. OI Orwoll, Eric/0000-0002-8520-7355 NR 141 TC 16 Z9 16 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-857X J9 RHEUM DIS CLIN N AM JI Rheum. Dis. Clin. North Am. PD AUG PY 1994 VL 20 IS 3 BP 671 EP 689 PG 19 WC Rheumatology SC Rheumatology GA PC560 UT WOS:A1994PC56000009 PM 7984784 ER PT J AU BRIDGES, AJ AF BRIDGES, AJ TI AUTOANTIBODIES IN PATIENTS WITH SILICONE IMPLANTS SO SEMINARS IN ARTHRITIS AND RHEUMATISM LA English DT Article; Proceedings Paper CT Symposium on Silicone-Related Disorders CY DEC 04, 1992 CL WASHINGTON, DC SP GEORGE WASHINGTON UNIV MED CTR DE SILICONE; AUTOANTIBODIES; CENTROMERE; RIBONUCLEOPROTEINS ID CONNECTIVE-TISSUE DISEASE; HUMAN ADJUVANT DISEASE; PROGRESSIVE SYSTEMIC-SCLEROSIS; GEL BREAST IMPLANTS; AUGMENTATION MAMMOPLASTY; ANTINUCLEAR ANTIBODIES; AUTOIMMUNE-DISEASES; LUPUS-ERYTHEMATOSUS; CHRONIC ARTHROPATHY; RHEUMATIC DISEASE C1 UNIV WISCONSIN,DEPT MED,RHEUMATOL SECT,MADISON,WI 53706. MIDDLETON VET ADM HOSP,MADISON,WI. NR 34 TC 18 Z9 19 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0049-0172 J9 SEMIN ARTHRITIS RHEU JI Semin. Arthritis Rheum. PD AUG PY 1994 VL 24 IS 1 SU 1 BP 54 EP 60 DI 10.1016/0049-0172(94)90110-4 PG 7 WC Rheumatology SC Rheumatology GA PC954 UT WOS:A1994PC95400009 PM 7801140 ER PT J AU MIRZABEKOV, T LIN, MC YUAN, WL MARSHALL, PJ CARMAN, M TOMASELLI, K LIEBERBURG, I KAGAN, BL AF MIRZABEKOV, T LIN, MC YUAN, WL MARSHALL, PJ CARMAN, M TOMASELLI, K LIEBERBURG, I KAGAN, BL TI CHANNEL FORMATION IN PLANAR LIPID BILAYERS BY A NEUROTOXIC FRAGMENT OF THE BETA-AMYLOID PEPTIDE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ALZHEIMERS-DISEASE; PROTEIN; PRECURSOR; MEMBRANES; AGGREGATION; NEURONS AB Alzheimer's disease (AD) pathology is characterized by plaques, tangles, and neuronal cell loss. The main constituent of plaques is beta-amyloid peptide (A beta), a 39-42 residue peptide which has been linked to disruption of calcium homeostasis and neurotoxicity in vitro. We demonstrate that a neurotoxic fragment of A beta, A beta (25-35) spontaneously inserted into planar lipid membranes to form weakly selective, voltage dependent, ion-permeable channels. We suggest that channel formation may be involved in the pathogenesis of AD and that A beta (25-35) may be the active channel forming segment. (C) 1994 Academic Press, Inc C1 UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90024. ATHENA NEUROSCI INC,S SAN FRANCISCO,CA 94080. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. FU NIMH NIH HHS [NIMH MH443433, NIMH MH01174] NR 25 TC 97 Z9 104 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JUL 29 PY 1994 VL 202 IS 2 BP 1142 EP 1148 DI 10.1006/bbrc.1994.2047 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NZ240 UT WOS:A1994NZ24000069 PM 7519420 ER PT J AU KOWLURU, A RABAGLIA, ME MUSE, KE METZ, SA AF KOWLURU, A RABAGLIA, ME MUSE, KE METZ, SA TI SUBCELLULAR-LOCALIZATION AND KINETIC CHARACTERIZATION OF GUANINE-NUCLEOTIDE-BINDING PROTEINS IN NORMAL RAT AND HUMAN PANCREATIC-ISLETS AND TRANSFORMED BETA-CELLS SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE PANCREATIC ISLET; GTPASE; G PROTEIN; SECRETORY GRANULE; INSULIN SECRETION ID INSULIN-SECRETING CELLS; LOW KM GTPASE; PERTUSSIS TOXIN; GRANULE MEMBRANES; HIT CELLS; CHROMAFFIN CELLS; PLASMA-MEMBRANES; ADP-RIBOSYLATION; CAMP METABOLISM; RINM5F CELLS AB The subcellular localization and the kinetics of the GTPase activities of monomeric and heterotrimeric GTP-binding proteins were investigated in normal rat and human pancreatic islets and were compared to those obtained using a transformed hamster beta cell line (HIT cells). The [alpha-P-32]GTP overlay technique revealed the presence of at least four low-molecular-mass proteins (approx. 20-27 kDa) in normal rat islets, which were enriched in the secretory granule fraction compared to the membrane fraction (with little abundance of these proteins in the cytosolic fraction). In contrast, in HIT cells, these proteins (at least six) were predominantly cytosolic. Three of these proteins were immunologically identified as rab3A, rac2 and CDC42Hs in islets as well as in HIT cells. In addition, pertussis toxin augmented the ribosylation of at least one heterotrimeric G-protein of about 39 kDa (probably G(i) and/or G(0)) in the membrane and secretory granule fractions of normal rat and human islets, whereas at least three such Ptx substrates (36-39 kDa) were found in HIT cell membranes. Kinetic analyses of the intrinsic specific GTPase activities revealed the presence of at least three such activities (K-m for GTP of 372 nM, 2.2 mu M, and 724 mu M) in islet homogenates which were differentially distributed in various subcellular fractions; similar activities were also demonstrable in HIT cell homogenates. Thus, these studies demonstrate the presence of both monomeric as well as trimeric G-proteins intrinsic to the secretory granules of normal rat islets which can be ascribed to beta cells; since these G-proteins are regulated by insulinotropic lipids (as described in the accompanying article), such proteins may couple the activation of phospholipases (endogenous to islets) to the exocytotic secretion of insulin. These findings also suggest that caution is necessary in extrapolating data concerning G-proteins from cultured, transformed beta cell lines to the physiology of normal islets, in view of both qualitative and quantitative differences between the two preparations. C1 UNIV WISCONSIN,SCH MED,ENDOCRINOL SECT,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI 53705. RP KOWLURU, A (reprint author), UNIV WISCONSIN,SCH MED,DEPT MED,H4-568 CLIN SCI CTR 600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIDDK NIH HHS [DK37312] NR 70 TC 38 Z9 38 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4889 J9 BBA-MOL CELL RES JI Biochim. Biophys. Acta-Mol. Cell Res. PD JUL 21 PY 1994 VL 1222 IS 3 BP 348 EP 359 DI 10.1016/0167-4889(94)90040-X PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PA034 UT WOS:A1994PA03400004 PM 8038203 ER PT J AU KOWLURU, A METZ, SA AF KOWLURU, A METZ, SA TI REGULATION OF GUANINE - NUCLEOTIDE-BINDING PROTEINS IN ISLET SUBCELLULAR-FRACTIONS BY PHOSPHOLIPASE-DERIVED LIPID MEDIATORS OF INSULIN-SECRETION SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE G PROTEIN; INSULIN SECRETION; LIPID MESSENGER; PANCREATIC ISLET; SECRETORY GRANULE; GTPASE ID PERMEABILIZED RAT ISLETS; ARACHIDONIC-ACID; PANCREATIC-ISLETS; GTPASE ACTIVITY; CHROMAFFIN GRANULES; CA-2+ MOBILIZATION; PLASMA-MEMBRANES; DUAL MECHANISMS; NADPH OXIDASE; RELEASE AB In the accompanying article (Kowluru, A., Rabaglia, M.E., Mose, K.E. and Metz, S.A. (1994) Biochim. Biophys. Acta 1222, 348-359) we identified three specific GTPase activities in islet subcellular fractions; most notably, two of these were enriched in the secretory granules. In the present study, we describe the regulation of GTPase activity in subcellular fractions of normal rat and human islets by insulinotropic lipids with a similar rank order as their insulin-releasing capacity. Arachidonic acid (AA), lysophosphatidylcholine (LPC), or phosphatidic acid (PA) inhibited the GTPase activities significantly (by 60-80%) in isIet homogenates; each also selectively inhibited certain GTPases in specific individual fractions. Less insulinotropic fatty acids, such as linoleic acid and oleic acid, inhibited GTPase to a lesser degree, whereas lysophosphatidic acid (LPA), phosphatidylcholine (PC) or palmitic acid, which do not acutely promote secretion, were ineffective. Similar inhibitory effects of these lipids were also demonstrable in fractions of human islets as well as those of transformed beta-cells (HIT cells). The effects of lipids were not attributable to their detergent properties (since several detergents failed to mimic lipid effects) or to inhibition of GTP binding (since they actually increased GTP gamma S binding modestly, and moreover, in reconstituted fractions, they potentiated GDP/GTP exchange activity up to 2-fold). These data indicate that the insulinotropic nature of the lipids might be due, in part, to their ability to maintain G-proteins in their GTP-bound (active) configuration by increasing GTP binding and decreasing its hydrolysis. These studies comprise the first evidence for the regulation by biologically active lipids of endocrine cell G-proteins at a locus distal to plasma membrane events (i.e., on endocrine secretory granules), and provide thereby a possible novel mechanism whereby the activation of islet endogenous phospholipases might culminate in insulin exocytosis. C1 UNIV WISCONSIN,SCH MED,ENDOCRINOL SECT,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP KOWLURU, A (reprint author), UNIV WISCONSIN,SCH MED,DEPT MED,H4-568 CLIN SCI CTR,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIDDK NIH HHS [DK 37312] NR 43 TC 26 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4889 J9 BBA-MOL CELL RES JI Biochim. Biophys. Acta-Mol. Cell Res. PD JUL 21 PY 1994 VL 1222 IS 3 BP 360 EP 368 DI 10.1016/0167-4889(94)90041-8 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PA034 UT WOS:A1994PA03400005 PM 8038204 ER PT J AU JACOBY, RF HOHMAN, C MARSHALL, DJ FRICK, TJ SCHLACK, S BRODA, M SMUTKO, J ELLIOTT, RW AF JACOBY, RF HOHMAN, C MARSHALL, DJ FRICK, TJ SCHLACK, S BRODA, M SMUTKO, J ELLIOTT, RW TI GENETIC-ANALYSIS OF COLON-CANCER SUSCEPTIBILITY IN MICE SO GENOMICS LA English DT Article ID MULTIPLE INTESTINAL NEOPLASIA; COLORECTAL-CANCER; INBRED STRAINS; APC GENE; MOUSE; 1,2-DIMETHYLHYDRAZINE; MUTATIONS; LINKAGE; MAP; CARCINOGENESIS AB Mouse models may aid in the identification of genes involved in colon cancer. Our mating scheme involved mouse strains selected for maximum differences in susceptibility to DMH-induced colon tumors, Tumors were found in 40 of 122 progeny from a backcross to the resistant strain. We examined progeny animals for segregation of 177 genetic markers distributed at intervals of 5-30 cM on all mouse chromosomes. Multiple loci contribute to the phenotype, with significant linkage to a novel locus, Ccs1, between D12Mit5 and D12Mit6 on mouse Chr 12. Comparative maps suggest that the human homologue of Ccs1 is near FOS on human chromosome 14q. (C) 1994 Academic Press, Inc. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,CTR COMPREHENS CANC,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. ROSWELL PK CANC INST,DEPT MOLEC & CELLULAR BIOL,BUFFALO,NY 14263. RP JACOBY, RF (reprint author), UNIV WISCONSIN,SCH MED,GASTROENTEROL SECT,H6-516 CLIN SCI CTR,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 39 TC 67 Z9 67 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JUL 15 PY 1994 VL 22 IS 2 BP 381 EP 387 DI 10.1006/geno.1994.1399 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA PB571 UT WOS:A1994PB57100018 PM 7806225 ER PT J AU BENMANSOUR, S BRUNSWICK, DJ AF BENMANSOUR, S BRUNSWICK, DJ TI THE MAO-B INHIBITOR DEPRENYL, BUT NOT THE MAO-A INHIBITOR CLORGYLINE, POTENTIATES THE NEUROTOXICITY OF P-CHLOROAMPHETAMINE SO BRAIN RESEARCH LA English DT Article DE P-CHLOROAMPHETAMINE; NEUROTOXICITY; SEROTONIN UPTAKE SITE; MONOAMINE OXIDASE; PARGYLINE; DEPRENYL; CLORGYLINE ID MONOAMINE-OXIDASE INHIBITORS; RAT-BRAIN; 3,4-METHYLENEDIOXYMETHAMPHETAMINE MDMA; EXTRACELLULAR 5-HYDROXYTRYPTAMINE; SEROTONIN; DOPAMINE; METABOLISM; RELEASE; METHYLENEDIOXYMETHAMPHETAMINE; 5,6-DIHYDROXYTRYPTAMINE AB The effect of co-administration of MAO inhibitors together with a low dose of the neurotoxic amphetamine p-chloroamphetamine (pCA) on neurotoxicity was examined. Neurotoxicity was assessed by measuring decreases in the binding of [H-3]cyanoimipramine to serotonin uptake sites using quantitative autoradiography. By itself, a low dose of pCA (2 mg/kg) did not produce any alterations in radioligand binding, measured 7 days after drug administration. However, co-administration of the MAO-B selective inhibitor deprenyl (1 mg/kg) or the non-selective inhibitor pargyline (50 mg/kg) produced significant decreases in radioligand binding. Measurements of the effects of these drugs on body temperature ruled out the possibility that deprenyl and pargyline were increasing neurotoxicity by producing a drug-induced hyperthermia. In contrast to the effects of deprenyl and pargyline, co-administration of the MAO-A selective inhibitor clorgyline (1 mg/kg) did not alter binding. By themselves none of the MAO inhibitors produced neurotoxic effects. There are a number of possible explanations for these results. Administration of deprenyl or pargyline, together with pCA, itself a MAO-A inhibitor, will lead to inhibition of both MAO-A and MAO-B activities. This will likely lead to an enhanced release of dopamine and serotonin compared with the release following administration of pCA alone or pCA together with clorgyline. Elevation of the extracellular levels of either or both of these monoamines could lead to enhanced neurotoxicity. Whatever the mechanism involved, our results show that the co-administration of a type-B MAOI enhances the neurotoxic effects of pCA on serotonin neurons. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT,PHILADELPHIA,PA 19104. FU NIDA NIH HHS [DA05137] NR 45 TC 14 Z9 14 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUL 11 PY 1994 VL 650 IS 2 BP 305 EP 312 DI 10.1016/0006-8993(94)91796-5 PG 8 WC Neurosciences SC Neurosciences & Neurology GA NW229 UT WOS:A1994NW22900015 PM 7953696 ER PT J AU MAYFIELD, C EBBINGHAUS, S GEE, J JONES, D RODU, B SQUIBB, M MILLER, D AF MAYFIELD, C EBBINGHAUS, S GEE, J JONES, D RODU, B SQUIBB, M MILLER, D TI TRIPLEX FORMATION BY THE HUMAN HA-RAS PROMOTER INHIBITS SP1 BINDING AND IN-VITRO TRANSCRIPTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DIHYDROFOLATE-REDUCTASE PROMOTER; PROTO-ONCOGENE PROMOTER; C-MYC PROMOTER; HELIX FORMATION; DNA; OLIGONUCLEOTIDES; SEQUENCE; OLIGODEOXYNUCLEOTIDES; CLEAVAGE; INVITRO AB The central role of the ras oncogenes in the pathogenesis of a wide variety of human malignancies is well established. Toward developing specific transcriptional inhibitors of the human Ha-ras oncogene, we have designed oligonucleotides to target a region of the Ha-ras promoter (-8 to -28) which contains two of the three Sp1 binding sites essential for transcriptional activity. Gel mobility analysis and DNase I footprinting demonstrate that an oligonucleotide (HR21ap) forms a sequence-specific triple helix with its target site in an antiparallel orientation with respect to the purine-rich duplex strand through predominantly G*G:C triplets. Within the Ha-ras promoter, HR21ap binds exclusively to the proximal target Sp1 sites over a similar nontarget distal sequence which, like the target, contains a consensus Sp1 site. Protein binding assays demonstrate that triplex formation by HR21ap inhibits Sp1 binding to the Ha-ras promoter. Moreover, oligonucleotide-directed triplex formation arrests Ha-ras promoter-dependent transcription in vitro, The results presented here suggest that tripler formation by the Ha-ras promoter targeted oligonucleotide may provide a means to specifically inhibit transcription of this oncogene in vivo. C1 UNIV ALABAMA, DEPT BIOCHEM, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, CTR COMPREHENS CANC, DEPT ORAL PATHOL, BIRMINGHAM, AL 35294 USA. BIRMINGHAM VET AFFAIRS MED CTR, BIRMINGHAM, AL 35294 USA. RP MAYFIELD, C (reprint author), UNIV ALABAMA, DEPT MED, BOLDEN LAB, BIRMINGHAM, AL 35294 USA. FU NCI NIH HHS [NCI-CN-25428-33, R01 CA42337, R01 CA42664] NR 34 TC 60 Z9 61 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUL 8 PY 1994 VL 269 IS 27 BP 18232 EP 18238 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NV422 UT WOS:A1994NV42200070 PM 8027084 ER PT J AU WANG, SJ SHOHAT, T VADHEIM, C SHELLOW, W EDWARDS, J ROTTER, JI AF WANG, SJ SHOHAT, T VADHEIM, C SHELLOW, W EDWARDS, J ROTTER, JI TI INCREASED RISK FOR TYPE-I (INSULIN-DEPENDENT) DIABETES IN RELATIVES OF PATIENTS WITH ALOPECIA-AREATA (AA) SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE ALOPECIA AREATA; IMMUNOLOGICAL DISEASE; TYPE 1 DIABETES; TYPE 2 DIABETES ID AUTOIMMUNITY; MELLITUS; PREVALENCE; JUVENILE; DISEASE; IDDM AB The prevalence of various chronic diseases was compared in 517 individuals with alopecia areata, and 2,969 of their first degree relatives. As previous reports have suggested an increased incidence of diabetes in relatives of patients with alopecia areata, special attention was given to the prevalence of Type 1 and Type 2 diabetes in the patients and in their relatives. Several immunologic diseases were increased in alopecia probands and relatives. Thyroid disease, vitiligo, Addison disease, and pernicious anemia were more prevalent in probands and in their relatives than in the general population. Specifically, a high rate of thyroid disease was found in probands (14.7%) and in their first degree relatives (4.2%). Only one proband had Type I diabetes, yet there were 14 sibs with Type 1 diabetes. Thus, Type 1 diabetes was significantly more prevalent in the sibs (1.2%) than in either the probands with alopecia (0.2%), or the general population (0.12-0.25%) (P < 0.05)). In contrast, Type 2 diabetes was not more common in probands or in sibs than in the general population. These data suggest that alopecia areata protects against Type 1 diabetes in predisposed individuals. The high rate of thyroid disease suggests that screening probands and first degree relatives for thyroid disease should be considered. (C) 1994 Wiley-Liss, Inc. C1 CEDARS SINAI MED CTR,DEPT MED,DIV MED GENET,CTR MED GENET BIRTH DEFECTS,LOS ANGELES,CA 90048. CEDARS SINAI MED CTR,DEPT PEDIAT,LOS ANGELES,CA 90048. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,DEPT DERMATOL,LOS ANGELES,CA. HAIR,ALOPECIA AREATA RES FDN,RALEIGH,NC. NR 41 TC 44 Z9 47 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 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JUL 1 PY 1994 VL 51 IS 3 BP 234 EP 239 DI 10.1002/ajmg.1320510313 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA NR121 UT WOS:A1994NR12100012 PM 8074151 ER PT J AU BARCHIESI, F COLOMBO, AL MCGOUGH, DA FOTHERGILL, AW RINALDI, MG AF BARCHIESI, F COLOMBO, AL MCGOUGH, DA FOTHERGILL, AW RINALDI, MG TI IN-VITRO ACTIVITY OF ITRACONAZOLE AGAINST FLUCONAZOLE-SUSCEPTIBLE AND FLUCONAZOLE-RESISTANT CANDIDA-ALBICANS ISOLATES FROM ORAL CAVITIES OF PATIENTS INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID KETOCONAZOLE; AIDS AB A broth macrodilution technique, which was performed by following the recommendations provided by the National Committee for Clinical Laboratory Standards (document M27-P), was applied to study the in vitro activity of itraconazole against fluconazole-susceptible and -resistant Candida albicans isolates from the oral cavities of 100 patients infected with human immunodeficiency virus. The in vitro data demonstrated that itraconazole had good activity against the tested isolates; for 90% of all strains of C. albicans, MICs were 1 mu g/ml, and only one isolate was highly resistant to this triazole (MIC, >16 mu g/ml). However, the itraconazole MICs for the fluconazole-susceptible isolates were significantly lower than those for the fluconazole-resistant isolates; the MICs for 50 and 90% of the isolates tested were less than or equal to 0.03 and 0.25 mu g/ml, respectively, for the fluconazole-susceptible isolates and 0.5 and 1 mu g/ml, respectively, for the fluconazole-resistant isolates (P = 0.00001). Our findings could be of clinical relevance because human immunodeficiency virus-infected patients who fail fluconazole therapy for oral and/or esophageal candidiasis may require itraconazole at doses higher than those used in standard therapy. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV ANCONA,IST MALATTIE INFET & MED PUBBL,ANCONA,ITALY. ESCOLA PAULISTA MED,BR-04023 SAO PAULO,BRAZIL. RP BARCHIESI, F (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,FUNGUS TESTING LAB,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 21 TC 86 Z9 89 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JUL PY 1994 VL 38 IS 7 BP 1530 EP 1533 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA NU598 UT WOS:A1994NU59800016 PM 7979284 ER PT J AU ATKINSON, BA BOCANEGRA, R COLOMBO, AL GRAYBILL, JR AF ATKINSON, BA BOCANEGRA, R COLOMBO, AL GRAYBILL, JR TI TREATMENT OF DISSEMINATED TORULOPSIS-GLABRATA INFECTION WITH DO870 AND AMPHOTERICIN-B SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID NEUTROPENIC MICE; CANDIDIASIS; MORTALITY AB Torulopsis glabrata, an opportunist pathogen in immunosuppressed patients, is resistant to many antifungal agents, and there are no established treatment regimens for this organism. The mouse model was used to evaluate treatment with DO870, amphotericin B, fluconazole, and their combination. Mice were immunosuppressed with 5 mg of gold sodium thiomalate given intraperitoneally 1 day prior to intravenous infection with 10(8) T. glabrata cells. Treatment with a new antifungal triazole, DO870, at doses ranging from 1 to 50 mg/kg of body weight administered per os either daily or on alternate days; fluconazole at 100 mg/kg twice a day per os; or amphotericin B at 3 mg/kg/day intraperitoneally was begun 1 day after infection. Treatment for 5 days was followed by sacrifice 2 days later for determining CFU counts in spleen and kidney tissue. For a fluconazole-sensitive isolate (MIC of DO870, < 1.25 mu g/ml), DO870 at 5 mg/kg/day significantly reduced counts in kidney and spleen tissue (P < 0.05), amphotericin B was modestly effective, and the combination of DO870 (25 mg/kg) and amphotericin B (3 mg/kg) was markedly more effective than either drug alone (P < 0.01). Three additional isolates were resistant in vitro to DO870 (MIC, 4 mu g/ml). No reduction in CFU in kidney or spleen tissue was observed with DO870 when compared with counts in control tissue. DO870 is effective in vivo against at least some isolates of T. glabrata and when combined with amphotericin B can exert additive effects. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. ESCOLA PAULISTA MED,BR-04023 SAO PAULO,BRAZIL. NR 19 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JUL PY 1994 VL 38 IS 7 BP 1604 EP 1607 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA NU598 UT WOS:A1994NU59800027 PM 7979293 ER PT J AU MILLS, BG FRAUSTO, A SINGER, FR OHSAKI, Y DEMULDER, A ROODMAN, GD AF MILLS, BG FRAUSTO, A SINGER, FR OHSAKI, Y DEMULDER, A ROODMAN, GD TI MULTINUCLEATED CELLS FORMED IN-VITRO FROM PAGETS BONE-MARROW EXPRESS VIRAL-ANTIGENS SO BONE LA English DT Article DE PAGETS BONE MARROW; GIANT CELLS IN VITRO; VIRAL ANTIGENS ID DISEASE; CULTURES AB Paget's disease of bone is characterized by large numbers of osteoclasts that have viral-like nuclear and/or cytoplasmic inclusions. Pagetic osteoclasts express respiratory syncytial viral (RSV) and measles viral (MV) nucleocapsid antigens. The data suggest a possible viral etiology for Paget's disease. However, studies to characterize further the putative viral inclusions in Paget's osteoclasts have been severely hampered by the extreme difficulty in isolating large numbers of osteoclasts from pagetic bone. The recent demonstration that osteoclast-like multinucleated cells (MNC), that had certain characteristics of pagetic osteoclasts formed in marrow cultures from Paget's patients, may permit studies to describe this virus further. Therefore, we have cultured marrow samples from involved and uninvolved bones from Paget's patients and from normal subjects to determine if the MNC formed in these cultures express viral antigens. RSV and/or MV antigens were expressed in the mononuclear cells and/or the MNC formed in 12 of 12 marrow cultures from active lesions of patients with Paget's disease, with 40-50% of the cells expressing viral antigens. In contrast, less than 5% of cells isolated from cultures from normal subjects expressed RSV and/or MV. These results suggest that MNC formed in long-term marrow cultures from patients with Paget's disease frequently express paramyxoviral antigens and are very similar to pagetic osteoclasts. Thus, these marrow cultures may be useful for further characterizing the virus in Paget's disease. C1 UNIV SO CALIF,ORTHOPED HOSP,LOS ANGELES,CA. VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. CEDARS SINAI MED CTR,LOS ANGELES,CA. RP MILLS, BG (reprint author), ORTHOPED HOSP,2400 S FLOWER ST,LOS ANGELES,CA 90007, USA. FU NCI NIH HHS [CA40035]; NIADDK NIH HHS [AM-19980]; NIAMS NIH HHS [AR-35188] NR 18 TC 46 Z9 46 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 8756-3282 J9 BONE JI Bone PD JUL-AUG PY 1994 VL 15 IS 4 BP 443 EP 448 DI 10.1016/8756-3282(94)90823-0 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NP070 UT WOS:A1994NP07000011 PM 7917585 ER PT J AU HANDFORTH, A CHENG, JT MANDELKERN, MA TREIMAN, DM AF HANDFORTH, A CHENG, JT MANDELKERN, MA TREIMAN, DM TI MARKEDLY INCREASED MESIOTEMPORAL LOBE METABOLISM IN A EASE WITH PLEDS - FURTHER EVIDENCE THAT PLEDS ARE A MANIFESTATION OF PARTIAL STATUS EPILEPTICUS SO EPILEPSIA LA English DT Article DE STATUS EPILEPTICUS; ELECTROENCEPHALOGRAPHY; PARTIAL SEIZURES; POSITRON EMISSION TOMOGRAPHY; TEMPORAL LOBE ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLUCOSE-METABOLISM; COMPLEX PARTIAL SEIZURES; CLINICAL-SIGNIFICANCE; F-18 FLUORODEOXYGLUCOSE; PARTIAL EPILEPSY; DISCHARGES; EEG; SPECT AB The pathophysiologic and clinical significance of periodic lateralized epileptiform discharges (PLEDs) is unclear; whether PLEDs represent an ictal condition that should be treated remains uncertain. We performed FDG-positron emission computed tomography (FDG-PET) in a patient with PLEDs at 3 days, 18 days, and 10 weeks after onset. During left temporal PLEDs, the initial scan showed intense hypermetabolism of the left mesiotemporal region. The second scan, performed when PLEDs were resolving, displayed reduced hypermetabolism. The follow-up scan, when PLEDs had resolved, showed left temporal hypometabolism. These findings, together with clinical evidence from the literature, are compatible with the interpretation that PLEDs represent partial status epilepticus (SE); whether vigorous therapy is required to prevent neuronal damage from this focal seizure activity remains uncertain. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF IRVINE,DEPT PHYS,IRVINE,CA 92717. RP HANDFORTH, A (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,WADSWORTH DIV,WILSHIRE & SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. NR 33 TC 94 Z9 94 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD JUL-AUG PY 1994 VL 35 IS 4 BP 876 EP 881 DI 10.1111/j.1528-1157.1994.tb02526.x PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA PF808 UT WOS:A1994PF80800027 PM 8082637 ER PT J AU RANDALL, GM JENSEN, DM MACHICADO, GA HIRABAYASHI, K JENSEN, ME YOU, S PELAYO, E AF RANDALL, GM JENSEN, DM MACHICADO, GA HIRABAYASHI, K JENSEN, ME YOU, S PELAYO, E TI PROSPECTIVE RANDOMIZED COMPARATIVE-STUDY OF BIPOLAR VERSUS DIRECT-CURRENT ELECTROCOAGULATION FOR TREATMENT OF BLEEDING INTERNAL HEMORRHOIDS SO GASTROINTESTINAL ENDOSCOPY LA English DT Article ID DIRECT-CURRENT ELECTROTHERAPY AB Internal hemorrhoids are the most common cause of lower gastrointestinal bleeding. Although new anoscopic therapies are available, few comparative randomized studies have evaluated them in regard to long-term efficacy, recurrence rates, and safety. Our purpose was to compare the treatment of internal hemorrhoids with direct current (Ultroid, Cabot Medical, Langhorn, Pa.) and bipolar (BICAP, Circon ACMI, Stamford, Conn.) hemorrhoid probes. One hundred patients with symptomatic internal hemorrhoids were randomized: 50 to direct current electrocoagulation and 50 to bipolar electrocoagulation. Follow-up and treatment were at 3- to 4-weekly intervals; two to three hemorrhoid segments were treated at each session until relief of symptoms (bleeding, prolapse, and discharge) and a reduction in hemorrhoid size to grade 1 or 0 were noted. The hemorrhoids of 98% of all patients studied were grade 2 or 3; 2% of patients had grade 1 hemorrhoids and none had grade 4 hemorrhoids. At 1 year after treatment, most patients had no (69%) or only mild (23%) recurrence, and a few had severe, symptomatic (8%) hemorrhoid recurrence. A greater recurrence rate was noted after direct current treatment (34%) than bipolar treatment (29%). In contrast, rebleeding at 1 year occurred less frequently after direct current treatment (5%) than after bipolar treatment (20%). Our conclusions were as follows: (1) Both direct current and bipolar probes were effective for control of chronic bleeding from grade 1 to 3 internal hemorrhoids. (2) Bipolar probe was significantly faster than direct current probe. (3) Direct current treatment produced fewer complications than bipolar treatment (12% versus 14%). (4) Recurrence rates were low after 1 year with either device (8%). (5) More recurrences were noted after direct current electrocoagulation (34%) than after bipolar electrocoagulation (29%). C1 UNIV CALIF LOS ANGELES,CTR ULCER RES & EDUC,W LOS ANGELES VET ADM,LOS ANGELES,CA 90024. VALLEY MED CTR,LOS ANGELES,CA. FU NIDDK NIH HHS [NIDDK 41301] NR 17 TC 25 Z9 29 U1 2 U2 5 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD JUL-AUG PY 1994 VL 40 IS 4 BP 403 EP 410 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NY866 UT WOS:A1994NY86600001 PM 7926528 ER PT J AU GARZATREVINO, ES AF GARZATREVINO, ES TI NEUROBIOLOGICAL FACTORS IN AGGRESSIVE-BEHAVIOR SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Review ID IMPULSIVE FIRE SETTERS; CEREBROSPINAL-FLUID; MONOAMINE METABOLITES; VIOLENT OFFENDERS; BRAIN-SEROTONIN; FAMILY HISTORY; CSF 5-HIAA; SUICIDE; ILLNESS; IMPAIRMENT AB The author's aim was to review literature in the neurosciences and psychiatric clinical research reports about biological factors in aggression and the pathophysiological mechanisms that accompany aggression in neuropsychiatric syndromes. Method: Studies were located through computer searches of relevant experimental reports and review articles mainly from the last 25 years. Results: Several studies using neuroimaging and neurophysiological and neuropathological research techniques have identified lesions in the limbic structures, temporal lobes, and frontal lobes of the brain in abnormally aggressive individuals. Several reports have associated deficiency or dysregulation of serotonin with homicidal, suicidal, and impulsive behavior. However, few studies have focused on polypeptides or second messenger systems, although abnormalities in these systems have been reported in patients with neuropsychiatric syndromes who have shown aggressive behavior. Even fewer studies focus on the correlation of brain structures and metabolic markers. Conclusions: The understanding of aggressive behavior in psychiatric patients is fragmented. Some explanations are speculative and extrapolated to clinical psychiatric syndromes from experimental data on the neurophysiology of cats, rats, and other mammals. Identification of biochemical markers that can be used in predicting patients' response to pharmacological interventions may be the next step in developing more rational treatment of violent patients. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP GARZATREVINO, ES (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 100 TC 27 Z9 29 U1 0 U2 3 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD JUL PY 1994 VL 45 IS 7 BP 690 EP 699 PG 10 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA NU776 UT WOS:A1994NU77600011 PM 7927294 ER PT J AU CHAMPION, CI BLANCO, DR SKARE, JT HAAKE, DA GILADI, M FOLEY, D MILLER, JN LOVETT, MA AF CHAMPION, CI BLANCO, DR SKARE, JT HAAKE, DA GILADI, M FOLEY, D MILLER, JN LOVETT, MA TI A 9.0-KILOBASE-PAIR CIRCULAR PLASMID OF BORRELIA-BURGDORFERI ENCODES AN EXPORTED PROTEIN - EVIDENCE FOR EXPRESSION ONLY DURING INFECTION SO INFECTION AND IMMUNITY LA English DT Article ID PHOSPHATE-BINDING PROTEIN; LYME-DISEASE SPIROCHETE; OUTER-MEMBRANE PROTEINS; ESCHERICHIA-COLI; MOLECULAR-CLONING; LINEAR-PLASMID; ALKALINE-PHOSPHATASE; SEQUENCE-ANALYSIS; SIGNAL PEPTIDES; SALMONELLA-TYPHIMURIUM AB In this study, we report the cloning, sequencing, and molecular analysis of a gene located on a 9.0-kbp circular plasmid of virulent Borrelia burgdorferi B31 designated eppA (exported plasmid protein A). This gene encodes a precursor protein of 174 amino acids including a signal peptide of 20 amino acids and a type I signal peptidase cleavage site. The mature EppA protein of 154 amino acids has a calculated molecular weight of 17,972. Several lines of evidence suggest that eppA is not expressed by B. burgdorferi B31 during in vitro cultivation. Immunoblot analysis using hyperimmune rabbit antiserum to recombinant EppA (rEppA) did not detect the presence of EppA in B. burgdorferi B31 cultivated in vitro. Northern blot analysis using total RNA isolated from in vitro cultivated virulent B. burgdorferi B31 failed to detect an eppA transcript. EppA was not detected in culture supernatants of virulent B. burgdorferi B31 in 9 sensitive antigen-capture enzyme-linked immunosorbent assay. In contrast, evidence for expression of eppA during infection,vas based on the observation that patients with Lyme disease as well as rabbits experimentally infected with B. burgdorferi B31 produced antibodies that recognized rEppA. Because the cellular location of EppA in B. burgdorferi cannot be determined in vivo because of very small numbers of organisms present in vertebrate infection, we examined the cellular location of rEppA expressed in Escherichia coli. In E. coli, rEppA is targeted to the outer membrane. In addition, purified E. coli outer membranes containing rEppA treated with chaotrophic agents did not result in rEppA release. These findings are consistent with the idea that EppA is not peripherally associated with the outer membrane of E. coli but rather has an integral outer membrane association. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,DIV INFECT DIS,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DIV INFECT DIS,LOS ANGELES,CA 90073. RP CHAMPION, CI (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024, USA. FU NIAID NIH HHS [5-T32-AI07323, AI-21352, AI-29733] NR 59 TC 101 Z9 101 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 1994 VL 62 IS 7 BP 2653 EP 2661 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NU014 UT WOS:A1994NU01400001 PM 8005657 ER PT J AU TURNIDGE, JD GUDMUNDSSON, S VOGELMAN, B CRAIG, WA AF TURNIDGE, JD GUDMUNDSSON, S VOGELMAN, B CRAIG, WA TI THE POSTANTIBIOTIC EFFECT OF ANTIFUNGAL AGENTS AGAINST COMMON PATHOGENIC YEASTS SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID CANDIDA-ALBICANS; 5-FLUOROCYTOSINE; INFECTIONS; NETILMICIN C1 DEPT MED LANDSPITALINN,IS-101 REYKJAVIK,ICELAND. MONASH MED CTR,DEPT INFECT DIS & MICROBIOL,CLAYTON,VIC 3168,AUSTRALIA. UNIV ICELAND,SCH MED,IS-101 REYKJAVIK,ICELAND. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. NR 24 TC 68 Z9 70 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 JUL PY 1994 VL 34 IS 1 BP 83 EP 92 DI 10.1093/jac/34.1.83 PG 10 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA NY308 UT WOS:A1994NY30800008 PM 7961219 ER PT J AU ANZUETO, A BRASSARD, JM ANDRADE, FH LAWRENCE, RA MAXWELL, LC LEVINE, SM JENKINSON, SG AF ANZUETO, A BRASSARD, JM ANDRADE, FH LAWRENCE, RA MAXWELL, LC LEVINE, SM JENKINSON, SG TI EFFECTS OF HYPEROXIA ON RAT DIAPHRAGM FUNCTION SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE FATIGUE; RESPIRATORY MUSCLES; FREE RADICALS; RESISTIVE BREATHING; GLUTATHIONE; CONTRACTILE PROPERTIES ID OXYGEN-TOXICITY; SKELETAL-MUSCLE; REACTIVE OXYGEN; BLOOD-FLOW; FATIGUE; GLUTATHIONE; LUNG; PERFORMANCE; 100-PERCENT AB The association of oxygen radical generation with impaired diaphragm performance has previously been reported after inspiratory resistive loading (IRL). We hypothesized that exposure of rats to normobaric hyperoxia (O-2) could produce impaired diaphragm function because of free radical production. Sprague-Dawley rats were divided into four groups: 1) room air (control), 2) > 95% O-2 for 24 h, 3) > 95% O-2 for 48 h, and 4) > 95% O-2 for 60 h. Each group was studied at rest after the O-2 exposure and then after IRL. During IRL, the animals breathed through an inspiratory resistor until they were unable to sustain > 70% of the maximum airway pressure. Diaphragm samples were obtained for analysis of glutathione (GSH) and glutathione disulfide (GSSG) concentrations. In vitro isometric contractile properties were also determined, including maximal tetanic tension (P-o) and maximal twitch tension (P-t), in GSSG content and in GSSG-to-GSH ratios. Hyperoxia for > 48 h resulted in significant decreases in P-o and P-t and an increase in GSSG content and in GSSG-to-GSH ratios compared with other groups. Those same animals subjected to IRL showed a further decrease in P-o and P-t. These data suggest that free radical generation may occur in the diaphragm during a hyperoxia exposure associated with activation of the GSH redox cycle and impairment of diaphragm function. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,DIV PULM DIS CRIT CARE,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,SAN ANTONIO,TX 78284. RP ANZUETO, A (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DIV PULM DIS CRIT CARE 111E,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 FU NHLBI NIH HHS [HL-32824] NR 31 TC 8 Z9 8 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JUL PY 1994 VL 77 IS 1 BP 63 EP 68 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA NX536 UT WOS:A1994NX53600011 PM 7961276 ER PT J AU TATERKA, J SUTCLIFFE, M RUBIN, DH AF TATERKA, J SUTCLIFFE, M RUBIN, DH TI SELECTIVE REOVIRUS INFECTION OF MURINE HEPATOCARCINOMA CELLS DURING CELL-DIVISION - A MODEL OF VIRAL LIVER INFECTION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE RECEPTORS; VIRUS; LIVER REGENERATION; CELL CYCLE; INTESTINAL INFECTION; CELLULAR DIFFERENTIATION ID ADULT HUMAN HEPATOCYTES; HEPATITIS-B VIRUS; GROWTH-FACTOR; ALCOHOLIC PATIENTS; DISEASE; BINDING; TYPE-3; CYCLE; MICE; TRANSCRIPTION AB Reovirus type 1, strain Lang (1/L), can infect hepatocytes in vivo only after hepatocellular damage is induced by hepatotoxins, surgical trauma, resection, or profound immunosuppression. To examine the role of cell cycle and cellular differentiation on liver cell susceptibility to reovirus infection, a murine hepatocarcinoma cell line, Hepa 1/A1, was infected with reovirus and assayed for the presence of infectious virus or reovirus antigen in cells. Despite a > 95% binding of reovirus to hepatocarcinoma cells as indicated by cytometric analysis; only 10% of hepatoma cells contained infectious virus by infectious center assay. In comparison, 100% of L cells were infected. Analysis of intracellular reovirus antigen revealed its presence in dividing but not in quiescent hepatocytes. This correlation of cellular division and cell capacity to support viral replication suggests that induction of hepatocyte proliferation may be a mechanism for liver susceptibility to reovirus infection. C1 VET AFFAIRS MED CTR,DEPT MED RES,ACOS RES,NASHVILLE,TN 37212. UNIV PENN,DEPT BIOL,PHILADELPHIA,PA 19104. UNIV PENN,DIV GASTROENTEROL MED,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,DEPT MED RES,PHILADELPHIA,PA 19104. VANDERBILT UNIV,MED CTR,DEPT MED,DIV INFECT DIS,NASHVILLE,TN 37212. VANDERBILT UNIV,MED CTR,DEPT MICROBIOL & IMMUNOL,NASHVILLE,TN 37212. FU NIAID NIH HHS [AI-23970]; NIDDK NIH HHS [T-32-DK-07066] NR 40 TC 14 Z9 14 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 JUL PY 1994 VL 94 IS 1 BP 353 EP 360 DI 10.1172/JCI117329 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NW496 UT WOS:A1994NW49600045 PM 8040276 ER PT J AU PFALLER, MA BALE, M BUSCHELMAN, B LANCASTER, M ESPINELINGROFF, A REX, JH RINALDI, MG AF PFALLER, MA BALE, M BUSCHELMAN, B LANCASTER, M ESPINELINGROFF, A REX, JH RINALDI, MG TI SELECTION OF CANDIDATE QUALITY-CONTROL ISOLATES AND TENTATIVE QUALITY-CONTROL RANGES FOR IN-VITRO SUSCEPTIBILITY TESTING OF YEAST ISOLATES BY NATIONAL COMMITTEE FOR CLINICAL LABORATORY STANDARDS PROPOSED STANDARD METHODS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; FUNGAL-INFECTIONS; FLUCONAZOLE RESISTANCE; BROTH MACRODILUTION; EPIDEMIOLOGY; PATHOGENS AB The National Committee for Clinical Laboratory Standards has developed a proposed standard method for in vitro antifungal susceptibility testing of yeast isolates (National Committee for Clinical Laboratory Standards, document M27-P, 1992). In order for antifungal testing by the M27-P method to be accepted, reliable quality control (QC) performance criteria must be developed. In the present study, five laboratories tested 10 candidate QC strains 20 times each against three antifungal agents: amphotericin B, fluconazole, and 5-fluorocytosine. All sites conformed to the M27-P standards and used a common lot of tube dilution reagents and RPMI 1640 broth medium. Overall, 98% of MIC results with amphotericin B, 95% with fluconazole, and 92% with 5-fluorocytosine fell within the desired 3-log(2) dilution range (mode +/- 1 log(2) dilution). Excellent performance with all three antifungal agents was observed for six strains: Candida albicans ATCC 90028, Candida parapsilosis ATCC 90018, C. parapsilosis ATCC 22019, Candida krusei ATCC 6258, Candida tropicalis ATCC 750, and Saccharomyces cerevisiae ATCC 9763. With these strains, 3-log, dilution ranges encompassing 94 to 100% of MICs for all three drugs were established. Additional studies with multiple lots of RPMI 1640 test medium will be required to establish definitive QC ranges. C1 ALAMAR BIOSCI INC,SACRAMENTO,CA 95834. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. UNIV TEXAS,SCH MED,HOUSTON,TX 77030. UNIV TEXAS,AUDIE L MURPHY MEM VET ADM MED CTR,CTR HLTH SCI,LAB SERV,SAN ANTONIO,TX 78284. RP PFALLER, MA (reprint author), UNIV IOWA,COLL MED,MRC 273,DEPT PATHOL,IOWA CITY,IA 52242, USA. NR 34 TC 50 Z9 51 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 1994 VL 32 IS 7 BP 1650 EP 1653 PG 4 WC Microbiology SC Microbiology GA NR924 UT WOS:A1994NR92400006 PM 7929752 ER PT J AU CHENG, LY OUTTERBRIDGE, LV COVATTA, ND MARTENS, DA GORDON, JT DRATMAN, MB AF CHENG, LY OUTTERBRIDGE, LV COVATTA, ND MARTENS, DA GORDON, JT DRATMAN, MB TI FILM AUTORADIOGRAPHY IDENTIFIES UNIQUE FEATURES OF [I-125] 3,3',5'-(REVERSE) TRIIODOTHYRONINE TRANSPORT FROM BLOOD TO BRAIN SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID CENTRAL-NERVOUS-SYSTEM; RETINOL-BINDING PROTEIN; THYROID-HORMONE ACTION; CHOROID-PLEXUS; RAT-BRAIN; REVERSE TRIIODOTHYRONINE; TRANSTHYRETIN SYNTHESIS; THYROXINE TRANSPORT; MEDIATED TRANSPORT; PRE-ALBUMIN AB I, Steady-state iodothyronine profiles in plasma are composed of thyroid gland-synthesized hormones (mainly thyroxine) and tissue iodothyronine metabolites (mainly triiodothyronine and reverse triiodothyronine) that have entered the bloodstream. The hormones circulate in noncovalently bound complexes with a panoply of carrier proteins. Transthyretin (TTR), the major high-affinity thyroid hormone binding protein in rat plasma, is formed in the liver. It is also actively and independently synthesized in choroid plexus, where its function as a chaperone of thyroid hormones from bloodstream to cerebrospinal fluid (CSF) is undergoing close scrutiny by several groups of investigators. Because TTR has high-affinity binding sites for both thyroxine and retinol binding protein, its potential role as a mediator of combined thyroid hormone and retinoic acid availability in brain is of further interest. 2. While they are in the free state relative to their binding proteins, iodothyronines in the cerebral circulation are putatively subject to transport across both the blood-brain barrier (BBB) and choroid plexus CSF barrier(CSFB) before entering the brain. Previous autoradiographic studies had already indicated that after intravenous administration the transport mechanisms governing thyroxine and triiodothyronine entry into brain were probably similar, whereas those for reverse triiodothyronine were very different, although the basis for the difference was not established at that time. Intense labeling seen over brain ventricles after intravenous administration of all three iodothyronines suggested that all were subject to transport across the CSFB. 3. To evaluate the role of the BBB and CSFB in determining iodothyronine access to brain parenchyma, autoradiograms prepared after intravenous administration of[I-125]-labeled hormones (revealing results of transport across both barriers) were compared with those prepared after intrathecal (icv) hormone injection (reflecting only their capacity to penetrate into the brain after successfully navigating the CSFB). 4. Those studies revealed that thyroxine and triiodothyronine were mainly transported across the BBB. They shared with reverse triiodothyronine a generally similar, limited pattern of penetration from CSF into the brain, with circumventricular organs likely to be the main recipients of iodothyronines (with or without retinol) transported across the CSFB. 5. Analysis of all of the images obtained after intravenous and icv hormone administration clarified the basis for the unique distribution of intravenously injected reverse triiodothyronine. The hormone is excluded by the BBB but may be subject to limited penetration into brain parenchyma via the CSF. 6. Overall the observations single out reverse triiodothyronine as the iodothyronine showing the most distinctive as well as the most limited pattern of transport from blood to brain. Although it is considered to be a largely inactive metabolic product formed in the service of thyroxine disposal, a number of considerations suggest that reverse triiodothyronine, actively formed from thyroxine within the brain at selected sites of inner ring monodeiodinase activity, may have as yet undiscovered functions. The present results raise the possibility that, as in the case of other known neuroactive molecules that are formed within the brain but excluded by the BBB, reverse triiodothyronine generated intracerebrally may exert important brain-specific and site-specific functional effects. C1 DEPT VET AFFAIRS MED CTR,MED RES SERV 151,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. UNIV PENN,DEPT MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. FU NIMH NIH HHS [MH-44210, MH-45252] NR 46 TC 17 Z9 17 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD JUL PY 1994 VL 72 IS 1 BP 380 EP 391 PG 12 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA NX819 UT WOS:A1994NX81900034 PM 7965021 ER PT J AU SCOTT, PA CHOU, JM TANG, H FRAZER, A AF SCOTT, PA CHOU, JM TANG, H FRAZER, A TI DIFFERENTIAL INDUCTION OF 5-HT1A-MEDIATED RESPONSES IN-VIVO BY 3 CHEMICALLY DISSIMILAR 5-HT1A AGONISTS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID POSTSYNAPTIC 5-HT(1A) RECEPTORS; MONOAMINE OXIDASE INHIBITOR; DORSAL RAPHE NEURONS; ELECTROPHYSIOLOGICAL EVIDENCE; L-TRYPTOPHAN; 5-HYDROXYTRYPTAMINE1A RECEPTORS; BEHAVIORAL SYNDROME; RAT-BRAIN; IN-VIVO; SEROTONIN AB In the rat, activation of 5-hydroxytryptamine(1A) (5-HT1A) receptors causes hypothermia and the 5-HT syndrome. The effects of three chemically dissimilar 5-HT1A agonists administered s.c. [8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), gepirone, and (+)4[n-5-(methoxychroman-3-yl)n-propylamino]butyl-8-azas-piro[4,5]decane-7,adione ((+) S-20499)] on both of these responses were studied. The same maximal drop in body temperature (similar to 2.5 degrees C) was elicited by all three agonists, 8-OH-DPAT being the most potent (EC(50) = 0.05 mg/kg), followed by gepirone (1.8 mg/kg) and (+) S-20499 (8 mg/kg). Both pindolol, a nonselective 5-HT1A receptor/beta adrenoceptor antagonist and n-t-butyl,- 3-[1-[4-(2-methoxy)phenyl]piperazinyl]-1-phenylpropionamide [(+) WAY 100135], a more selective 5-HT1A receptor antagonist, dose dependently attenuated the hypothermia induced by all three agonists. From these data, we inferred that all three agonists caused hypothermia via activation of 5-HT1A receptors. The syndrome was observed reliably in rats at doses of 2 to 4 mg/kg 8-OH-DPAT; doses up to 100 mg/kg of gepirone or (+) S-20499 did not produce the syndrome. In reserpine-pretreated animals, 8-OH-DPAT (maximal effect at 2-4 mg/kg) and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) (5 mg/kg) induced forepaw treading, whereas gepirone (10 mg/kg) and (+) S-20499 (75 mg/kg) did not. (+) WAY 100135 competitively antagonized the forepaw treading caused by 8-OH-DPAT in reserpine-pretreated rats. This indicates that forepaw treading, like hypothermia, is mediated by activation of 5-HT1A receptors. Gepirone (5-10 mg/kg) attenuated the forepaw treading induced by either 3-OH-DPAT (4 mg/kg) or 5-MeODMT (5 mg/kg); by contrast, (+) S-20499, at doses up to 75 mg/kg, did not attenuate the forepaw treading induced by either 8-OH-DPAT or 5-MeODMT. The inability of (+) S-20499 either to induce the 5-HT syndrome or forepaw treading or to attenuate the forepaw treading induced by other agonists could be due to several factors, one of which is that different subtypes of the 5HT(1A) receptor mediate hypothermia and the 5-HT syndrome. C1 DEPT VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DAVID MAHONEY INST NEUROL SCI,PHILADELPHIA,PA 19104. RP SCOTT, PA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIMH NIH HHS [MH48125] NR 54 TC 38 Z9 38 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 JUL PY 1994 VL 270 IS 1 BP 198 EP 208 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA PC025 UT WOS:A1994PC02500027 PM 8035316 ER PT J AU HARLEY, JB AF HARLEY, JB TI AUTOANTIBODIES ARE CENTRAL TO THE DIAGNOSIS AND CLINICAL MANIFESTATIONS OF LUPUS SO JOURNAL OF RHEUMATOLOGY LA English DT Editorial Material ID DISEASE HETEROGENEITY; ERYTHEMATOSUS; PROTEIN C1 US DEPT VET AFFAIRS,OKLAHOMA CITY,OK. RP HARLEY, JB (reprint author), UNIV OKLAHOMA,OKLAHOMA MED RES FDN,OKLAHOMA CITY,OK, USA. NR 9 TC 8 Z9 8 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 1994 VL 21 IS 7 BP 1183 EP 1185 PG 3 WC Rheumatology SC Rheumatology GA NW809 UT WOS:A1994NW80900003 PM 7966055 ER PT J AU KUTNER, NG SCHECHTMAN, KB ORY, MG BAKER, DI MILLER, JP PROVINCE, MA ARFKEN, CL ROSSITER, J HORNBROOK, MC STEVENS, VJ WINGFIELD, DJ GREENLICK, MR TINETTI, ME CLAUS, EB HORWITZ, RI BUCHNER, DM WAGNER, EH DELATEUR, BJ CRESS, ME PRICE, R ABRASS, IB ESSELMAN, P MARGUERITA, T MULROW, CD GERETY, MB CORNELL, JE SATTIN, RW DENINO, LA KANTEN, D WOLF, SL GREEN, RC MCNEELY, E COOGLER, C FIATARONE, MA ONEILL, EF RYAN, ND CLEMENTS, KM LIPSITZ, LA KEHAYIAS, JJ ROBERTS, SB EVANS, WJ WALLACE, R ROSS, JE HUSTON, JC KUNDEL, CJ SELLBERG, MS WOLFSON, LI WHIPPLE, RH AMERMAN, PM JUDGE, JO DERBY, CA KING, MB HADLEY, EC TAMBOLI, A WEISS, S AF KUTNER, NG SCHECHTMAN, KB ORY, MG BAKER, DI MILLER, JP PROVINCE, MA ARFKEN, CL ROSSITER, J HORNBROOK, MC STEVENS, VJ WINGFIELD, DJ GREENLICK, MR TINETTI, ME CLAUS, EB HORWITZ, RI BUCHNER, DM WAGNER, EH DELATEUR, BJ CRESS, ME PRICE, R ABRASS, IB ESSELMAN, P MARGUERITA, T MULROW, CD GERETY, MB CORNELL, JE SATTIN, RW DENINO, LA KANTEN, D WOLF, SL GREEN, RC MCNEELY, E COOGLER, C FIATARONE, MA ONEILL, EF RYAN, ND CLEMENTS, KM LIPSITZ, LA KEHAYIAS, JJ ROBERTS, SB EVANS, WJ WALLACE, R ROSS, JE HUSTON, JC KUNDEL, CJ SELLBERG, MS WOLFSON, LI WHIPPLE, RH AMERMAN, PM JUDGE, JO DERBY, CA KING, MB HADLEY, EC TAMBOLI, A WEISS, S TI OLDER ADULTS PERCEPTIONS OF THEIR HEALTH AND FUNCTIONING IN RELATION TO SLEEP DISTURBANCE, FALLING, AND URINARY-INCONTINENCE SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article; Proceedings Paper CT Annual Meeting of the Gerontological-Society-of-America CY NOV 20, 1992 CL WASHINGTON, DC SP GERONTOL SOC AMER ID FICSIT TRIALS; INTERVENTIONS; DISORDERS; FRAILTY; ELDERS AB OBJECTIVE: To investigate variation in older adults' perceived health and functioning that is associated with self-reported sleep disturbance, falling, and urinary incontinence, controlling for self-reported depression, ambulation difficulty, number of chronic conditions, and subjects' sociodemographic characteristics. DESIGN: Multicenter prospective study (FICSIT). SETTING: Persons age 70 and older living in the community evaluated at baseline. PARTICIPANTS: 239 women, 113 men; mean age = 77. MEASUREMENTS: Sleep disturbance score based on EPESE questions, recent falls history (Y/N), incontinent episodes (Y/N), CES-D score, SIP Ambulation score, and 4 MOS SF-36 scale scores. RESULTS: Women were significantly more likely than men to report multiple conditions (sleep disturbance, falling, incontinence) and to report lower levels of functioning as measured by 3 of 4 SF-36 scales. In regression analyses, sleep disturbance and urinary incontinence were significant predictors of perceived limitation in usual role activities because of physical health problems. Depression and ambulation measures significantly predicted scores on all 4 SF-36 scales. CONCLUSIONS: Our analysis suggests that it is important to address depressive symptomatology and ambulation difficulty-which in turn are related to sleep disturbance, falling, and urinary incontinence-in efforts to enhance older adults' perceived health and functioning. C1 WASHINGTON UNIV,DIV BIOSTAT,ST LOUIS,MO. NIA,BETHESDA,MD 20892. YALE UNIV,SCH NURSING,NEW HAVEN,CT 06536. WASHINGTON UNIV,SCH MED,DIV BIOSTAT,ST LOUIS,MO 63130. KAISER PERMANENTE CTR HLTH RES,PORTLAND,OR. YALE UNIV,SCH MED,PROGRAM AGING,NEW HAVEN,CT 06520. WASHINGTON UNIV,DEPT HLTH SCI,ST LOUIS,MO 63130. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX. CTR DIS CONTROL & PREVENT,ATLANTA,GA. UNIV CONNECTICUT,CTR HLTH,DEPT NEUROL,STORRS,CT 06269. NIA,NCNR,BETHESDA,MD. HARVARD UNIV,SCH MED,HEBREW REHABIL CTR AGED,USDA HUMAN NUTR RES CTR AGING,CAMBRIDGE,MA. UNIV IOWA,IOWA CITY,IA 52242. UNIV IOWA,IOWA STATE UNIV SCI & TECHNOL,IOWA CITY,IA. RP KUTNER, NG (reprint author), EMORY UNIV,SCH MED,DEPT REHABIL MED,1441 CLIFTON RD NE,ATLANTA,GA 30322, USA. RI Wolf, Steven/F-6588-2010 OI Wolf, Steven/0000-0002-9446-8995; Miller, J Philip/0000-0003-4568-6846 FU NIA NIH HHS [U01-AG09089] NR 27 TC 42 Z9 44 U1 2 U2 3 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 1994 VL 42 IS 7 BP 757 EP 762 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NW339 UT WOS:A1994NW33900012 PM 8014352 ER PT J AU OSTERWEIL, D MULFORD, P SYNDULKO, K MARTIN, M AF OSTERWEIL, D MULFORD, P SYNDULKO, K MARTIN, M TI COGNITIVE FUNCTION IN OLD AND VERY OLD RESIDENTS OF A RESIDENTIAL FACILITY - RELATIONSHIP TO AGE, EDUCATION, AND DEMENTIA SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID MINI-MENTAL-STATE; COMMUNITY POPULATION; ALZHEIMERS-DISEASE; LIMITS; NORMS AB OBJECTIVE: To determine if age, education, and dementia status affect neuropsychological performance in old and very old frail residential care subjects. DESIGN: Descriptive study of performance at the time of preadmission assessment. SETTING: Jewish Home for the Aging, Reseda, California. PARTICIPANTS: 201 applicants to the Jewish Home for the Aging residential care setting. Mean age was 84.7 years; SD was 5.6. Ninety-five subjects were 84 years of age or younger, while 106 were age 85 and older. There were 141 nondemented, 21 demented, and 39 were possibly demented applicants. Levels of education were as follows: 0-4 years: n = 25; 5-8: n = 69; 9-12: n = 77; and, 13-20: n = 23. MEASUREMENTS: Independent variables were age, education, and dementia status. Outcome measures were Folstein MMSE, Inglis P-A Learning Test, Digit Span, Cube Copying, selected Boston Diagnostic Aphasia Exam subtests. RESULTS: Subjects with 0 to 4 years of education scored more poorly on cognitive tests than other subjects. The very old tended to score more poorly than the old. Neuropsychological tests discriminated between those with normal cognitive function, possible dementia, and established dementia. About one-third of nondemented elderly scored below the traditional impairment cut-off of 24 points on the Mini-Mental State Exam. CONCLUSIONS: Questions are raised about how to interpret the poorer cognitive performance of very old and often frail subjects, especially in long-term-care settings where there are fewer demands upon residents whose impairments might otherwise cause them more functional difficulty. C1 UNIV CALIF LOS ANGELES,DEPT MED,DIV GERIATR,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. RP OSTERWEIL, D (reprint author), JEWISH HOMES AGING,7150 TAMPA AVE,RESEDA,CA 91335, USA. FU NIA NIH HHS [NIA 1K08AG00259-01A1] NR 32 TC 43 Z9 44 U1 5 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JUL PY 1994 VL 42 IS 7 BP 766 EP 773 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NW339 UT WOS:A1994NW33900014 PM 8014354 ER PT J AU ROYALL, DR MAHURIN, R AF ROYALL, DR MAHURIN, R TI QUALITATIVE ASSESSMENT OF DEMENTIA SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Letter ID BEDSIDE ASSESSMENT; IMPAIRMENT C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX, USA. NR 9 TC 2 Z9 2 U1 1 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 JUL PY 1994 VL 42 IS 7 BP 798 EP 799 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NW339 UT WOS:A1994NW33900023 PM 8014361 ER PT J AU GREGERMAN, RI AF GREGERMAN, RI TI AGING AND HORMONE-SENSITIVE LIPOLYSIS - RECONCILING THE LITERATURE SO JOURNALS OF GERONTOLOGY LA English DT Review ID DEPENDENT PROTEIN-KINASE; RAT ADIPOCYTES; STIMULATED LIPOLYSIS; ADIPOSE-TISSUE; AGE; INHIBITION; ADENOSINE; RABBITS C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP GREGERMAN, RI (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,GRECC 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 16 TC 16 Z9 16 U1 0 U2 0 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 JUL PY 1994 VL 49 IS 4 BP B135 EP B139 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NV799 UT WOS:A1994NV79900001 PM 8014384 ER PT J AU CHOUDHURY, GG BISWAS, P GRANDALIANO, G FOUQUERAY, B HARVEY, SA ABBOUD, HE AF CHOUDHURY, GG BISWAS, P GRANDALIANO, G FOUQUERAY, B HARVEY, SA ABBOUD, HE TI PDGF-MEDIATED ACTIVATION OF PHOSPHATIDYLINOSITOL 3-KINASE IN HUMAN MESANGIAL CELLS SO KIDNEY INTERNATIONAL LA English DT Article ID RECEPTOR TYROSINE KINASES; GROWTH-FACTOR RECEPTORS; PHOSPHOLIPASE-C-GAMMA; MIDDLE T-ANTIGEN; HUMAN PLATELETS; SH3 DOMAINS; SIGNAL TRANSDUCTION; PROTEIN; BINDING; PHOSPHORYLATION AB Platelet-derived growth factor (PDGF) stimulates mitogenesis and exerts other biologic activities in glomerular mesangial cells. The precise mechanism of PDGF-induced mitogenesis in these cells is not clear. The activation of a signal transducing enzyme, phosphatidylinositol 3 kinase (PI 3 kinase) is associated with mitogenesis. Activation of PI 3 kinase results from stimulation of tyrosine kinase and G-protein-coupled classes of receptors. The synthesis of D3 phosphorylated inositides, the products of this enzymatic reaction, in non-nucleated cells such as blood platelets is dependent upon protein kinase C activation and G-proteins. We studied the activation of PI 3 kinase in response to PDGF in human glomerular mesangial cells. Using a PI 3 kinase 85 kD subunit specific antibody, we detected mesangial cell PI 3 kinase protein as 110 and 85 kD heterodimer. PDGF stimulated PI 3 kinase activity in antiphosphotyrosine immunoprecipitates in a dose-dependent manner showing maximum activation at 12 ng/ml. The antiphosphotyrosine associated PI 3 kinase activity showed biphasic kinetics with a fast peak within two minutes followed by a second peak at 10 minutes. Antiphosphotyrosine and PI 3 kinase immunoprecipitation studies indicated the association of the 85 kD PI 3 kinase subunit with PDGFR. Direct immunoprecipitation with PDGFR beta antibody showed the association of PI 3 kinase activity with the PDGF-receptor. The isoquinoline sulfonyl piperazine compound H7 at concentrations that inhibit PDGF-stimulated PKC activity had no effect on PDGF-stimulated PI 3 kinase activity in antiphospotyrosine immunoprecipates. These data indicate that PI3 kinase activation is insensitive to PKC. Treatment of mesangial cells with pertussis toxin at concentrations that partially inhibited PDGF-induced DNA synthesis in human mesangial cells did not inhibit PDGF-induced PI 3 kinase activation. These data indicate that PDGF activates PI 3 kinase in mesangial cells and that pertussis toxin-sensitive G-proteins are not involved in PI 3 kinase activation. The data further dissociate activation of PI 3 kinase from mitogenesis in human mesangial cells. C1 UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP CHOUDHURY, GG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,SAN ANTONIO,TX 78284, USA. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK 43988, DK 33665] NR 49 TC 33 Z9 34 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JUL PY 1994 VL 46 IS 1 BP 37 EP 47 DI 10.1038/ki.1994.242 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA NT128 UT WOS:A1994NT12800005 PM 7933847 ER PT J AU KREISBERG, JI RADNIK, RA AYO, SH GARONI, JA SAIKUMAR, P AF KREISBERG, JI RADNIK, RA AYO, SH GARONI, JA SAIKUMAR, P TI HIGH GLUCOSE ELEVATES C-FOS AND C-JUN TRANSCRIPTS AND PROTEINS IN MESANGIAL CELL-CULTURES SO KIDNEY INTERNATIONAL LA English DT Article ID GENE-EXPRESSION; DIACYLGLYCEROL MASS; SIGNAL TRANSDUCTION; DIABETES-MELLITUS; MESSENGER-RNA; KINASE-C; ACTIVATION; GLOMERULI; ONCOGENES; INCREASE AB It has been previously shown that rat glomerular mesangial cells synthesized increased amounts of fibronectin, laminin, and type IV collagen when grown in medium containing 30 mM glucose. High glucose exerted its effect at the mRNA level since transcripts for all three extracellular matrix (ECM) proteins were similarly elevated. High glucose appeared to exert its effect on ECM mRNA levels through protein kinase C activation. Using quantitative reverse transcription (RT) PCR, we now report that mRNA levels for c-fos and c-Jun were increased approximately twofold after treatment with high glucose. The fos levels were elevated 15 minutes after addition of high glucose and were maintained elevated through 30 minutes; by one hour mRNA levels for fos returned to control levels, c-jun, on the other hand, was increased at two hours and remained elevated at 24 and 48 hours. Fibronectin mRNA levels were increased three- to fourfold at 24 and 48 hours. Immunofluorescence studies with polyclonal antibodies to c-fos and c-jun revealed that high glucose treatment for four hours increased nuclear staining intensity two- to threefold for both proteins. Nuclear staining for fos returned to control levels by 24 hours while staining for jun remained elevated. These determinations were made on images obtained on a confocal laser scanning microscope. Thus, high glucose may effect gene expression of ECM proteins by elevating the transcription factors c-fos and c-jun which complex with one another to form activator protein 1 (AP-1). C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP KREISBERG, JI (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 28 TC 103 Z9 105 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JUL PY 1994 VL 46 IS 1 BP 105 EP 112 DI 10.1038/ki.1994.249 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA NT128 UT WOS:A1994NT12800012 PM 7933827 ER PT J AU HAO, EH MENKE, JB SMITH, AM JONES, C GEFFNER, ME HERSHMAN, JM WUERTH, JP SAMUELS, HH WAYS, DK USALA, SJ AF HAO, EH MENKE, JB SMITH, AM JONES, C GEFFNER, ME HERSHMAN, JM WUERTH, JP SAMUELS, HH WAYS, DK USALA, SJ TI DIVERGENT DIMERIZATION PROPERTIES OF MUTANT BETA-1 THYROID-HORMONE RECEPTORS ARE ASSOCIATED WITH DIFFERENT DOMINANT-NEGATIVE ACTIVITIES SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID RETINOIC ACID RECEPTORS; LIGAND-BINDING DOMAIN; GENERALIZED RESISTANCE; RESPONSE ELEMENTS; X-RECEPTOR; HISTIDINE MUTATION; AUXILIARY PROTEIN; ENHANCES BINDING; GENE; DNA AB Syndromes of resistance to thyroid hormones are caused by mutations in the T-3-binding domain of the c-erbA beta thyroid hormone receptor gene. The S receptor (deletion of THR332) is a potent dominant negative protein cloned from a kindred with generalized resistance to thyroid hormones. The G-H receptor (ARG311HIS) has compromised dominant negative function and was found in both normal individuals and in a patient with severe pituitary resistance to thyroid hormones. We have investigated the mechanism responsible for the difference in receptor phenotypes by analyzing the binding of S and G-H receptors to thyroid hormone response elements with electrophoretic mobility shift analysis. Wild-type human c-erbA beta 1 (WT), S, and G-H receptors were synthesized in reticulocyte lysate, reacted with a thyroid hormone response element consisting of a direct repeat with 4 base pairs (DR+4; AGGTCA CAGG AGGTCA), and the products analyzed by gel shift. G-H receptor homodimerization was greatly impaired; G-H formed predominantly monomeric complex compared with monomeric and homodimeric WT complexes. The G-H receptor was able to form heterodimeric complexes with cellular thyroid hormone receptor auxiliary protein (TRAP) factors including the human retinoid X receptor-alpha. When TRAP was limiting, the levels of G-H heterodimeric complex were 2- to 3-fold reduced compared with Wi receptor. In contrast to the WT and G-H receptors, the S receptor formed almost exclusively homodimeric complex with DR+4; the approximate ratio of S:WT:G-H homodimeric complexes at equivalent concentrations of receptors was 60:20:1. A measurable increase (1.2- to 2.6-fold) in heterodimeric complex formation was observed with the S receptor relative to WT when TRAP was at limiting concentration. As reported previously by others, thyroid hormone significantly reduced the WT homodimeric complex with DR+4. There was no effect on the S homodimeric complex. Finally, the WT, S, and G-H receptors formed different complexes with the element consisting of an inverted repeat with 5 base pairs (IR+5; AGGTCA ACAGT TGACCT) and the IR element (AGGTCA TGACCT), which were differently regulated by thyroid hormone. The S receptor bound as a homodimer with IR+5, whereas the WT receptor bound as a homodimer only with thyroid hormone. No homodimeric complex formed with IR+5 and the G-H receptor. Qualitatively similar results were observed with the IR element. We conclude that the ARG311HIS mutation severely perturbs the homodimerization and, to a much less degree, heterodimerization functions of the c-erbAB1 receptor. Furthermore, the THR332 deletion mutation augments homodimerization of the c-erbA81 receptor. These results indicate that different mutations in the c-erbAB1 thyroid hormone receptor have divergently affected dimerization activities which seem to influence the level of dominant negative activity in man. C1 E CAROLINA UNIV, SCH MED, DEPT MED, ENDOCRINOL SECT, GREENVILLE, NC 27858 USA. E CAROLINA UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, GREENVILLE, NC 27858 USA. UNIV CALIF LOS ANGELES, MED CTR, DEPT PEDIAT, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. NYU, MED CTR, DEPT MED, NEW YORK, NY 10016 USA. NYU, MED CTR, DEPT MED, DIV MOLEC ENDOCRINOL, NEW YORK, NY 10016 USA. NYU, MED CTR, DEPT PHARMACOL, NEW YORK, NY 10016 USA. FU NCI NIH HHS [CA-43823]; NIDDK NIH HHS [DK-42807, DK-16636] NR 50 TC 35 Z9 35 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD JUL PY 1994 VL 8 IS 7 BP 841 EP 851 DI 10.1210/me.8.7.841 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NY971 UT WOS:A1994NY97100003 PM 7984146 ER PT J AU BENHAMOU, PY WATT, PC MULLEN, Y INGLES, S WATANABE, Y NOMURA, Y HOBER, C MIYAMOTO, M KENMOCHI, T PASSARO, EP ZINNER, MJ BRUNICARDI, FC AF BENHAMOU, PY WATT, PC MULLEN, Y INGLES, S WATANABE, Y NOMURA, Y HOBER, C MIYAMOTO, M KENMOCHI, T PASSARO, EP ZINNER, MJ BRUNICARDI, FC TI HUMAN ISLET ISOLATION IN 104 CONSECUTIVE CASES - FACTORS AFFECTING ISOLATION SUCCESS SO TRANSPLANTATION LA English DT Article ID PANCREATIC-ISLETS; ACUTE STROKE; TRANSPLANTATION; HYPERGLYCEMIA; LANGERHANS; VIABILITY; ANIMALS; TYPE-1; RATS AB One of the major steps toward successful islet trans plantation for the treatment of type diabetes is to obtain islets of sufficient number and viability. Using a standardized method of isolating islets, the goal of this study was to analyze the factors influencing the outcome of islet isolation. A total of 104 cadaveric human pancreata were processed for islets by the same team. Data from the islet-processing charts were reviewed retrospectively. The two endpoints were the recovery of islets, viable after 2 days of culture (group V=viable, group NV=nonviable) and the islet yield. Viable islets were recovered in 61% of cases (n=63). Minimal blood glucose recorded during hospitalization was very significantly lower in group V (124+/-5 vs. 148+/-9, P=0.01). Lack of significant medical history in the donor was associated with better viability as compared with vari ous donor predispositions (chi-(2) 4.21, P=0.04). Cold ischemia time (8.1+/-0.5 hr in group V vs. 9.8+/-0.9 hr in group NV, P=0.07) and collagenase lot (5 lots tested, chi-(2) 13.1, P=0.01) also affected the recovery of viable islets. Hospital time was shorter in group V (65.3+/-6.8 vs. 80.9+/-17.9 hr, P=0.35). Multivariate logistic regression analyses of viable islet recovery identified minimal blood glucose (P=0.03) and collagenase lot (P=0.06) as the most significant risk factors. However, the best multivariate predictive model-which includes blood glucose, collagenase lot, donor age and surgical procurement team-correctly predicted 66.2% of cases only. Multivariate analysis of final islet yield designed hospitalization length, cardiorespiratory arrest, surgical procurement team, and collagenase lot as the best predictors. These data obtained in a large series of pancreata emphasized several donor and technical factors that should target the attention of islet transplant researchers in order to improve islet yield and viability. C1 UNIV CALIF LOS ANGELES,SCH MED,DIABET RES CTR,DEPT SURG,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DIABET RES CTR,DEPT BIOMATH,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DEPT SURG,LOS ANGELES,CA 90024. NR 23 TC 99 Z9 102 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD JUN 27 PY 1994 VL 57 IS 12 BP 1804 EP 1810 DI 10.1097/00007890-199457120-00021 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA NV568 UT WOS:A1994NV56800021 PM 8016887 ER PT J AU FLEISCHMANN, J CAMPBELL, DA AF FLEISCHMANN, J CAMPBELL, DA TI EXPRESSION OF THE LEISHMANIA-TARENTOLAE UBIQUITIN-ENCODING AND MINI-EXON GENES SO GENE LA English DT Article DE CHROMOSOME LOCATION; KINETOPLASTID; MESSENGER-RNA; SPLICED LEADER; TRYPANOSOMATID; GECKO ID TRYPANOSOMA-BRUCEI; RNA GENE; GENOMIC ORGANIZATION; NUCLEOTIDE-SEQUENCE; POLYUBIQUITIN GENE; MESSENGER-RNAS; TRANSCRIPTION; CHROMOSOMES; CALMODULIN; DONOVANI AB To develop models for transcription and trans-splicing in kinetoplastid protozoa, we have characterized ubiquitin (Ubi) gene organization and mRNA processing in Leishmania tarentolae (Lt). Three ubi loci were characterized: two discrete Ubi-extension protein 52 (EP52)-encoding genes (ubiA and ubiB) and a polymorphic polyubiquitin-encoding gene (ubiC). The three loci resided on chromosomes of 2.05 Mb, 630 kb and 2.9 Mb, respectively. On the basis of upstream flanking gene identity, ubiB appears to be the homologue of the tandemly repeated ubi-EP52/1 and 2 in Trypanosoma brucei (Tb). Similar to Trypanosoma cruzi, Lt did not contain a homologue of the ubi-EP76 that has been found in Saccharomyces cerevisiae and multicellular organisms. All three Lt ubi loci were transcribed. The primary transcripts from the ubi loci were processed at the 5'-end by trans-splicing with the mini-exon. A Lt mini-exon gene (min) that gave rise to a 95-nt primary transcript, which is the second template in the trans-splicing reaction, was also characterized. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,INST MOLEC BIOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. NR 24 TC 14 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD JUN 24 PY 1994 VL 144 IS 1 BP 45 EP 51 DI 10.1016/0378-1119(94)90201-1 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA NW550 UT WOS:A1994NW55000007 PM 8026757 ER PT J AU WU, GD CHEN, LL FORSLUND, K TRABER, PG AF WU, GD CHEN, LL FORSLUND, K TRABER, PG TI HEPATOCYTE NUCLEAR FACTOR-1-ALPHA (HNF-1-ALPHA) AND HNF-1-BETA REGULATE TRANSCRIPTION VIA 2 ELEMENTS IN AN INTESTINE-SPECIFIC PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SUCRASE-ISOMALTASE GENE; HUMAN-COLON CARCINOMA; DNA-BINDING PROTEINS; CRYPT-VILLUS AXIS; MESSENGER-RNA; MOLECULAR-CLONING; LEUCINE ZIPPER; CELL-LINE; FACTOR-I; EXPRESSION AB Hepatocyte nuclear factor-1 alpha (HNF-1 alpha) and HNF-1 beta are transcription factors that contain a divergent homeodomain, bind to DNA as homo- or heterodimers, and act to regulate transcription of many genes that are expressed primarily in liver. We show that HNF-1 alpha and HNF-1 beta act as regulatory factors for transcription of sucrase-isomaltase (SI), the gene for which is expressed exclusively in absorptive enterocytes of the small intestine. HNF-1 alpha and HNF-1 beta bind to two evolutionarily conserved sites in the SI promoter, previously named SIF2 and SIF3, with different relative affinities. HNF-1 alpha binds to the SIF3 element with greater affinity than to the SIF2 element, whereas HNF-1 beta binds to both elements equally. Co-transfection experiments demonstrated that HNF-1 alpha is able to increase transcriptional initiation from a minimal SI intestine-specific promoter. In contrast, HNF-1 beta has no functional effect on transcription of the SI promoter. The functional and DNA binding differences of HNF-1 alpha and HNF-1 beta on elements in the SI promoter suggest that these transcription factors may play a role in the complex spatial patterns of SI gene expression in the intestine. C1 UNIV PENN, SCH MED, DEPT INTERNAL MED, DIV GASTROENTEROL, PHILADELPHIA, PA 19104 USA. DEPT VET AFFAIRS MED CTR, PHILADELPHIA, PA 19104 USA. FU NIDDK NIH HHS [DK44621] NR 40 TC 104 Z9 106 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 24 PY 1994 VL 269 IS 25 BP 17080 EP 17085 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NT846 UT WOS:A1994NT84600018 PM 8006012 ER PT J AU KRAUT, JA COBURN, JW AF KRAUT, JA COBURN, JW TI BONE, ACID, AND OSTEOPOROSIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID SODIUM-BICARBONATE; CALCIUM BALANCE; WOMEN RP KRAUT, JA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90072, USA. NR 10 TC 22 Z9 22 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 JUN 23 PY 1994 VL 330 IS 25 BP 1821 EP 1822 DI 10.1056/NEJM199406233302510 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NR295 UT WOS:A1994NR29500010 PM 8190161 ER PT J AU MILLER, SR SALO, AL BOGGAN, WO PATRICK, KS AF MILLER, SR SALO, AL BOGGAN, WO PATRICK, KS TI DETERMINATION OF PLASMA COCAINE AND ETHYLCOCAINE (COCAETHYLENE) IN MICE USING GAS-CHROMATOGRAPHY MASS-SPECTROMETRY AND DEUTERATED INTERNAL STANDARDS SO JOURNAL OF CHROMATOGRAPHY B-BIOMEDICAL APPLICATIONS LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; PHASE EXTRACTION COLUMNS; ECGONINE METHYL-ESTER; ETHANOL INGESTION; HUMAN LIVER; METABOLITES; BENZOYLECGONINE; DOPAMINE; SERUM; URINE AB A gas chromatographic-mass spectrometric method is described for the determination of cocaine and ethylcocaine (cocaethylene) from mouse plasma microsamples (50 mu l). [H-2(3)]Cocaine and [H-2(5)]ethylcocaine served as internal standards, analytical separations were performed on a (5% phenyl)methylpolysiloxane capillary column, and detection was by selected-ion monitoring of electron-impact generated fragment ions [M - CO(2)Ph]. Pilot study plasma concentrations of ethylcocaine following coadministration of cocaine and ethanol were less than 5% of the parent drug. C1 MED UNIV S CAROLINA,DEPT PHARMACEUT SCI,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC 29425. RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC 29401. FU NIAAA NIH HHS [1RO1AA09487]; NIDA NIH HHS [1RO1DA08034] NR 31 TC 6 Z9 6 U1 2 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR B JI J. Chromatogr. B-Biomed. Appl. PD JUN 17 PY 1994 VL 656 IS 2 BP 335 EP 341 DI 10.1016/0378-4347(94)00133-2 PG 7 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA NW845 UT WOS:A1994NW84500006 PM 7987485 ER PT J AU SINGH, BN AF SINGH, BN TI IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS - NOT THE ULTIMATE GOLD STANDARD FOR GAUGING THERAPY OF VT/FIBRILLATION SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Editorial Material ID VENTRICULAR TACHYARRHYTHMIAS; ANTIARRHYTHMIC DRUGS; EFFICACY; LIFE C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90024 USA. RP SINGH, BN (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, DIV CARDIOL 691 111E, WILSHIRE & SAWTELLE BLVD, LOS ANGELES, CA 90073 USA. NR 17 TC 11 Z9 11 U1 0 U2 0 PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC PI BRIDGEWATER PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA SN 0002-9149 EI 1879-1913 J9 AM J CARDIOL JI Am. J. Cardiol. PD JUN 15 PY 1994 VL 73 IS 16 BP 1211 EP 1213 DI 10.1016/0002-9149(94)90184-8 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NP976 UT WOS:A1994NP97600014 PM 8203341 ER PT J AU TAKAHASHI, R HEYDARI, AR GUTSMANN, A SABIA, M RICHARDSON, A AF TAKAHASHI, R HEYDARI, AR GUTSMANN, A SABIA, M RICHARDSON, A TI THE HEAT-SHOCK TRANSCRIPTION FACTOR IN LIVER EXISTS IN A FORM THAT HAS DNA-BINDING ACTIVITY BUT NO TRANSCRIPTIONAL ACTIVITY SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PROTEIN; ACTIVATION; PROMOTER; YEAST; AGE; OLIGOMERIZATION; HEPATOCYTES; STRESS; GENES; CELLS AB The binding activity of the heat shock transcription factor (HSF) to the heat shock element (HSE) is observed in non-stressed Liver and freshly isolated hepatocytes when the expression of hsp70 is undetectable, HSF binding activity in non-stressed liver/hepatocytes is specific for HSE and similar to the HSF binding activity observed in heat shocked hepatocytes that is associated with hsp70 transcription. However, the HSF binding activity in non-stressed and heat shock cells can be distinguished on the basis of the thermal stability in vitro. The HSE binding activity of cell extracts isolated from non-stressed liver/hepatocytes was lost rapidly when the extracts were incubated at 37 degrees C. In contrast, the HSF binding activity of cell extracts isolated from heat shocked hepatocytes was relatively stable at 37 degrees C. Based on our observations, we propose that the activation of HSF is a multistep process that involves a change in conformation after oligomerization and the acquisition of DNA binding to a form that is more thermostable and is associated with increased hsp70 transcription. (C) 1994 Academic Press, Inc. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. TOHO UNIV,SCH PHARMACEUT SCI,CHIBA 274,JAPAN. FU NIA NIH HHS [AG01548]; NIEHS NIH HHS [ES06277] NR 19 TC 10 Z9 10 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JUN 15 PY 1994 VL 201 IS 2 BP 552 EP 558 DI 10.1006/bbrc.1994.1737 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NQ805 UT WOS:A1994NQ80500010 PM 8002986 ER PT J AU AFRIDI, I QUINONES, MA ZOGHBI, WA CHEIRIF, J AF AFRIDI, I QUINONES, MA ZOGHBI, WA CHEIRIF, J TI DOBUTAMINE STRESS ECHOCARDIOGRAPHY - SENSITIVITY, SPECIFICITY, AND PREDICTIVE VALUE FOR FUTURE CARDIAC EVENTS SO AMERICAN HEART JOURNAL LA English DT Article ID CORONARY-ARTERY DISEASE; ACUTE MYOCARDIAL-INFARCTION; EXERCISE ECHOCARDIOGRAPHY; PROGNOSTIC VALUE AB We conducted a retrospective study to determine whether dobutamine stress echocardiography (DE) can be used for risk stratification of patients with known or suspected coronary artery disease (CAD). The study population consisted of 77 patients who underwent DE at our institution. The protocol consisted of an echocardiogram at baseline followed by imaging during intravenous dobutamine infusion starting at 10 mu g/kg/min with increments of 10 mu g/kg/min every 3 minutes to a maximum dose of 40 mu g/kg/min. The reasons for performing DE included preoperative cardiac evaluation (30), chest pain (23), assessment of ischemia (18), and suspected, restenosis (6). DE was classified according to wall motion response as normal (before and during DE), fixed abnormal (abnormal before with no change during DE), or ischemic (new wall-motion abnormality during DE). Mean duration of follow-up was 10 months. Cardiac events occurred in 14 patients. These included congestive heart failure in seven patients, myocardial infarction-in six, and cardiac death in one. A normal wall-motion response (n = 40) was associated with a low incidence of cardiac events (5%), whereas 5 of 10 patients (50%) with an ischemic response had events. The risk of cardiac events was intermediate (26%) in patients with fixed abnormal wall motion. Overall sensitivity of DE for predicting future cardiac events was 85%. In 45 patients who underwent coronary angiography within 2 months of DE, the test detected CAD with a sensitivity of 71%. In conclusion, the wall-motion response during DE may be used for identifying patients at high risk for future cardiac events. C1 BAYLOR COLL MED,VET ADM HOSP,DEPT INTERNAL MED,CARDIOL SECT,HOUSTON,TX. FU NCRR NIH HHS [RR-00350] NR 17 TC 76 Z9 77 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 JUN PY 1994 VL 127 IS 6 BP 1510 EP 1515 DI 10.1016/0002-8703(94)90378-6 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NQ301 UT WOS:A1994NQ30100011 PM 8197976 ER PT J AU PUGH, JA TULEY, MR BASU, S AF PUGH, JA TULEY, MR BASU, S TI SURVIVAL AMONG MEXICAN-AMERICANS, NON-HISPANIC WHITES, AND AFRICAN-AMERICANS WITH END-STAGE RENAL DISEASE - THE EMERGENCE OF A MINORITY PATTERN OF INCREASED INCIDENCE AND PROLONGED SURVIVAL SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE SURVIVAL; END-STAGE RENAL DISEASE; HISPANIC; MEXICAN-AMERICAN; MINORITIES ID RENAL-DISEASE; DIALYSIS; THERAPY C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,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 FU AHRQ HHS [1U01HS0739701]; NIDDK NIH HHS [DK38392] NR 17 TC 44 Z9 44 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 JUN PY 1994 VL 23 IS 6 BP 803 EP 807 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA NQ744 UT WOS:A1994NQ74400006 PM 8203362 ER PT J AU KITTEN, AM HYMER, TK KATZ, MS AF KITTEN, AM HYMER, TK KATZ, MS TI BIDIRECTIONAL MODULATION OF PARATHYROID HORMONE-RESPONSIVE ADENYLYL-CYCLASE BY PROTEIN-KINASE-C SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PHORBOL ESTER; PARATHYROID HORMONE RECEPTOR; DIACYLGLYCEROL; G PROTEINS; OSTEOBLAST ID OSTEOBLAST-LIKE CELLS; CYCLIC-AMP PRODUCTION; INDUCED HOMOLOGOUS DESENSITIZATION; SIGNAL TRANSDUCTION SYSTEMS; OSTEOSARCOMA CELLS; PHORBOL ESTER; PTH RECEPTOR; SARCOMA CELLS; CAMP; STIMULATION AB The temporal pattern with which phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), modulates parathyroid hormone (PTH)-responsive adenylyl cyclase (AC) was evaluated in a clonal osteoblast-like cell line (UMR-106). Brief (less than or equal to 1 h) exposure of UMR-106 cells to PMA enhanced PTH simulation of AC, whereas more prolonged PMA treatment decreased the PTH response, with maximum inhibition occurring at less than or equal to 6 h. PMA treatment also resulted in initial activation followed by downregulation of PKC. Exposure of cells to 1,2-dioctanoyl-sn-glycerol, which activated but did not downregulate PKC, resulted in bidirectional modulation of PTH-responsive AC identical to that produced by PMA. Prolonged PMA exposure decreased PTH receptor number, as determined by radioligand binding studies, and reduced PTH receptor mRNA levels, assessed by Northern blot analysis. Forskolin activation of the catalytic subunit of AC was also decreased after prolonged PMA treatment. The results suggest that activation of PKC sequentially stimulates and then inhibits PTH responsiveness. Inhibition of the PTH response occurs by PKC actions exerted on the PTH receptor and the AC catalytic subunit. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,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. NR 33 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 JUN PY 1994 VL 266 IS 6 BP E897 EP E904 PN 1 PG 8 WC Physiology SC Physiology GA NV809 UT WOS:A1994NV80900045 PM 8023920 ER PT J AU MARDER, SR MEIBACH, RC AF MARDER, SR MEIBACH, RC TI RISPERIDONE IN THE TREATMENT OF SCHIZOPHRENIA SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID NEGATIVE SYNDROME SCALE; RITANSERIN R-55667; SEROTONIN-S2; HALOPERIDOL; ANTAGONIST; EFFICACY; PLACEBO; SAFETY AB Objective: The purpose of this study was to investigate the safety and efficacy of risperidone in the treatment of schizophrenic Patients and determine its optimal dose. Method: This double-blind study included 388 schizophrenic patients drawn from 20 sites in the United States. Patients were randomly assigned to 8 weeks' treatment with placebo, one Of four doses of risperidone (2, 6, 10, or 16 mg), or 20 mg of haloperidol daily. Results: Clinical improvement (20% reduction in total scores on the Positive and Negative Syndrome Scale for Schizophrenia) at the study end point was shown by 35% of the patients receiving 2 mg of risperidone, 57% receiving 6 mg, 40% receiving 10 mg, and 51% receiving 16 mg; and by 30% receiving haloperidol and 22% receiving placebo. Statistically significant differences in clinical improvement were found between 6 and 16 mg of risperidone versus placebo and versus haloperidol. Positive symptom scores were significantly lower after 6, 10, and 16 mg of risperidone and 20 mg of haloperidol than placebo; negative symptom scores, however, were reduced significantly, compared with placebo, only after 6 and 16 mg of risperidone. The incidence of extrapyramidal side effects (measured by the Extrapyramidal Symptom Rating Scale) was significantly higher in patients treated with 16 mg of risperidone or 20 mg of haloperidol than placebo. The results indicate that the optimal daily dose of risperidone for most schizophrenic patients in this study was 6 mg; this dose was as effective as 16 mg, and the incidence of extrapyramidal symptoms in patients receiving 6 mg of risperidone was no higher than that in patients receiving Placebo. Conclusions: Risperidone is a safe antipsychotic that is effective against both the positive and negative symptoms of schizophrenia. C1 JANSSEN RES FDN,TITUSVILLE,NJ. RP MARDER, SR (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV 116A,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 29 TC 1045 Z9 1070 U1 9 U2 54 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 JUN PY 1994 VL 151 IS 6 BP 825 EP 835 PG 11 WC Psychiatry SC Psychiatry GA NN755 UT WOS:A1994NN75500006 PM 7514366 ER PT J AU HANDFORTH, A FINCH, DM PETERS, R TAN, AM TREIMAN, DM AF HANDFORTH, A FINCH, DM PETERS, R TAN, AM TREIMAN, DM TI INTERICTAL SPIKING INCREASES 2-DEOXY(C-14)GLUCOSE UPTAKE AND C-FOS-LIKE REACTIVITY SO ANNALS OF NEUROLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLUCOSE-UTILIZATION; STATUS EPILEPTICUS; PARTIAL SEIZURES; PARTIAL EPILEPSY; MESSENGER-RNA; DENTATE GYRUS; RAT-BRAIN; EXPRESSION; STIMULATION AB Although interictal spikes are thought to share pathophysiological mechanisms with partial-onset seizure discharges, positron emission tomographic studies of the interictal state have paradoxically shown focal hypometabolism whereas seizures produce hypermetabolism To address this question, we performed functional mapping studies in an interictal spiking model in the rat. Recording screw electrodes were inserted through the skull bone so as to depress underlying cortex. Interictal spiking was subsequently induced by systemic administration of bicuculline methiodide. 2-deoxy[C-14]glucose studies revealed increased glucose utilization in superficial and middle cortical layers at spiking screw sites. Nonspiking screw sites in the same animals and in controls did not show increased uptake. Convulsive seizures caused additional 2-deoxy[C-14]glucose uptake at screw sites and in widespread forebrain areas. c-fos immunoreactivity occurred in superficial cortex at interictal spiking, but not nonspiking, sites. Convulsive seizures induced widespread forebrain c-fos immunoreactivity. These data suggest interictal epileptiform activity occurs in cells adjacent to cortical injury; these activate deeper layers via local connections. Interictal and ictal epileptiform states share common mechanisms, as both induce glucose hypermetabolism and immediate-early gene product activation. Possible reasons for failure to detect hypermetabolism in interictal human subjects are discussed. C1 W LOS ANGELES DEPT VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. RP HANDFORTH, A (reprint author), DEPT VET AFFAIRS MED CTR,W LOS ANGELES WADSWORTH DIV,NEUROL SERV,SAWTELLE & WILSHIRE BLVDS,LOS ANGELES,CA 90073, USA. FU NINDS NIH HHS [NS 16721] NR 28 TC 23 Z9 23 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JUN PY 1994 VL 35 IS 6 BP 724 EP 731 DI 10.1002/ana.410350614 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NQ973 UT WOS:A1994NQ97300013 PM 8210230 ER PT J AU BERENGUER, J ALI, NM ALLENDE, MC LEE, J GARRETT, K BATTAGLIA, S PISCITELLI, SC RINALDI, MG PIZZO, PA WALSH, TJ AF BERENGUER, J ALI, NM ALLENDE, MC LEE, J GARRETT, K BATTAGLIA, S PISCITELLI, SC RINALDI, MG PIZZO, PA WALSH, TJ TI ITRACONAZOLE FOR EXPERIMENTAL PULMONARY ASPERGILLOSIS - COMPARISON WITH AMPHOTERICIN-B, INTERACTION WITH CYCLOSPORINE-A, AND CORRELATION BETWEEN THERAPEUTIC RESPONSE AND ITRACONAZOLE CONCENTRATIONS IN PLASMA SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID INVASIVE ASPERGILLOSIS; SYSTEMIC MYCOSES; ANTIFUNGAL; INVITRO; CRYPTOCOCCOSIS; AZOLES; PHARMACOKINETICS; INVIVO AB Itraconazole and amphotericin B were compared by using a newly developed model of invasive pulmonary aspergillosis in rabbits immunosuppressed with methylprednisolone and cyclosporin A (CsA). Both itraconazole at 40 mg/kg (given orally) and amphotericin B at 1 mg/kg (given intravenously) had in vivo antifungal activity in comparison with controls, At these dosages, amphotericin B was more effective than itraconazole in reducing the tissue burden (log(10) CFU per gram) of Aspergillus fumigatus (P < 0.05) and the number of pulmonary lesions (P < 0.01). However, there was considerable variation in the near-peak concentrations of itraconazole in plasma (median, 4.15 mu g/ml; range, <0.5 to 16.8 mu g/ml) and a strong inverse correlation between concentrations of itraconazole in plasma and the tissue burden of A. fumigatus. An inhibitory sigmoid maximum-effect model predicted a significant pharmacodynamic relationship (r = 0.87, P < 0.001) between itraconazole concentrations in plasma and antifungal activity as a function of the tissue burden of A, fumigatus. This model demonstrated that levels in plasma of greater than 6 mu g/ml were associated with a significantly greater antifungal effect. Levels in plasma of less than 6 mu g/ml were associated with a rapid decline in the antifungal effect. Itraconazole, in comparison with amphotericin B, caused a twofold elevation of CsA levels (P < 0.01) but was less nephrotoxic (P < 0.01). This study of experimental pulmonary aspergillosis demonstrated that amphotericin B at 1 mg/kg/day was more active but more nephrotoxic than itraconazole at 40 mg/kg/day, that itraconazole increased concentrations of CsA in plasma, and that the antifungal activity of itraconazole strongly correlated with concentrations in plasma in an inhibitory sigmoid maximum-effect model. These findings further indicate the importance of monitoring concentrations of itraconazole in plasma as a guide to increasing dosage, improving bioavailability, and optimizing antifungal efficacy in the treatment of invasive pulmonary aspergillosis. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT PHARM,PHARMACOKINET RES LAB,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78229. AUDIE L MURPHY MEM VET ADM MED CTR,LAB SERV,SAN ANTONIO,TX 78221. OI Berenguer, Juan/0000-0001-8541-8200 NR 32 TC 60 Z9 61 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 JUN PY 1994 VL 38 IS 6 BP 1303 EP 1308 PG 6 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA NN770 UT WOS:A1994NN77000015 PM 8092829 ER PT J AU ARNASON, JA PATEL, A SUNDSTROM, WR AF ARNASON, JA PATEL, A SUNDSTROM, WR TI TRANSTHORACIC AND TRANSESOPHAGEAL ECHOCARDIOGRAPHIC EVALUATION OF THE AORTIC ROOT AND SUBVALVULAR STRUCTURES IN ANKYLOSING-SPONDYLITIS SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD JUN PY 1994 VL 37 IS 6 SU S BP R13 EP R13 PG 1 WC Rheumatology SC Rheumatology GA NP830 UT WOS:A1994NP83000034 ER PT J AU BORIGINI, MJ PAULUS, HE CLEMENTS, PJ PERSSELIN, JE AF BORIGINI, MJ PAULUS, HE CLEMENTS, PJ PERSSELIN, JE TI CLINICAL EFFICACY OF IMMUNOADSORPTION OF RHEUMATOID-ARTHRITIS (RA) PLASMA ON PROTEIN-A COLUMNS MAY BE RELATED TO ALTERATIONS IN PLASMA ANTI-IGG ANTIBODY-LEVELS SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD JUN PY 1994 VL 37 IS 6 SU S BP R7 EP R7 PG 1 WC Rheumatology SC Rheumatology GA NP830 UT WOS:A1994NP83000016 ER PT J AU DUNKIN, JJ LEUCHTER, AF NEWTON, TF COOK, IA AF DUNKIN, JJ LEUCHTER, AF NEWTON, TF COOK, IA TI REDUCED EEG COHERENCE IN DEMENTIA - STATE OR TRAIT MARKER SO BIOLOGICAL PSYCHIATRY LA English DT Article DE EEG COHERENCE; ALZHEIMERS DISEASE; DEMENTIA; QUANTITATIVE EEG; QEEG RELIABILITY ID MULTI-INFARCT DEMENTIA; MILD SENILE DEMENTIA; ALZHEIMER-TYPE; DIFFERENTIAL-DIAGNOSIS; ELDERLY SUBJECTS; HUMAN-BRAIN; DISEASE; RELIABILITY; PATTERNS; TASK AB Recent work from our laboratory demonstrated that quantitative electroencephalographic (EEG) coherence between brain areas linked by long cortico-cortical fibers (termed ''fascicle'' coherence) was differentially reduced in subjects with Alzheimer's disease, whereas coherence between brain areas linked by short cortico-cortical and cortico-subcortical fibers in postcentral areas (termed ''visual'' coherence) was differentially reduced in subjects with multi-infarct dementia. In this study, we investigated whether these differences in coherence represent ''trait'' or ''state'' markers for dementia. Visual coherence demonstrated high stability in both demented groups as assessed by both one-year test-retest reliabilities and analysis of group mean change. Fascicle coherence demonstrated good stability in multi-infarct dementia and control subjects, but some variability was observed in Alzheimer's subjects, suggesting both state and trait factors may be involved. These findings complement neuropathologic studies, and suggest that decreases in coherence may serve as a diagnostic trait markers for these two types of dementia. The role of state factors in Alzheimer's disease requires further investigation. C1 UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,QUANTITAT EEG LAB,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. OI newton, thomas/0000-0002-3198-5901 FU NIA NIH HHS [P30 AG 10123]; NIMH NIH HHS [NIMH MH 40705, NIMH MH 00665] NR 25 TC 65 Z9 73 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JUN 1 PY 1994 VL 35 IS 11 BP 870 EP 879 DI 10.1016/0006-3223(94)90023-X PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NN547 UT WOS:A1994NN54700007 PM 8054410 ER PT J AU DIAMOND, D DOANE, JA AF DIAMOND, D DOANE, JA TI DISTURBED ATTACHMENT AND NEGATIVE AFFECTIVE STYLE - AN INTERGENERATIONAL SPIRAL SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID EXPRESSED EMOTION; FAMILY; DISORDERS; ILLNESS; SCHIZOPHRENIA; DEPRESSIVES; PREDICTORS; RELAPSE; BONDS AB The relationship between the quality of parents' attachment to their own parents and the quality of affective style was examined with a sample of 49 severely disturbed young adults and adolescents and their families receiving long-term in-patient treatment. Measures reflecting disturbances in attachment of parents to their own parents, derived from a five-minute speech sample task, were strongly associated with measures of negative affective style (e.g., criticism, intrusiveness and guilt induction) in face-to-face interactions with the disturbed offspring, as assessed through videotaped discussions of conflictual family issues after three months of treatment. The most significant findings involved the linkages between disturbances in the mother's attachment to her own mother and the degree of negative affect directed at the child patient. The association between disturbed intergenerational parental attachments and negative affective style supports the hypothesis that the parent's own internal burdens, stemming from disturbed attachment representations, particularly of the same-sex parent, may be a driving force behind the negative affect they display in interactions with their disturbed offspring. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP DIAMOND, D (reprint author), CORNELL UNIV,NEW YORK HOSP,COLL MED,DEPT PSYCHIAT,WESTCHESTER DIV,21 BLOOMINGDALE RD,WHITE PLAINS,NY 10605, USA. FU NIMH NIH HHS [MH44991] NR 54 TC 22 Z9 22 U1 3 U2 4 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD JUN PY 1994 VL 164 BP 770 EP 781 DI 10.1192/bjp.164.6.770 PG 12 WC Psychiatry SC Psychiatry GA NR864 UT WOS:A1994NR86400008 PM 7952983 ER PT J AU COOLEY, ME DAVIS, LE DESTEFANO, M ABRAHM, J AF COOLEY, ME DAVIS, LE DESTEFANO, M ABRAHM, J TI CISPLATIN - A CLINICAL REVIEW .1. CURRENT USES OF CISPLATIN AND ADMINISTRATION GUIDELINES SO CANCER NURSING LA English DT Review DE CISPLATIN; USES; ADMINISTRATION ID CELL LUNG-CANCER; HIGH-DOSE CISPLATIN; REFRACTORY OVARIAN-CARCINOMA; RANDOMIZED TRIAL; CIS-PLATINUM; INTRAPERITONEAL CHEMOTHERAPY; ONCOLOGY-GROUP; SALVAGE THERAPY; BRAIN-TUMORS; PHASE-I AB Cisplatin is one of the most active cancer treatment agents available. Unfortunately, however, cisplatin causes many untoward side effects. Nurses play a major role in administering cisplatin and in preventing and managing the adverse effects associated with this drug. In order to maximize the quality of life of patients undergoing cisplatin treatment, nurses need a thorough knowledge of its uses, administration, and side effects. This article is the first of a two-part series about cisplatin. Part I will provide a review of the mechanism of action, current uses, and administration guidelines. Part II will discuss the most common side effects of cisplatin and the appropriate nursing assessment and management of patients undergoing treatment with this agent. In addition, future directions for the use of cisplatin and the use of alternative agents will be discussed. C1 PHILADELPHIA VET AFFAIRS MED CTR,LUNG TUMOR CLIN,PHILADELPHIA,PA. DELAWARE CTY MEM HOSP,DREXEL HILL,PA. PHILADELPHIA VET AFFAIRS MED CTR,HEMATOL ONCOL SECT,PHILADELPHIA,PA. PHILADELPHIA COLL PHARM & SCI,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. NR 78 TC 10 Z9 10 U1 2 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0162-220X J9 CANCER NURS JI Cancer Nurs. PD JUN PY 1994 VL 17 IS 3 BP 173 EP 184 PG 12 WC Oncology; Nursing SC Oncology; Nursing GA NP075 UT WOS:A1994NP07500001 PM 8055487 ER PT J AU VOLK, MJ PUGH, TD KIM, M FRITH, CH DAYNES, RA ERSHLER, WB WEINDRUCH, R AF VOLK, MJ PUGH, TD KIM, M FRITH, CH DAYNES, RA ERSHLER, WB WEINDRUCH, R TI DIETARY RESTRICTION FROM MIDDLE-AGE ATTENUATES AGE-ASSOCIATED LYMPHOMA DEVELOPMENT AND INTERLEUKIN-6 DYSREGULATION IN C57BL/6 MICE SO CANCER RESEARCH LA English DT Article ID B-CELLS; HODGKINS-DISEASE; TRANSGENIC MICE; SURVIVAL; INCREASE; DIFFERENTIATION; CLASSIFICATION; TUMORIGENICITY; EXPRESSION; NEOPLASMS AB Dietary restriction (DR) started in middle age profoundly reduces the occurrence of lymphoma in C57BL/6 mice. Here, we report immunocellular and molecular changes associated with this mode of cancer prevention. Twelve-month-old male C57BL/6 mice were either fed a control diet or subjected to moderate DR (similar to 25% < control intake). DR significantly reduced lymphoma development (incidence at 25 months, 19% of 72 control mice versus 5% of 60 DR mice). Flow cytometry of splenocytes showed that DR increased the percentage of CD4(+) and CD8(+) cells. Lymphomatous spleens displayed varied labeling patterns and high percentages of cells in S phase. Splenocyte c-myc expression tended to increase with age in controls and was reduced by DR Lymphopenia and markedly reduced nucleated cell yields from peripheral lymphoid tissues were induced by DR. Serum interleukin 6 levels increased with age and were quite high (>2500 pg/ml) in several mice with lymphoma and other histopathological findings. DR attenuated this age-associated increase. Immunohistochemical studies of lymphomatous spleens showed the presence of interleukin 6 in monocytic appearing cells but not in lymphoma cells. These observations support the possibility that an age-associated interleukin 6 dysregulation is important in lymphomagenesis. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT NUTR SCI,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI 53705. TOXICOL PATHOL ASSOCIATES,LITTLE ROCK,AR 72211. UNIV UTAH,SCH MED,DEPT PATHOL,SALT LAKE CITY,UT 84132. NR 42 TC 51 Z9 52 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 JUN 1 PY 1994 VL 54 IS 11 BP 3054 EP 3061 PG 8 WC Oncology SC Oncology GA NN724 UT WOS:A1994NN72400044 PM 8187095 ER PT J AU CIVEN, R BERLIN, G PANOSIAN, C AF CIVEN, R BERLIN, G PANOSIAN, C TI VERTEBRAL OSTEOMYELITIS AFTER INTRAVESICAL ADMINISTRATION OF BACILLE CALMETTE-GUERIN SO CLINICAL INFECTIOUS DISEASES LA English DT Letter ID BLADDER-CANCER; THERAPY; COMPLICATIONS; IMMUNOTHERAPY; INFECTION C1 W LOS ANGELES VET AFFAIRS MED CTR,DIV INFECT DIS,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DIV INFECT DIS,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,MED CTR,DEPT PATHOL & LAB MED,CLIN MICROBIOL SECT,LOS ANGELES,CA 90024. NR 10 TC 16 Z9 16 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JUN PY 1994 VL 18 IS 6 BP 1013 EP 1014 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NQ826 UT WOS:A1994NQ82600035 PM 8086533 ER PT J AU WEXLER, HM MOLITORIS, E FINEGOLD, SM AF WEXLER, HM MOLITORIS, E FINEGOLD, SM TI IN-VITRO ACTIVITY OF GREPAFLOXACIN (OPC-17116) AGAINST ANAEROBIC-BACTERIA SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Note ID COMPARATIVE INVITRO ACTIVITIES; QUINOLONE AB In vitro activity of the quinolone grepafloxacin (OPC-17116) was compared with that of ciprofloxacin, fleroxacin, clindamycin, imipenem, and metronidazole by using the NCCLS-approved Brucella-base-laked blood agar dilution method and breakpoints, when available. Clindamycin, metronidazole, and imipenem inhibited greater than or equal to 98% of Bacteroides fragilis at the breakpoint; grepafloxacin, ciprofloxacin, and fleroxacin inhibited 83%, 6%, and 0, respectively, at 2 mu g/ml. Grepafloxacin inhibited 39% of other B. fragilis group species isolates (80) at breakpoint (less than or equal to 2 mu g/ml) compared with 100% for metronidazole and imipenem, 83% for clindamycin, 6% for ciprofloxacin, and 1% for fleroxacin. Grepafloxacin demonstrated substantially better activity against B. fragilis than did ciprofloxacin or fleroxacin; overall activity against anaerobes was marginally better than that of ciprofloxacin or fleroxacin. C1 VET ADM MED CTR,MED SERV,WADSWORTH DIV,LOS ANGELES,CA 91343. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. RP WEXLER, HM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MICROBIAL DIS RES LAB,RES SERV,WADSWORTH DIV,BLDG 304,LOS ANGELES,CA 90073, USA. NR 10 TC 6 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD JUN PY 1994 VL 19 IS 2 BP 129 EP 133 DI 10.1016/0732-8893(94)90123-6 PG 5 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA PD356 UT WOS:A1994PD35600009 PM 7805357 ER PT J AU NASU, M SUGAWARA, M AF NASU, M SUGAWARA, M TI EXOGENOUS FREE IODOTYROSINE INHIBITS IODIDE TRANSPORT THROUGH THE SEQUENTIAL INTRACELLULAR EVENTS SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article ID THYROID AUTO-REGULATION; CELLS; ADENOSINE-3',5'-MONOPHOSPHATE; THYROGLOBULIN; THYROTROPIN; MECHANISM; HORMONE AB We describe a new function of exogenous iodotyrosine as a regulator of iodide transport. Porcine thyroid follicles in culture were preincubated with 0-20 mu mol/l monoiodotyrosine or diiodotyrosine (DIT) in the presence of bovine thyrotropin (TSH) for 24 h; these iodotyrosines inhibited iodide uptake in a dose-response manner. Extracellular [I-125]DIT was actively transported to the thyroid follicle in the presence of TSH or (Bu)(2) cAMP. Inhibition of iodide uptake by iodotyrosine required preincubation with iodotyrosine in the presence of TSH; without TSH, iodotyrosine was ineffective. Follicles preincubated with DIT for 24 h inhibited TSH-mediated cAMP production, which is an important signal for iodide transport. Inhibition of iodide uptake and cAMP generation by iodotyrosine was negated characteristically by 3-nitro-L-tyrosine, an inhibitor of iodotyrosine deiodinase, or by methimazole, an inhibitor of thyroid peroxidase. Our findings suggest that iodotyrosine regulates iodide transport through the following sequential intracellular events: TSH-dependent iodotyrosine transport into the thyroid cell; deiodination of iodotyrosine and release in iodide; iodine organification by the peroxidase system; inhibition of cAMP generation by organified iodine; and inhibition of iodide transport. Thus, exogenous iodotyrosine can serve as an inhibitor of thyroid hormone formation only when TSH is present. C1 W LOS ANGELES VET AFFAIRS MED CTR,DIV ENDOCRINOL & METAB,RES SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,DIV ENDOCRINOL & METAB,MED SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. NR 26 TC 2 Z9 2 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0804-4643 J9 EUR J ENDOCRINOL JI Eur. J. Endocrinol. PD JUN PY 1994 VL 130 IS 6 BP 601 EP 607 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NT430 UT WOS:A1994NT43000012 PM 8205262 ER PT J AU OBERLEY, TD SCHULTZ, JL OBERLEY, LW AF OBERLEY, TD SCHULTZ, JL OBERLEY, LW TI IN-VITRO MODULATION OF ANTIOXIDANT ENZYME LEVELS IN NORMAL HAMSTER-KIDNEY AND ESTROGEN-INDUCED HAMSTER-KIDNEY TUMOR SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE ANTIOXIDANT ENZYMES; MANGANESE SUPEROXIDE DISMUTASE; KIDNEY; TUMOR; DIETHYLSTILBESTROL; FREE RADICALS ID MANGANESE SUPEROXIDE-DISMUTASE; SYRIAN-HAMSTER; IMMUNOHISTOCHEMICAL LOCALIZATION; GLUTATHIONE-PEROXIDASE; LUNG FIBROBLASTS; CELLS; INVITRO; PROLIFERATION; DIFFERENTIATION; INDUCTION AB Antioxidant enzyme (AE) activities were studied in normal hamster kidney proximal tubules and in estrogen-induced hamster kidney cancer. In vivo, kidney tumor had lower activities of manganese superoxide dismutase (MnSOD), copper, zinc superoxide dismutase, catalase, and glutathione peroxidase than kidney proximal tubules. Differences in AE activities were, in general, maintained in tissue culture, with AE activities remaining low in tumor cells compared to normal cells. Normal proximal tubular cells showed significant induction of MnSOD activity as a function of time in culture or following exposure to diethylstilbestrol, a synthetic estrogen, while MnSOD activity remained low in tumor cells under these conditions. Our results suggest that antioxidant enzymes, particularly MnSOD, are regulated differently in estrogen-induced hamster kidney tumor cells than in normal kidney proximal tubular cells, demonstrating that cancers arising from hormonal influence have similar AE profiles to those previously described in cancers arising from viral or chemical etiologies. C1 UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53706. UNIV IOWA,COLL MED,RADIAT RES LAB,IOWA CITY,IA. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL & LAB MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA 41267] NR 37 TC 20 Z9 22 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JUN PY 1994 VL 16 IS 6 BP 741 EP 751 DI 10.1016/0891-5849(94)90189-9 PG 11 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA NL951 UT WOS:A1994NL95100008 PM 8070677 ER PT J AU BAKER, PJ HRABA, T TAYLOR, CE STASHAK, PW FAUNTLEROY, MB ZAHRINGER, U TAKAYAMA, K SIEVERT, TR HRONOWSKI, XP COTTER, RJ PEREZPEREZ, G AF BAKER, PJ HRABA, T TAYLOR, CE STASHAK, PW FAUNTLEROY, MB ZAHRINGER, U TAKAYAMA, K SIEVERT, TR HRONOWSKI, XP COTTER, RJ PEREZPEREZ, G TI MOLECULAR-STRUCTURES THAT INFLUENCE THE IMMUNOMODULATORY PROPERTIES OF THE LIPID-A AND INNER-CORE REGION OLIGOSACCHARIDES OF BACTERIAL LIPOPOLYSACCHARIDES SO INFECTION AND IMMUNITY LA English DT Article ID III PNEUMOCOCCAL POLYSACCHARIDE; SUPPRESSOR T-CELLS; ANTIBODY-PRODUCING CELLS; GRAM-NEGATIVE BACTERIA; A-SUBUNIT ANALOGS; PSEUDOMONAS-AERUGINOSA; ESCHERICHIA-COLI; HELICOBACTER-PYLORI; CELLULAR LEVEL; MICE AB The relationship between chain length as well as the position of fatty acyl groups to the ability of lipid A to abolish the expression of suppressor T-cell (Ts) activity was examined. Fatty acyl chain lengths of C-12 to C-14, as in the lipid A of Escherichia coli and Salmonella minnesota, appear to be optimal for this bioactivity, since lipid A preparations with fatty acyl groups of relatively short chain length (C-10 to C-12 for Pseudomonas aeruginosa and Chromobacterium violaceum) or predominantly long chain length (C-18 for Helicobacter pylori) are without effect. The presence of an acyloxyacyl group of appropriate chain length at the 3' position of the glucosamine disaccharide backbone of lipid A also plays a decisive role. By contrast, the lipid A proximal inner core region oligosaccharides of some bacterial lipopolysaccharides increase the expression of Ts activity; this is due mainly to the capacity of such oligosaccharides, which are relatively conserved in structure among gram-negative bacteria, to enlarge or expand upon the population of CD8(+) Ts generated during the course of a normal antibody response to unrelated microbial antigens. The minimal structure required for the expression of the added immunosuppression observed appears to be a hexasaccharide containing one 2-keto-3-deoxyoctonate residue, two glucose residues, and three heptose residues to which are attached two pyrophosphorylethanolamine groups. The relevance of these findings to virulence and to the pathogenesis of gram-negative infections is discussed. C1 NIAID, TWINBROOK RES FACIL 2, IMMUNOGENET LAB, ROCKVILLE, MD USA. FORSCHUNGSINST BORSTEL, INST EXPTL BIOL & MED, W-2061 BORSTEL, GERMANY. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MYCOBACTERIOL RES LAB, MADISON, WI 53705 USA. UNIV WISCONSIN, COLL AGR & LIFE SCI, DEPT BACTERIOL, MADISON, WI 53706 USA. JOHNS HOPKINS SCH MED, DEPT PHARMACOL & MOLEC SCI, BALTIMORE, MD 21205 USA. VANDERBILT UNIV, SCH MED, DEPT MED, DIV INFECT DIS, NASHVILLE, TN 37232 USA. FU NIGMS NIH HHS [GM-36054] NR 60 TC 31 Z9 32 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUN PY 1994 VL 62 IS 6 BP 2257 EP 2269 PG 13 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NM782 UT WOS:A1994NM78200017 PM 8188347 ER PT J AU DHANANI, S HUANG, M WANG, JY DUBINETT, SM AF DHANANI, S HUANG, M WANG, JY DUBINETT, SM TI INTERFERON-ALPHA INHIBITS MURINE MACROPHAGE TRANSFORMING GROWTH-FACTOR-BETA MESSENGER-RNA EXPRESSION SO INFLAMMATION LA English DT Article ID NECROSIS-FACTOR-ALPHA; TOXIC T-CELLS; EXTRACELLULAR-MATRIX; TGF-BETA; THYMOCYTE PROLIFERATION; PULMONARY FIBROSIS; FACTOR-BETA-1 GENE; KILLER CELLS; GENERATION; COLLAGEN AB Transforming growth factor-beta (TGF-beta), a multifunctional polypeptide is produced by a wide variety of cells and regulates a broad array of physiological and pathological functions. TGF-beta appears to play a central role in pulmonary fibrosis and may contribute to tumor-associated immunosuppression. Alveolar macrophages are a rich source of TGF-beta and are intimately involved in lung inflammation. We therefore chose to study TGF-beta regulation in murine alveolar macrophages as well as an immortalized peritoned macrophage cell line (IC-21). Murine macrophages were incubated with cytokines to evaluate their role in regulating TGF-beta mRNA expression. We conclude that IFN-alpha downregulates TGF-beta mRNA expression in murine macrophages. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP DHANANI, S (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DIV PULM & CRIT CARE MED,LOS ANGELES,CA 90073, USA. NR 43 TC 18 Z9 19 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0360-3997 J9 INFLAMMATION JI Inflammation PD JUN PY 1994 VL 18 IS 3 BP 301 EP 309 DI 10.1007/BF01534271 PG 9 WC Cell Biology; Immunology SC Cell Biology; Immunology GA NQ871 UT WOS:A1994NQ87100005 PM 8088926 ER PT J AU HOOPER, DC RUBIN, DH CEBRA, JJ AF HOOPER, DC RUBIN, DH CEBRA, JJ TI SPONTANEOUS PROLIFERATION OF PEYERS PATCH CELLS IN-VITRO SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE AUTOLOGOUS MIXED LYMPHOCYTE REACTION; DENDRITIC CELLS; MUCOSAL IMMUNITY; T-CELLS ID AUTOREACTIVE T-CELLS; AUTOLOGOUS ERYTHROCYTES; LYMPHOID-TISSUES; DENDRITIC CELLS; CLONAL DELETION; SELF-TOLERANCE; LYMPHOCYTES-T; B-CELLS; ANTIGEN; MOUSE AB Under normal circumstances most lymphoid cell populations do not exhibit strong proliferative reactions in culture unless provoked by antigen or mitogen. The autologous mixed lymphocyte reaction (AMLR) mediated by adult T cells is a relatively weak proliferative response that occurs in the absence of known heterologous stimuli. In this investigation we demonstrate that Peyer's patch (PP) cells possess an inherent capacity to commence dividing in vitro and to display an exceptionally vigorous AMLR. The magnitude and kinetics of this spontaneous proliferation resemble that of a secondary response to a strong mucosal immunogen such as reovirus type 1/Lang. Analysis of the cellular components of the PP cultures implicates CD4+CD8- T cells as the major responding population and dendritic cells (DC) as stimulators. Mixing experiments indicate that spleen contains a cell population which can stimulate PP T cells, albeit to a lesser extent than PP cells. Similarly, splenic T cells have a reduced but significant capacity to respond to PP DC, in comparison to PP T cells. These differences suggest the possibility that there may be a decreasing gradient of antigenicity between the gut and the spleen which is reflected in the spontaneous activity of PP versus splenic T cells in vitro. We propose that PP cells are in fact responding in vitro to heterologous antigens derived from food, enteric microbes and other environmental sources. This notion is supported by the observation that PP cells from antigen-minimized germ-free mice fail to proliferate spontaneously in culture. C1 UNIV PENN,DEPT BIOL,LEIDY LAB BIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. OI Hooper, Douglas/0000-0002-8578-5104 FU NIAID NIH HHS [AI-23970, AI-17997] NR 40 TC 12 Z9 12 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD JUN PY 1994 VL 6 IS 6 BP 873 EP 880 DI 10.1093/intimm/6.6.873 PG 8 WC Immunology SC Immunology GA NT226 UT WOS:A1994NT22600009 PM 8086375 ER PT J AU HARRIS, SE BONEWALD, LF HARRIS, MA SABATINI, M DALLAS, S FENG, JQ GHOSHCHOUDHURY, N WOZNEY, J MUNDY, GR AF HARRIS, SE BONEWALD, LF HARRIS, MA SABATINI, M DALLAS, S FENG, JQ GHOSHCHOUDHURY, N WOZNEY, J MUNDY, GR TI EFFECTS OF TRANSFORMING GROWTH-FACTOR-BETA ON BONE NODULE FORMATION AND EXPRESSION OF BONE MORPHOGENETIC PROTEIN-2, OSTEOCALCIN, OSTEOPONTIN, ALKALINE-PHOSPHATASE, AND TYPE-1 COLLAGEN MESSENGER-RNA IN LONG-TERM CULTURES OF FETAL-RAT CALVARIAL OSTEOBLASTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID CELL-PROLIFERATION; GENE-EXPRESSION; FORMED INVITRO; VITAMIN-D; STIMULATION; INHIBITION; INVIVO; MATRIX; REPLICATION; TGF-BETA-1 AB Transforming growth factor beta (TGF-beta) is one of the most abundant of the known growth regulatory factors stored within the bone matrix. When bone is resorbed, TGF-beta is released in an active form and is a powerful bone growth stimulant. When injected into the subcutaneous tissue over the calvarial surface of rodents, it rapidly causes proliferation of the periosteal layer and accumulation of new woven bone. In this report, we describe the effects of TGF-beta(1) on first subcultures of fetal rat osteoblasts obtained from calvarial bones and cultured from confluence with ascorbic acid and beta-glycerophosphate. Under these conditions, nodules with characteristics of normal bone appear by day 8. Similar to experiments described by Antosz et al., TGF-beta added to confluent cultures inhibited the formation of bone nodules. Both the number and total area of the nodules were quantitated and shown to be completely inhibited by 2 ng/ml of TGF-beta(1). TGF-beta also impaired the expression of genes associated with bone formation, including type I collagen, alkaline phosphatase, osteopontin, and osteocalcin. TGF-beta also inhibited the expression of mRNA for the bone morphogenetic protein 2 (BMP-2). These results, showing suppression of markers representative of osteoblast differentiation, suggest that the effects of TGF-beta to stimulate bone formation in vivo are not likely a result of effects on differentiated mineralizing osteoblasts but, as suggested by previous studies, more likely are caused by effects on osteoblast precursors. These results also suggest that endogenous BMP-2 expression in fetal rat calvaria cells is important for bone cell differentiation. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT VET AFFAIRS,SAN ANTONIO,TX. INST RECH SERVIER,F-92150 SURESNES,FRANCE. GENET INST INC,CAMBRIDGE,MA 02140. FU NIAMS NIH HHS [AR39529]; NIDCR NIH HHS [DE08569] NR 33 TC 244 Z9 250 U1 4 U2 16 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JUN PY 1994 VL 9 IS 6 BP 855 EP 863 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NN314 UT WOS:A1994NN31400010 PM 8079661 ER PT J AU TSUTSUI, H SPINALE, FG NAGATSU, M SCHMID, PG ISHIHARA, K DEFREYTE, G COOPER, G CARABELLO, BA AF TSUTSUI, H SPINALE, FG NAGATSU, M SCHMID, PG ISHIHARA, K DEFREYTE, G COOPER, G CARABELLO, BA TI EFFECTS OF CHRONIC BETA-ADRENERGIC-BLOCKADE ON THE LEFT-VENTRICULAR AND CARDIOCYTE ABNORMALITIES OF CHRONIC CANINE MITRAL REGURGITATION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE MITRAL VALVE INSUFFICIENCY; ADRENERGIC BETA RECEPTOR BLOCKADERS; VENTRICULAR FUNCTION; LEFT HEART FAILURE; CONGESTIVE HYPERTROPHY ID TACHYCARDIA-INDUCED CARDIOMYOPATHY; IDIOPATHIC DILATED CARDIOMYOPATHY; EXPERIMENTAL VOLUME OVERLOAD; CONGESTIVE-HEART-FAILURE; SUPRAVENTRICULAR TACHYCARDIA; CONTRACTILE DYSFUNCTION; RECEPTOR DENSITY; MYOCARDIAL-CELLS; MYOCYTE SIZE; WALL STRESS AB The mechanism by which beta blockade improves left ventricular dysfunction in various cardiomyopathies has been ascribed to improved contractile function of the myocardium or to improved beta-adrenergic responsiveness. In this study we tested two hypotheses: (a) that chronic beta blockade would improve the left ventricular dysfunction which develops in mitral regurgitation, and (b) that an important mechanism of this effect would be improved innate contractile function of the myocardium. Two groups of six dogs with chronic severe mitral regurgitation were studied. After 3 mo both groups had developed similar and significant left ventricular dysfunction. One group was then gradually beta-blocked while the second group continued to be observed without further intervention. In the group that remained unblocked, contractile function remained depressed. However, in the group that received chronic beta blockade, contractile function improved substantially. The contractility of cardiocytes isolated from the unblocked hearts and then studied in the absence of beta receptor stimulation was extremely depressed. However, contractility of cardiocytes isolated from the beta-blocked ventricles was virtually normal. Consistent with these data, myofibrillar density was much higher, 55 +/- 4% in the beta-blocked group vs. 39 +/- 2% (P < 0.01) in the unblocked group; thus, there were more contractile elements to generate force in the beta-blocked group. We conclude that chronic beta blockade improves left ventricular function in chronic experimental mitral regurgitation. This improvement was associated with an improvement in the innate contractile function of isolated cardiocytes, which in turn is associated with an increase in the number of contractile elements. C1 MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT MED,DIV CARDIOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT SURG,DIV CARDIOTHORAC,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29403. UNIV IOWA,VET AFFAIRS MED CTR,DEPT INTERNAL MED,IOWA CITY,IA 52246. RI Tsutsui, Hiroyuki/A-4070-2012 FU NHLBI NIH HHS [NHLBI R01 HL-38185] NR 64 TC 131 Z9 132 U1 1 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1994 VL 93 IS 6 BP 2639 EP 2648 DI 10.1172/JCI117277 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NP577 UT WOS:A1994NP57700047 PM 7911128 ER PT J AU SNYDER, SL ROSENBAUM, DH ROWAN, AJ STRAIN, JJ AF SNYDER, SL ROSENBAUM, DH ROWAN, AJ STRAIN, JJ TI SCID DIAGNOSIS OF PANIC DISORDER IN PSYCHOGENIC SEIZURE PATIENTS SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID HYSTERICAL SEIZURES; DSM-III; PSEUDOSEIZURES AB The authors administered the Structured Clinic Interview for DSM-III-R (SCID) to 20 outpatients with nonepileptic seizures documented by video-EEG. Fourteen (70%) had one or more non-somatoform DSM-III-R diagnoses. All 14 met criteria for panic disorder. Comorbid mood, psychotic, substance abuse, and eating disorders were also noted. Meticulous use of the SCID, with extensive follow-up, may have resulted in enhanced detection of panic disorder in patients who do not spontaneously report panic symptoms. Panic attacks may play a more important role in nonepileptic seizures than has been generally recognized, especially in outpatients with a chronic course of illness. C1 MT SINAI MED CTR,DEPT NEUROL,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,DEPT NEUROL,BRONX,NY. RP SNYDER, SL (reprint author), MT SINAI MED CTR,DEPT PSYCHIAT,DIV BEHAV MED & CONSULTAT PSYCHIAT,BOX 1228,1 G L LEVY PL,NEW YORK,NY 10029, USA. NR 31 TC 30 Z9 30 U1 1 U2 3 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 SUM PY 1994 VL 6 IS 3 BP 261 EP 266 PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NY895 UT WOS:A1994NY89500007 PM 7950349 ER PT J AU PAHLAVANI, MA RICHARDSON, A AF PAHLAVANI, MA RICHARDSON, A TI AGE-RELATED DECREASE IN THE NAIVE (OX22+) T-CELLS IN F344 RATS SO MECHANISMS OF AGEING AND DEVELOPMENT LA English DT Article DE AGING; NAIVE (OX22+) T CELLS; RAT ID LYMPHOCYTE SUBSETS; PERIPHERAL-BLOOD; IMMUNE FUNCTION; EXPRESSION; INTERLEUKIN-2; MICE; ANTIGEN; YOUNG; RESTRICTION; PATTERNS AB The frequency of the cells bearing the naive marker (OX22+) in T cells, helper, and cytotoxic/suppressor T cell subsets isolated from the spleens of young and old F344 rats were measured by flow cytometry. The percentage of naive cells in T cells decreased significantly with age and this decline occurred primarily in the helper subset. C1 UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. RP PAHLAVANI, MA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,GRECC 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [AG-01548, AG-00165] NR 35 TC 22 Z9 22 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0047-6374 J9 MECH AGEING DEV JI Mech. Ageing. Dev. PD JUN PY 1994 VL 74 IS 3 BP 171 EP 176 DI 10.1016/0047-6374(94)90088-4 PG 6 WC Cell Biology; Geriatrics & Gerontology SC Cell Biology; Geriatrics & Gerontology GA NV131 UT WOS:A1994NV13100003 PM 7934214 ER PT J AU BLANK, AS AF BLANK, AS TI CLINICAL DETECTION, DIAGNOSIS, AND DIFFERENTIAL-DIAGNOSIS OF POSTTRAUMATIC-STRESS-DISORDER SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID BORDERLINE PERSONALITY-DISORDER; CHILD SEXUAL ABUSE; WORLD-WAR-II; POSTTRAUMATIC-STRESS; VIETNAM VETERANS; MULTIPLE PERSONALITY; DSM-IV; PSYCHOPHYSIOLOGICAL ASSESSMENT; COMBAT VETERANS; PHYSICAL ABUSE C1 US DEPT VET AFFAIRS,READJUSTMENT COUNSELING SERV,WASHINGTON,DC. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20007. NR 208 TC 26 Z9 30 U1 3 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 JUN PY 1994 VL 17 IS 2 BP 351 EP 383 PG 33 WC Psychiatry SC Psychiatry GA NR151 UT WOS:A1994NR15100010 PM 7937364 ER PT J AU SCHUMACHER, HR BAUTISTA, BB KRAUSER, RE MATHUR, AK GALL, EP AF SCHUMACHER, HR BAUTISTA, BB KRAUSER, RE MATHUR, AK GALL, EP TI HISTOLOGICAL APPEARANCE OF THE SYNOVIUM IN EARLY RHEUMATOID-ARTHRITIS SO SEMINARS IN ARTHRITIS AND RHEUMATISM LA English DT Article DE SYNOVIAL MEMBRANE; SYNOVIAL FLUID; MICROVASCULATURE; INFLAMMATION ID REITERS-SYNDROME; CLINICAL COURSE; MEMBRANE; FLUID; DISEASE; EXPRESSION; FEATURES; ANTIGEN; THERAPY; ONSET C1 UNIV PENN,SCH MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. PAOLI MEM HOSP,PAOLI,PA. MON VALLEY HOSP,MONONGAHELA,PA. UNIV ARIZONA,CTR HLTH SCI,DIV RHEUMATOL ALLERGY & IMMUNOL,TUCSON,AZ. RP SCHUMACHER, HR (reprint author), VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA 19104, USA. FU NIAMS NIH HHS [AR 40770, AR 07062, AR 40525] NR 23 TC 32 Z9 34 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 JUN PY 1994 VL 23 IS 6 SU 2 BP 3 EP 10 DI 10.1016/0049-0172(94)90079-5 PG 8 WC Rheumatology SC Rheumatology GA NU451 UT WOS:A1994NU45100002 PM 7939728 ER PT J AU DROPCHO, EJ AF DROPCHO, EJ TI PARANEOPLASTIC DISORDERS - ANTINEURONAL ANTIBODIES AND THERAPEUTIC OPTIONS SO SEMINARS IN NEUROLOGY LA English DT Review ID NEOPLASTIC CEREBELLAR DEGENERATION; CELL LUNG-CANCER; ANTI-HU ANTIBODY; ENCEPHALOMYELITIS SENSORY NEURONOPATHY; EATON MYASTHENIC SYNDROME; CENTRAL-NERVOUS-SYSTEM; STIFF-MAN SYNDROME; NEURO-BLASTOMA; BREAST-CANCER; ANTICEREBELLAR ANTIBODIES C1 BIRMINGHAM VET AFFAIRS MED CTR,BIRMINGHAM,AL. UNIV ALABAMA,CTR COMPREHENS CANC,NEUROONCOL PROGRAM,BIRMINGHAM,AL 35294. NR 115 TC 10 Z9 10 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0271-8235 J9 SEMIN NEUROL JI Semin. Neurol. PD JUN PY 1994 VL 14 IS 2 BP 179 EP 187 DI 10.1055/s-2008-1041076 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA PB358 UT WOS:A1994PB35800014 PM 7984833 ER PT J AU HERSHMAN, JM AF HERSHMAN, JM TI HIGHLIGHTS OF THIS ISSUE SO THYROID LA English DT Editorial Material RP HERSHMAN, JM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BLDG 114,ROOM 200,WILSHIRE & SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD SUM PY 1994 VL 4 IS 2 BP 141 EP 141 DI 10.1089/thy.1994.4.141 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NV962 UT WOS:A1994NV96200001 ER PT J AU BALASUBRAMANIAN, V WIEGESHAUS, EH TAYLOR, BT SMITH, DW AF BALASUBRAMANIAN, V WIEGESHAUS, EH TAYLOR, BT SMITH, DW TI PATHOGENESIS OF TUBERCULOSIS - PATHWAY TO APICAL LOCALIZATION SO TUBERCLE AND LUNG DISEASE LA English DT Review ID EXPERIMENTAL AIRBORNE TUBERCULOSIS; HOST-PARASITE RELATIONSHIPS; MYCOBACTERIUM-TUBERCULOSIS; GUINEA-PIGS; EXOGENOUS REINFECTION; INFECTION; SPUTUM AB We have examined the published work of investigators which dealt with the pathogenesis of tuberculosis, especially the following: the infective dose, the yield of bacilli from the primary lesion and primary complex, the predominant location of the minimal lesion, the hypotheses of a vulnerable region in the lung and the specific pathways (endogenous or exogenous) by which tubercle bacilli cause disease. More knowledge of the pathogenic pathway to tuberculosis would provide clues to the development of new vaccines and drug regimens that can intervene at a specific stage in the pathogenesis. Based on the examination of the literature on pathogenesis of human tuberculosis and our findings in a guinea-pig model of experimental airborne tuberculosis, we have proposed an hypothesis which integrates the endogenous and exogenous pathways to tuberculosis. This hypothesis is based on the following observations: 1. The infectious dose is very low, usually 1-5 tubercle bacilli. 2. The first implant can occur anywhere in the lungs. 3. The cavitary lesion, characteristic of tuberculous disease, is often located in the apical regions in the lungs. 4. Whereas the primary implant can occur anywhere in the lungs, for the progression from infection to disease, the tubercle bacilli must gain access to the 'vulnerable' regions in the apex of the lungs. Our hypothesis states that in areas of the world where there is a low risk of infection with tubercle bacilli low incidence of vaccination or sensitization to environmental mycobacteria, or high incidence of high virulent isolates, the virulent tubercle bacilli reach the vulnerable region via a bacillemia during the first infection. In areas of the world where there is a high risk of infection with tubercle bacilli, high incidence of vaccination or sensitization to environmental mycobacteria or a high incidence of low virulent isolates, the tubercle bacilli reach the vulnerable region via the airway, which requires repeated episodes of infection as the probability of a first implant occurring in the vulnerable regions is low. C1 UNIV WISCONSIN,DEPT MED MICROBIOL & IMMUNOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. NR 48 TC 106 Z9 110 U1 1 U2 5 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0962-8479 J9 TUBERCLE LUNG DIS JI Tubercle Lung Dis. PD JUN PY 1994 VL 75 IS 3 BP 168 EP 178 DI 10.1016/0962-8479(94)90002-7 PG 11 WC Respiratory System SC Respiratory System GA NV896 UT WOS:A1994NV89600002 PM 7919306 ER PT J AU BLITZER, RD WONG, T NOURANIFAR, R LANDAU, EM AF BLITZER, RD WONG, T NOURANIFAR, R LANDAU, EM TI THE CHOLINERGIC INHIBITION OF AFTERHYPERPOLARIZATION IN RAT HIPPOCAMPUS IS INDEPENDENT OF CAMP-DEPENDENT PROTEIN-KINASE SO BRAIN RESEARCH LA English DT Note DE NOREPINEPHRINE; CARBACHOL; CAMP-DEPENDENT PROTEIN KINASE; WHOLE CELL RECORDING; CAI; RP-CAMPS ID PYRAMIDAL CELLS; GUINEA-PIG; NEURONS; CALCIUM; HYPERPOLARIZATION; NORADRENALINE; STIMULATION; SUBUNIT; SLICES AB The possible involvement of protein kinase A (PKA) in the muscarinic inhibition of the slow afterhyperpolarizing current (I-AHP) was investigated in rat hippocampal pyramidal cells. I-AHP was recorded using the whole cell method in hippocampal slices, and Rp-cAMPS, a PKA antagonist, was applied intracellularly. The inhibition of I-AHP by carbachol was not affected by Rp-cAMPS. In contrast, Rp-cAMPS reduced the cAMP-dependent inhibition of I-AHP by norepinephrine. The results show that phosphorylation by PKA does not contribute to the muscarinic effect on I-AHP. C1 MT SINAI MED CTR,DEPT PHARMACOL,NEW YORK,NY 10029. BRONX VET ADM MED CTR,PSYCHIAT SERV,NEW YORK,NY 10029. RP BLITZER, RD (reprint author), MT SINAI MED CTR,DEPT PSYCHIAT,BOX 1230,1 GUSTAVE LEVY PL,NEW YORK,NY 10029, USA. NR 26 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAY 23 PY 1994 VL 646 IS 2 BP 312 EP 314 DI 10.1016/0006-8993(94)90096-5 PG 3 WC Neurosciences SC Neurosciences & Neurology GA NM416 UT WOS:A1994NM41600021 PM 8069680 ER PT J AU COREY, JL DAVIDSON, N LESTER, HA BRECHA, N QUICK, MW AF COREY, JL DAVIDSON, N LESTER, HA BRECHA, N QUICK, MW TI PROTEIN-KINASE-C MODULATES THE ACTIVITY OF A CLONED GAMMA-AMINOBUTYRIC-ACID TRANSPORTER EXPRESSED IN XENOPUS-OOCYTES VIA REGULATED SUBCELLULAR REDISTRIBUTION OF THE TRANSPORTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RAT ADIPOSE CELL; FREE FATTY-ACIDS; GLUCOSE TRANSPORTER; PLASMA-MEMBRANE; PHORBOL ESTERS; INDUCED TRANSLOCATION; INSULIN ACTION; 3T3-L1 CELLS; AFFINITY; PHOSPHORYLATION AB We report that activators and inhibitors of protein kinase C (PKC) and protein phosphatases regulate the activity of a cloned rat brain gamma-aminobutyric acid (GABA) transporter (GAT1) expressed in Xenopus oocytes. Four compounds known to activate PKC increased GABA uptake 2-3.5-fold over basal control levels. Inhibition of PKC by bisindolylmaleimide reduced basal GABA uptake 80% and blocked the phorbol 12-myristate 13-acetate (PMA)-induced stimulation of transport. Okadaic acid, a protein phosphatase inhibitor, stimulated transport 2.5-fold; a 4-fold increase in GABA uptake occurred when oocytes were treated with cyclosporin A, a specific inhibitor of protein phosphatase 2B. Modulation resulted in changes to V-max but not to K-m and was influenced by the functional expression level of the transporter protein; as expression level increased, the ability to up-regulate transporter activity decreased. Down-regulation of transporter activity was independent of expression level. Modulation did not occur through phosphorylation of the three consensus PKC sites predicted by the primary protein sequence since their removal had no effect on the susceptibility of the transporter to modulation by PMA or bisindolylmaleimide. Subcellular fractionation of oocyte membranes demonstrated that under basal level conditions, the majority of GAT1 was targeted to a cytoplasmic compartment corresponding to the trans-Golgi or low density vesicles. Stimulation of PKC with PMA resulted in a translocation of transporters from this compartment to the plasma membrane. At higher expression levels of GAT1 protein, a larger portion of GAT1 was found on the plasma membrane during basal level conditions and treatment with bisindolylmaleimide resulted in removal of these transporters from the plasma membrane. At expression levels demonstrated to be resistant to modulation by PMA, PMA-treatment still resulted in translocation of transporters from the cytoplasm to the plasma membrane. Thus, the inability of PMA to increase uptake at high expression of the GAT1 protein is due to saturation at a step subsequent to translocation. These findings 1) demonstrate the presence of a novel regulated secretory pathway in oocytes and 2) suggest a modulatory mechanism for neurotransmitter transporters that could have significant effects upon synaptic function. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,INST BRAIN RES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,CTR ULCER RES,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP COREY, JL (reprint author), CALTECH,DIV BIOL,156-29,PASADENA,CA 91125, USA. FU NINDS NIH HHS [NS-11756] NR 40 TC 184 Z9 187 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 MAY 20 PY 1994 VL 269 IS 20 BP 14759 EP 14767 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NM065 UT WOS:A1994NM06500071 PM 8182081 ER PT J AU ABRUTYN, E MOSSEY, J BERLIN, JA BOSCIA, J LEVISON, M PITSAKIS, P KAYE, D AF ABRUTYN, E MOSSEY, J BERLIN, JA BOSCIA, J LEVISON, M PITSAKIS, P KAYE, D TI DOES ASYMPTOMATIC BACTERIURIA PREDICT MORTALITY AND DOES ANTIMICROBIAL TREATMENT REDUCE MORTALITY IN ELDERLY AMBULATORY WOMEN SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE BACTERIURIA; URINARY TRACT INFECTIONS; RISK FACTORS; HEALTH STATUS INDICATORS; OUTCOME AND PROCESS ASSESSMENT (HEALTH CARE) ID URINARY-TRACT INFECTIONS; NO THERAPY; SURVIVAL; EPIDEMIOLOGY; POPULATION; HEALTH AB Objective: To determine whether asymptomatic bacteriuria in elderly ambulatory women is a marker of increased mortality and, if so, whether it is because of an association with other determinants of mortality or because asymptomatic bacteriuria is itself an independent cause, the removal of which might improve longevity. Design: A cohort study and a controlled clinical trial of the effect of antimicrobial treatment. Setting: A geriatric center and 21 continuing care retirement communities. Participants: Women without urinary tract catheters. Measurements: Urine cultures every 6 months (the same organism at 10(5) colony-forming units or more per mL on two midstream urine specimens defined asymptomatic bacteriuria), comorbidity, and mortality. Results: In the observational study, infected residents (n = 318) were older, and sicker, and had higher mortality (18.7 per 100 000 resident-days) than uninfected residents (n = 1173; 10.1 per 100 000 resident-days). However, in a multivariate Cox analysis, infection was not related to mortality (relative risk, 1.1; P > 0.2), whereas age at entry and self-rated health (score 1 [excellent] to 4 [bad or poor]) were strong predictors. In the clinical trial, mortality in 166 treated residents (13.8 per 100 000 resident-days) was comparable to that of 192 untreated residents (15.1 per 100 000 resident-days); the relative rate was 0.92 (95% CI, 0.57 to 1.47). The cure rates among treated and untreated residents were 82.9% and 15.6%, respectively. Conclusion: Urinary tract infection was not an independent risk factor for mortality, and its treatment did not lower the mortality rate. Screening and treatment of asymptomatic bacteriuria in ambulatory elderly women to decrease mortality do not appear warranted. C1 MED COLL PENN,EASTERN PENN PSYCHIAT INST,PHILADELPHIA,PA 19129. UNIV PENN,SCH MED,CTR CLIN EPIDEMIOL & BIOSTAT,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. RP ABRUTYN, E (reprint author), DEPT VET AFFAIRS MED CTR,38TH & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIA NIH HHS [AG03934] NR 31 TC 119 Z9 120 U1 0 U2 4 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 1994 VL 120 IS 10 BP 827 EP 833 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA NK458 UT WOS:A1994NK45800003 PM 7818631 ER PT J AU DUFFIN, J DOUSE, MA VANALPHEN, J AF DUFFIN, J DOUSE, MA VANALPHEN, J TI EXCITATION OF UPPER CERVICAL INSPIRATORY NEURONS BY VAGAL-STIMULATION IN THE CAT SO NEUROREPORT LA English DT Article DE UPPER CERVICAL INSPIRATORY NEURONS; VAGUS NERVE STIMULATION; PERI-STIMULUS HISTOGRAM; CAT ID EXPIRATORY NEURONS; CROSS-CORRELATION; RESPIRATORY NEURONS; NODOSE GANGLION; RAT; CONNECTIONS; NERVE; CORD AB THE responses of 57 upper cervical inspiratory neurones to single shock stimuli applied to the ipsilateral cervical vagus nerve were recorded using peri-stimulus histograms in 19 cats. Many (47%) of the histograms showed a late latency (17.9 +/- 3.4 ms; mean +/- S.D.) broad peak following the stimulation preceding a similar peak in the histogram for the phrenic activity. Nine (16%) showed a short latency (5.2 +/- 1.2 ms) peak preceding that for the phrenic activity. These peaks were of narrow half-amplitude width (1.0 +/- 0.4 ms), indicative of a paucisynaptic pathway between the cervical vagus and the ipsilateral upper cervical inspiratory neurones. Such results suggest that the upper cervical inspiratory neurones are either monosynaptically excited via vagal fibres, or disynaptically excited via dorsal group inspiratory C1 UNIV TORONTO,DEPT ANAESTHESIA,TORONTO M5S 1A8,ON,CANADA. DENVER VA MED CTR,DENVER,CO 80220. RP DUFFIN, J (reprint author), UNIV TORONTO,DEPT PHYSIOL,MED SCI BLDG,TORONTO M5S 1A8,ON,CANADA. OI Duffin, James/0000-0003-2270-7392 NR 22 TC 5 Z9 5 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAY 9 PY 1994 VL 5 IS 9 BP 1133 EP 1136 DI 10.1097/00001756-199405000-00028 PG 4 WC Neurosciences SC Neurosciences & Neurology GA NN159 UT WOS:A1994NN15900029 PM 8080973 ER PT J AU MORROW, NS NOVIN, D GARRICK, T AF MORROW, NS NOVIN, D GARRICK, T TI MICROINJECTION OF THYROTROPIN-RELEASING-HORMONE IN THE PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS STIMULATES GASTRIC CONTRACTILITY SO BRAIN RESEARCH LA English DT Article DE PARAVENTRICULAR NUCLEUS; THYROTROPIN-RELEASING HORMONE; GASTRIC CONTRACTILITY; VAGOTOMY ID CENTRAL NERVOUS-SYSTEM; ACID SECRETION; OXYTOCIN ANTAGONIST; RAT HYPOTHALAMUS; IMMUNOREACTIVE INNERVATION; LESION FORMATION; VAGUS NERVE; TRH; NEURONS; MOTILITY AB Changes in gastric contractility following microinjection of thyrotropin-releasing hormone (TRH) into the paraventricular nucleus of the hypothalamus (PVN) were examined in fasted, urethane-anesthetized rats. Gastric contractility was measured with extraluminal force transducers and analysed by computer. Unilateral and bilateral PVN microinjections of TRH (0.5 and 1.0 mu g) significantly increased the force index of gastric contractions from 0 to 60 min postinjection, when compared with animals microinjected with 0.1 mu g TRH, 0.1% BSA or TRH (0.5 and 1.0 mu g TRH) in sites adjacent to the PVN. The gastric force index was also significantly elevated from 61 to 120 min postinjection in rats receiving bilateral PVN microinjections of TRH (0.5 and 1.0 mu g) Peak gastric responses occurred within 10-20 min postinjection and represented an approximately eight-fold increase over basal values. In the remaining groups, the force index was not significantly altered from preinjection values. The excitatory action of TRH (1.0 mu g) on gastric contractility was completely abolished by subdiaphragmatic vagotomy. These results suggest that TRH acts within the PVN to stimulate gastric contractility via vagal-dependent pathways. C1 W LOS ANGELES VET AFFAIRS MED CTR,CURE,CTR GASTROENTER BIOL,DEPT PSYCHIAT,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,DEPT RES,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. RP MORROW, NS (reprint author), UNIV CALIF LOS ANGELES,DEPT PSYCHOL,405 HILGARD AVE,1285 FRANZ HALL,LOS ANGELES,CA 90024, USA. FU NIDDK NIH HHS [DK 41301]; NIMH NIH HHS [NIMH 5T32 M17140] NR 38 TC 10 Z9 12 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 MAY 2 PY 1994 VL 644 IS 2 BP 243 EP 250 DI 10.1016/0006-8993(94)91686-1 PG 8 WC Neurosciences SC Neurosciences & Neurology GA NJ164 UT WOS:A1994NJ16400009 PM 8050036 ER PT J AU ORWOLL, E RIDDLE, M PRINCE, M AF ORWOLL, E RIDDLE, M PRINCE, M TI EFFECTS OF VITAMIN-D ON INSULIN AND GLUCAGON-SECRETION IN NON-INSULIN-DEPENDENT DIABETES-MELLITUS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE VITAMIN-D; INSULIN; GLUCAGON; DIABETES ID CALCIUM-BINDING PROTEIN; PERFUSED RAT PANCREAS; D-DEFICIENT RAT; GLUCOSE-TOLERANCE; 1,25-DIHYDROXYVITAMIN-D3; MODE; RADIOIMMUNOASSAY; CALCIFEROL; REPLETION; KIDNEY AB Vitamin D has been shown to increase insulin release from pancreatic islet cells in vitro, and to improve insulin secretion in vitamin D-deficient animals. Few attempts have been made to evaluate this issue directly in humans. We studied 35 otherwise healthy diabetic subjects in the early spring at the seasonal nadir of 25-hydroxyvitamin D [25(OH)D] concentrations (mean 35 +/- 7 nmol/L). Easting glucose, insulin, C-peptide, and glucagon concentrations, and their responses to Sustacal stimulation were not related to indexes of mineral metabolism. In 20 subjects, a double-blinded, placebo-controlled, crossover trial of 1,25-dihydroxyvitamin D [1,25(OH)(2)D] treatment (1 mu g/d for 4 d) had no effect on fasting or stimulated glucose, insulin, C-peptide, or glucagon concentrations. However, insulin and C-peptide responses to Sustacal after 1,25(OH)(2)D treatment were related to duration of diabetes (r(2) = 0.28, P = 0.052 and r(2) = 0.25, P = 0.002, respectively) in that short duration correlated with improvement after 1,25(OH)(2)D treatment. Hence, vitamin D nutrition, or 1,25(OH)(2)D therapy, had no major effect on glucose homeostasis in non-insulin-dependent diabetes mellitus. C1 PORTLAND VA MED CTR, PORTLAND, OR USA. OREGON HLTH SCI UNIV, PORTLAND, OR 97201 USA. INDIANA UNIV, DEPT MED, INDIANAPOLIS, IN USA. OI Orwoll, Eric/0000-0002-8520-7355 NR 31 TC 106 Z9 107 U1 0 U2 3 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAY PY 1994 VL 59 IS 5 BP 1083 EP 1087 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA NJ050 UT WOS:A1994NJ05000022 PM 8172095 ER PT J AU HERBERT, V AF HERBERT, V TI VITAMIN-B-12 AND ELDERLY PEOPLE SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Letter ID PROTEIN-BOUND VITAMIN-B12; MALABSORPTION RP HERBERT, V (reprint author), BRONX VET ADM MED CTR, 130 W KINGSBRIDGE RD, BRONX, NY 10468 USA. NR 11 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAY PY 1994 VL 59 IS 5 BP 1093 EP 1094 PG 2 WC Nutrition & Dietetics SC Nutrition & Dietetics GA NJ050 UT WOS:A1994NJ05000025 PM 8172098 ER PT J AU HERBERT, V AF HERBERT, V TI STAGING VITAMIN-B-12 (COBALAMIN) STATUS IN VEGETARIANS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE VITAMIN B-12; SERUM HOLOTRANSCOBALAMIN II; TRANSCOBALAMIN II; COBALAMIN; VEGANS; SERUM TOTAL VITAMIN B-12; SERUM HOLOHAPTOCORRIN; B-12 HAPTOCORRIN; HAPTOCORRIN ID INTRINSIC-FACTOR; HOLOTRANSCOBALAMIN-II; TRANSCOBALAMIN-II; R-BINDER; SERUM; DEFICIENCY; AIDS; GLUTATHIONE; ABSORPTION; DEPLETION AB When one stops eating vitamin B-12 (cobalamins), one passes through four stages of negative cobalamin balance: serum depletion [low holotranscobalamin II, ie, low vitamin B-12 on transcobalamin II (TCII)], cell depletion (decreasing holohaptocorrin and low red cell vitamin B-12 concentrations), biochemical deficiency (slowed DNA synthesis, elevated serum homocysteine and methylmalonate concentrations), and, finally, clinical deficiency (anemia). Serum vitamin B-12 is on two proteins: the circulating vitamin B-12 delivery protein, TCII, and the circulating vitamin B-12 storage protein, haptocorrin. Because TCII is depleted of vitamin B-12 within days after absorption stops, the best screening test for early negative vitamin B-12 balance is a measurement of vitamin B-12 on TCII (holoTCII). HoloTCII falls below the bottom of its normal range long before total serum vitamin B-12 (which is mainly vitamin B-12 on haptocorrin) falls below the bottom of its normal range. C1 MT SINAI MED CTR, NEW YORK, NY 10029 USA. BRONX VET AFFAIRS MED CTR, NEW YORK, NY USA. NR 68 TC 142 Z9 142 U1 2 U2 10 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAY PY 1994 VL 59 IS 5 SU S BP 1213S EP 1222S PG 10 WC Nutrition & Dietetics SC Nutrition & Dietetics GA NK656 UT WOS:A1994NK65600019 PM 8172125 ER PT J AU FEIGIN, AM NINOMIYA, Y BEZRUKOV, SM BRYANT, BP MOORE, PA KOMAI, M WACHOWIAK, M TEETER, JH VODYANOY, I BRAND, JG AF FEIGIN, AM NINOMIYA, Y BEZRUKOV, SM BRYANT, BP MOORE, PA KOMAI, M WACHOWIAK, M TEETER, JH VODYANOY, I BRAND, JG TI ENHANCEMENT OF GUSTATORY NERVE-FIBERS TO NACL AND FORMATION OF ION CHANNELS BY COMMERCIAL NOVOBIOCIN SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE SALT TASTE TRANSDUCTION; AMILORIDE ID ELECTRICAL TONGUE STIMULATIONS; CHORDA TYMPANI FIBERS; TASTE RECEPTOR-CELLS; AMILORIDE INHIBITION; NA+ CHANNEL; SALT TASTE; SODIUM; RESPONSES; ORGANIZATION; TRANSDUCTION AB Single fibers of the rat chorda tympani nerve were used to study the mechanism of action of the antibiotic novobiocin on salt taste transduction. In the rat, novobiocin selectively enhanced the responses of sodium-specific and amiloride-sensitive chorda tympani nerve fibers (N type) without affecting more broadly responsive cation-sensitive and amiloride-insensitive fibers (E type). In the presence of amiloride, novobiocin was ineffective at enhancing the response of N-type fibers toward sodium chloride. Novobiocin also increased the conductance of bilayers formed from neutral lipids by forming nonrectifying ion channels with low conductance (similar to 7 pS in 110 mM NaCl), long open times (several seconds and longer), and high cation selectivity. Amiloride did not alter either the conductance or kinetics of these novobiocin channels. These observations suggest that even though novobiocin is able to form cation channels in lipid bilayers, and possibly in cell membranes as well, its action on the salt-taste response is through modulation of existing amiloride-sensitive sodium channels. C1 DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. ASAHI UNIV,DEPT ORAL PHYSIOL,GIFU 50102,JAPAN. NIH,BETHESDA,MD 20892. ST PETERSBURG NUCL PHYS INST,ST PETERSBURG 188350,RUSSIA. OFF NAVAL RES,ARLINGTON,VA 22217. RP FEIGIN, AM (reprint author), UNIV PENN,MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. NR 33 TC 13 Z9 13 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAY PY 1994 VL 266 IS 5 BP C1165 EP C1172 PN 1 PG 8 WC Physiology SC Physiology GA NP995 UT WOS:A1994NP99500003 ER PT J AU LIBERMAN, RP VANPUTTEN, T MARSHALL, BD MINTZ, J BOWEN, L KUEHNEL, TG ARAVAGIRI, M MARDER, SR AF LIBERMAN, RP VANPUTTEN, T MARSHALL, BD MINTZ, J BOWEN, L KUEHNEL, TG ARAVAGIRI, M MARDER, SR TI OPTIMAL DRUG AND BEHAVIOR-THERAPY FOR TREATMENT-REFRACTORY SCHIZOPHRENIC-PATIENTS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note ID HALOPERIDOL; PLASMA AB Thirteen treatment-refractory schizophrenic patients (10 melt and three women) who were receiving more than 50 mg/day of haloperidol and who had been hospitalized for more than 1 year successfully tolerated a mean dose reduction of 63% with consequent improvement in psychopathology and side effects. The addition of intensive behavior therapy to the optimal dose of haloperidol yielded further improvements in functional behavior, such as self-care and social interaction, C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,CAMARILLO STATE HOSP,CAMARILLO RES CTR,LOS ANGELES,CA. RP LIBERMAN, RP (reprint author), UNIV CALIF LOS ANGELES,CAMARILLO RES CTR,DEPT PSYCHIAT & BIOBEHAV SCI,POB 6022,CAMARILLO,CA 93011, USA. NR 22 TC 27 Z9 27 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAY PY 1994 VL 151 IS 5 BP 756 EP 759 PG 4 WC Psychiatry SC Psychiatry GA NJ089 UT WOS:A1994NJ08900022 PM 8166320 ER PT J AU SCHWARDT, JD NEUFELD, GR BAUMGARDNER, JE SCHERER, PW AF SCHWARDT, JD NEUFELD, GR BAUMGARDNER, JE SCHERER, PW TI NONINVASIVE RECOVERY OF ACINAR ANATOMIC INFORMATION FROM CO2 EXPIROGRAMS SO ANNALS OF BIOMEDICAL ENGINEERING LA English DT Article DE AIRWAY CONVECTION-DIFFUSION; PULMONARY FUNCTION; EMPHYSEMA; NONINVASIVE PULMONARY MEASUREMENT ID GAS; AIRWAYS; DISPERSION; DIFFUSION; DISEASE; WASHOUT; VOLUME; MODEL AB A numerical single path model of respiratory gas exchange with distributed alveolar gas sources was used to estimate the anatomical changes in small peripheral airways such as occur in chronic obstructive pulmonary diseases (COPD). A previous sensitivity analysis of the single path model showed that decreasing total acinar airway cross-sectional area by an area reduction factor, R, results in computed gas expirograms with Phase III steepening similar to that observed in COPD patients. From experimental steady state CO2 washout data recorded from six healthy subjects and six COPD patients, optimized area reduction factors for the single path model were found that characterize peripheral airway anatomy for each subject. Area reduction factors were then combined with measured functional residual capacity data to calculate the normalized peripheral airspace diameters in a given subject, relative to the airspace diameters in the generations of an idealized standard lung. Mean area reduction factors for the patient subgroup were 63% of those for the healthy subgroup, which is related to the gas transport limitation observed in disease. Mean airspace sizes for the patient subgroup were 235% of the healthy subgroup, which characterizes the increase in size and reduction in number of peripheral airspaces due to tissue erosion in emphysema. From these results, the air-phase diffusive conductance in COPD patients was calculated to be 32% of the mean value in the healthy subjects. These findings correlated well with standard pulmonary function test data for the patients and yield the recovery of acinar airway information from gas washout by combining the single path model with experimental measurements. 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 36 TC 27 Z9 27 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0090-6964 J9 ANN BIOMED ENG JI Ann. Biomed. Eng. PD MAY-JUN PY 1994 VL 22 IS 3 BP 293 EP 306 DI 10.1007/BF02368236 PG 14 WC Engineering, Biomedical SC Engineering GA PB687 UT WOS:A1994PB68700008 PM 7978550 ER PT J AU HANDELSMAN, L BERNSTEIN, D HOLLOWAY, K SHEIKH, I TRESTMAN, R SIEVER, L COOPER, T AF HANDELSMAN, L BERNSTEIN, D HOLLOWAY, K SHEIKH, I TRESTMAN, R SIEVER, L COOPER, T TI HOSTILE IMPULSIVE TRAITS IN ADDICTS - 5-HT BEHAVIORAL PHARMACOLOGY SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,BRONX,NY. NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY 10032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 625 EP 625 DI 10.1016/0006-3223(94)90694-7 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200038 ER PT J AU ADLER, LE HOPE, C HOFFER, LD STEPHEN, C YOUNG, D GERHARDT, G AF ADLER, LE HOPE, C HOFFER, LD STEPHEN, C YOUNG, D GERHARDT, G TI BROMOCRIPTINE IMPAIRS P50 AUDITORY SENSORY GATING IN NORMAL CONTROL SUBJECTS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV COLORADO,HLTH SCI CTR,DEPT PSYCHIAT,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT PHARMACOL,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT BIOMETR,DENVER,CO. DENVER VAMC,DENVER,CO. NR 0 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 630 EP 630 DI 10.1016/0006-3223(94)90714-5 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200058 ER PT J AU LI, G SILVERMAN, JM ALTSTIEL, L HAROUTUNIAN, H BIRSTEIN, S MOHS, R DAVIS, KL AF LI, G SILVERMAN, JM ALTSTIEL, L HAROUTUNIAN, H BIRSTEIN, S MOHS, R DAVIS, KL TI APOLIPOPROTEIN EPSILON-4 ALLELE AND FAMILIAL RISK IN ALZHEIMERS-DISEASE SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,NEW YORK,NY 10468. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 664 EP 664 DI 10.1016/0006-3223(94)90837-0 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200179 ER PT J AU GARVER, DL GRIFFITH, J HIRSCHOWITZ, J AF GARVER, DL GRIFFITH, J HIRSCHOWITZ, J TI MINIMUM EFFECTIVE DOSE OF HALOPERIDOL IN TREATMENT OF PSYCHOSES SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV TEXAS,SW MED CTR,DALLAS,TX 75235. DALLAS VA MED CTR,DALLAS,TX. BRONX VET ADM MED CTR,NEW YORK,NY. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 667 EP 667 DI 10.1016/0006-3223(94)90846-X PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200188 ER PT J AU STEINBERG, BJ TRESTMAN, RL MITROPOULOU, V COCCARO, E SIEVER, LJ AF STEINBERG, BJ TRESTMAN, RL MITROPOULOU, V COCCARO, E SIEVER, LJ TI DIURNAL MHPG, CORTISOL AND AUTONOMIC RHYTHMS IN ACUTE AND REMITTED DEPRESSION SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET ADM MED CTR,BRONX,NY. MED COLL PENN,PHILADELPHIA,PA 19129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 669 EP 669 DI 10.1016/0006-3223(94)90853-2 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200195 ER PT J AU TRESTMAN, RL BUCHSBAUM, M SIEGEL, B LOSONCZY, M SCHAEFER, C SIEVER, LJ AF TRESTMAN, RL BUCHSBAUM, M SIEGEL, B LOSONCZY, M SCHAEFER, C SIEVER, LJ TI FUNCTIONAL IMAGING WITH SPECT OF COGNITIVE ACTIVITY IN SCHIZOTYPALS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,BRONX,NY. MT SINAI MED CTR,NEW YORK,NY 10029. FDR VA MED CTR,MONTROSE,NY. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 683 EP 684 DI 10.1016/0006-3223(94)90905-9 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200247 ER PT J AU AMIN, F SILVERMAN, J WENTZEL, C SMITH, CJ KNOTT, P SIEVER, LJ AF AMIN, F SILVERMAN, J WENTZEL, C SMITH, CJ KNOTT, P SIEVER, LJ TI DOPAMINE METABOLISM IN THE 1ST-DEGREE RELATIVES OF SCHIZOPHRENIC PROBANDS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,PSYCHIAT SERV 116A,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 690 EP 691 DI 10.1016/0006-3223(94)90929-6 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200271 ER PT J AU HIRSCHOWITZ, J VALLABHAJOSULA, S INTRATOR, J HITZEMANN, R DACOSTA, M MACHAC, J AF HIRSCHOWITZ, J VALLABHAJOSULA, S INTRATOR, J HITZEMANN, R DACOSTA, M MACHAC, J TI ANTIPSYCHOTIC DRUG-THERAPY IN SCHIZOPHRENICS - STUDIES OF RECEPTOR OCCUPANCY SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,NEW YORK,NY 10468. MT SINAI MED CTR,NEW YORK,NY 10029. SUNY STONY BROOK,STONY BROOK,NY 11768. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 691 EP 691 DI 10.1016/0006-3223(94)90930-X PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200272 ER PT J AU AMES, D MANSCHRECK, TC BUCHANAN, RW AF AMES, D MANSCHRECK, TC BUCHANAN, RW TI NEUROLOGIC ABNORMALITIES IN SCHIZOPHRENIA SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 W LOS ANGELES VAMC,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90073. NEW HAMPSHIRE HOSP,CONCORD,NH 03301. MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21228. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 714 EP 714 DI 10.1016/0006-3223(94)91013-8 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200355 ER PT J AU AMES, D WIRSHING, WC WATERS, B MOHGIMI, R BERISFORD, MA AF AMES, D WIRSHING, WC WATERS, B MOHGIMI, R BERISFORD, MA TI NEUROLOGIC DEFICITS, TARDIVE-DYSKINESIA, AND MEDICATION STATUS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 715 EP 715 DI 10.1016/0006-3223(94)91018-9 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200360 ER PT J AU LANDAU, EM WONG, T NOURANIFAR, R IYENGAR, R BLITZER, RD AF LANDAU, EM WONG, T NOURANIFAR, R IYENGAR, R BLITZER, RD TI POSTSYNAPTIC CAMP-DEPENDENT PROTEIN-KINASE PARTICIPATES IN LONG-TERM POTENTIATION SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,BRONX,NY 10468. MT SINAI SCH MED,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 733 EP 733 DI 10.1016/0006-3223(94)91082-0 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200424 ER PT J AU SILVERMAN, JM GREENBERG, DA ALTSTIEL, LD SMITH, CJ ZHOU, G ZACCARIO, ML YANG, XP HOLLANDER, T BELLO, J SIEVER, LJ MOHS, RC DAVIS, KL AF SILVERMAN, JM GREENBERG, DA ALTSTIEL, LD SMITH, CJ ZHOU, G ZACCARIO, ML YANG, XP HOLLANDER, T BELLO, J SIEVER, LJ MOHS, RC DAVIS, KL TI A LINKAGE MARKER FOR SCHIZOPHRENIA AND RELATED DISORDERS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET ADM MED CTR,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 740 EP 741 DI 10.1016/0006-3223(94)91110-X PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200452 ER PT J AU STEINBERG, BJ TRESTMAN, RL LOPEZ, I PAVELL, E SIEVER, LJ AF STEINBERG, BJ TRESTMAN, RL LOPEZ, I PAVELL, E SIEVER, LJ TI CHOLINERGIC CHALLENGE AND AFFECTIVE INSTABILITY IN PERSONALITY-DISORDER PATIENTS SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. BRONX VET ADM MED CTR,BRONX,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 740 EP 740 DI 10.1016/0006-3223(94)91108-8 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200450 ER PT J AU STERN, RG SCHMEIDLER, J DAVIDSON, M AF STERN, RG SCHMEIDLER, J DAVIDSON, M TI A REVIEW OF STATISTICAL DESIGN IN CONTROLLED TREATMENT TRIALS IN SCHIZOPHRENIA SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET ADM MED CTR,NEW YORK,NY 10029. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1994 VL 35 IS 9 BP 741 EP 741 DI 10.1016/0006-3223(94)91112-6 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ172 UT WOS:A1994NJ17200454 ER PT J AU SPEEG, KV MALDONADO, AL AF SPEEG, KV MALDONADO, AL TI EFFECT OF THE NONIMMUNOSUPPRESSIVE CYCLOSPORINE ANALOG SDZ PSC-833 ON COLCHICINE AND DOXORUBICIN BILIARY-SECRETION BY THE RAT IN-VIVO SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE SDZ PSC-833; COLCHICINE; DOXORUBICIN; MDR; LIVER; KIDNEY ID MEDIATED MULTIDRUG RESISTANCE; TRANSPORTER STUDIED INVIVO; P-GLYCOPROTEIN; DRUG-RESISTANCE; GENE-PRODUCT; LOCALIZATION; LEUKEMIA; ANTIBODY; TISSUES; TUMOR AB Colchicine and doxorubicin are secreted into bile as a major pathway of their elimination. Colchicine and doxorubicin are also substrates for P-glycoprotein, and P-glycoprotein has been demonstrated to be present at the liver canalicular membrane. Cyclosporin (CsA) inhibits colchicine biliary secretion in vivo. In the present study, the effects of SDZ PSC-833, a nonimmunosuppressive cyclosporin D analog, on the biliary secretion of colchicine and doxorubicin were investigated. SDZ PSC-833 given at a bolus dose of 2 mg/kg promptly decreased colchicine biliary clearance from 9.05+/-0.2 to 2.41+/-0.43 ml min(-1) kg(-1) (P<0.001) and the colchicine bile/plasma ratio from 146+/-8 to 35+/-5 (P<0.001). SDZ PSC-833 also inhibited doxorubicin biliary clearance (basal: 10.5+/-3 vs post-SDZ PSC-833: 2.48+/-0.94 m1 min(-1) kg(-1); P = 0.06) and the doxorubicin bile/plasma ratio (basal: 228+/-64 vs post-SDZ PSC-833: 48+/-22; P<0.01). Colchicine renal secretion was completely inhibited by SDZ PSC-833. Thus, SDZ PSC-833 inhibits the constitutive transport of the multidrug-resistance substrates colchicine and doxorubicin and is more potent than cyclosporin in this regard. The possibility of increased toxicity to normal tissues because of impaired elimination of cytotoxic agents will need to be considered if SDZ PSC-833 is used to chemosensitize cancer cells. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP SPEEG, KV (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 17 TC 50 Z9 51 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD MAY PY 1994 VL 34 IS 2 BP 133 EP 136 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA NM002 UT WOS:A1994NM00200007 PM 7910787 ER PT J AU FINEGOLD, SM AF FINEGOLD, SM TI CENTENNIAL SYMPOSIUM ON ANAEROBES - A MEMORIAL TO VEILLON,ANDRE - THE SECRET PATHOGENS - INTRODUCTION SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT IMMUNOL,LOS ANGELES,CA. RP FINEGOLD, SM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,ROOM 136,BLDG 114,LOS ANGELES,CA 90073, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAY PY 1994 VL 18 SU 4 BP S245 EP S247 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NL750 UT WOS:A1994NL75000001 PM 8086570 ER PT J AU FINEGOLD, SM AF FINEGOLD, SM TI REVIEW OF EARLY RESEARCH ON ANAEROBES SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT Centennial Symposium on Anaerobes: A Memorial to Andre Veillon, the Secret Pathogens CY MAR 27, 1993 CL PARIS, FRANCE AB It has been one hundred years since the appearance of the first clinical paper on infection involving anaerobic bacteria, an article that also detailed recovery of and description of the organisms responsible for the infection. We pay tribute to the author of that landmark paper, Andre Veillon, in celebration of the centennial of this important occasion. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. RP FINEGOLD, SM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,ROOM 136,BLDG 114,LOS ANGELES,CA 90073, USA. NR 12 TC 1 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAY PY 1994 VL 18 SU 4 BP S248 EP S249 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NL750 UT WOS:A1994NL75000002 PM 8086571 ER PT J AU SILVA, JA LEONG, GB AF SILVA, JA LEONG, GB TI UNTITLED SO COMPREHENSIVE PSYCHIATRY LA English DT Letter ID MISIDENTIFICATION SYNDROMES; CAPGRAS SYNDROME C1 VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV,SAN ANTONIO,TX 78284, 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 0010-440X J9 COMPR PSYCHIAT JI Compr. Psychiat. PD MAY-JUN PY 1994 VL 35 IS 3 BP 244 EP 244 DI 10.1016/0010-440X(94)90198-8 PG 1 WC Psychiatry SC Psychiatry GA NL809 UT WOS:A1994NL80900012 PM 8045116 ER PT J AU CUMMINGS, JL AF CUMMINGS, JL TI VASCULAR SUBCORTICAL DEMENTIAS - CLINICAL ASPECTS SO DEMENTIA LA English DT Article; Proceedings Paper CT 2nd Symposium on Ageing and Ageing Disorders CY AUG 19-20, 1993 CL STOCKHOLM, SWEDEN SP FDN GAMLA TJANARINNOR DE SUBCORTICAL DEMENTIA; LACUNES; BINSWANGERS DISEASE; FRONTAL-SUBCORTICAL CIRCUITS; EXECUTIVE FUNCTION ID MULTI-INFARCT DEMENTIA; SYMPTOMS PREDOMINATE; BINSWANGERS DISEASE; BASAL GANGLIA; PARKINSONISM; DIAGNOSIS; LACUNES AB Vascular dementia (VAD) is common, and small vessel disease is one of the most frequent etiologies of the disorder. Lacunar state and Binswanger's disease are the two types of VAD associated with small vessel disease. Lacunar state and Binswanger's disease produce a dementia syndrome with characteristics of subcortical dementia including slowing of information processing, impaired memory, and poor sustained attention. Executive dysfunction includes poor word list generation and verbal fluency (design generation), impaired motor programming with perseveration and impersistence, and difficulty with set shifting. Memory loss in subcortical VAD is characterized by poor retrieval and intact recognition. Apathy is ubiquitous in VAD and depression and psychosis are common. Parkinsonism with prominent gait disturbances in conjunction with pyramidal tract signs, dysarthria, pseudobulbar affect, and incontinence are frequent motor manifestations of VAD with small vessel disease. The lesions of subcortical VAD affect the structures - caudate nucleus, globus pallidus, thalamus - and connecting fibers of frontal-subcortical circuits and produce a clinical syndrome similar to that seen in other subcortical diseases. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,BEHAV NEUROSCI SECT,LOS ANGELES,CA. RP CUMMINGS, JL (reprint author), UNIV CALIF LOS ANGELES,SCH MED,REED NEUROL RES CTR,DEPT NEUROL,710 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. FU NIA NIH HHS [AG10123] NR 25 TC 123 Z9 131 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1013-7424 J9 DEMENTIA JI Dementia PD MAY-AUG PY 1994 VL 5 IS 3-4 BP 177 EP 180 DI 10.1159/000106718 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NP580 UT WOS:A1994NP58000011 PM 8087175 ER PT J AU GIULIAN, D LI, J LI, X GEORGE, J RUTECKI, PA AF GIULIAN, D LI, J LI, X GEORGE, J RUTECKI, PA TI THE IMPACT OF MICROGLIA-DERIVED CYTOKINES UPON GLIOSIS IN THE CNS SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE AIDS; ALZHEIMERS DISEASE; BRAIN INJURY; CYTOKINES; GLIA; MICROGLIA; NEURON; STROKE ID TUMOR NECROSIS FACTOR; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; MAMMALIAN BRAIN; AMEBOID MICROGLIA; FACTOR-ALPHA; INTERLEUKIN-1; ASTROCYTES; INJURY; CELLS AB Injury to the CNS elicits a complex cellular response involving both astrocytes and microglia. Reactive glial populations make up the so-called 'glial scar' that has long been implicated as a barrier to axonal regeneration or as a causal factor in the genesis of epilepsy. Using in vitro models involving highly enriched populations of brain cells we have observed that astroglial growth is regulated in part by an immunomodulatory growth factor, or cytokine, called interleukin-1 (IL-1). A second cytokine, granulocyte-macrophage colony-stimulating factor (GM-CSF) serves as a potent microglial mitogen and regulator of the microglial component of the glial scar. Employing cytokines as tools to manipulate reactive gliosis, we found that IL-1 supported neuronal growth by action upon astroglia, while GM-CSF initiated epileptic-like discharges through mechanisms involving reactive microglia. We propose that a 'cytokine network' involving IL-1 and GM-CSF mediates the composition of glial scars at sites of CNS injury; these reactive glia, in turn, influence the survival and function of neighboring neurons, C1 UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET ADM HOSP,FM FORSTER EPILEPSY CTR,DEPT NEUROL,MADISON,WI. RP GIULIAN, D (reprint author), BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030, USA. FU NINDS NIH HHS [NS23113, NS28580, NS25637] NR 29 TC 146 Z9 148 U1 1 U2 11 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PD MAY-AUG PY 1994 VL 16 IS 3-4 BP 128 EP 136 DI 10.1159/000112099 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA PZ611 UT WOS:A1994PZ61100003 PM 7535679 ER PT J AU PFALLER, MA BUSCHELMAN, B BALE, MJ LANCASTER, M ESPINELINGROFF, A REX, JH RINALDI, MG AF PFALLER, MA BUSCHELMAN, B BALE, MJ LANCASTER, M ESPINELINGROFF, A REX, JH RINALDI, MG TI MULTICENTER COMPARISON OF A COLORIMETRIC MICRODILUTION BROTH METHOD WITH THE REFERENCE MACRODILUTION METHOD FOR IN-VITRO SUSCEPTIBILITY TESTING OF YEAST ISOLATES SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Article AB This multicenter study was performed to compare a colorimetric microdilution method with the NCCLS M27-P reference macrodilution method for the testing of yeast isolates against amphotericin B, fluconazole, and 5-fluorocytosine (5FC). Testing was performed on ten yeast isolates in five independent laboratories. All sites tested each isolate a total of 20 times with both methods. MICs were read after 48 h incubation. The macrodilution MIC reference range was defined as the modal MIC +/- 1-log(2) dilution for each organism-antifungal agent combination. Agreement between the M27-P reference range results and the microdilution MICs was 86% with amphotericin B, 90% with fluconazole, and 93% with 5FC. Based on these data, it is apparent that new approaches, such as the colorimetric microdilution method, will provide MIC values comparable to the M27-P macrodilution method in a format that is more practical for use in a busy clinical laboratory. C1 ALAMAR BIOSCI,SACRAMENTO,CA. VIRGINIA COMMONWEALTH UNIV MED COLL VIRGINIA,RICHMOND,VA. UNIV TEXAS,SCH MED,HOUSTON,TX. UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,CTR HLTH SCI,LAB SERV 113,SAN ANTONIO,TX 78285. RP PFALLER, MA (reprint author), UNIV IOWA,COLL MED,DEPT PATHOL,273 MRC,IOWA CITY,IA 52242, USA. NR 4 TC 28 Z9 28 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD MAY PY 1994 VL 19 IS 1 BP 9 EP 13 DI 10.1016/0732-8893(94)90044-2 PG 5 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA NX242 UT WOS:A1994NX24200003 PM 7956018 ER PT J AU LEAF, DA AF LEAF, DA TI LIPID DISORDERS - APPLYING NEW GUIDELINES TO YOUR OLDER PATIENTS SO GERIATRICS LA English DT Article ID CORONARY HEART-DISEASE; RISK-FACTORS; LIPOPROTEIN CHOLESTEROL; MYOCARDIAL-INFARCTION; FATTY-ACIDS; FRAMINGHAM; AGE; HEALTH AB The National Cholesterol Education Program Expert Panel has revised its recommendations for managing hypercholesterolemia in adults, including those at midlife and older. In utilizing these guidelines, it is important for the physician to develop an individualized approach to the older patient with hypercholesterolemia. Patient characteristics to consider include lifespan limitations, presence and severity of concomitant disease, mental status and cognitive ability, and the patient's expectations from medical care. Dietary intervention is the first step, with the major focus on restricting saturated fat and cholesterol. Lipid-lowering agents may be warranted in some patients to achieve target LDL levels. Minimize the risk of side effects by careful monitoring and using medications cautiously. C1 W LOS ANGELES VA MED CTR,LOS ANGELES,CA. RP LEAF, DA (reprint author), UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024, USA. NR 26 TC 2 Z9 2 U1 0 U2 0 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 SN 0016-867X J9 GERIATRICS JI Geriatrics PD MAY PY 1994 VL 49 IS 5 BP 35 EP & PG 0 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA NK594 UT WOS:A1994NK59400013 PM 8174939 ER PT J AU HARTZ, D BANYS, P HALL, SM AF HARTZ, D BANYS, P HALL, SM TI CORRELATES OF HOMELESSNESS AMONG SUBSTANCE-ABUSE PATIENTS AT A VA MEDICAL-CENTER SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Note ID MENTAL-DISORDERS; HEALTH-STATUS; DRUG-ABUSE; ALCOHOL; ADULTS C1 UNIV CALIF SAN FRANCISCO,LANGLEY PORTER PSYCHIAT INST,SAN FRANCISCO,CA 94143. SAN FRANCISCO VA MED CTR,PSYCHIAT SERV,SAN FRANCISCO,CA. FU NIDA NIH HHS [1R18-DA06097] NR 10 TC 10 Z9 10 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 MAY PY 1994 VL 45 IS 5 BP 491 EP 493 PG 3 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA NJ221 UT WOS:A1994NJ22100016 PM 8045549 ER PT J AU PATTERSON, JE SANCHEZ, RO HERNANDEZ, J GROTA, P ROSS, KA AF PATTERSON, JE SANCHEZ, RO HERNANDEZ, J GROTA, P ROSS, KA TI SPECIAL ORGANISM ISOLATION - ATTEMPTING TO BRIDGE THE GAP SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID INTENSIVE-CARE UNIT; INFECTION; RESISTANT; PRECAUTIONS; VANCOMYCIN; GENTAMICIN; ANITRATUS; OUTBREAK C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV HOSP,DEPT QUAL RISK MANAGEMENT INFECT CONTROL,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT INFECT CONTROL,SAN ANTONIO,TX 78284. VET AFFAIRS MED CTR,DEPT INFECT CONTROL,W HAVEN,CT. RP PATTERSON, JE (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED INFECT DIS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 13 TC 8 Z9 8 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 MAY PY 1994 VL 15 IS 5 BP 335 EP 338 PG 4 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA NM781 UT WOS:A1994NM78100015 PM 8077647 ER PT J AU REDDY, SV TAKAHASHI, S DALLAS, M WILLIAMS, RE NECKERS, L ROODMAN, GD AF REDDY, SV TAKAHASHI, S DALLAS, M WILLIAMS, RE NECKERS, L ROODMAN, GD TI INTERLEUKIN-6 ANTISENSE DEOXYOLIGONUCLEOTIDES INHIBIT BONE-RESORPTION BY GIANT-CELLS FROM HUMAN GIANT-CELL TUMORS OF BONE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID OSTEOBLASTS; IL-6 AB The effects of antisense constructs to IL-6 on the bone-resorbing capacity of purified giant cells from giant cell tumors of bone were examined to further define the role of IL-6 in human osteoclastic bone resorption. In addition, we wanted to determine the utility of antisense constructs to cytokines produced by osteoclasts as probes to identify the molecular events responsible for the bone-resorptive process. Giant cells were cultured on sperm whale dentin for 24 h in the presence of fluoresceinated antisense or scrambled antisense deoxyoligonucleotides complementary to IL-6 mRNA. The giant cells actively incorporated these oligonucleotides, as evidenced by their intense fluorescence. The number of resorptive lacunae formed and the area of the dentin resorbed were significantly decreased in cultures of giant cells treated with antisense IL-6 constructs compared with control cultures treated with scrambled antisense constructs to IL-6 (60 +/- 13 versus 12 +/- 6 lacunae and 1.2 +/- 0.3 versus 0.26 +/- 0.1 x 10(5) mu m(2)). IL-6 levels in conditioned media from giant cell cultures treated with IL-6 antisense constructs were fourfold lower than those in control media obtained from giant cells treated with scrambled antisense constructs to IL-6. These data confirm the capacity of IL-6 antisense oligomers to block IL-6 production by these cells. These observations show that IL-6 plays an important role in the bone-resorptive process of human osteoclasts and suggest that antisense constructs to cytokines produced by bone cells may be useful for determining the molecular events occurring during bone resorption. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED HEMATOL,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NIH,BETHESDA,MD. NR 13 TC 53 Z9 53 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 MAY PY 1994 VL 9 IS 5 BP 753 EP 757 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NF563 UT WOS:A1994NF56300021 PM 8053406 ER PT J AU SAMUELS, MH KRAMER, P WILSON, D SEXTON, G AF SAMUELS, MH KRAMER, P WILSON, D SEXTON, G TI EFFECTS OF NALOXONE INFUSIONS ON PULSATILE THYROTROPIN SECRETION SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Note ID THYROID-STIMULATING HORMONE; OPIATE RECEPTOR BLOCKADE; LUTEINIZING-HORMONE; BETA-ENDORPHIN; GROWTH-HORMONE; OPIOID-PEPTIDES; CORTISOL-LEVELS; TSH RELEASE; PITUITARY; PROLACTIN AB Endogenous opioids are known to modulate the secretion of some anterior pituitary hormones, but they are not thought to have significant effects on TSH secretion. However, dynamic TSH secretion has not been characterized during naloxone infusions. Therefore, we measured TSH levels every 15 min over 24 h in nine healthy young men at baseline and during infusions of naloxone at 2 mg/h. A TRH test was performed after each study. TSH pulses were located by Cluster analysis. Naloxone infusions decreased 24-h mean TSH levels by 28%, from 1.68 +/- 0.20 to 1.21 +/- 0.19 mU/L. Mean daytime TSH levels did not change, but nocturnal TSH levels were decreased by 39%, from 2.21 +/- 0.30 to 1.35 +/- 0.21 mU/L. There were no changes in TSH pulse frequency, but naloxone infusions decreased 24-h TSH pulse amplitude by 32%, from 2.02 +/- 0.26 to 1.37 +/- 0.21 mU/L. Daytime TSH pulse amplitude was relatively unaffected (1.27 +/- 0.15 us. 1.16 +/- 0.21 mU/L), whereas nocturnal TSH pulse amplitude was decreased by 42%, from 2.72 +/- 0.40 to 1.57 +/- 0.23 mU/L. TSH responses to acute TRH administration were decreased after naloxone infusions (12.38 +/- 1.93 us. 9.17 +/- 1.36 mU/L). Serum T-3 levels fell by 21% during naloxone infusions, from 1.9 +/- 0.1 to 1.5 +/- 0.1 nmol/L, whereas other thyroid hormone levels and cortisol levels were unchanged. These findings suggest that endogenous opioids have significant stimulatory effects on TSH secretion, predominantly during the nocturnal TSH surge. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP SAMUELS, MH (reprint author), OREGON HLTH SCI UNIV, DIV ENDOCRINOL, L607, 3181 SW SAM JACKSON PK RD, PORTLAND, OR 97201 USA. FU NCRR NIH HHS [MO1-RR-01-346, MO1-RR-00-334] NR 33 TC 12 Z9 14 U1 1 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD MAY PY 1994 VL 78 IS 5 BP 1249 EP 1252 DI 10.1210/jc.78.5.1249 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NK241 UT WOS:A1994NK24100044 PM 8175985 ER PT J AU BRATOEVA, MP WOLF, MK MARKS, JK CANTEY, JR AF BRATOEVA, MP WOLF, MK MARKS, JK CANTEY, JR TI A CASE OF DIARRHEA, BACTEREMIA, AND FEVER CAUSED BY A NOVEL STRAIN OF ESCHERICHIA-COLI SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID TISSUE-CULTURE CELLS; DNA PROBE; EAE GENE; ADHERENCE FACTOR; HEP-2 CELLS; INVASION; CLONING; O157-H7 AB A nonenteropathogenic strain of Escherichia coli from a patient with diarrhea and bacteremia possessed the attaching-effacing ene gene, was invasive in the gentamicin invasion assay, and expressed two types of pili and K1 antigen. This unique combination places the strain in a new category of attaching-effacing E. coli. C1 MED UNIV S CAROLINA,DEPT MED,DIV INFECT DIS,CHARLESTON,SC 29425. RALPH H JOHNSON VET ADM MED CTR,CHARLESTON,SC. WALTER REED ARMY INST RES,WASHINGTON,DC. NR 20 TC 2 Z9 2 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 MAY PY 1994 VL 32 IS 5 BP 1383 EP 1386 PG 4 WC Microbiology SC Microbiology GA NG217 UT WOS:A1994NG21700050 PM 7914208 ER PT J AU HEFLE, SL BUSH, RK YUNGINGER, JW CHU, FS AF HEFLE, SL BUSH, RK YUNGINGER, JW CHU, FS TI A SANDWICH ENZYME-LINKED-IMMUNOSORBENT-ASSAY (ELISA) FOR THE QUANTITATION OF SELECTED PEANUT PROTEINS IN FOODS SO JOURNAL OF FOOD PROTECTION LA English DT Article DE ALLERGENS; PEANUT; ELISA; FOOD ALLERGY; MONOCLONAL ANTIBODY ID INDUCED ANAPHYLAXIS; PRODUCTS AB A sandwich-type, enzyme-linked immunosorbent assay (ELISA) was developed for the detection of selected peanut proteins in foods. Monoclonal antibodies against a series of allergenic peanut proteins were used as the capture antibody. Food sample extracts were then added, and polyclonal rabbit antibodies directed against roasted peanut proteins were employed as secondary antibodies. The amount of allergen bound to the solid-phase was determined by a biotin and streptavidin-peroxidase system. Radioallergosorbent assay (RAST) inhibition studies of the food extracts were done as a comparison. The coefficient of determination for the ELISA and RAST assays was 0.85. Selected food samples were tested by RAST inhibition at another laboratory for comparison. Skin tests were done with selected samples in peanut-allergic adults, and the results correlated to the ELISA and RAST inhibition results. In other studies, defatted peanut protein (0.01 to 5.0%) were added to vanilla ice cream, then extracted and analyzed using ELISA and skin tests. The sensitivity of the ELISA in ice cream was approximately 40 mug/ml. In six of seven peanut-sensitive adults tested, the lowest level of added peanut protein (0.01%, 21 mug/ml) still caused a positive skin test reaction. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,INST FOOD RES,MADISON,WI 53706. MAYO CLIN & MAYO GRAD SCH MED,DEPT PEDIAT,ALLERG DIS RES LAB,ROCHESTER,MN 55901. MAYO CLIN & MAYO GRAD SCH MED,DEPT INTERNAL MED,ROCHESTER,MN 55901. NR 20 TC 41 Z9 43 U1 2 U2 4 PU INT ASSOC MILK FOOD ENVIRONMENTAL SANITARIANS, INC PI DES MOINES PA 6200 AURORA AVE SUITE 200W, DES MOINES, IA 50322-2838 SN 0362-028X J9 J FOOD PROTECT JI J. Food Prot. PD MAY PY 1994 VL 57 IS 5 BP 419 EP 423 PG 5 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA NN281 UT WOS:A1994NN28100011 ER PT J AU MIRRA, SS GEARING, M MCKEEL, DW CRAIN, BJ HUGHES, JP VANBELLE, G HEYMAN, A BALL, MJ CLARK, AW HANSEN, LA HEDREEN, JC JOACHIM, CL KIM, RC KIRKPATRICK, JB MARKESBERY, WR DAVIS, D MARTINEZ, AJ MILLER, CA MOOSSY, J MORRIS, J NOCHLIN, D PERL, DP PUROHIT, D PETITO, CK RAO, GR ROBITAILLE, Y SCHELPER, RL SUMI, SM VOGEL, FS WHITE, CR AF MIRRA, SS GEARING, M MCKEEL, DW CRAIN, BJ HUGHES, JP VANBELLE, G HEYMAN, A BALL, MJ CLARK, AW HANSEN, LA HEDREEN, JC JOACHIM, CL KIM, RC KIRKPATRICK, JB MARKESBERY, WR DAVIS, D MARTINEZ, AJ MILLER, CA MOOSSY, J MORRIS, J NOCHLIN, D PERL, DP PUROHIT, D PETITO, CK RAO, GR ROBITAILLE, Y SCHELPER, RL SUMI, SM VOGEL, FS WHITE, CR TI INTERLABORATORY COMPARISON OF NEUROPATHOLOGY ASSESSMENTS IN ALZHEIMERS-DISEASE - A STUDY OF THE CONSORTIUM TO ESTABLISH A REGISTRY FOR ALZHEIMERS-DISEASE (CERAD) SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ALZHEIMERS DISEASE; MULTICENTER STUDY; QUALITY IMPROVEMENT; SENILE PLAQUES; SILVER STAINS ID SENILE PLAQUES; NEUROFIBRILLARY TANGLES; SYNAPSE LOSS; DIAGNOSIS; DEMENTIA; CRITERIA AB Concerns about intercenter variation in methods and interpretation prompted CERAD investigators to examine standardization of the neuropathological assessment of Alzheimer's disease (AD). Contiguous frontal lobe sections derived from autopsy brains of eight patients clinically diagnosed as having probable AD and two cognitively normal individuals were distributed to 24 neuropathologists from 18 medical centers in the United States and Canada. Using their routine staining method(s), neuropathologists determined the rank order of severity of AD neuropathology in these cases, as well as semiquantitative and quantitative senile plaque and neurofibrillary tangle frequencies. Ranking of the ten cases revealed 75% inter-rater reliability among the 24 raters. Semiquantitative analyses showed reasonable inter-rater agreement, whereas quantitative measures yielded significant differences between raters for plaque and tangle counts (p < 0.0001). These differences reflected variation in stain sensitivity, staining technique (even when the same stain was used), and interpretation of the histological findings. Ratings on the cases with the highest proportions of diffuse plaques showed the greatest dependence upon stain sensitivity and variability in interpretation. This study indicates that greater attention to quality improvement is needed for the neuropathological evaluation of AD, particularly when pooling data in multicenter studies such as CERAD. C1 EMORY UNIV,SCH MED,ATLANTA,GA. WASHINGTON UNIV,SCH MED,ST LOUIS,MO. DUKE UNIV,MED CTR,DURHAM,NC. OREGON HLTH SCI UNIV,PORTLAND,OR. UNIV CALGARY,HLTH SCI CTR,CALGARY,AB,CANADA. UNIV CALIF SAN DIEGO,LA JOLLA,CA. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA. VET AFFAIRS MED CTR,LONG BEACH,CA. BAYLOR COLL MED,HOUSTON,TX. UNIV KENTUCKY,MED CTR,LEXINGTON,KY. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA. UNIV SO CALIF,MED CTR,LOS ANGELES,CA. UNIV WASHINGTON,SCH MED,SEATTLE,WA. MT SINAI MED CTR,NEW YORK,NY. BRONX VET AFFAIRS MED CTR,NEW YORK,NY. CORNELL UNIV,MED CTR,NEW YORK,NY. VET AFFAIRS MED CTR,PITTSBURGH,PA. MONTREAL NEUROL HOSP & INST,MONTREAL,PQ,CANADA. UNIV IOWA HOSP & CLIN,IOWA CITY,IA. UNIV TEXAS,SOUTHWESTERN MED CTR,DALLAS,TX. RP MIRRA, SS (reprint author), VET AFFAIRS MED CTR,1670 CLAIRMONT RD,DECATUR,GA 30033, USA. FU NIA NIH HHS [AG05681, AG06790, AG10130] NR 25 TC 105 Z9 105 U1 1 U2 1 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1994 VL 53 IS 3 BP 303 EP 315 DI 10.1097/00005072-199405000-00012 PG 13 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA NL027 UT WOS:A1994NL02700012 PM 8176413 ER PT J AU BHATTATHIRY, M GLASS, E KIRGAN, D MORTON, D HOH, C MADDAHI, J BROWN, C KHONSARY, A BLAHD, W AF BHATTATHIRY, M GLASS, E KIRGAN, D MORTON, D HOH, C MADDAHI, J BROWN, C KHONSARY, A BLAHD, W TI EFFICACY OF FDG WHOLE-BODY PET IN STAGING AND CLINICAL MANAGEMENT OF METASTATIC MALIGNANT-MELANOMA SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,MED CTR,JOHN WAYNE CANC INST,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1994 VL 35 IS 5 SU S BP P230 EP P230 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NK909 UT WOS:A1994NK90900941 ER PT J AU BROWN, CV KHONSARY, SA BHATTATHIRY, M ROPCHAN, JR FARAHI, JB QUINONES, N RIBE, JY COLOURIS, GC GLASS, EC COYLE, JJ MANDELKERN, MA BLAHD, WH AF BROWN, CV KHONSARY, SA BHATTATHIRY, M ROPCHAN, JR FARAHI, JB QUINONES, N RIBE, JY COLOURIS, GC GLASS, EC COYLE, JJ MANDELKERN, MA BLAHD, WH TI WHOLE-BODY FDG-PET ONCOLOGY ATLAS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1994 VL 35 IS 5 SU S BP P273 EP P273 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NK909 UT WOS:A1994NK90901111 ER PT J AU CHAUDHURI, TR ZINN, KR MORRIS, JS MCDONALD, GA LLORENS, AS CHAUDHURI, TK AF CHAUDHURI, TR ZINN, KR MORRIS, JS MCDONALD, GA LLORENS, AS CHAUDHURI, TK TI DEVELOPMENT AND CHARACTERIZATION OF RADIOLABELED HUMAN MONOCLONAL-ANTIBODY AGAINST OVARIAN-CANCER SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 UNIV MISSOURI, COLUMBIA, MO USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. VET ADM MED CTR, SAN ANTONIO, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 EI 1535-5667 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1994 VL 35 IS 5 SU S BP P218 EP P219 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NK909 UT WOS:A1994NK90900889 ER PT J AU SIMEON, PS GEFFNER, ME LEVIN, SR LINDSEY, AM AF SIMEON, PS GEFFNER, ME LEVIN, SR LINDSEY, AM TI CONTINUOUS INSULIN INFUSIONS IN NEONATES - PHARMACOLOGICAL AVAILABILITY OF INSULIN IN INTRAVENOUS SOLUTIONS SO JOURNAL OF PEDIATRICS LA English DT Article ID GLUCOSE-INTOLERANCE; INFANTS AB Continuous insulin infusion is sometimes used in very low birth weight infants with glucose intolerance. We studied the availability of insulin to the neonate by means of a laboratory-simulated clinical infusion under both flushed and nonflushed conditions. Although loss of insulin was noted with both solutions (0.5 U/ml), under the nonflushed condition only 55.9% of the prescribed dose for the first 2 hours was delivered before the delivery rate of the flushed system, 71.4%, was approached. These findings have implications for neonatal insulin administration. C1 UNIV CALIF LOS ANGELES, MED CTR, SCH NURSING, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, DEPT PEDIAT, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, DEPT MED, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 9 TC 11 Z9 11 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD MAY PY 1994 VL 124 IS 5 BP 818 EP 820 DI 10.1016/S0022-3476(05)81382-4 PN 1 PG 3 WC Pediatrics SC Pediatrics GA NK479 UT WOS:A1994NK47900030 PM 8176576 ER PT J AU BROWN, LJ GARCIA, R AF BROWN, LJ GARCIA, R TI UTILIZATION OF DENTAL SERVICES AS A RISK FACTOR FOR PERIODONTITIS SO JOURNAL OF PERIODONTOLOGY LA English DT Article DE DELIVERY OF HEALTH CARE; ORAL HEALTH SURVEYS; PATIENT ACCEPTANCE OF HEALTH CARE; UTILIZATION REVIEW ID SUBGINGIVAL PLAQUE CONTROL; ORAL HYGIENE; LINEAR-MODELS; DISEASE; HEALTH; POPULATION; ADULTS; TEETH AB THE RELATION BETWEEN UTILIZATION OF DENTAL SERVICES from community dentists and the extent and severity of alveolar bone loss is reported for a panel of men followed for over 6 years. Oral health data were collected by the Department of Veterans Affairs, Dental Longitudinal Study, which began in 1969 and still continues. Participants have received regular oral examinations approximately every 3 years. A variety of oral health conditions were assessed, including plaque, calculus, gingival inflammation, probing depth, tooth mobility, clinical attachment level, and alveolar bone loss. Utilization data were abstracted from the dental records of dental offices that participants attended from 1979 through 1988. Multivariate modeling as well as comparisons of high utilizers and non-utilizers indicate that utilization of routine diagnostic and preventive services was not predictive of the extent and severity of periodontitis. C1 US DEPT VET AFFAIRS,WASHINGTON,DC. TUFTS UNIV,BOSTON,MA 02111. RP BROWN, LJ (reprint author), NIDR,WESTWOOD BLDG,ROOM 528,5333 WESTBARD AVE,BETHESDA,MD 20892, USA. NR 71 TC 14 Z9 15 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 MAY PY 1994 VL 65 IS 5 SU S BP 551 EP 563 PG 13 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA NM524 UT WOS:A1994NM52400012 PM 8046572 ER PT J AU MEYER, JS TAKASHIMA, S TERAYAMA, Y OBARA, K MURAMATSU, K WEATHERS, S AF MEYER, JS TAKASHIMA, S TERAYAMA, Y OBARA, K MURAMATSU, K WEATHERS, S TI CT CHANGES ASSOCIATED WITH NORMAL AGING OF THE HUMAN BRAIN SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE COMPUTED TOMOGRAPHY; POLIO-ARAIOSIS; LEUKOARAIOSIS; CEREBRAL PERFUSION; DENSITOMETRY ID COMPUTED-TOMOGRAPHY; LEUKO-ARAIOSIS; ALZHEIMERS-DISEASE; WHITE MATTER; RISK-FACTORS; CELL COUNTS; DEMENTIA; ATROPHY; LUCENCIES; NUMBERS AB CT was used to measure changes in cerebral gray and white matter tissue densities associated with normal aging, using a cross-sectional design, in order to provide normative data for comparisons with abnormal aging such as dementias of Alzheimer's and vascular types. Cerebral compartmental densities were measured using plain CT; and their perfusion values were recorded during stable xenon inhalation (CT-CBF), among 81 neurologically and cognitively normal volunteers of different ages. Results led to the conclusion that cortical gray matter tissue densities progressively decline (polio-araiosis) after age 60. Cortical polio-araiosis is coupled with regional hypoperfusion but not with cortical atrophy. It is speculated that the cortical hypodensity identified by CT imaging parallels declines in cortical synaptic density, as reported from autopsy studies using anti-synaptophysin staining of cerebral cortex obtained from normal people above and below age 60. The coupling of cortical hypoperfusion with polio-araiosis is believed to reflect age-related reductions of cortical metabolic demands as reported by PET. During normal aging leuko-araiosis correlates directly with cortical atrophy, suggesting that anterograde axonal degeneration resulting from cortical neuronal dearborization play a role in its causation. C1 BAYLOR COLL MED & NEUROL,DEPT NEUROL,HOUSTON,TX. BAYLOR COLL MED & NEUROL,DEPT RADIOL,HOUSTON,TX. RP MEYER, JS (reprint author), DEPT VET AFFAIRS MED CTR,SERV RADIOL,CEREBAL BLOOD FLOW LAB,2002 HOLCOMBE BLVD 151A,HOUSTON,TX 77030, USA. NR 40 TC 27 Z9 27 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD MAY PY 1994 VL 123 IS 1-2 BP 200 EP 208 DI 10.1016/0022-510X(94)90224-0 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NL359 UT WOS:A1994NL35900031 PM 8064316 ER PT J AU HAFFNER, SM VALDEZ, RA MYKKANEN, L STERN, MP KATZ, MS AF HAFFNER, SM VALDEZ, RA MYKKANEN, L STERN, MP KATZ, MS TI DECREASED TESTOSTERONE AND DEHYDROEPIANDROSTERONE-SULFATE CONCENTRATIONS ARE ASSOCIATED WITH INCREASED INSULIN AND GLUCOSE-CONCENTRATIONS IN NONDIABETIC MEN SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID HORMONE-BINDING GLOBULIN; BODY-FAT DISTRIBUTION; SEX-HORMONES; POSTMENOPAUSAL WOMEN; MEXICAN-AMERICANS; RESISTANCE; HYPERINSULINEMIA; ADIPOSITY; OBESITY; LIPOPROTEIN C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIAT & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN EPIDEMIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. FU NHLBI NIH HHS [R37-HL36820, R01 HL-24799] NR 38 TC 181 Z9 183 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD MAY PY 1994 VL 43 IS 5 BP 599 EP 603 DI 10.1016/0026-0495(94)90202-X PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NL244 UT WOS:A1994NL24400013 PM 8177048 ER PT J AU PEKARY, AE BERG, L SANTINI, F CHOPRA, I HERSHMAN, JM AF PEKARY, AE BERG, L SANTINI, F CHOPRA, I HERSHMAN, JM TI CYTOKINES MODULATE TYPE-I IODOTHYRONINE DEIODINASE MESSENGER-RNA LEVELS AND ENZYME-ACTIVITY IN FRTL-5 RAT-THYROID CELLS SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Note DE RAT; THYROID; TYPE I IODOTHYRONINE DEIODINASE; MESSENGER RNA; ENZYME ACTIVITY; CYTOKINE ID NECROSIS-FACTOR-ALPHA AB Tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interferon-gamma (INF-gamma) have inhibitory effects on thyroid function both in vivo and in vitro. We have studied the effects of these cytokines on type I 5'-deiodinase (5'-DI) mRNA expression and enzyme activity in FRTL-5 cells maintained in standard cell culture medium containing 0 (5H) or 2 mIU/ml bovine TSH (6H). Northern blots were hybridized with 5'-DI cDNA. 5'-DI mRNA levels were reduced to 20% of control values after treating cells with 100 ng/ml TNF-alpha in 6H for 2 days while the corresponding enzyme activity was reduced 50%. Other cytokines, including IL-1 beta and interferon-gamma, also significantly inhibited expression of 5'-DI in FRTL-5 cells grown in 6H medium. Because the majority of circulating T, in the rat is secreted by the thyroid gland, the highly significant decline in the serum T-3/T-4 ratio following in vivo administration of cytokines may be due to their direct inhibitory effect on thyroidal 5'-DI expression. C1 UNIV CALIF LOS ANGELES,DEPT MED,DIV ENDOCRINOL,LOS ANGELES,CA 90073. RP PEKARY, AE (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VA MED CTR,ENDOCRINOL RES LAB,BLDG 114,RM 200,LOS ANGELES,CA 90073, USA. NR 19 TC 37 Z9 37 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD MAY PY 1994 VL 101 IS 1-2 BP R31 EP R35 DI 10.1016/0303-7207(94)90256-9 PG 5 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA NJ789 UT WOS:A1994NJ78900045 PM 9397972 ER PT J AU WEINBERGER, LE SREENIVASAN, S AF WEINBERGER, LE SREENIVASAN, S TI ETHICAL AND PROFESSIONAL CONFLICTS IN CORRECTIONAL PSYCHOLOGY SO PROFESSIONAL PSYCHOLOGY-RESEARCH AND PRACTICE LA English DT Article ID PRISON AB The role of the mental health professional in a prison setting has changed to reflect the prevailing ideology of the correctional administration that deemphasizes treatment and emphasizes security and custodial concerns. As a consequence, mental health professionals who work in corrections have experienced unique ethical and professional conflicts. Standards were developed to address the conflicts and provide guidelines for professional conduct, but dilemmas continue to exist. The authors believe this can be attributed to (a) the standards being vague and (b) correctional personnel not understanding or supporting the standards or the psychologist's role as a mental health professional. This article examines these propositions in more detail, using vignettes and discussion, and offers other approaches to resolving the dilemmas and improving the delivery of mental health services to incarcerated individuals. C1 W LOS ANGELES DEPT VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. RP WEINBERGER, LE (reprint author), UNIV SO CALIF,INST PSYCHIAT LAW & BEHAV SCI,POB 86125,LOS ANGELES,CA 90089, USA. NR 27 TC 15 Z9 15 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7028 J9 PROF PSYCHOL-RES PR JI Prof. Psychol.-Res. Pract. PD MAY PY 1994 VL 25 IS 2 BP 161 EP 167 DI 10.1037//0735-7028.25.2.161 PG 7 WC Psychology, Multidisciplinary SC Psychology GA NL399 UT WOS:A1994NL39900011 ER PT J AU LIBERMAN, RP AF LIBERMAN, RP TI PSYCHOSOCIAL TREATMENTS FOR SCHIZOPHRENIA SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article ID CONTROLLED TRIAL; MAINTENANCE CHEMOTHERAPY; FAMILY PSYCHOEDUCATION; PSYCHIATRIC-PATIENTS; AFTERCARE TREATMENT; EXPRESSED EMOTION; MENTALLY-ILL; FOLLOW-UP; SKILLS; RELAPSE AB BASED upon educational and social learning principles, social skills training and family management modalities have been validated as effective in improving coping skills and symptomatic course and outcome of schizophrenia. Combined with judicious doses of antipsychotic medication, these modalities have been designed from the conceptualization of schizophrenia as a stress-related, biomedical disorder, with those afflicted having enduring vulnerability to the emergence or exacerbation of psychotic symptoms with associated social disability. Behaviorally oriented modalities require integration with a comprehensive psychiatric service delivery system to confer protection against relapse. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. CAMARILLO STATE HOSP,CAMARILLO,CA 93010. RP LIBERMAN, RP (reprint author), W LOS ANGELES VA MED CTR,REHABILITAT COMMUNITY & PSYCHIATRY B116V,WILSHIRE & SAWTELLE BLVDS,LOS ANGELES,CA 90073, USA. FU NIMH NIH HHS [NIMH MH 30911] NR 59 TC 54 Z9 55 U1 2 U2 3 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 MAY PY 1994 VL 57 IS 2 BP 104 EP 114 PG 11 WC Psychiatry SC Psychiatry GA NX017 UT WOS:A1994NX01700003 PM 7938330 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R SHARMA, KK KLEIN, RL AF SILVA, JA LEONG, GB WEINSTOCK, R SHARMA, KK KLEIN, RL TI DELUSIONAL MISIDENTIFICATION SYNDROMES AND DANGEROUSNESS SO PSYCHOPATHOLOGY LA English DT Article; Proceedings Paper CT Conference on Delusional Misidentification Syndromes CY 1993 CL HOSPITAL SAINTE ANNE, PARIS, FRANCE HO HOSPITAL SAINTE ANNE AB Dangerousness in the delusional misidentification syndromes is studied by reviewing a sample of 82 cases defined by either verbal threats or physical violence caused by a misidentification delusion. Eighty cases were obtained from a review of the anglophone psychiatric literature in which the patients exhibited some degree of dangerousness, to which we added 2 previously unreported cases. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA 90073. UNIV SO CALIF,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA. UNIV CALIF IRVINE,GRAD SCH MANAGEMENT,IRVINE,CA 92717. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 14 TC 20 Z9 20 U1 1 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD MAY-OCT PY 1994 VL 27 IS 3-5 BP 215 EP 219 PG 5 WC Psychiatry SC Psychiatry GA PN447 UT WOS:A1994PN44700017 PM 7846240 ER PT J AU WALDO, MC CAWTHRA, E ADLER, LE DUBESTER, S STAUNTON, M NAGAMOTO, H BAKER, N MADISON, A SIMON, J SCHERZINGER, A DREBING, C GERHARDT, G FREEDMAN, R AF WALDO, MC CAWTHRA, E ADLER, LE DUBESTER, S STAUNTON, M NAGAMOTO, H BAKER, N MADISON, A SIMON, J SCHERZINGER, A DREBING, C GERHARDT, G FREEDMAN, R TI AUDITORY SENSORY GATING, HIPPOCAMPAL VOLUME, AND CATECHOLAMINE METABOLISM IN SCHIZOPHRENICS AND THEIR SIBLINGS SO SCHIZOPHRENIA RESEARCH LA English DT Article DE PATHOPHYSIOLOGY; AUDITORY EVOKED POTENTIAL; HIPPOCAMPUS; DOPAMINE; HOMOVANILLIC ACID; (SCHIZOPHRENIA) ID EYE-TRACKING DYSFUNCTIONS; PLASMA HOMOVANILLIC-ACID; EVOKED-RESPONSES; NEUROPHYSIOLOGICAL EVIDENCE; P50 SUPPRESSION; LIMBIC SYSTEM; POTENTIALS; NOREPINEPHRINE; ABNORMALITIES; STIMULATION AB Schizophrenia may result from the concerted action of several pathophysiological factors. This pilot study compared the distribution of measurements of three such putative factors in 11 schizophrenics and their siblings: a neurophysiological deficit in auditory sensory gating, diminished hippocampal volume, and increased catecholamine metabolism. Abnormal auditory sensory gating was found in all schizophrenics in the 11 families studied and in 8 of their 20 siblings. Compared with the schizophrenics, the clinically unaffected siblings with abnormal auditory gating had larger hippocampal volume. There was no similar difference for the siblings with normal gating. The siblings with abnormal auditory gating also had lower homovanillic acid levels than the other siblings. The data suggest that a familial neuronal deficit, identified by diminished sensory gating, may be a necessary, but not sufficient factor in the pathogenesis of schizophrenia. Individuals with this deficit are generally clinically unaffected, except for schizophrenics, who also have other abnormalities, such as diminished hippocampal volume and increased catecholamine metabolism. C1 DENVER VA MED CTR,DEPT PSYCHIAT,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR C26871,DENVER,CO 80262. DENVER VA MED CTR,DEPT PHARMACOL,DENVER,CO. DENVER VA MED CTR,DEPT RADIOL,DENVER,CO. FU NIMH NIH HHS [MH00728, MH44212, MH38321] NR 60 TC 100 Z9 100 U1 0 U2 1 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 PY 1994 VL 12 IS 2 BP 93 EP 106 DI 10.1016/0920-9964(94)90067-1 PG 14 WC Psychiatry SC Psychiatry GA NK059 UT WOS:A1994NK05900001 PM 8043530 ER PT J AU HAROUTUNIAN, V DAVIDSON, M KANOF, PD PERL, DP POWCHIK, P LOSONCZY, M MCCRYSTAL, J PUROHIT, DP BIERER, LM DAVIS, KL AF HAROUTUNIAN, V DAVIDSON, M KANOF, PD PERL, DP POWCHIK, P LOSONCZY, M MCCRYSTAL, J PUROHIT, DP BIERER, LM DAVIS, KL TI CORTICAL CHOLINERGIC MARKERS IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Article DE ALZHEIMERS DISEASE; ACETYLCHOLINE; CHOLINERGIC; CHOLINE ACETYLTRANSFERASE; ACETYLCHOLINESTERASE; CORTEX; POSTMORTEM; (SCHIZOPHRENIA) ID ALZHEIMERS-DISEASE; NUCLEUS BASALIS; SENILE DEMENTIA; LONG-TERM; SYSTEM; MEMORY; BRAIN; IMPAIRMENT; DEFICITS; BINDING AB Cortical cholinergic deficits have been implicated in the cognitive deficits produced by a variety of neurodegenerative diseases including Alzheimer's disease (AD). Recent studies have suggested that many of the chronically institutionalized geriatric schizophrenic patients are also cognitvely impaired. In this postmortem study we compared cholinergic marker activity in six different cortical regions derived from elderly controls, chronically institutionalized geriatric schizophrenic patients, and AD patients. All of the Alzheimer's disease cases met neuropathological criteria for AD, while none of the schizophrenic cases met criteria for AD. Cholinergic marker activity (choline acetyltransferase and acetylcholinesterase) was significantly diminished in the AD cohort but not in the schizophrenic cohort. Additionally, cortical choline acetyltransferase activity was significantly and negatively correlated with Clinical Dementia Rating scores (CDR), whereas no such correlations were evident in the schizophrenic cohort. These results suggest that cognitive deficits in geriatric schizophrenics are not due to diminished cortical cholinergic activity. C1 CUNY MT SINAI SCH MED,DEPT PATHOL,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,BRONX,NY. PILGRIM PSYCHIAT CTR,W BRENTWOOD,NY. RP HAROUTUNIAN, V (reprint author), CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029, USA. FU NIA NIH HHS [AG00408] NR 48 TC 61 Z9 61 U1 6 U2 6 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 PY 1994 VL 12 IS 2 BP 137 EP 144 DI 10.1016/0920-9964(94)90071-X PG 8 WC Psychiatry SC Psychiatry GA NK059 UT WOS:A1994NK05900005 PM 8043524 ER PT J AU KATZ, MS LOWENTHAL, DT AF KATZ, MS LOWENTHAL, DT TI INFLUENCES OF AGE AND EXERCISE ON GLUCOSE-METABOLISM - IMPLICATIONS FOR MANAGEMENT OF OLDER DIABETICS SO SOUTHERN MEDICAL JOURNAL LA English DT Article; Proceedings Paper CT Symposium on Exercise and Aging CY SEP, 1992 CL GAINESVILLE, FL SP GAINESVILLE VA MED CTR GERIATR RES EDUC & CLIN CTR, UNIV FLORIDA, CTR EXERCISE SCI, UNIV FLORIDA, COLL HLTH & HUMAN PERFORMANCE, UNIV FLORIDA, COLL MED, GERIATR EDUC CTR, BIRMINGHAM REG MED EDUC CTR ID PHYSICAL-ACTIVITY; INSULIN SENSITIVITY; SKELETAL-MUSCLE; TOLERANCE; MELLITUS; MEN; INTOLERANCE; TRANSPORT; MORTALITY AB The well-characterized decline in glucose tolerance during aping is due primarily to impaired insulin-mediated glucose uptake in peripheral tissues. Elderly persons with reduced insulin sensitivity are predisposed to the development of noninsulin-dependent diabetes mellitus (NIDDM), which is common in the geriatric population. Numerous studies suggest that exercise and physical training increase insulin sensitivity in young adult and middle-aged nondiabetics, older subjects with impaired glucose tolerance, and middle-aged persons with NIDDM. These investigations provide presumptive evidence that elderly persons with NIDDM may benefit from exercise training, although no published studies have specifically addressed the effects of exercise in older diabetics. Physical activity may also be effective in preventing the development of NIDDM. In addition, exercise training improves several cardiovascular risk factors, such as plasma lipid abnormalities, hypertension, and obesity. The risks of exercise in older diabetics include hypoglycemia in insulin-treated patients, exacerbation of preexisting cardiovascular disease, and worsening of long-term diabetic complications. Any exercise prescription in the older diabetic must be individualized to the patient's physical capabilities, limitations, and preferences. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV FLORIDA,COLL MED,DEPT MED,GAINESVILLE,FL. UNIV FLORIDA,COLL MED,DEPT PHARMACOL,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT EXERCISE SCI,GAINESVILLE,FL. VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,GAINESVILLE,FL 32608. RP KATZ, MS (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 32 TC 9 Z9 9 U1 0 U2 2 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 MAY PY 1994 VL 87 IS 5 BP S70 EP S73 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA NL879 UT WOS:A1994NL87900016 PM 8178206 ER PT J AU HENSLER, JG FERRY, RC LABOW, DM KOVACHICH, GB FRAZER, A AF HENSLER, JG FERRY, RC LABOW, DM KOVACHICH, GB FRAZER, A TI QUANTITATIVE AUTORADIOGRAPHY OF THE SEROTONIN TRANSPORTER TO ASSESS THE DISTRIBUTION OF SEROTONERGIC PROJECTIONS FROM THE DORSAL RAPHE NUCLEUS SO SYNAPSE LA English DT Article DE H-3 CYANOIMIPRAMINE; PARA-CHLOROAMPHETAMINE; 5,7-DIHYDROXYTRYPTAMINE; 5-HT1A RECEPTORS ID OBSESSIVE-COMPULSIVE DISORDER; RAT-BRAIN; MIDBRAIN RAPHE; BINDING-SITES; ASCENDING PROJECTIONS; UPTAKE INHIBITORS; EXTRACELLULAR 5-HYDROXYTRYPTAMINE; DIFFERENTIAL PROJECTIONS; FILM AUTORADIOGRAPHY; CEREBRAL-CORTEX AB The binding of H-3-CN-IMI to 5-HT uptake sites, as measured by quantitative autoradiography, was used as a marker of serotonergic neurons. Within the dorsal raphe nucleus the binding of H-3-CN-IMI was compared in adjacent coronal sections of rat brain to the binding of H-3-DPAT to 5-HT1A receptors, which have a known somatodendritic localization. The heterogeneous pattern of binding of these two radioligands within the dorsal raphe nucleus was similar and corresponded to the distribution of serotonergic cell bodies as visualized by 5-HT immunohistochemistry. Intracerebroventricular administration of 5,7-dihydroxytryptamine (5,7-DHT), which caused a dramatic loss of 5-HT immunoreactivity and H-3-DPAT binding to 5-HT1A receptors, resulted in a marked reduction of H-3-CN-IMI binding in this nucleus. Treatment of rats with a dose of parachloroamphetamine (PCA) which has been reported to selectively lesion serotonergic processes arising from the dorsal raphe nucleus, while sparing serotonergic cell bodies and projections from the median raphe nucleus, did not alter the binding of H-3-DPAT or H-3-CN-IMI in the dorsal raphe nucleus; serotonergic cell bodies appeared morphologically unaffected. The lack of effect of PCA treatment on the binding of H-3-DPAT and H-3-CN-IMI is consistent with a somatodendritic localization of the 5-HT transporter in the dorsal raphe nucleus. PCA treatment appeared to produce a moderate loss of serotonergic innervation in serotonergic terminal field areas as visualized by serotonin immunohistochemistry. The reductions in H-3-CN-IMI binding observed in terminal field areas (24 to 69%) following treatment of rats with PCA did not reflect a marked differential innervation of forebrain areas by the dorsal and medial raphe nuclei as expected from previous biochemical studies, and were not entirely consistent with the findings of neuroanatomical studies using histochemical techniques. Site-specific injection of 5,7-DHT into the dorsal raphe nucleus produced an 80 +/- 11% reduction in the binding of H-3-CN-IMI in this nucleus, whereas the binding of H-3-CN-IMI in the median raphe nucleus was not reduced. The reductions in H-3-CN-IMI binding measured in the caudate putamen, frontal and entorhinal cortex as a result of specific lesion of the dorsal raphe nucleus were suggestive of a heavy innervation of these areas by the dorsal raphe nucleus as indicated in neuroanatomical studies. In the hippocampus, our data were consistent with an over-lapping innervation of these areas by both the dorsal and median raphe nuclei and are not reflective of predominant innervation by the medial raphe nucleus. (C) 1994 Wiley-Liss, Inc. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. FU NIMH NIH HHS [MH48125, MH14654] NR 64 TC 88 Z9 88 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 0887-4476 J9 SYNAPSE JI Synapse PD MAY PY 1994 VL 17 IS 1 BP 1 EP 15 DI 10.1002/syn.890170102 PG 15 WC Neurosciences SC Neurosciences & Neurology GA NG540 UT WOS:A1994NG54000001 PM 8042142 ER PT J AU VINTERS, HV SECOR, DL READ, SL FRAZEE, JG TOMIYASU, U STANLEY, TM FERREIRO, JA AKERS, MA AF VINTERS, HV SECOR, DL READ, SL FRAZEE, JG TOMIYASU, U STANLEY, TM FERREIRO, JA AKERS, MA TI MICROVASCULATURE IN BRAIN BIOPSY SPECIMENS FROM PATIENTS WITH ALZHEIMERS-DISEASE - AN IMMUNOHISTOCHEMICAL AND ULTRASTRUCTURAL-STUDY SO ULTRASTRUCTURAL PATHOLOGY LA English DT Article DE ALZHEIMERS DISEASE; AMYLOID ANGIOPATHY; BLOOD-BRAIN BARRIER; BRAIN BIOPSY; CEREBRAL MICROVASCULATURE ID CEREBRAL AMYLOID ANGIOPATHY; BETA-PROTEIN PRECURSOR; PLAQUE CORE PROTEIN; NEURITIC PLAQUES; SENILE PLAQUES; GAMMA-TRACE; DUTCH TYPE; DEMENTIA; PEPTIDE; HEMORRHAGE AB Brain biopsy specimens from five patients with Alzheimer's disease obtained in the course of a trial of intracerebroventricular bethanechol were studied by immunohistochemical (antibody to A, peptide) and ultrastructural techniques, with particular emphasis on the microvessels. In some cases, numbers of A(4)-immunoreactive lesions (senile plaques) correlated well with numbers of plaques demonstrable by silver stains. Prominent A(4)-immunoreactive amyloid angiopathy was seen in one patient. The patient with severe cerebral amyloid angiopathy (CAA) showed extensive arteriolar deposition of amyloid filaments with apparent destruction of the media but remarkably intact endothelium. A cell of origin for amyloid filaments was not apparent, although close proximity to smooth muscle cell remnants in the arteriolar media suggested this as one possible cell of origin. Frequent vessels showed medial or adventitial collagen deposition, even when the amount of amyloid was minimal or negligible. Thus relatively severe CAA can exist in the absence of overt endothelial injury, although related studies on this tissue indicate definite abnormalities of the blood-brain barrier. Conversely, destruction of smooth muscle cells and collagen deposition in vessel walls may be the cellular correlates of arteriolar weakening that can lead to CAA-related brain hemorrhage. C1 UNIV CALIF LOS ANGELES,MED CTR,BRAIN RES INST,LOS ANGELES,CA 90024. JOHN DOUGLAS FRENCH CTR,LOS ALAMITOS,CA. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP VINTERS, HV (reprint author), UNIV CALIF LOS ANGELES,MED CTR,DEPT PATHOL & LAB MED,CHS 18-170,LOS ANGELES,CA 90024, USA. FU NIA NIH HHS [AG 10123]; NINDS NIH HHS [R29 NS 26312] NR 74 TC 98 Z9 98 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0191-3123 J9 ULTRASTRUCT PATHOL JI Ultrastruct. Pathol. PD MAY-JUN PY 1994 VL 18 IS 3 BP 333 EP 348 PG 16 WC Microscopy; Pathology SC Microscopy; Pathology GA NL204 UT WOS:A1994NL20400003 PM 8066824 ER PT J AU HARRIS, HW ZEIDEL, ML JO, IH HAMMOND, TG AF HARRIS, HW ZEIDEL, ML JO, IH HAMMOND, TG TI CHARACTERIZATION OF PURIFIED ENDOSOMES CONTAINING THE ANTIDIURETIC HORMONE-SENSITIVE WATER CHANNEL FROM RAT RENAL PAPILLA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INTEGRAL MEMBRANE-PROTEIN; STIMULATED TOAD BLADDER; DUCT PRINCIPAL CELLS; COLLECTING DUCT; PERMEABILITY RESPONSE; ENDOCYTIC VESICLES; CHIP28 PROTEIN; COATED PITS; PROTON; CONTAIN AB Antidiuretic hormone (ADH) stimulation of renal epithelial cells elicits a large increase in apical membrane osmotic water permeability (P-f) produced by the fusion of water channel containing vesicles with the apical membrane. Removal of ADH stimulation results in retrieval of apical water channels into a specialized nonacidic endosomal compartment. Previous studies (Sabolic, I., Wuarin, E., and Shi, L, B. (1992) J. Cell Biol. 119, 111-122) have shown that water channel containing papillary endosomes labeled with fluorescein-dextran can be isolated from rat renal papilla. We have utilized small particle flow sorting methodology to both monitor and improve upon the purification of these water channel containing endosomes (WCV). Flow cytometry analysis on a vesicle-by-vesicle basis demonstrates that WCV are homogenous with respect to entrapped fluorescein-dextran, the apical membrane enzyme marker leucine amino peptidase and ultrastructural morphology. WCV do not acidify their luminal contents after addition of Mg-ATP but contain abundant functional water channels (P-f 0.28 cm/s at 23 degrees C) as determined by stopped flow fluorimetry. SDS-polyacrylamide gel electrophoresis analysis shows that purified WCV are composed of 20 major protein bands. To determine the identity of WCV water channels, WCV proteins were probed with affinity purified antisera recognizing two renal water channel proteins. These include Aquaporin-CHIP found in the proximal tubule and thin descending limb of Henle and the candidate ADH water channel protein WCH-1 or Aquaporin- (AQP) CD present in the ADH-responsive epithelial cells of the collecting duct. These data reveal that WCV contained little or no AQP-CHIP protein. In contrast, WCV are highly enriched for AQP-CD protein. Together, these data define the protein composition of the papillary WCV and link directly the presence of functional apical membrane water channels with the presence of the AQP-CD protein. C1 BROCKTON W ROXBURY VET ADM MED CTR,DIV NEPHROL,BOSTON,MA 02115. UNIV PITTSBURGH,SCH MED,DIV RENAL & ELECTROLYTE,PITTSBURGH,PA 15213. UNIV WISCONSIN HOSP & CLIN,WILLIAM S MIDDLETON MEM VET ADM HOSP,MADISON,WI 53792. RP HARRIS, HW (reprint author), CHILDRENS HOSP,DIV NEPHROL,HUNNEWELL 3,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK 46117, DK 43955, DK 38874] NR 48 TC 45 Z9 45 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 APR 22 PY 1994 VL 269 IS 16 BP 11993 EP 12000 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NG377 UT WOS:A1994NG37700051 PM 8163502 ER PT J AU STEELE, RM SCHUNA, AA SCHREIBER, RT AF STEELE, RM SCHUNA, AA SCHREIBER, RT TI CALCIUM ANTAGONIST-INDUCED GINGIVAL HYPERPLASIA SO ANNALS OF INTERNAL MEDICINE LA English DT Note ID NIFEDIPINE; OVERGROWTH C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP STEELE, RM (reprint author), COOK CTY HOSP,DEPT PHARM,1900 W POLK,SUITE 552,CHICAGO,IL 60612, USA. NR 10 TC 32 Z9 34 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 APR 15 PY 1994 VL 120 IS 8 BP 663 EP 664 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NE850 UT WOS:A1994NE85000006 PM 8135450 ER PT J AU SANZ, I WANG, SS MENESES, G FISCHBACH, M AF SANZ, I WANG, SS MENESES, G FISCHBACH, M TI MOLECULAR CHARACTERIZATION OF HUMAN IG HEAVY-CHAIN DIR GENES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID X-LINKED AGAMMAGLOBULINEMIA; B-CELL DEVELOPMENT; D-MU PROTEIN; DIVERSITY; SEGMENT; RECOMBINATION; REARRANGEMENT; AUTOANTIBODIES; SEQUENCE; VH AB Antibody VDJ recombination is ensured by evolutionarily conserved recombination signals (RS). The 12/23 rule postulates that only gene segments with asymmetrically spaced RS recombine with one another. Two unusually long D genes (170 bp) with irregular RS (DIR) have been reported in humans and have been postulated to participate actively in VDJ recombination, thus frequently contributing to the Ab heavy chain third hypervariable region (CDR3). However, the limited sequence information retained in the CDR3 along with significant sequence diversity has precluded an accurate assessment of the actual role and genomic diversity of DIR genes. Furthermore, DIR genes pose an interesting puzzle in terms of their precise mechanism of recombination because they possess multiple and imperfect RS, often located up to 30 bp away from the recombining fragment within the DIR coding region. Here we present conclusive evidence for the existence of additional human germ-line DIR genes and preliminary evidence that suggests the absence of DIR-like sequences in nonprimate animals. We also show that DIR genes are under the transcriptional control of V-H-independent promoters and have the potential to encode a D mu protein of 105 amino acids. Finally, DIR genes seem at least in early fetal life to recombine preferentially through the conventional 3' RS. C1 UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP SANZ, I (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [AI-29003] NR 27 TC 31 Z9 31 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 1994 VL 152 IS 8 BP 3958 EP 3969 PG 12 WC Immunology SC Immunology GA NF018 UT WOS:A1994NF01800027 PM 8144963 ER PT J AU SCHECHTER, NM WANG, ZM BLACHER, RW LESSIN, SR LAZARUS, GS RUBIN, H AF SCHECHTER, NM WANG, ZM BLACHER, RW LESSIN, SR LAZARUS, GS RUBIN, H TI DETERMINATION OF THE PRIMARY STRUCTURES OF HUMAN SKIN CHYMASE AND CATHEPSIN-G FROM CUTANEOUS MAST-CELLS OF URTICARIA PIGMENTOSA LESIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NEUTROPHIL ELASTASE GENE; AMINO-ACID-SEQUENCE; MOLECULAR-CLONING; SERINE PROTEASE; NUCLEOTIDE-SEQUENCE; ANGIOTENSIN-II; HUMAN HEART; MCTC TYPE; HUMAN-T; MOUSE AB This study establishes the primary structure of human skin chymase and provides further evidence for the presence of a cathepsin G-like proteinase within human mast cells. The amino acid sequence of human skin chymase was established by protein methods and by analysis of PCR amplification products obtained with cDNA-derived from urticaria pigmentosa (UP) lesions. UP is a disease characterized by skin lesions containing high numbers of mast cells. Proteolytic digests of human chymase purified from normal skin yielded 10 resolvable peptides that were sequenced by automated Edman degradation. The amino acid sequences for these peptides combined with the sequence obtained for the protein's NH2-terminal region (35 residues) accounted for 137 residues of the human skin chymase sequence. This partial amino acid sequence corresponded to the sequence of human heart chymase, a proteinase isolated from heart tissue with immunologic and hydrolytic properties similar to skin chymase. PCR amplification of UP-derived cDNA with primers based on the cDNA structure of heart chymase demonstrated a single amplification product of expected size which was subcloned and sequenced. The amino acid sequence (135 residues) deduced from this product was identical to that of heart chymase in the region between the primers. This sequence, along with that established for the purified protein, constituted 99% of the heart chymase primary structure, strongly indicating that human skin and heart chymases have identical primary structures. Amplification of the same UP-cDNA with primers coding for the NH2- and COOH-terminal sequences of human neutrophil cathepsin G also produced a specific amplification product which was sequenced. The deduced amino acid sequence between the primers was identical to that reported for neutrophil cathepsin G, indicating that the protein of cutaneous mast cells previously shown to be immunologically cross-reactive with neutrophil cathepsin G has a comparable amino acid sequence. UP-cDNA demonstrating amplification products for cathepsin G did not demonstrate amplification products for human neutrophil elastase, suggesting that the cathepsin G PCR amplification product was not derived from neutrophils or monocytes possibly contaminating the lesion. These studies provide further evidence that human skin mast cells contain two different chymotrypsin-like proteinases. C1 UNIV PENN,DEPT BIOCHEM & BIOPHYS,PHILADELPHIA,PA 19104. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. ATHENA NEUROSCI INC,S SAN FRANCISCO,CA 94080. RP SCHECHTER, NM (reprint author), UNIV PENN,DEPT DERMATOL,CLIN RES BLDG,422 CURIE BLVD,PHILADELPHIA,PA 19104, USA. FU NCI NIH HHS [CA55071]; NIAMS NIH HHS [AR39647] NR 43 TC 30 Z9 33 U1 1 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 APR 15 PY 1994 VL 152 IS 8 BP 4062 EP 4069 PG 8 WC Immunology SC Immunology GA NF018 UT WOS:A1994NF01800038 PM 8144971 ER PT J AU MCENTEE, CM CANTWELLIBDAH, R HUDSON, AP AF MCENTEE, CM CANTWELLIBDAH, R HUDSON, AP TI REGULATION OF STRINGENT MITOCHONDRIAL TRANSCRIPTION IN YEAST FOLLOWING AMINO-ACID DEPRIVATION SO GENE LA English DT Note DE STARVATION; CYCLIC AMP; RNA; SACCHAROMYCES CEREVISIAE; PROTEIN KINASE ID DEPENDENT PROTEIN-KINASE; SACCHAROMYCES-CEREVISIAE; RNA-POLYMERASE; GENE; PHOSPHODIESTERASE; SUBUNIT; CLONING AB In the yeast Saccharomyces cerevisiae, a phenotypically identical stringent response is induced by either nutritional downshift or starvation for a required auxotrophic amino acid (aa); in each case, the response selectively includes transcriptional curtailment for the mitochondrial (mt) genome. We have shown previously that the downshift-induced mt stringent response is governed by changing cellular cyclic AMP (cAMP) levels, via a mt cAMP-dependent protein kinase. In contrast, we demonstrate here that cAMP levels are not altered in yeast following starvation for a required aa, and we use in vitro mt transcription assays with organelles from wild-type and mutant strains to confirm that the aa starvation-induced mt stringent response is not governed by cAMP. Rather, such stringent organellar transcriptional attenuation may result from altered availability of an unidentified small molecule which is probably a product of the cytoplasmic and/or mt protein synthesis systems. C1 DEPT VET AFFAIRS MED CTR,RES SERV,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. NR 19 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD APR 8 PY 1994 VL 141 IS 1 BP 129 EP 132 DI 10.1016/0378-1119(94)90140-6 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA NG425 UT WOS:A1994NG42500021 PM 8163164 ER PT J AU ALASSI, MT GENTA, RM GRAHAM, DY AF ALASSI, MT GENTA, RM GRAHAM, DY TI OMEPRAZOLE-TETRACYCLINE COMBINATIONS ARE INADEQUATE AS THERAPY FOR HELICOBACTER-PYLORI INFECTION SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Note ID CAMPYLOBACTER-PYLORI; DUODENAL-ULCER; ERADICATION; SUSCEPTIBILITY; LANSOPRAZOLE; AMOXICILLIN; GASTRITIS AB Background: Current triple antimicrobial therapies cure Helicobacter pylori infection in 60-90% of cases but are cumbersome. Addition of omeprazole to amoxycillin has been shown to enhance effectiveness when compared to amoxycillin alone. Method: We studied omeprazole 20 mg t.d.s. plus tetracycline 500 mg q.d.s. for 14 days (OMP/TCN) and omeprazole 40 mg in the morning plus tetracycline 500 mg q.d.s. along with bismuth subsalicylate tablets 2 q.d.s. (OMP/TCN/BSS) for 14 days. Forty-four patients (19 OMP/TCN, 25 OMP/TCN/BSS) with H. pylori peptic ulcer disease were studied. H. pylori status was evaluated at least 4 weeks after ending antimicrobial therapy. Results: In the OMP/TCN group cure of H. pylori infection was achieved in 5/19 (26%). Adding bismuth to the regimen improved the results; 4 weeks after ending therapy cure of H. pylori infection was achieved in 12/25 (48%). Conclusions: Neither regimen can be recommended for routine cure of H. pylori infection. Although one cannot predict which antimicrobial therapies will be enhanced by the addition of omeprazole, these data suggest that future studies should evaluate drugs whose effectiveness is compromised by low pH. C1 VET AFFAIRS MED CTR 111D,DEPT MED,HOUSTON,TX 77030. VET AFFAIRS MED CTR,DEPT PATHOL,HOUSTON,TX. VET AFFAIRS MED CTR,DIV MOLEC VIROL,HOUSTON,TX. BAYLOR COLL MED,HOUSTON,TX. NR 36 TC 19 Z9 19 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-2813 J9 ALIMENT PHARM THERAP JI Aliment. Pharmacol. Ther. PD APR PY 1994 VL 8 IS 2 BP 259 EP 262 PG 4 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA NH776 UT WOS:A1994NH77600015 PM 8038358 ER PT J AU BELL, NH HOLLIS, BW SHARY, JR EYRE, DR EASTELL, R COLWELL, A RUSSELL, RGG AF BELL, NH HOLLIS, BW SHARY, JR EYRE, DR EASTELL, R COLWELL, A RUSSELL, RGG TI DICLOFENAC SODIUM INHIBITS BONE-RESORPTION IN POSTMENOPAUSAL WOMEN SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; PROSTAGLANDIN PRODUCTION; OSTEOCLASTS; COLLAGEN; ESTROGEN; RATS; 1,25-DIHYDROXYVITAMIN-D; QUANTITATION; CROSSLINKS; CALCITONIN AB Background: The results of experimental studies with animals indicated that prostaglandins stimulate bone resorption, that skeletal production of prostaglandin E, is enhanced by ovariectomy and is diminished by 17 beta-estradiol, and that the nonsteroidal anti-inflammatory drug (NSAID) naproxyn prevents bone loss after ovariectomy. Studies were carried out to investigate the effects of the NSAID diclofenac sodium on bone and mineral metabolism in premenopausal women and to compare the effects of diclofenac sodium and conjugated estrogens on bone and mineral metabolism in postmenopausal women. Patients and methods: Ten healthy premenopausal women and 17 healthy postmenopausal women were studied while not being treated and again after 4 weeks of treatment with diclofenac sodium, 150 mg per day in divided doses (both groups), and conjugated estrogens, 0.625 mg per day (postmenopausal women). Cross-linked N-telopeptides of type I collagen were measured in the urine as an index of bone resorption. The postmenopausal women were separated into two groups, responders and nonresponders, based on their response to conjugated estrogens as assessed by linear discriminant analysis for groups. Conjugated estrogens lowered urinary N-telopeptides of type I collagen in responders, but not in nonresponders. Results: Urinary cross-linked N-telopeptides were higher in the eight postmenopausal women responders than in the nine postmenopausal nonresponders or in the premenopausal women, and were not altered by diclofenac sodium in premenopausal women. In the eight postmenopausal women with higher rates of bone resorption, diclofenac sodium and conjugated estrogens significantly lowered both urinary calcium concentration and urinary cross-linked N-telopeptides. The effects of the two drugs were comparable. Conclusion: The preliminary results demonstrate that, at the dose used, diclofenac sodium is almost as effective as conjugated estrogens for decreasing bone loss in postmenopausal women. Further studies will be needed to determine whether diclofenac sodium can prevent postmenopausal bone loss. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. UNIV WASHINGTON,DEPT ORTHOPED,SEATTLE,WA 98195. UNIV SHEFFIELD,SCH MED,DEPT HUMAN METAB & CLIN BIOCHEM,SHEFFIELD S10 2UL,ENGLAND. NO GEN HOSP,CTR CLIN SCI,SHEFFIELD,S YORKSHIRE,ENGLAND. RP BELL, NH (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. RI Eastell, Richard/G-5851-2011 OI Eastell, Richard/0000-0002-0323-3366 FU NCRR NIH HHS [M01 RR 01070]; NIAMS NIH HHS [R37 AR037318, AR 36066, R01 AR036794] NR 26 TC 34 Z9 35 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 APR PY 1994 VL 96 IS 4 BP 349 EP 353 DI 10.1016/0002-9343(94)90065-5 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA NG901 UT WOS:A1994NG90100009 PM 8166154 ER PT J AU KLEYMAN, TR SMITH, PR BENOS, DJ AF KLEYMAN, TR SMITH, PR BENOS, DJ TI CHARACTERIZATION AND LOCALIZATION OF EPITHELIAL NA+ CHANNELS IN TOAD URINARY-BLADDER SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE TBM CELLS; AMILORIDE; 2'-METHOXY-5'-NITROBENZAMIL; BENZAMIL; BROMOBENZAMIL; ANTI-SODIUM CHANNEL ANTIBODY ID ANTI-AMILORIDE ANTIBODIES; SODIUM-CHANNEL; PROTEIN; TRANSPORT; BINDING; PNEUMOCYTES; ANALOGS; SUBUNIT; KIDNEY; CELLS AB The toad urinary bladder and epithelial cell lines derived from the urinary bladder, including TBM, serve as model systems for the study of transepithelial Na+ transport. We examined biochemical characteristics of epithelial Na+ channels in toad urinary bladder and TBM cells and their cellular localization in the urinary bladder. The radiolabeled amiloride analogue [H-3]benzamil bound to a single class of high-affinity binding sites in membrane vesicles from toad urinary bladder with a dissociation constant (K-d) Of 10 nM. Photoactive benzamil analogues specifically labeled a 135,000-Da polypeptide in toad urinary bladder and TBM cells. A monoclonal anti-Na+ channel antibody directed against the amiloride-binding component of the channel specifically recognized a 135,000-Da polypeptide in TBM cells. Polyclonal anti-Na+ channel antibodies generated against purified bovine epithelial Na+ channel specifically recognized a 235,000-Da polypeptide in toad urinary bladder and localized Na+ channels to the apical plasma membrane of urinary bladder epithelial cells. The biochemical characteristics and the cellular localization of epithelial Na+ channels in toad urinary bladder are similar to those previously described in mammalian kidney and in the A6 cell line. C1 UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. UNIV ALABAMA,DEPT PHYSIOL & BIOPHYS,BIRMINGHAM,AL 35294. RP KLEYMAN, TR (reprint author), DEPT VET AFFAIRS MED CTR,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 31 TC 15 Z9 15 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP C1105 EP C1111 PN 1 PG 7 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400025 ER PT J AU KEMNITZ, JW ROECKER, EB WEINDRUCH, R ELSON, DF BAUM, ST BERGMAN, RN AF KEMNITZ, JW ROECKER, EB WEINDRUCH, R ELSON, DF BAUM, ST BERGMAN, RN TI DIETARY RESTRICTION INCREASES INSULIN SENSITIVITY AND LOWERS BLOOD-GLUCOSE IN RHESUS-MONKEYS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE AGING; MINIMAL MODEL; ADIPOSITY ID FOOD RESTRICTION; FAT DISTRIBUTION; MINIMAL-MODEL; AGE; RESISTANCE; TOLERANCE; OBESITY; HYPOTHESIS; DISEASE AB Insulin sensitivity and glucose tolerance typically decline during later life. In a multidimensional randomized trial of the effects of dietary restriction started in adulthood on the processes of aging, we are studying insulin sensitivity and glucoregulation longitudinally in control (C, n = 15, fed a defined diet ad libitum for 6-8 h/day) and restricted (R, n = 15, fed 30% less than C) monkeys using the Modified Minimal Model method. Linear rates of change were calculated for individual animals through 30 mo of diet treatment and compared between treatment groups. Basal glucose, basal insulin, and insulin responses to glucose and tolbutamide increased for C and decreased for R animals (P less than or equal to 0.002), whereas insulin sensitivity decreased for C and increased for R (P = 0.008). Glycosylated hemoglobin at 30 mo was marginally lower in R (P = 0.06) and was positively correlated with fasting plasma glucose (r = 0.508, P < 0.001). Insulin changes were significantly correlated with changes in adiposity (weight and abdominal circumference). Identification of the mechanisms through which these effects are achieved may aid in ameliorating glucose intolerance, insulin resistance, and associated illnesses in older persons. C1 UNIV WISCONSIN,WISCONSIN REG PRIMATE RES CTR,DEPT BIOSTAT,MADISON,WI 53715. WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI 53705. UNIV SO CALIF,SCH MED,DEPT PHYSIOL & BIOPHYS,LOS ANGELES,CA 90033. RP KEMNITZ, JW (reprint author), UNIV WISCONSIN,WISCONSIN REG PRIMATE RES CTR,DEPT MED,1223 CAPITOL COURT,MADISON,WI 53715, USA. FU NIA NIH HHS [AG-00213, AG-07831]; NIDDK NIH HHS [DK-29867] NR 34 TC 170 Z9 173 U1 1 U2 4 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP E540 EP E547 PN 1 PG 8 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400032 PM 8178974 ER PT J AU EMMONS, C STOKES, JB AF EMMONS, C STOKES, JB TI CELLULAR ACTIONS OF CAMP ON HCO(3)(-)SECRETING CELLS OF RABBIT CCD - DEPENDENCE ON IN-VIVO ACID-BASE STATUS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE; INTERCALATED CELLS; ALKALOSIS; CORTICAL COLLECTING DUCT; SODIUM-DEPENDENT CHLORIDE, BICARBONATE ION EXCHANGE ID CORTICAL COLLECTING TUBULES; INTERCALATED CELLS; INTRACELLULAR PH; BICARBONATE TRANSPORT; H+-ATPASE; ALKALI LOADS; DUCT; SECRETION; EXCHANGE; BAND-3 AB HCO3- secretion by cortical collecting duct (CCD) occurs via beta-intercalated cells. In vitro CCD HCO3- secretion is modulated by both the in vivo acid-base status of the animal and by adenosine 3',5'-cyclic monophosphate (cAMP). To investigate the mechanism of cAMP-induced HCO3- secretion, we measured intracellular pH (pH(i)) of individual beta-intercalated cells of CCDs dissected from alkali-loaded rabbits perfused in vitro. beta-Intercalated cells were identified by demonstrating the presence of an apical anion exchanger (cell alkalinization in response to removal of lumen Cl-). After 180 min of perfusion to permit decrease of endogenous cAMP, acute addition of 0.1 mM 8-bromo-cAMP or 1 mu M isoproterenol to the bath caused a transient cellular alkalinization (> 0.20 pH units). In the symmetrical absence of either Na+, HCO3-, or Cl-, cAMP produced no change in pH(i). Basolateral dihydrogen 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) for 15 min before cAMP addition also prevented this alkalinization. In contrast to the response of cells from alkali-loaded rabbits, addition of basolateral cAMP to CCDs dissected from normal rabbits resulted in an acidification of beta-intercalated cells (similar to 0.20 pH units). The present studies demonstrate the importance of the in vivo acid-base status of the animal in the regulation of CCD HCO3- secretion by beta-intercalated cells. The results identify the possible existence of a previously unrecognized Na+-dependent Cl-/HCO3- exchanger on the basolateral membrane of beta-intercalated cells in alkali-loaded rabbits. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,DIV NEPHROL,LOS ANGELES,CA 90024. UNIV IOWA,DEPT INTERNAL MED,EPITHELIAL TRANSPORT LAB,IOWA CITY,IA 52242. VET AFFAIRS MED CTR,IOWA CITY,IA 52242. RP EMMONS, C (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DIV NEPHROL,10833 LECONTE AVE,FACTOR 7-155,LOS ANGELES,CA 90024, USA. FU NIDDK NIH HHS [DK-25231] NR 32 TC 13 Z9 13 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP F528 EP F535 PN 2 PG 8 WC Physiology SC Physiology GA NJ996 UT WOS:A1994NJ99600098 PM 8184884 ER PT J AU ANZUETO, A SUPINSKI, GS LEVINE, SM JENKINSON, SG AF ANZUETO, A SUPINSKI, GS LEVINE, SM JENKINSON, SG TI MECHANISMS OF DISEASE - ARE OXYGEN-DERIVED FREE-RADICALS INVOLVED IN DIAPHRAGMATIC DYSFUNCTION SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Editorial Material ID VITAMIN-E; LIPID-PEROXIDATION; SKELETAL-MUSCLE; SUPEROXIDE-DISMUTASE; N-ACETYLCYSTEINE; REACTIVE OXYGEN; EXERCISE; FATIGUE; RATS; METABOLISM C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. METROHLTH MED CTR,CLEVELAND,OH. RP ANZUETO, A (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 40 TC 36 Z9 36 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD APR PY 1994 VL 149 IS 4 BP 1048 EP 1052 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NP836 UT WOS:A1994NP83600033 PM 8143041 ER PT J AU HOGAN, Q DOTSON, R ERICKSON, S KETTLER, R HOGAN, K AF HOGAN, Q DOTSON, R ERICKSON, S KETTLER, R HOGAN, K TI LOCAL-ANESTHETIC MYOTOXICITY - A CASE AND REVIEW SO ANESTHESIOLOGY LA English DT Note DE ANESTHETICS, LOCAL, BUPIVACAINE; ANESTHETICS, LOCAL, MYOTOXICITY; MUSCLE, SKELETAL, LOCAL ANESTHETIC TOXICITY; TOXICITY, LOCAL ANESTHETICS ID FROG SKELETAL-MUSCLE; CALCIUM RELEASE; SARCOPLASMIC-RETICULUM; REGENERATION; FIBERS; RHABDOMYOLYSIS; DEGENERATION; INJECTIONS; TETRACAINE; MARCAINE C1 MED COLL WISCONSIN,DEPT NEUROL,MILWAUKEE,WI 53226. MED COLL WISCONSIN,DEPT RADIOL,MILWAUKEE,WI 53226. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT ANESTHESIOL,MADISON,WI. UNIV WISCONSIN,MADISON,WI. RP HOGAN, Q (reprint author), MED COLL WISCONSIN,MILWAUKEE CTY MED COMPLEX,DEPT ANESTHESIOL,8700 W WISCONSIN AVE,MILWAUKEE,WI 53226, USA. NR 48 TC 76 Z9 77 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 1994 VL 80 IS 4 BP 942 EP 947 DI 10.1097/00000542-199404000-00029 PG 6 WC Anesthesiology SC Anesthesiology GA NG521 UT WOS:A1994NG52100029 PM 8024149 ER PT J AU REYNOLDS, PP AF REYNOLDS, PP TI REAFFIRMING PROFESSIONALISM THROUGH THE EDUCATION COMMUNITY SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material ID INTERNAL MEDICINE; RESIDENT; IMPACT; AIDS; TIME AB Objective: To determine the role of the clinical training environment and a medical education community in reaffirming medical professionalism among physicians-in-training and faculty. Data sources: Published articles on undergraduate and graduate medical education and sociology works on professionalism were identified through research. Study selection: Studies were selected that illustrated barriers to professionalism in medical education and patient care and the professional conduct of medical students, residents, and faculty. Results: Factors that undermined the medical education community were the specialization of medicine, the faculty reward systems, and the service demands of residency because of the economics of health care. Conclusions: Establishment of a firm system with a core teaching faculty, creation of mentoring and role modeling programs, implementation of a longitudinal curriculum on medical professionalism, evaluation of physicians on professional conduct, and evaluation of the clinical training environment are suggested as strategies to re-establish an education community and reaffirm professionalism in medicine. C1 VET AFFAIRS MED CTR, PHILADELPHIA, PA 19104 USA. RP REYNOLDS, PP (reprint author), UNIV PENN, SCH MED, ROBERT WOOD JOHNSON FDN, CLIN SCHOLARS PROGRAM, 3615 CHESTNUT ST, PHILADELPHIA, PA 19104 USA. NR 47 TC 80 Z9 80 U1 0 U2 3 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 EI 1539-3704 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1994 VL 120 IS 7 BP 609 EP 614 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA NC764 UT WOS:A1994NC76400013 PM 8117001 ER PT J AU MARDER, SR WIRSHING, WC VANPUTTEN, T MINTZ, J MCKENZIE, J JOHNSTONCRONK, K LEBELL, M LIBERMAN, RP AF MARDER, SR WIRSHING, WC VANPUTTEN, T MINTZ, J MCKENZIE, J JOHNSTONCRONK, K LEBELL, M LIBERMAN, RP TI FLUPHENAZINE VS PLACEBO SUPPLEMENTATION FOR PRODROMAL SIGNS OF RELAPSE IN SCHIZOPHRENIA SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID INTERMITTENT; SYMPTOMS; TRIAL AB Background: We studied the effectiveness of treating patients with low doses of fluphenazine decanoate and supplementing them with oral fluphenazine when there was evidence of prodromal symptoms of psychotic exacerbations Methods: Eighty schizophrenic patients who were receiving 5 to 10 mg of fluphenazine decanoate every 2 weeks were monitored for prodromal symptoms using an idiosyncratic prodromal rating scale. When patients met our criteria for a prodromal episode, they were randomly assigned to a double-blind comparison of oral fluphenazine hydrochloride (5 mg twice daily) or a placebo for the current and future prodromal episodes. We compared rates of psychotic exacerbations in the two treatment groups. Results: Thirty-six patients (45%) met the criteria for a prodrome at some point during the trial and were randomized to drug or placebo. Using survival analysis during the entire 2 years, we did not find a significant difference between fluphenazine and placebo in the likelihood that a prodrome would continue to an exacerbation. Survival analysis beginning at the start of the second year of treatment did indicate a significant reduction in exacerbation risk for patients receiving drug supplementation (P=.032). Similarly, there was no difference between the two groups in the proportion of time at risk spent in exacerbation during the first year, but patients receiving active drug supplementation spent less time in an exacerbated state in the second year (P=.05). Conclusions: Our treatment strategy appeared to be effective for some patients, particularly those who were able to remain in the study beyond the first year. Although the occurrence of a prodrome was a fairly good marker that a patient was at high risk of ultimate exacerbation with our low-dose maintenance protocol, prodromes were not highly sensitive indicators of imminent exacerbation. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP MARDER, SR (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV 116A,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. FU NIMH NIH HHS [MH-41573, MH-30911] NR 20 TC 60 Z9 60 U1 8 U2 8 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 APR PY 1994 VL 51 IS 4 BP 280 EP 287 PG 8 WC Psychiatry SC Psychiatry GA NF265 UT WOS:A1994NF26500003 PM 8161288 ER PT J AU HISNANICK, J CODDINGTON, DA GERGEN, PJ AF HISNANICK, J CODDINGTON, DA GERGEN, PJ TI TRENDS IN ASTHMA-RELATED ADMISSIONS AMONG AMERICAN-INDIAN AND ALASKAN NATIVE CHILDREN FROM 1979 TO 1989 - UNIVERSAL HEALTH-CARE IN THE FACE OF POVERTY SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID ACUTE CHILDHOOD ASTHMA; LOW-BIRTH-WEIGHT; CHANGING PATTERNS; HOSPITALIZATION; PREVALENCE; MORTALITY; SMOKING; SEVERITY; ILLNESS; SERVICE AB Objective: To describe changes in asthma-related hospitalizations in Indian Health Service facilities and compare with national trends. Design: Trend analysis. Patients and Setting: Hospital discharge records of patients aged 17 years and younger treated by the Indian Health Service between 1979 and 1989. Main Outcome Measures: Patients discharged with asthma as the first listed diagnosis. Results: The rates of asthma-related hospitalizations increased an average of 2.6% (95% confidence interval [CI], 0.1 to 5.2) per year between 1979 and 1989 among American Indian and Alaskan Native children aged 0 to 17 years. The increase was 3.7% among the 0- to 4-year age group (95% CI, 2.0 to 5.5) and 0.3% (95% CI, 0.26 to 0.3) among the 5- to 17-year age group. Boys tended to have a higher rate of increase (4.3% [95% CI, -0.1 to 8.7]) compared with girls (2.6% [95% CI, -0.2 to 5.4]). The rates for any hospitalization decreased during this period for 0- to di-year-olds (-7.5% [95% CI, -10.5 to -4.5]). Little change was noted in hospitalization rates for lower respiratory tract diseases. Diagnostic transfer from bronchitis/bronchiolitis to asthma could not explain the increase. Both first admission and readmission for treatment of asthma contributed to the increase. Compared with previously published data, 0- to 4-year-old American Indian and Alaskan Native children more closely approximate white children than black children in both rates of hospitalization (1979-1987) and annual percentage increase in hospitalization (1979-1989 for American Indian and Alaskan Native children and 1979-1987 for white and black children) for the treatment of asthma. Conclusions: American Indian and Alaskan Native children who are cared for by the Indian Health Service have asthma-related hospitalization patterns that are similar to those seen in white children despite having socioeconomic characteristics more similar to those of black children. C1 INDIAN HLTH SERV,OFF HLTH PROGRAM,TUCSON,AZ. CHILDRENS NATL MED CTR,DEPT GEN PEDIAT,WASHINGTON,DC 20010. NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,BETHESDA,MD 20892. RP HISNANICK, J (reprint author), US DEPT VET AFFAIRS,NVCAS 008C12,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 44 TC 17 Z9 17 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 1994 VL 148 IS 4 BP 357 EP 363 PG 7 WC Pediatrics SC Pediatrics GA NF055 UT WOS:A1994NF05500003 PM 8148934 ER PT J AU ORSON, FM AF ORSON, FM TI PHOTODOCUMENTATION OF UV SHADOWING WITH DNA GELS SO BIOTECHNIQUES LA English DT Note ID TRANSCRIPTION; INHIBITION C1 BAYLOR COLL MED,DEPT INTERNAL MED,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,HOUSTON,TX 77030. NR 9 TC 2 Z9 2 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD APR PY 1994 VL 16 IS 4 BP 592 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NE764 UT WOS:A1994NE76400008 PM 8024774 ER PT J AU DURANTE, W SCHINI, VB KROLL, MH CATOVSKY, S SCOTTBURDEN, T WHITE, JG VANHOUTTE, PM SCHAFER, AI AF DURANTE, W SCHINI, VB KROLL, MH CATOVSKY, S SCOTTBURDEN, T WHITE, JG VANHOUTTE, PM SCHAFER, AI TI PLATELETS INHIBIT THE INDUCTION OF NITRIC-OXIDE SYNTHESIS BY INTERLEUKIN-1-BETA IN VASCULAR SMOOTH-MUSCLE CELLS SO BLOOD LA English DT Article ID MOLECULAR-WEIGHT COMPLEX; L-ARGININE; ENDOTHELIAL-CELLS; RELAXING FACTOR; GROWTH-FACTOR; SYNTHASE ACTIVITY; RELAXATION; VASODILATORS; AGGREGATION; EXPRESSION C1 HOUSTON VET AFFAIRS MED CTR,MED SERV,2002 HOLCOMBE BLVD,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MED & PHARMACOL,HOUSTON,TX 77030. BAYLOR COLL MED,CTR EXPTL THERAPEUT,HOUSTON,TX 77030. UNIV MINNESOTA,SCH MED,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT PEDIAT,MINNEAPOLIS,MN 55455. UNIV FREIBURG,DEPT APPL PHYSIOL,W-7800 FREIBURG,GERMANY. RI Vanhoutte, Paul/B-4533-2009 FU NHLBI NIH HHS [HL-46356, HL-31183, HL-36045] NR 42 TC 20 Z9 20 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1994 VL 83 IS 7 BP 1831 EP 1838 PG 8 WC Hematology SC Hematology GA NE411 UT WOS:A1994NE41100016 PM 8142651 ER PT J AU RANDOLPH, ET ETH, S GLYNN, SM PAZ, GG LEONG, GB SHANER, AL STRACHAN, A VANVORT, W ESCOBAR, JI LIBERMAN, RP AF RANDOLPH, ET ETH, S GLYNN, SM PAZ, GG LEONG, GB SHANER, AL STRACHAN, A VANVORT, W ESCOBAR, JI LIBERMAN, RP TI BEHAVIORAL FAMILY MANAGEMENT IN SCHIZOPHRENIA - OUTCOME OF A CLINIC-BASED INTERVENTION SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID CONTROLLED TRIAL; PREVENTION AB To test further the highly successful outcomes of a controlled study of in-home behavioural family management (BFM) for schizophrenic patients, a clinic-based version of this intervention was compared with customary care alone for 41 schizophrenic patients in a Veterans Administration (VA) mental health clinic. Monthly Brief Psychiatric Rating Scale (BPRS) ratings, conducted by clinic psychiatrists who were 'blind' to the patients' assignment, revealed that 3 (14%) patients who received behavioural family management as well as customary care, as compared with 11 (55%) patients who received customary care alone, had symptomatic exacerbations during the first year of treatment. C1 SANTA MONICA FAMILY CONSULTANTS,SANTA MONICA,CA 90405. UNIV CONNECTICUT,DEPT PSYCHIAT,FARMINGTON,CT 06107. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,CLIN RES CTR SCHIZOPHRENIA,LOS ANGELES,CA 90025. RP RANDOLPH, ET (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 19 TC 92 Z9 95 U1 1 U2 3 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD APR PY 1994 VL 164 BP 501 EP 506 DI 10.1192/bjp.164.4.501 PG 6 WC Psychiatry SC Psychiatry GA NF414 UT WOS:A1994NF41400013 PM 8038939 ER PT J AU RAGO, RP MILES, JM SUFIT, RL SPRIGGS, DR WILDING, G AF RAGO, RP MILES, JM SUFIT, RL SPRIGGS, DR WILDING, G TI SURAMIN-INDUCED WEAKNESS FROM HYPOPHOSPHATEMIA AND MITOCHONDRIAL MYOPATHY - ASSOCIATION OF SURAMIN WITH MITOCHONDRIAL TOXICITY IN HUMANS SO CANCER LA English DT Article DE SURAMIN; MITOCHONDRIAL MYOPATHY; HYPOPHOSPHATEMIA; FANCONIS SYNDROME; WEAKNESS; NEOPLASM ID CARCINOMA-CELLS; DISRUPTION; MECHANISM; THERAPY; DRUG AB Background. Suramin is an antiparasitic drug being evaluated as an antitumor compound. Suramin therapy commonly causes weakness and is known to cause neuropathy. Two potential causes of suramin-induced muscular weakness are described. Methods. Suramin was administered to 15 patients with advanced cancer as part of a Phase I study. Weekly dosing was adjusted to achieve mean plasma concentrations of 210 mug/ml. Results. Serum phosphate levels fell significantly (P < 0.0001) in all 15 patients on the 42nd day of treatment from a pretreatment average of 4.0 mg/dl (standard deviation [SD] +/- 0.37) to 3.0 mg/dl (SD +/- 0.20). Absolute hypophosphatemia developed in two patients with more prolonged suramin treatment due to Fanconi's syndrome. The patient who received the largest amount of suramin (19.2 g over 14 weeks) had severe proximal muscle weakness despite 6 weeks of effective phosphate repletion. A muscle biopsy was performed, which demonstrated markedly decreased cytochrome c oxidase activity by muscle histochemistry and biochemistry. Electron microscopy revealed subsarcolemmal collections of abnormal mitochondria. This mitochondrial myopathy resolved clinically 7 weeks after discontinuing suramin. Conclusions. This report indicates that suramin is associated with hypophosphatemia of Fanconi's syndrome and a mitochondrial myopathy. The clinical combination of mitochondrial myopathy and Fanconi's syndrome is similar to descriptions of congenital mitochondrial cytochrome c oxidase deficiency of de Toni-Fanconi-Debre syndrome. These findings in humans correlate with the authors' in vitro observations that suramin causes toxic mitochondrial changes, indicating a mechanism of suramin's toxicity and possibly its antitumor effect. C1 UNIV WISCONSIN,CTR COMPREHENS CANC,K4-666 CSC,600 HIGHLAND AVE,MADISON,WI 53792. UNIV WISCONSIN HOSP & CLIN,DEPT PATHOL,MADISON,WI. UNIV WISCONSIN HOSP & CLIN,DEPT NEUROL,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NCI NIH HHS [CA-50590, N01-CM-57735, T32-CA-09614] NR 21 TC 23 Z9 23 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1994 VL 73 IS 7 BP 1954 EP 1959 DI 10.1002/1097-0142(19940401)73:7<1954::AID-CNCR2820730729>3.0.CO;2-H PG 6 WC Oncology SC Oncology GA NC857 UT WOS:A1994NC85700028 PM 8137223 ER PT J AU ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH AF ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH TI HEMIN INHIBITION OF TARTRATE-RESISTANT ACID-PHOSPHATASE (TRAP) EXPRESSION IS MEDIATED BY BINDING OF A NUCLEAR-PROTEIN TO A SPECIFIC TANDEM REPEAT IN THE 5'-FLANKING REGION OF THE MTRAP GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 3 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 1994 VL 42 IS 2 BP A120 EP A120 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000047 ER PT J AU BISWAS, P CHOUDHURY, GG WENZEL, U GRANDALIANO, G ABBOUD, HE AF BISWAS, P CHOUDHURY, GG WENZEL, U GRANDALIANO, G ABBOUD, HE TI DIFFERENTIAL EFFECT OF THROMBIN ON PROTEIN-KINASE-C ISOFORMS IN MESANGIAL CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RI Grandaliano, Giuseppe/G-2963-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A144 EP A144 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000184 ER PT J AU HUANG, SC PAN, Z HARLEY, JB SCOFIELD, RH AF HUANG, SC PAN, Z HARLEY, JB SCOFIELD, RH TI IMMUNIZATION WITH VESICULAR STOMATITIS-VIRUS NUCLEOCAPSID PROTEIN INDUCES AUTOANTIBODIES TO 60 KD RO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV OKLAHOMA,HLTH SCI CTR,OKLAHOMA MED RES FDN,OKLAHOMA CITY,OK 73190. US DEPT VET AFFAIRS,OKLAHOMA CITY,OK. 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 1994 VL 42 IS 2 BP A278 EP A278 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000946 ER PT J AU KASINATH, BS GRELLIER, P TERHUNE, WC GHOSHCHOUDHURY, G MALDONADO, R ABBOUD, S AF KASINATH, BS GRELLIER, P TERHUNE, WC GHOSHCHOUDHURY, G MALDONADO, R ABBOUD, S TI REGULATION OF BASEMENT-MEMBRANE (BM) HEPARAN-SULFATE PROTEOGLYCAN (HSPG) CORE PROTEIN GENE-EXPRESSION BY HIGH GLUCOSE MEDIUM IN GLOMERULAR EPITHELIAL-CELLS (GEC) 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 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 1994 VL 42 IS 2 BP A143 EP A143 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000181 ER PT J AU LICHTENSTEIN, MJ MONTERROSA, A ESPINO, DV HAZUDA, HP AF LICHTENSTEIN, MJ MONTERROSA, A ESPINO, DV HAZUDA, HP TI ASSOCIATION OF VISUAL-ACUITY WITH STATIC AND DYNAMIC MEASURES OF BALANCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. UTHSC,DEPT MED,SAN ANTONIO,TX. 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 APR PY 1994 VL 42 IS 2 BP A218 EP A218 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000608 ER PT J AU REDDY, SV HUNDLEY, JE WINDLE, JJ LEACH, RJ ALCANTARA, O BOLDT, DH ROODMAN, GD AF REDDY, SV HUNDLEY, JE WINDLE, JJ LEACH, RJ ALCANTARA, O BOLDT, DH ROODMAN, GD TI THE MOUSE TARTRATE-RESISTANT ACID-PHOSPHATASE GENE (TRAP) CONTAINS 2 ACTIVE PROMOTERS AND IS REGULATED BY IRON 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. CANC THERAPY & RES CTR S TEXAS,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 APR PY 1994 VL 42 IS 2 BP A210 EP A210 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000562 ER PT J AU WENZEL, UO VALENTE, AJ ABBOUD, HE AF WENZEL, UO VALENTE, AJ ABBOUD, HE TI THROMBIN INDUCES MONOCYTE CHEMOTACTIC PEPTIDE (MCP-1) PRODUCTION IN HUMAN VASCULAR SMOOTH-MUSCLE CELLS (VSMC) 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 PATHOL,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 1994 VL 42 IS 2 BP A266 EP A266 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000879 ER PT J AU ROYALL, DR AF ROYALL, DR TI PRECIS OF EXECUTIVE DYSCONTROL AS A CAUSE OF PROBLEM BEHAVIOR IN DEMENTIA SO EXPERIMENTAL AGING RESEARCH LA English DT Article ID SUBCORTICAL DEMENTIA; FRONTAL LOBES; ALZHEIMERS-DISEASE; SCHIZOPHRENIC SYNDROMES; COGNITIVE IMPAIRMENT; VASCULAR DEMENTIA; HUMAN AUTONOMY; CORTEX; LESIONS; DYSFUNCTION AB Frontal lobe executive control functions (ECF) are proposed as a source of problem behavior in dementia. The behavior and personality changes that follow frontal lobe brain damage overlap with those seen in dementia, and frontal lobe structural and metabolic lesions can be demonstrated across a variety of dementing illnesses. ECF help explain the importance of social and environmental cues in the production of disruptive behavior and suggest interpersonal strategies for their control. This model has considerable face validity and leads to several testable hypotheses. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT PSYCHIAT,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT MED,SAN ANTONIO,TX. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 90 TC 47 Z9 47 U1 6 U2 7 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0361-073X J9 EXP AGING RES JI Exp. Aging Res. PD APR-JUN PY 1994 VL 20 IS 2 BP 73 EP 94 DI 10.1080/03610739408253955 PG 22 WC Geriatrics & Gerontology; Psychology SC Geriatrics & Gerontology; Psychology GA NE556 UT WOS:A1994NE55600001 PM 8020543 ER PT J AU ROYALL, DR MAHURIN, RK CORNELL, J AF ROYALL, DR MAHURIN, RK CORNELL, J TI BEDSIDE ASSESSMENT OF FRONTAL DEGENERATION - DISTINGUISHING ALZHEIMERS-DISEASE FROM NON-ALZHEIMERS CORTICAL DEMENTIA SO EXPERIMENTAL AGING RESEARCH LA English DT Article ID COGNITIVE IMPAIRMENT; FEATURES AB Two instruments, the Executive Interview (EXIT) and the Qualitative Evaluation of Dementia (QED), that are useful in the evaluation of frontal system failure are discussed. The ability of these instruments to discriminate frontal-type dementia (FTD) from Alzheimer's disease (AD) and the dementia of major depression (DMD) was examined in 100 consecutive elderly dementia patients presenting to a multidisciplinary geriatric clinic. All groups showed executive impairment by the EXIT, and 46% of the FTD patients were found to be unimpaired by the Mini-Mental State Examination (MMSE). The AD and FTD groups differed significantly from the DMD group on the QED. The QED alone could not distinguish AD from FTD cases. However, mapping of scores against MMSE (errors) scores revealed that AD and FTD follow very different regression lines. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT PSYCHIAT,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT MED,SAN ANTONIO,TX. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 20 TC 47 Z9 47 U1 1 U2 1 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0361-073X J9 EXP AGING RES JI Exp. Aging Res. PD APR-JUN PY 1994 VL 20 IS 2 BP 95 EP 103 DI 10.1080/03610739408253956 PG 9 WC Geriatrics & Gerontology; Psychology SC Geriatrics & Gerontology; Psychology GA NE556 UT WOS:A1994NE55600002 PM 8020544 ER PT J AU JACOBY, RF MARSHALL, DJ SCHLACK, S HARMS, B LOVE, RR AF JACOBY, RF MARSHALL, DJ SCHLACK, S HARMS, B LOVE, RR TI DNA-REPLICATION ERRORS DURING ADENOMA TO CARCINOMA PROGRESSION IN HNPCC SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT HUMAN ONCOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI 53706. 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A398 EP A398 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901580 ER PT J AU SINGARAM, C SWEET, MA SNIPES, RL GAUMNITZ, EA AF SINGARAM, C SWEET, MA SNIPES, RL GAUMNITZ, EA TI COLONIC PEPTIDERGIC MUCOSAL INNERVATION IN CONSTIPATION PREDOMINANT IRRITABLE-BOWEL-SYNDROME (IBS) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A567 EP A567 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902253 ER PT J AU CHANG, MP YAMAGUCHI, DT YEH, M TAYLOR, AN NORMAN, DC AF CHANG, MP YAMAGUCHI, DT YEH, M TAYLOR, AN NORMAN, DC TI MECHANISM OF THE IMPAIRED T-CELL PROLIFERATION IN ADULT-RATS EXPOSED TO ALCOHOL IN-UTERO SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID HUMAN LYMPHOCYTE-T; MEDIATED SIGNAL TRANSDUCTION; CYTOSOLIC FREE CALCIUM; INTERLEUKIN-2 RECEPTOR; FETAL ALCOHOL; TYROSINE PHOSPHORYLATION; ANTIGEN RECEPTOR; PRENATAL ETHANOL; BETA-CHAIN; ACTIVATION AB Although attempts have been made to assess the effect of ethanol on the immune responses in individuals with fetal alcohol syndrome, there is no consensus as to the effect of ethanol on the immune system. Evidence that fetal alcohol-exposed (FAE) humans and animals have diminished proliferative response of T-cells to mitogenic lectins is well established. However, little is known about the mechanism of a toxic effect of ethanol on T-cell growth. Thus, a rat model was used to delineate the mode of ethanol action on T-cell proliferation. We found that the diminished T-cell proliferation in young adult FAE rats was due to a decreased responsiveness to interleukin 2 (IL2), but not to an impaired production of IL2 and expression of IL2 receptors (IL2R). Furthermore, the decreased proliferative response did not result from the presence of an excessive suppressor T-cell activity. Measurements of [Ca+2](i) and T-cell proliferation were concurrently performed in batches of cells from the same animals. It was demonstrated that an increase in [Ca+2](i) induced by Concanavalin A (Con A) in T-cells from FAE rats was not impaired, although the T-cell proliferation induced by Con A was significantly diminished. The results of the IL2-binding study showed that the K-d values and the number of both high- and low-affinity IL2R binding sites on the T-cells of FAE rats were comparable to those of pair-, or chow-fed rats. Finally, the results of the kinetics and rate of the internalization of IL2 showed that (1) the amount of the internalized IL2 was significantly reduced in T-cells from FAE rats, and (2) the half-time (t(1/2)) for dissociation of IL2 from the receptors in the T-cells from FAE rats was also greater than that of the control rats. These results taken together indicate that ethanol suppresses T-cell proliferation by interfering with events following the IL2 - IL2R interaction. C1 W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH RES DIV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90073. RP CHANG, MP (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 53 TC 16 Z9 17 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PD APR PY 1994 VL 16 IS 4 BP 345 EP 357 PG 13 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA NG597 UT WOS:A1994NG59700010 PM 8045674 ER PT J AU BADR, MS SKATRUD, JB DEMPSEY, JA AF BADR, MS SKATRUD, JB DEMPSEY, JA TI EFFECT OF CHEMORECEPTOR STIMULATION AND INHIBITION ON TOTAL PULMONARY RESISTANCE IN HUMANS DURING NREM SLEEP SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE HYPOXIA; HYPOCAPNIA; UPPER AIRWAY PATENCY ID UPPER AIRWAY-RESISTANCE; RESPIRATORY DRIVE; NORMAL MEN; HYPERCAPNIA; HYPOXIA; COLLAPSIBILITY; HYPOGLOSSAL; OBSTRUCTION; RESPONSES; MECHANICS AB We investigated the effect of chemoreceptor stimulation and inhibition on total pulmonary resistance (RL) during non-rapid-eye-movement (NREM) sleep in healthy subjects. Chemoreceptor stimulation was accomplished with brief isocapnic hypoxia (n = 8). Minute ventilation increased to 150% of room air control. RL at peak inspiratory flow decreased to 66% of room air control. Resistive pressure-inspiratory flow plots demonstrated lower resistive pressures for a given inspiratory flow. Chemoreceptor inhibition was accomplished by abruptly terminating brief hypocapnic hypoxia with 100% O-2 (n = 7). Minute ventilation decreased to 63% of room air control. RL calculated at peak inspiratory or fixed flow did not change significantly, and pressure-flow plots at nadir ventilation showed no systematic change from room air control. We conclude that I) hypoxic chemoreceptor stimulation is associated with decreased RL and enhancement of pressure-flow relationships, suggesting increased upper airway caliber; 2) upper airway patency is not compromised during periods of low ventilatory drive in normal subjects; and 3) upper airway dilating muscles and thoracic pump muscles are optionally coordinated with increased and decreased ventilatory drive. C1 UNIV WISCONSIN,SCH MED,WILLIAM S MIDDLETON MEM VET ADM HOSP,MED SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT MED,JOHN RANKIN LAB PREVENT MED,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PREVENT MED,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. FU NHLBI NIH HHS [NHLBI 42242, NHLBI HL-02588] NR 34 TC 30 Z9 30 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 APR PY 1994 VL 76 IS 4 BP 1682 EP 1692 PG 11 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA NG707 UT WOS:A1994NG70700042 PM 8045848 ER PT J AU YOSHIMURA, M PEKARY, AE PANG, XP BERG, L GOODWIN, TM HERSHMAN, JM AF YOSHIMURA, M PEKARY, AE PANG, XP BERG, L GOODWIN, TM HERSHMAN, JM TI THYROTROPIC ACTIVITY OF BASIC ISOELECTRIC FORMS OF HUMAN CHORIONIC-GONADOTROPIN EXTRACTED FROM HYDATIDIFORM MOLE TISSUES SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID STIMULATOR; VARIANTS; CELLS AB hCG is known to have thyroid-stimulating activity and may cause hyperthyroidism in patients with trophoblastic diseases. hCG occurs in normal and molar pregnancy with breaks or nicks in the alpha- or beta-subunit peptide linkage and with substantial heterogeneity in the composition and degree of branching within the oligosaccharide side-chains. The bioactivity of hCG is markedly influenced by these structural variations. We purified hCG from five hydatidiform moles, using chromatofocusing separation after gel filtration. The hCG molecules were fractionated according to their isoelectric points, with a linear pH gradient from 3.2-6.1 and a final 1.0 mol/L NaCl step elution. The hCG immunoreactivity of each fraction was measured by RIA, and the thyroid-stimulating activity of hCG was determined by means of the cAMP response in Chinese hamster ovary cells expressing functional human TSH receptors (Chinese hamster ovary-JP09 cells). The chromatofocusing profile showed that hCG from the moles was eluted in six or seven major peaks at pH 6.1, 5.5, 5.3, 4.8, 3.8, and 3.2 and with 1.0 mol/L NaCl, whereas hCG extracted from serum of hydatidiform moles and standard hCG preparation CR-127 extracted from pregnancy urine showed only small peaks at pH greater than 5.3. Each fraction increased cAMP production significantly in Chinese hamster ovary-JP09 cells. The relative bioactivity/immunoreactivity, represented as the ratio of cAMP/hCG (picomoles per IU), was significantly higher in basic components (pI 6.1, 6.2 +/- 1.2; pI 5.5, 4.4 +/- 2.7; pI 5.3, 5.8 +/- 0.3) than in hCG CR-127 (bioactivity/immunoreactivity, 0.42; P < 0.05). The difference in pI of each hCG isoform was attributable to the extent of sialylation; basic hCG isoforms contained less sialic acid by immunological detection using lectins. These results indicate that isoforms of hCG with more thyrotropic activity were produced by trophoblastic tissues in patients with hydatidiform mole. We speculate that these isoforms of hCG may be responsible for the hyperthyroidism in some patients with hydatidiform moles. C1 W LOS ANGELES VET AFFAIRS MED CTR, ENDOCRINOL RES LAB, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV SO CALIF, SCH MED, DEPT OBSTET & GYNECOL, LOS ANGELES, CA 90033 USA. NR 27 TC 47 Z9 47 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1994 VL 78 IS 4 BP 862 EP 866 DI 10.1210/jc.78.4.862 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NF021 UT WOS:A1994NF02100013 PM 8157712 ER PT J AU SCHENKER, S BAY, M AF SCHENKER, S BAY, M TI DRUG DISPOSITION AND HEPATOTOXICITY IN THE ELDERLY SO JOURNAL OF CLINICAL GASTROENTEROLOGY LA English DT Article DE HEPATOTOXICITY; DRUG DISPOSITION; ELDERLY ID AGE-RELATED-CHANGES; ANTIOXIDANT ENZYMES; DIETARY RESTRICTION; LIVER-DISEASE; RAT-LIVER; EXPRESSION; INJURY; METABOLISM AB Overall, the aged liver seems to function remarkably well in the elderly. Decreased drug disposition is selective and modest and there is no compelling evidence of greater susceptibility to drug-induced or other types of injury. Drug-drug interactions and concurrent derangements accompanying advanced age may, however, contribute to adverse drug effects. Still, the aged, consume about three times as many therapeutic agents as other people. Most of these are metabolized in the liver before excretion. With increasing age, hepatic blood flow falls and so does hepatic volume. Moreover, binding of some agents normally carried on albumin may decrease. In contrast, increasing age has relatively modest effects on hepatic drug metabolism and these are highly selective. In the healthy aged, hepatic drug elimination is only modestly, if at all, impaired and this is likely to especially affect agents dependent on liver blood flow. Other factors that affect drug elimination in the aged are drug-drug interaction and the frailty and functional impairment of many elderly, as a result of poor diet, infection, multiple hospitalizations, or other events. Decreased host defense systems in the aged liver may lead to decreased adaptation to stress and slower regeneration after injury. 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,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07514] NR 40 TC 14 Z9 14 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-0790 J9 J CLIN GASTROENTEROL JI J. Clin. Gastroenterol. PD APR PY 1994 VL 18 IS 3 BP 232 EP 237 DI 10.1097/00004836-199404000-00013 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NE689 UT WOS:A1994NE68900012 PM 8034922 ER PT J AU WOLFE, JT CHOOBACK, L FINN, DT BENOIT, BM JAWORSKY, C ROOK, AH LESSIN, SR AF WOLFE, JT CHOOBACK, L FINN, DT BENOIT, BM JAWORSKY, C ROOK, AH LESSIN, SR TI LARGE-CELL TRANSFORMATION (LCT) IN CUTANEOUS T-CELL LYMPHOMA (CTCL) - DEMONSTRATION OF A SINGLE NEOPLASTIC T-CELL CLONE EXPRESSING THE IDENTICAL T-CELL RECEPTOR (TCA) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV PENN,DEPT DERMATOL,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 623 EP 623 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600623 ER PT J AU KIM, JJ MODLIN, RL MOU, RL DUBINETT, S TOMONO, S UYEMURA, K AF KIM, JJ MODLIN, RL MOU, RL DUBINETT, S TOMONO, S UYEMURA, K TI IL-10 PRODUCTION BY BASAL-CELL CARCINOMA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,DIV DERMATOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 633 EP 633 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600678 ER PT J AU GABRIEL, SM BIERER, LM DAVIDSON, M PUROHIT, DP PERL, DP HAROTUNIAN, V AF GABRIEL, SM BIERER, LM DAVIDSON, M PUROHIT, DP PERL, DP HAROTUNIAN, V TI GALANIN-LIKE IMMUNOREACTIVITY IS INCREASED IN THE POSTMORTEM CEREBRAL-CORTEX FROM PATIENTS WITH ALZHEIMERS-DISEASE SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE ALZHEIMERS DISEASE; GALANIN; DEMENTIA; NEUROPEPTIDES; NEURODEGENERATION ID CENTRAL-NERVOUS-SYSTEM; NITRIC-OXIDE SYNTHASE; NEURONAL NADPH DIAPHORASE; BASAL FOREBRAIN COMPLEX; ACETYLCHOLINE-RELEASE; CHOLINERGIC NEURONS; NEUROPEPTIDE-Y; SPINAL-CORD; PHOSPHOINOSITIDE TURNOVER; HUNTINGTONS-DISEASE AB Galanin is a peptide that is associated with cholinergic neurons of the basal forebrain and, thus, of interest for the neuropathology of Alzheimer's disease. In the present study, human galanin-like immunoreactivity was measured in postmortem human cerebral cortical tissues by using a homologous radioimmunoassay. In an initial study, six cerebral cortical regions were evaluated from nine elderly controls, 13 neuropathologically verified Alzheimer's disease patients, and 19 elderly schizophrenics. A significant 65% increase in galanin was found in frontal cortex Brodmann area 8 of Alzheimer's disease patients compared with controls. In contrast, cerebral cortical tissues from elderly schizophrenics were not different from those from elderly controls in any region. In a second study, 10 cerebral cortical regions were evaluated from 50 neuropathologically verified Alzheimer's disease patients and nine elderly controls. Concentrations of galanin were increased significantly 26-61% in six of 10 cerebral cortical regions examined (Brodmann areas F8, F44, T20, T21, T36, and P22). Purification of brain extracts by size-exclusion Sephadex G-50 chromatography revealed that human galanin-like immunoreactivity eluted in two peaks of different molecular weights. These studies reveal increased concentrations of galanin in the cerebral cortex of Alzheimer's disease, similar to previous findings in basal forebrain tissue. Because galanin inhibits cholinergic neurotransmission, these findings may have important implications in the understanding of Alzheimer's disease neuropathology and associated cognitive deficits. RP GABRIEL, SM (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIA NIH HHS [NIA AG05138, NIA AG02219, NIA AG00408] NR 57 TC 52 Z9 52 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1994 VL 62 IS 4 BP 1516 EP 1523 PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NB403 UT WOS:A1994NB40300036 PM 7510783 ER PT J AU BUDIMANMAK, E ROACH, KE STUCK, R SPENCER, F POLIZOS, T CONRAD, KJ AF BUDIMANMAK, E ROACH, KE STUCK, R SPENCER, F POLIZOS, T CONRAD, KJ TI RADIOGRAPHIC MEASUREMENT OF HALLUX-VALGUS IN THE RHEUMATOID ARTHRITIC FOOT SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE RADIOGRAPHS; HALLUX VALGUS ID OBSERVER AB Objective. To develop a method which is objective and quantifiable, as well as reliable and valid for measuring the severity and progression of hallux valgus deformity (HVD). HVD is defined as an increase in the hallux abductus angle (HAA). Methods. HAA drawn on plain anterioposterior radiographs of the foot was measured in 94 patients with rheumatoid arthritis. The intra and interrater reliability were analyzed. Results. Findings were significant with interclass correlation coefficients ranging from 0.9 to 0.99. Detection of changes in HAA using this method were comparable to the judgment of a panel of experienced clinicians. Conclusion. This method is useful in detecting progression of HVD. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MIDWEST HLTH SERV RES & DEV,HINES,IL 60141. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MIDWEST HLTH SERV RES & DEV,FIELD PROGRAM,HINES,IL 60141. RP BUDIMANMAK, E (reprint author), US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MIDWEST HLTH SERV RES & DEV,HINES,IL 60141, USA. NR 13 TC 5 Z9 5 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 APR PY 1994 VL 21 IS 4 BP 623 EP 626 PG 4 WC Rheumatology SC Rheumatology GA NG016 UT WOS:A1994NG01600008 PM 8035383 ER PT J AU BLACKBURN, WD BERNREUTER, WK ROMINGER, M LOOSE, LL AF BLACKBURN, WD BERNREUTER, WK ROMINGER, M LOOSE, LL TI ARTHROSCOPIC EVALUATION OF KNEE ARTICULAR-CARTILAGE - A COMPARISON WITH PLAIN RADIOGRAPHS AND MAGNETIC-RESONANCE-IMAGING SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE ARTHROSCOPY; MAGNETIC RESONANCE IMAGING; OSTEOARTHRITIS ID OSTEO-ARTHRITIS; HYALINE CARTILAGE; MR; OSTEOARTHRITIS; JOINT; DEGENERATION; SEVERITY; DEFECTS AB Objective. To compare radiographic, magnetic resonance imaging (MRT), and outpatient direct arthroscopic evaluation of cartilage in patients with osteoarthritis (OA) of the knee. Methods. Thirty-three patients with OA of the knee were evaluated by plain weight bearing radiographs and arthroscopy using a 1.9 mm arthroscope under local anesthesia. Sixteen of these patients also had MRI of the knee performed. Knee compartments were evaluated using AP weight bearing and lateral radiographs of the knee. MRI and outpatient arthroscopic grading of cartilage were performed within 2 weeks of the plain radiographs. The MRI and arthroscopic evaluations were performed independently and were graded without knowledge of the other. Results. In patients in whom plain radiographs, MRI, and arthroscopy were compared, the plain radiographs and MRI significantly underestimated the extent of cartilage abnormalities. There was a moderate correlation between imaged cartilage scores and the arthroscopy scores (Pearson correlation coefficient = 0.40). The arthroscopic scores were reproducible with good intra and interobserver reliability. The arthroscopic procedure was well tolerated and actually preferred over the MRI by the majority of patients. No significant complications were noted as a result of arthroscopy. Conclusions. Our results indicate that outpatient arthroscopic evaluation is a useful method in evaluating surface cartilage abnormalities and is more sensitive in detecting these abnormalities than either plain radiographs or MRI. Outpatient arthroscopic evaluation of cartilage appears to be a safe, sensitive, and a well tolerated tool for evaluating patients with OA of the knee and may prove to be particularly useful in evaluating response to therapeutic interventions. C1 UNIV ALABAMA,DEPT RADIOL,BIRMINGHAM,AL. UNIV ALABAMA,DIV CLIN IMMUNOL & RHEUMATOL,BIRMINGHAM,AL. PFIZER INC,DIV CENT RES,GROTON,CT 06340. RP BLACKBURN, WD (reprint author), BIRMINGHAM VET AFFAIRS MED CTR,RES SERV 151F,700 19TH ST S,BIRMINGHAM,AL 35233, USA. NR 25 TC 78 Z9 80 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 APR PY 1994 VL 21 IS 4 BP 675 EP 679 PG 5 WC Rheumatology SC Rheumatology GA NG016 UT WOS:A1994NG01600019 PM 8035392 ER PT J AU MULROW, CD GERETY, MB CORNELL, JE LAWRENCE, VA KANTEN, DN AF MULROW, CD GERETY, MB CORNELL, JE LAWRENCE, VA KANTEN, DN TI THE RELATIONSHIP BETWEEN DISEASE AND FUNCTION AND PERCEIVED HEALTH IN VERY FRAIL ELDERS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article; Proceedings Paper CT Southern-Section of the Society-of-General-Internal-Medicine Meeting CY JAN, 1993 CL NEW ORLEANS, LA SP SOC GEN INTERNAL MED, SO SECT ID PRIMARY CARE PATIENTS; COMORBIDITY; VALIDATION; OUTCOMES; SEVERITY; IMPACT; INDEX AB Objective: To study associations between disease and observed function and self-perceived health in very frail elders. Design and Setting: Cross-sectional survey of nine nursing homes in San Antonio, TX. Participants: 194 elderly long-stay nursing home residents dependent in at least two ADLs and without severe cognitive impairment. Measures: Burden of disease (BOD) was chart abstracted using a standardized protocol that assessed types and severities of 59 categorizations of chronic and acute medical conditions. Observed function and self-perceived health status were assessed independently by the Katz Activities of Daily Living scale (ADL) and the Sickness Impact Profile (SIP), respectively. Results: Summary BOD scores had a low, but statistically significant, univariate correlation with ADL scores (r = 0.21, P = 0.003) and no significant correlation with SIP scores (R = -0.008). Multiple linear regression analyses, including the 24 most frequent disease categories, showed that disease explained significant amounts of ADL (r2 = 0.25, P = 0.001) and borderline significant amounts of SIP (r2 = 0.16, P = 0.11). Models including both disease and sociodemographic, cognitive, and affective variables showed disease added significant incremental explanation beyond the other factors to ADL (incremental r2 = 0.14, P = 0.04), but not to SIP (incremental r2 = 0.08, P > 0.10). Conclusions: Disease, observed function, and self-perceived health status are separate, but interrelated entities, with disease having a stronger relationship to observed function than self-perceived health. Comprehensive assessment of frail elders may need to include all three areas, and studies that focus on one area should take into account the other two as potential important covariates. C1 UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,AMBULATORY CARE 11C,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [NIA UO1AG09117-01] NR 35 TC 57 Z9 60 U1 1 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 APR PY 1994 VL 42 IS 4 BP 374 EP 380 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NE417 UT WOS:A1994NE41700003 PM 8144821 ER PT J AU MISRA, AK MISHRA, SK EIGEN, AC TOURTELLOTTE, WW AF MISRA, AK MISHRA, SK EIGEN, AC TOURTELLOTTE, WW TI SUCCESSFUL IMMUNOSUPPRESSIVE THERAPY FOR HTLV-I-ASSOCIATED MYELOPATHY SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE HTLV-I ASSOCIATED MYELOPATHY (HAM); IMMUNOSUPPRESSION; CYCLOPHOSPHAMIDE; PREDNISONE ID VIRUS TYPE-I AB We report here a patient with HTLV-I associated myelopathy (HAM), who showed remarkable improvement clinically and immunologically with combined cyclophosphamide and prednisone therapy. C1 DEPT VET AFFAIRS OUTPATIENT CLIN,SCH MED,NEUROL SERV 752-127,351 E TEMPLE ST,LOS ANGELES,CA 90012. W LOS ANGELES DEPT VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA. UNIV SO CALIF,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90033. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. NR 7 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD APR PY 1994 VL 122 IS 2 BP 155 EP 156 DI 10.1016/0022-510X(94)90293-3 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA ND187 UT WOS:A1994ND18700006 PM 8021699 ER PT J AU SCHLANGER, LE KLEYMAN, TR LING, BN AF SCHLANGER, LE KLEYMAN, TR LING, BN TI K+-SPARING DIURETIC ACTIONS OF TRIMETHOPRIM - INHIBITION OF NA+ CHANNELS IN A6 DISTAL NEPHRON CELLS SO KIDNEY INTERNATIONAL LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; POTASSIUM CHANNELS; THERAPY; HYPERKALEMIA AB Hyperkalemia complicates trimethoprim-sulfamethoxazole (TMP-SMX) therapy in over 20% of HIV-infected patients. TMP is a heterocyclic weak base, similar to amiloride, a ''K+-sparing'' diuretic and Na+ channel blocker. Apical TMP is known to inhibit amiloride-sensitive short circuit current in A6 cells, a tissue culture model for mammalian cortical collecting tubule principal cells [1]. We used cell-attached patch clamp techniques to investigate the effect of TMP on the 4 pS, highly selective Na+ channel in the apical membrane of A6 cells grown on permeable supports in the presence of 1.5 mu M aldosterone. Baseline channel activity at resting membrane potential, measured as NPo (N of channels x open probability), was 1.09 +/- 0.50 (N = 18). NPo (0.92 +/- 0.38; N = 9) was unchanged when 10(-3) M TMP was added to the basolateral bath for 30 minutes. However, apical exposure with pipettes containing 10(-3) or 10(-5) M TMP reduced NPo approximate to tenfold (0.12 +/- 0.08; N = 7 and 0.18 +/- 0.14; N = 12, respectively). Kinetic analysis revealed the appearance of a new closed state after apical TMP treatment. Another group of A6 cells were pretreated with 10(-3) M apical TMP for 30 minutes prior to patching with pipettes filled with TMP-free saline. NP, progressively rose from 0.07 +/- 0.09 to 0.87 +/- 0.23 (N = 5) as the residual TMP was diluted within the pipette. Apical or basolateral pretreatment (30 min) with 10(-3) M SMX did not change Na+ channel activity. In conclusion, in A6 distal nephron cells: (1) TMP reversibly blocks highly selective Na+ channels; (2) direct interaction with the outer channel pore is required since inhibition was observed with apical, but not basolateral TMP; (3) the SMX component of TMP-SMX preparations has no direct effect on Na+ channel activity; (4) This K+-sparing diuretic effect likely contributes to the hyperkalemia associated with TMP therapy in HIV-infected patients. C1 EMORY UNIV,SCH MED,DEPT MED,DIV RENAL,ATLANTA,GA 30322. VET AFFAIRS MED CTR,ATLANTA,GA 30033. UNIV PENN,DEPT MED,DIV RENAL & ELECTROLYTE,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. FU NIDDK NIH HHS [K08-DK02111, R01-DK37963, T32-DK07656] NR 25 TC 37 Z9 38 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD APR PY 1994 VL 45 IS 4 BP 1070 EP 1076 DI 10.1038/ki.1994.143 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA NB502 UT WOS:A1994NB50200016 PM 8007576 ER PT J AU BARNES, JL HEVEY, KA HASTINGS, RR BOCANEGRA, RA AF BARNES, JL HEVEY, KA HASTINGS, RR BOCANEGRA, RA TI MESANGIAL CELL-MIGRATION PRECEDES PROLIFERATION IN HABU SNAKE VENOM-INDUCED GLOMERULAR INJURY SO LABORATORY INVESTIGATION LA English DT Article DE PLATELETS; GLOMERULONEPHRITIS; CELL PROLIFERATION ID EXTRACELLULAR-MATRIX COMPONENTS; PLATELET SECRETORY PROTEINS; IMMUNE-COMPLEX NEPHRITIS; GROWTH-FACTOR; EXPRESSION; RAT; GLOMERULONEPHRITIS; ANTIBODIES; LESIONS; ACTIN AB BACKGROUND: Mesangial cells migrate in response to platelet released products in vitro (Am J Pathol 1991;138:859). Cell migration, in addition to proliferation might play a role in cell remodeling during the course of proliferative glomerular disease. EXPERIMENTAL DESIGN: In this study, we examined mesangial cell migration in vivo in a platelet-dependent model of proliferative glomerulonephritis induced by Habu snake venom. Mesangial cell migration was assessed by phenotypic identification and temporal location of mesangial cells within glomerular lesions in serial time studies from 8 to 48 hours after Habu snake venom. Autoradiography of [H-3]thymidine incorporation into cells was employed to identify and temporally separate cell division and proliferation from cell motility and other related events. RESULTS: Early (8-hour) lesions consisted of microaneurysms devoid of mesangial cells. By 24 hours, glomeruli showed mesangial cells at the margins of lesions adjacent to intact glomerular tufts, followed by the presence of clusters of cells at 30 and 36 hours. By 48 hours, most lesions were filled with proliferating mesangial cells. Cells containing [H-3]thymidine were rarely observed until 30 hours, at which point they were found in advanced lesions. Marginating cells did not contain [H-3]thymidine, suggesting that the location of these cells was not related to cell division but rather to migration. Platelet depletion eliminated platelets from lesions and substantially retarded mesangial cell migration into glomerular lesions indicating mesangial cell migration is, in part, dependent on platelets or their secretory products. CONCLUSIONS: These studies show that mesangial cells can migrate in vivo and suggest that cell migration is an important early step in cell redistribution and remodeling during glomerular injury in this model of proliferative glomerulonephritis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RHODE ISL HOSP,DEPT PATHOL,PROVIDENCE,RI 02902. RP BARNES, JL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [NIDDK DK37859] NR 32 TC 34 Z9 34 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD APR PY 1994 VL 70 IS 4 BP 460 EP 467 PG 8 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA NK099 UT WOS:A1994NK09900004 PM 8176886 ER PT J AU PANG, XP YOSHIMURA, M WANG, JY DUBINETT, SM AF PANG, XP YOSHIMURA, M WANG, JY DUBINETT, SM TI TNF-ALPHA-INDUCED ANTIPROLIFERATION IS NOT DEPENDENT ON THE AUTOCRINE ACTION OF TGF-BETA-1 IN A THYROID-CANCER SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR-BETA; FACTOR-KAPPA-B; PROGNOSTIC FACTORS; CELLS; PAPILLARY; CARCINOMA; INHIBITOR AB The autocrine inhibitory action of transforming growth factor-beta 1 (TGF-beta 1) may play an important role in maintaining the normal state of thyroid follicular epithelial cells. Deficiency of this regulatory mechanism has been implicated in the pathogenesis of nontoxic nodular goiter and thyroid epithelial cell cancer. Tumor necrosis factor-alpha (TNF-alpha) has an antiproliferative action in a human papillary thyroid carcinoma cell line, NP-PTC cells, through a receptor-mediated mechanism. In the present work, we studied the antiproliferative action of TNF-alpha. and TGF-beta 1 in NP-PTC cells. TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1. Both TNF-alpha and TGF-beta 1 inhibited the proliferation of NP-PTC cells. A neutralizing antibody specific to human TGF-beta 1 blocked the antiproliferative action of TGF-beta 1 on NP-PTC cells, but it failed to block TNF-alpha-induced antiproliferation. Further, TNF-alpha and TGF-beta 1 acted synergistically to inhibit NP-PTC cell proliferation. The results show that both TNF-alpha and TGF-beta 1 inhibit the proliferation of NP-PTC cells. However, the actions of TGF-beta 1 and TNF-alpha differ in NP-PTC cells; TNF-alpha activates nuclear factor kappa B (NF-kappa B) and TGF-beta 1 does not. Although TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1, the antiproliferative action of TNF-alpha is not dependent on the autocrine action of TGF-beta 1 in NP-PTC cells. C1 W LOS ANGELES VET AFFAIRS MED CTR,IMMUNOL PULM LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90073. RP PANG, XP (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINE RES LAB,BLDG 114,ROOM 200,LOS ANGELES,CA 90073, USA. NR 24 TC 8 Z9 9 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 APR PY 1994 VL 13 IS 2 BP 93 EP 97 PG 5 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA NL491 UT WOS:A1994NL49100005 PM 8061120 ER PT J AU ASHTON, CM KUYKENDALL, DH WRAY, NP AF ASHTON, CM KUYKENDALL, DH WRAY, NP TI MISCLASSIFICATION OF PATIENTS CAN AFFECT GROUP QUALITY OF CARE SCORES SO MEDICAL CARE LA English DT Letter RP ASHTON, CM (reprint author), DEPT VET AFFAIRS MED CTR,HOUSTON CTR QUAL CARE & UTILIZAT STUDIES,HOUSTON,TX, USA. NR 1 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 APR PY 1994 VL 32 IS 4 BP 405 EP 405 DI 10.1097/00005650-199404000-00009 PG 1 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA NE246 UT WOS:A1994NE24600009 PM 8139305 ER PT J AU ASCH, DA BARON, J HERSHEY, JC KUNREUTHER, H MESZAROS, J RITOV, I SPRANCA, M AF ASCH, DA BARON, J HERSHEY, JC KUNREUTHER, H MESZAROS, J RITOV, I SPRANCA, M TI OMISSION BIAS AND PERTUSSIS VACCINATION SO MEDICAL DECISION MAKING LA English DT Article DE BEHAVIORAL SCIENCES; DECISION MAKING; DECISION THEORY; ETHICS; HEALTH POLICY; JUDGMENT; PERTUSSIS VACCINE; PROBABILITY; PSYCHOLOGY; PUBLIC HEALTH; RISK; VACCINATION; WHOOPING COUGH ID ENCEPHALOPATHY; VACCINES; CHOICE AB Background: Several laboratory studies have suggested that many people favor potentially harmful omissions over less harmful acts. The authors studied the role of this omission bias in parents' decisions whether to vaccinate their children against pertussis. Methods: Two hundred mail surveys were sent to subscribers to a magazine that had published articles favoring and opposing pertussis vaccination. Subjects were asked about their beliefs about the vaccine and the disease, and whether they had vaccinated their own children or planned to, and they were given test items to identify omission bias in their reasoning. Results: One hundred and three subjects (52%) responded to the survey. Respondents who reported they did not or would not allow their children to be vaccinated (n = 43; 41%) were more likely to believe that vaccinating was more dangerous than not vaccinating (p < 0.001). They were also more likely to exhibit omission bias (p = 0.004), holding constant their stated beliefs about the danger of the vaccine. Conclusions: Omission bias plays a role in decisions not to vaccinate with pertussis vaccine, beyond the role played by belief about the risk of vaccination. C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNIV PENN,SCH ARTS & SCI,DEPT PSYCHOL,PHILADELPHIA,PA 19104. UNIV PENN,WHARTON SCH,PHILADELPHIA,PA 19104. UNIV PENN,WHARTON RISK & DECIS PROC CTR,PHILADELPHIA,PA 19104. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. RP ASCH, DA (reprint author), UNIV PENN,SCH MED,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104, USA. NR 23 TC 91 Z9 91 U1 2 U2 11 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 APR-JUN PY 1994 VL 14 IS 2 BP 118 EP 123 DI 10.1177/0272989X9401400204 PG 6 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA NG124 UT WOS:A1994NG12400004 PM 8028464 ER EF